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521
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listlengths 1
22
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stringlengths 9
22.1k
| documents
listlengths 1
133
| snippets
listlengths 0
125
| asq_challenge
int64 5
13
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stringclasses 6
values | concepts
listlengths 0
23
⌀ | triples
listlengths 0
4.35k
⌀ | id
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24
| __index_level_0__
int64 6
5.4k
|
|---|---|---|---|---|---|---|---|---|---|---|---|---|
factoid
|
What is the function of the protein calreticulin?
|
['chaperone and Ca2+ buffer to assist correct protein folding within the ER']
|
[
"chaperone",
"calcium buffer",
"Ca2+ buffer",
"endoplasmic reticulum chaperone",
"protein folding chaperone",
"chaperonin",
"molecular chaperone",
"chaperone protein",
"chaperone and Ca2+ buffer to assist correct protein folding within the ER"
] |
['Calreticulin (CALR) is an endoplasmic reticulum (ER)-resident protein involved in a spectrum of cellular processes. In healthy cells, CALR operates as a chaperone and Ca2+ buffer to assist correct protein folding within the ER.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33360823",
"http://www.ncbi.nlm.nih.gov/pubmed/34472223",
"http://www.ncbi.nlm.nih.gov/pubmed/34495528",
"http://www.ncbi.nlm.nih.gov/pubmed/32733014"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34495528",
"endSection": "abstract",
"offsetInBeginSection": 718,
"offsetInEndSection": 938,
"text": "Subsequently, the N-glycosylated nascent proteins enter the folding step, in which N-glycans contribute largely to attaining the correct protein fold by recruiting the lectin-like chaperones, calnexin, and calreticulin. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33360823",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "The lectin chaperones calnexin (CNX) and calreticulin (CRT) localized in the endoplasmic reticulum play important roles in glycoprotein quality control. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34472223",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 155,
"text": "Calreticulin (CRT), an endoplasmic reticulum-resident protein generally overexpressed in cancer cells, is associated with radiation resistance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32733014",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "Calreticulin (CALR) is an endoplasmic reticulum (ER)-resident protein involved in a spectrum of cellular processes. In healthy cells, CALR operates as a chaperone and Ca2+ buffer to assist correct protein folding within the ER."
}
] | 11
|
BioASQ-training11b
| null | null |
623dfd2ef0baec9a1b000004
| 4,660
|
factoid
|
What is the effect of epiregulin on leptin secretion?
|
['induction', 'increase']
|
[
"induction",
"increase",
"induction increase",
"augmentation",
"amplification",
"enhancement",
"boost",
"escalation",
"growth",
"rise"
] |
['Epiregulin induces leptin secretion.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30400011"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30400011",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Epiregulin induces leptin secretion and energy expenditure in high-fat diet-fed mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30400011",
"endSection": "abstract",
"offsetInBeginSection": 723,
"offsetInEndSection": 845,
"text": " EREG increased leptin production and secretion in a dose-dependent manner in iAb fat explants via the EGFR/MAPK pathway. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30400011",
"endSection": "abstract",
"offsetInBeginSection": 1522,
"offsetInEndSection": 1633,
"text": "Our data revealed a new role of EREG in induction of leptin secretion leading to the energy expenditure state. "
}
] | 11
|
BioASQ-training11b
| null | null |
6237ab873a8413c6530000b6
| 4,662
|
factoid
|
Which JASPAR release is JASPAR 2022?
|
['9th']
|
[
"9th",
"ninth"
] |
["JASPAR (http://jaspar.genereg.net/) is an open-access database containing manually curated, non-redundant transcription factor (TF) binding profiles for TFs across six taxonomic groups. In JASPAR 2022, JASPAR's 9th release, the CORE collection was expanded with 341 new profiles (148 for plants, 101 for vertebrates, 85 for urochordates, and 7 for insects), which corresponds to a 19% expansion over the previous release."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34850907"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34850907",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "JASPAR 2022: the 9th release of the open-access database of transcription factor binding profiles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34850907",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1313,
"text": "JASPAR (http://jaspar.genereg.net/) is an open-access database containing manually curated, non-redundant transcription factor (TF) binding profiles for TFs across six taxonomic groups. In this 9th release, we expanded the CORE collection with 341 new profiles (148 for plants, 101 for vertebrates, 85 for urochordates, and 7 for insects), which corresponds to a 19% expansion over the previous release. We added 298 new profiles to the Unvalidated collection when no orthogonal evidence was found in the literature. All the profiles were clustered to provide familial binding profiles for each taxonomic group. Moreover, we revised the structural classification of DNA binding domains to consider plant-specific TFs. This release introduces word clouds to represent the scientific knowledge associated with each TF. We updated the genome tracks of TFBSs predicted with JASPAR profiles in eight organisms; the human and mouse TFBS predictions can be visualized as native tracks in the UCSC Genome Browser. Finally, we provide a new tool to perform JASPAR TFBS enrichment analysis in user-provided genomic regions. All the data is accessible through the JASPAR website, its associated RESTful API, the R/Bioconductor data package, and a new Python package, pyJASPAR, that facilitates serverless access to the data."
}
] | 11
|
BioASQ-training11b
| null | null |
6202f600c9dfcb9c0900002b
| 4,663
|
factoid
|
What is the SPRTN protein function?
|
['DNA-protein crosslink proteolysis repair']
|
[
"DNA-protein crosslink proteolysis repair",
"DNA-protein crosslink repair",
"DNA-protein crosslink repair pathway",
"DNA-protein crosslink repair mechanism",
"DNA-protein crosslink repair process"
] |
['The protease SPRTN emerged as the essential enzyme for DNA-protein crosslink proteolysis repair.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33348378",
"http://www.ncbi.nlm.nih.gov/pubmed/33183910",
"http://www.ncbi.nlm.nih.gov/pubmed/34551432",
"http://www.ncbi.nlm.nih.gov/pubmed/34189469"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34551432",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 512,
"text": "we explored the role of Spartan (SPRTN), a metalloprotease associated with DNA replication, which removes proteins forming DPCs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33348378",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Repair of covalent DNA-protein crosslinks (DPCs) by the metalloprotease SPRTN prevents genome instability, premature aging and carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33183910",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "The protease SPRTN emerged as the essential enzyme for DNA-protein crosslink proteolysis repair"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34189469",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Covalent DNA-protein crosslinks (DPCs) have emerged as pervasive sources of genome instability. DPCs are targeted for repair by DNA-dependent proteases of the Wss1/SPRTN family."
}
] | 11
|
BioASQ-training11b
| null | null |
622deabc3a8413c6530000a6
| 4,665
|
factoid
|
What part of the body is associated with Cauda equina
|
['spine']
|
[
"spine",
"vertebral column",
"backbone",
"spinal column",
"spinal cord",
"spinal vertebrae"
] |
['The cauda equina is the sack of nerve roots (nerves that leave the spinal cord between spaces in the bones of the spine to connect to other parts of the body) at the lower end of the spinal cord.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"http://www.ncbi.nlm.nih.gov/pubmed/22254963",
"http://www.ncbi.nlm.nih.gov/pubmed/27753733",
"http://www.ncbi.nlm.nih.gov/pubmed/3356808",
"http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"http://www.ncbi.nlm.nih.gov/pubmed/3806684",
"http://www.ncbi.nlm.nih.gov/pubmed/32541159",
"http://www.ncbi.nlm.nih.gov/pubmed/33261250",
"http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"http://www.ncbi.nlm.nih.gov/pubmed/18664636",
"http://www.ncbi.nlm.nih.gov/pubmed/10797973",
"http://www.ncbi.nlm.nih.gov/pubmed/34321945",
"http://www.ncbi.nlm.nih.gov/pubmed/22764663"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33261250",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 346,
"text": "the right pedicle of L4, moved inside the vertebral canal (bridging the cauda equina) stopping just in front of the body of S2. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 124,
"text": "Thermoesthesia-and-algesthesia status in the dermatomes of cauda equina roots in patients with lumbar spine osteochondrosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Thermoesthesia-and-algesthesia disorders have been registered in the dermatomes of cauda equina roots of patients with lumbar spine osteochondrosis in all the cases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22764663",
"endSection": "abstract",
"offsetInBeginSection": 581,
"offsetInEndSection": 722,
"text": " Magnetic resonance images of the lumbar spine showed an intradural cystic lesion displacing and compressing the lower cord and cauda equina."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Cauda equina syndrome is a well described state of neurologic compromise due to lumbosacral root compression."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Acute cauda equina syndrome secondary to a lumbar synovial cyst"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 296,
"text": "INTRODUCTION: Schwannoma is a relatively common benign spinal cord and/or cauda equina tumor; however, giant cauda equina schwannoma with extensive scalloping of the lumbar vertebral body is a rare pathology, and the treatment strategy, including the use of surgical procedures, is controversial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 509,
"text": "In this report, we present a rare case of a giant lumbar schwannoma of the cauda equina with extremely large scalloping of the vertebral body, and we discuss the surgical strategy we used to treat this pathology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3356808",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 791,
"text": "In contrast, the caudal cord of Rana is reduced to a filum terminale consisting of little more than an ependymal tube; spinal nerves to all caudal myotomes leave the cord in the sacral region and reach their motor targets via a cauda equina and caudal plexus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3806684",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 791,
"text": "The spinal cords of other teleosts, the sun-fish and angler, also are abbreviated and possess a filum terminale and cauda equina."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10797973",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1126,
"text": "Penetrating spinal cord injury with foreign body included or myelography stop or showing cauda equina syndrome should be operated on."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27753733",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Cauda Equina Conduction Time Determined by F-Waves in Normal Subjects and Patients With Neurogenic Intermittent Claudication Caused by Lumbar Spinal Stenosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22254963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "After spinal cord injury, electrical stimulation of the roots inside the spinal column at the level of the cauda equina is a safe and effective way to regain some degree of control over lower body function, e.g. bladder and bowel management and leg movement. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32541159",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Malignant spinal cord compression(MSCC)is defined as a compression of the spinal cord or cauda equina with neuropathy caused by tumor spreading to the vertebral body. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"endSection": "abstract",
"offsetInBeginSection": 37,
"offsetInEndSection": 187,
"text": "nction of the cauda equina, the collection of ventral and dorsal lumbar, sacral and coccygeal nerve roots that surround the filum terminale. This most"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "INTRODUCTION: Schwannoma is a relatively common benign spinal cord and/or cauda equina tumor; however, giant cauda equina schwannoma with extensive scalloping of the lumbar vertebral body is a rare pathology, and the treatment strategy, including the use of surgical procedures, is controversial"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18664636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Cauda equina syndrome is a relatively uncommon condition typically associated with a large, space-occupying lesion within the canal of the lumbosacral spine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Cauda equina syndrome refers to dysfunction of the cauda equina, the collection of ventral and dorsal lumbar, sacral and coccygeal nerve roots that surround the filum terminale."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"endSection": "abstract",
"offsetInBeginSection": 1320,
"offsetInEndSection": 1510,
"text": "The involvement of intrinsic spinal cord neurons in the compression-induced cauda equina syndrome includes anterograde, retrograde and transneuronal degeneration in the lumbosacral segments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Single or double-level compression of the lumbosacral nerve roots located in the dural sac results in a polyradicular symptomatology clinically diagnosed as cauda equina syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34321945",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 470,
"text": "The cauda equina is an anatomic structure located in the lower part of the spinal canal consisting of multiple lumbar and sacral nerve roots."
}
] | 11
|
BioASQ-training11b
| null | null |
6238a0033a8413c6530000b8
| 4,666
|
factoid
|
What does RUNX1T1 stand for?
|
['runt-related transcription factor 1']
|
[
"runt-related transcription factor 1",
"RUNX1",
"AML1",
"CBFA2",
"runt domain transcription factor 1",
"runt-related transcription factor alpha",
"runt-related transcription factor 1 alpha"
] |
['RUNX1T1 stands for runt-related transcription factor 1.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32589708"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32589708",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 96,
"text": "Runt-related transcription factor 1 (RUNX1T1) isoforms are involved in adipogenesis."
}
] | 11
|
BioASQ-training11b
| null | null |
62265b4a3a8413c653000083
| 4,667
|
factoid
|
Is METTL3 an m6A writer, reader or eraser?
|
['Writer']
|
[
"Writer",
"Author",
"Scribe",
"Penman",
"Wordsmith",
"Novelist",
"Playwright",
"Poet",
"Scriptwriter"
] |
['The methyltransferase METTL3 is an m6A writer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34535671"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34535671",
"endSection": "abstract",
"offsetInBeginSection": 200,
"offsetInEndSection": 401,
"text": "Here we report decreased expression of the m6A \"writer\" METTL3 in tumor-infiltrating NK cells, and a positive correlation between protein expression levels of METTL3 and effector molecules in NK cells."
}
] | 11
|
BioASQ-training11b
| null | null |
62265c953a8413c653000084
| 4,672
|
factoid
|
What is the drug gantenerumab targeting?
|
['Gantenerumab significantly reduced amyloid plaques, cerebrospinal fluid total tau, and phospho-tau181 and attenuated increases of neurofilament light chain.']
|
[
"Gantenerumab",
"Gantenerumab (RG1450)",
"Gantenerumab (RO4917838)"
] |
['Gantenerumab significantly reduced amyloid plaques, cerebrospinal fluid total tau, and phospho-tau181 and attenuated increases of neurofilament light chain.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33336218",
"http://www.ncbi.nlm.nih.gov/pubmed/34198582",
"http://www.ncbi.nlm.nih.gov/pubmed/34155411"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34155411",
"endSection": "abstract",
"offsetInBeginSection": 1026,
"offsetInEndSection": 1183,
"text": "Gantenerumab significantly reduced amyloid plaques, cerebrospinal fluid total tau, and phospho-tau181 and attenuated increases of neurofilament light chain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34198582",
"endSection": "abstract",
"offsetInBeginSection": 1066,
"offsetInEndSection": 1327,
"text": "The late-stage agents with positive clinical or biomarker data include four antibodies that engage Aβ oligomers (aducanumab, lecanemab, gantenerumab, and donanemab) and ALZ-801, an oral agent that fully blocks the formation of Aβ oligomers at the clinical dose."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33336218",
"endSection": "title",
"offsetInBeginSection": 77,
"offsetInEndSection": 136,
"text": "Reduction in Amyloid Burden with Subcutaneous Gantenerumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33336218",
"endSection": "abstract",
"offsetInBeginSection": 770,
"offsetInEndSection": 929,
"text": "These results demonstrate that prolonged gantenerumab treatment, at doses up to 1200 mg, reduces amyloid plaque levels below the amyloid positivity threshold. "
}
] | 11
|
BioASQ-training11b
| null | null |
622dfb133a8413c6530000a8
| 4,675
|
factoid
|
Which protein is targeted by Herceptin?
|
['Her2']
|
[
"Her2",
"HER2",
"human epidermal growth factor receptor 2",
"ErbB2",
"neu",
"c-erbB-2"
] |
['Her2 is targeted by Herceptin.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33468562",
"http://www.ncbi.nlm.nih.gov/pubmed/34532642"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34532642",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 347,
"text": "HER2-targeting agents such as Herceptin®, Kadcyla® and ENHERTU® have been approved by the FDA for the treatment of breast cancer,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33468562",
"endSection": "abstract",
"offsetInBeginSection": 799,
"offsetInEndSection": 851,
"text": " Herceptin toward ErbB2-positive breast cancer cells"
}
] | 11
|
BioASQ-training11b
| null | null |
622b99f73a8413c653000093
| 4,680
|
factoid
|
What does PCAT6 stand for?
|
['rostate cancer-associated transcript 6']
|
[
"prostate cancer-associated transcript 6",
"PCAT-6",
"PCAT6",
"Prostate cancer-associated transcript 6"
] |
['PCAT6 stands for prostate cancer-associated transcript 6.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34620745"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34620745",
"endSection": "abstract",
"offsetInBeginSection": 240,
"offsetInEndSection": 391,
"text": "In this work, we investigated the role and regulatory mechanism of lncRNA prostate cancer-associated transcript 6 (PCAT6) in breast cancer progression."
}
] | 11
|
BioASQ-training11b
| null | null |
622668b13a8413c653000088
| 4,687
|
factoid
|
What organ is associated with a Gleason pattern or Gleason Score?
|
['prostate']
|
[
"prostate",
"prostate gland",
"prostatic gland"
] |
['The Gleason score is an important parameter for clinical outcome in prostate cancer patients', 'The Gleason score is an important parameter for clinical outcome in prostate cancer patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10652560",
"http://www.ncbi.nlm.nih.gov/pubmed/12385930",
"http://www.ncbi.nlm.nih.gov/pubmed/25189638",
"http://www.ncbi.nlm.nih.gov/pubmed/32350585",
"http://www.ncbi.nlm.nih.gov/pubmed/22367295",
"http://www.ncbi.nlm.nih.gov/pubmed/25228336",
"http://www.ncbi.nlm.nih.gov/pubmed/32686748",
"http://www.ncbi.nlm.nih.gov/pubmed/15475927",
"http://www.ncbi.nlm.nih.gov/pubmed/14562287",
"http://www.ncbi.nlm.nih.gov/pubmed/21862072",
"http://www.ncbi.nlm.nih.gov/pubmed/30363387",
"http://www.ncbi.nlm.nih.gov/pubmed/17277764",
"http://www.ncbi.nlm.nih.gov/pubmed/26439747"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32686748",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "The Gleason score is an important parameter for clinical outcome in prostate cancer patients"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32686748",
"endSection": "title",
"offsetInBeginSection": 83,
"offsetInEndSection": 124,
"text": "Gleason score 8 prostate cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32686748",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 390,
"text": "Gleason score 8 prostate cancer patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32350585",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 114,
"text": "Men with Gleason score 9-10 prostate cancer have worse outcomes compared to those with Gleason 8 disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12385930",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "OBJECTIVES: Most adenocarcinomas of the prostate with a Gleason score greater than 8 at radical prostatectomy have extraprostatic extension and a high risk of progression."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26439747",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Preoperative low serum testosterone is associated with high-grade prostate cancer and an increased Gleason score upgrading."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26439747",
"endSection": "abstract",
"offsetInBeginSection": 571,
"offsetInEndSection": 730,
"text": "eason score (GS) and predominant Gleason pattern were determined in prostate biopsies and in prostate tissue specimens, crosschecked by two uro-pathologists.RE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25189638",
"endSection": "abstract",
"offsetInBeginSection": 1712,
"offsetInEndSection": 1918,
"text": "In conclusion, cribriform growth in Gleason grade 4 is a strong prognostic marker for distant metastasis and disease-specific death in patients with Gleason score 7 prostate cancer at radical prostatectomy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25228336",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Accurate recognition of Gleason pattern 5 (GP5) prostate adenocarcinoma (PCa) on core biopsy (NBX) is critical because it is associated with disease progression and the worst clinical outcome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17277764",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1498,
"text": " the first time that reelin is expressed in prostate cancer and not in benign prostate tissue and its expression occurs in higher Gleason score and correlates significantly with increasing of single Gleason patterns. This suggests reelin may b"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30363387",
"endSection": "abstract",
"offsetInBeginSection": 89,
"offsetInEndSection": 426,
"text": "ne of the recent important modifications in the Gleason grading system recommended from the International Society of Urological Pathology consensus conference is recording the percentage of Gleason pattern 4 in the pathology reports of prostate needle biopsy and radical prostatectomy cases with Gleason score 7 prostatic adenocarcinoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22367295",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Usual and unusual histologic patterns of high Gleason score 8 to 10 adenocarcinoma of the prostate in needle biopsy tissue"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15475927",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "The Gleason score of prostate adenocarcinomas is an important preoperative predictor of cancer behavior, and is used to help guide treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17277764",
"endSection": "abstract",
"offsetInBeginSection": 935,
"offsetInEndSection": 1093,
"text": " frequently found in high Gleason score prostate cancers, we explored whether reelin expression is influenced by single Gleason patterns. While Gleason 3 patt"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10652560",
"endSection": "abstract",
"offsetInBeginSection": 2843,
"offsetInEndSection": 3036,
"text": " of prostate cancer would occur within Gleason scores 3 to 10 even though higher scores are usually considered more aggressive forms of prostate cancers. Since our study is based upon a very li"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21862072",
"endSection": "abstract",
"offsetInBeginSection": 713,
"offsetInEndSection": 934,
"text": "3 + 4 = 7 and Gleason score 4 + 3 = 7. Gleason score 4 + 3 = 7 showed an overall correlation with pathological stage (organ confined, focal extraprostatic extension, nonfocal extraprostatic extension, seminal vesicle inva"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14562287",
"endSection": "abstract",
"offsetInBeginSection": 300,
"offsetInEndSection": 490,
"text": "We compared the Gleason scores found on needle biopsy with the grade and stage (organ-confined, extra-prostatic extension, positive seminal vesicles or lymph nodes) at radical prostatectomy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12385930",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Prediction of outcome after radical prostatectomy in men with organ-confined Gleason score 8 to 10 adenocarcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12385930",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "OBJECTIVES: Most adenocarcinomas of the prostate with a Gleason score greater than 8 at radical prostatectomy have extraprostatic extension and a high risk of "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22367295",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Usual and unusual histologic patterns of high Gleason score 8 to 10 adenocarcinoma of the prostate in needle biopsy tissue."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25189638",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Cribriform growth is highly predictive for postoperative metastasis and disease-specific death in Gleason score 7 prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10652560",
"endSection": "abstract",
"offsetInBeginSection": 1697,
"offsetInEndSection": 1893,
"text": "A were similar in normal prostate and benign prostatic hyperplasia (BPH) whereas they varied consistently within and between Gleason histologic scores for prostate cancer. These variations showed "
}
] | 11
|
BioASQ-training11b
| null | null |
622b9d593a8413c653000095
| 4,691
|
factoid
|
Which tool has been developed to identify the glycan shielding of glycosylated proteins?
|
['GLYCO']
|
[
"GLYCO",
"Glycogen",
"Glycoconjugate",
"Glycoprotein",
"Glycolipid",
"Glycosylation",
"Glycosaminoglycan",
"Glycolysis"
] |
['GLYCO (GLYcan COverage) is an in silico approach to quantify the glycan shielding of a protein surface. The software provides insights into glycan-dense/sparse regions of the entire protein surface or a subset of the protein surface. GLYCO calculates glycan shielding from a single coordinate file or from multiple coordinate files, for instance, as obtained from molecular dynamics simulations or by nuclear magnetic resonance spectroscopy structure determination, enabling analysis of glycan dynamics.', 'GLYCO calculates glycan shielding from a single coordinate file or from multiple coordinate files, for instance, as obtained from molecular dynamics simulations or by nuclear magnetic resonance spectroscopy structure determination, enabling analysis of glycan dynamics.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34864901"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34864901",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "GLYCO: a tool to quantify glycan shielding of glycosylated proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34864901",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 910,
"text": "Here, we developed an in silico approach, GLYCO (GLYcan COverage), to quantify the glycan shielding of a protein surface. The software provides insights into glycan-dense/sparse regions of the entire protein surface or a subset of the protein surface. GLYCO calculates glycan shielding from a single coordinate file or from multiple coordinate files, for instance, as obtained from molecular dynamics simulations or by nuclear magnetic resonance spectroscopy structure determination, enabling analysis of glycan dynamics."
}
] | 11
|
BioASQ-training11b
| null | null |
621e59ce3a8413c65300004c
| 4,693
|
factoid
|
What does the gene symbol EREG stand for?
|
['epiregulin']
|
[
"epiregulin",
"EREG",
"epiregulin precursor",
"epiregulin protein",
"epiregulin isoform"
] |
['The gene symbol EREG stands for the gene epiregulin.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34667080"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34667080",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 569,
"text": "We found that epidermal growth factor (EGF)-deficient cells exhibited lower basal ERK activity than the cells deficient in heparin-binding EGF (HBEGF), transforming growth factor alpha (TGFα) or epiregulin (EREG), but all cell lines deficient in a single EGFR ligand retained the ERK activation waves."
}
] | 11
|
BioASQ-training11b
| null | null |
6237a5513a8413c6530000b0
| 4,697
|
factoid
|
Which tool has been developed for proteome-wide detection of membrane lipid-binding proteins?
|
['MBPpred']
|
[
"MBPpred",
"Molecular Biology Prediction",
"MBP prediction",
"MBPpred software",
"MBPpred tool"
] |
['MBPpred is a profile Hidden Markov Model based method capable of detecting Membrane Binding Proteins (MBPs) from information encoded in their amino acid sequence.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27048983"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27048983",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "MBPpred: Proteome-wide detection of membrane lipid-binding proteins using profile Hidden Markov Models."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27048983",
"endSection": "abstract",
"offsetInBeginSection": 355,
"offsetInEndSection": 1018,
"text": "Here we report a profile Hidden Markov Model based method capable of detecting Membrane Binding Proteins (MBPs) from information encoded in their amino acid sequence, called MBPpred. The method identifies MBPs that contain one or more of the Membrane Binding Domains (MBDs) that have been described to date, and further classifies these proteins based on their position in respect to the membrane, either as peripheral or transmembrane. MBPpred is available online at http://bioinformatics.biol.uoa.gr/MBPpred. This method was applied in selected eukaryotic proteomes, in order to examine the characteristics they exhibit in various eukaryotic kingdoms and phyla."
}
] | 11
|
BioASQ-training11b
| null | null |
62005e02c9dfcb9c09000018
| 4,698
|
factoid
|
What disease can be treated with Avacopan?
|
['ANCA-associated vasculitis']
|
[
"ANCA-associated vasculitis",
"Antineutrophil cytoplasmic antibody-associated vasculitis",
"ANCA vasculitis",
"ANCA vasculitis syndromes",
"ANCA-related vasculitis"
] |
['Avacopan is effective for ANCA-associated vasculitis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33625803",
"http://www.ncbi.nlm.nih.gov/pubmed/28400446",
"http://www.ncbi.nlm.nih.gov/pubmed/34484454",
"http://www.ncbi.nlm.nih.gov/pubmed/34473462",
"http://www.ncbi.nlm.nih.gov/pubmed/34826105",
"http://www.ncbi.nlm.nih.gov/pubmed/34006155",
"http://www.ncbi.nlm.nih.gov/pubmed/33164993",
"http://www.ncbi.nlm.nih.gov/pubmed/33596356",
"http://www.ncbi.nlm.nih.gov/pubmed/29718732",
"http://www.ncbi.nlm.nih.gov/pubmed/34224265",
"http://www.ncbi.nlm.nih.gov/pubmed/34553355",
"http://www.ncbi.nlm.nih.gov/pubmed/33128347",
"http://www.ncbi.nlm.nih.gov/pubmed/32088663"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34473462",
"endSection": "abstract",
"offsetInBeginSection": 1009,
"offsetInEndSection": 1397,
"text": "Current therapies are often effective in inducing and maintaining remission but are associated with a range of toxicities. Several new therapies are in development for ANCA vasculitis. Avacopan, an orally administered inhibitor of the complement fragment 5a (C5a) receptor, has been assessed in a phase 3 clinical trial and may play a role in reducing the cumulative glucocorticoid dose. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34484454",
"endSection": "abstract",
"offsetInBeginSection": 846,
"offsetInEndSection": 973,
"text": "New treatment approaches, such as the C5a receptor inhibitor avacopan could enable a minimized steroid treatment in the future."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34553355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "GPA/MPA INDUCTION OF REMISSION: As demonstrated in the ADVOCATE-trial avacopan allows for a substantial reduction of glucocorticoid (GC) use during induction of remission. A future role of avacopan in the treatment of GPA and MPA is likely."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33164993",
"endSection": "abstract",
"offsetInBeginSection": 1058,
"offsetInEndSection": 1216,
"text": "Avacopan has shown significant promise in ANCA-associated vasculitis as part of a glucocorticoid-free induction regimen in a recently completed phase 3 trial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34224265",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "In ANCA-associated vasculitis, avacopan was superior to prednisone taper for sustained remission"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34224265",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "SOURCE CITATION: Jayne DRW, Merkel PA, Schall TJ, et al. Avacopan for the treatment of ANCA-associated vasculitis. N Engl J Med. 2021;384:599-609. 33596356."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33596356",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 57,
"text": "Avacopan for the Treatment of ANCA-Associated Vasculitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33596356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "BACKGROUND: The C5a receptor inhibitor avacopan is being studied for the treatment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33596356",
"endSection": "abstract",
"offsetInBeginSection": 1886,
"offsetInEndSection": 2149,
"text": "CONCLUSIONS: In this trial involving patients with ANCA-associated vasculitis, avacopan was noninferior but not superior to prednisone taper with respect to remission at week 26 and was superior to prednisone taper with respect to sustained remission at week 52. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28400446",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Randomized Trial of C5a Receptor Inhibitor Avacopan in ANCA-Associated Vasculitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33625803",
"endSection": "abstract",
"offsetInBeginSection": 431,
"offsetInEndSection": 592,
"text": "tly, new molecules are being developed and some of them have already demonstrated clinical efficacy, such as avacopan (C5aR blocker) in ANCA vasculitis. As for k"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34826105",
"endSection": "abstract",
"offsetInBeginSection": 448,
"offsetInEndSection": 769,
"text": "ber 2021, avacopan received its first approval in Japan for the treatment of microscopic polyangiitis (MPA) and granulomatosis with polyangiitis (GPA), the two most common forms of ANCA-associated vasculitis, where it is being commercialized by Kissei Pharmaceutical through a partnership with Vifor Pharma. In October 20"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34006155",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Avacopan for the treatment of ANCA-associated vasculitis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33596356",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Avacopan for the Treatment of ANCA-Associated Vasculitis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29718732",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "Avacopan in the treatment of ANCA-associated vasculitis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34224265",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "In ANCA-associated vasculitis, avacopan was superior to prednisone taper for sustained remission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34826105",
"endSection": "abstract",
"offsetInBeginSection": 772,
"offsetInEndSection": 1045,
"text": " avacopan was approved in the USA as an adjunctive treatment in adults for severe active ANCA-associated vasculitis (specifically MPA and GPA) in combination with standard therapy including glucocorticoids (avacopan does not eliminate glucocorticoid use). Avacopan has rece"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34826105",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 218,
"text": "Avacopan (TAVNEOS™) is a complement 5a receptor (C5aR) antagonist developed by ChemoCentryx for the treatment of autoimmune diseases including anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis. The "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32088663",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 938,
"text": "al will evaluate if avacopan replaces the need for chronic glucocorticoids in the treatment of ANCA-associated vasculitis.OBJECTI"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34006155",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 57,
"text": "Avacopan for the treatment of ANCA-associated vasculitis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29718732",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Avacopan in the treatment of ANCA-associated vasculitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33128347",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 290,
"text": "OBJECTIVE: This study aimed to evaluate the safety of avacopan, an orally administered C5a receptor inhibitor, for the treatment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis in addition to standard-of-care (SOC) treatment with glucocorticoids with cyclophosphamide or"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33596356",
"endSection": "abstract",
"offsetInBeginSection": 1876,
"offsetInEndSection": 2024,
"text": "rednisone.CONCLUSIONS: In this trial involving patients with ANCA-associated vasculitis, avacopan was noninferior but not superior to prednisone tap"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34826105",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "Avacopan (TAVNEOS™) is a complement 5a receptor (C5aR) antagonist developed by ChemoCentryx for the treatment of autoimmune diseases including anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34826105",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 755,
"text": "In September 2021, avacopan received its first approval in Japan for the treatment of microscopic polyangiitis (MPA) and granulomatosis with polyangiitis (GPA), the two most common forms of ANCA-associated vasculitis, where it is being commercialized by Kissei Pharmaceutical through a partnership with Vifor Pharma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34826105",
"endSection": "abstract",
"offsetInBeginSection": 756,
"offsetInEndSection": 1027,
"text": "In October 2021, avacopan was approved in the USA as an adjunctive treatment in adults for severe active ANCA-associated vasculitis (specifically MPA and GPA) in combination with standard therapy including glucocorticoids (avacopan does not eliminate glucocorticoid use)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33596356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 343,
"text": "BACKGROUND: The C5a receptor inhibitor avacopan is being studied for the treatment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.METHODS: In this randomized, controlled trial, we assigned patients with ANCA-associated vasculitis in a 1:1 ratio to receive oral avacopan at a dose of 30 mg twice daily or oral prednisone on"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33128347",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 470,
"text": "OBJECTIVE: This study aimed to evaluate the safety of avacopan, an orally administered C5a receptor inhibitor, for the treatment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis in addition to standard-of-care (SOC) treatment with glucocorticoids with cyclophosphamide or rituximab.METHODS: In this randomized 12-week study, twice daily avacopan (10 mg or 30 mg) plus SOC was assessed versus SOC only in patients with newly diagnosed/relapsing ANCA-as"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32088663",
"endSection": "abstract",
"offsetInBeginSection": 789,
"offsetInEndSection": 1505,
"text": "onephritis. This trial will evaluate if avacopan replaces the need for chronic glucocorticoids in the treatment of ANCA-associated vasculitis.OBJECTIVE: The aim of this study is to determine the proportions of patients in remission at week 26 and with sustained remission at week 52, defined as Birmingham Vasculitis Activity Score=0, and not taking glucocorticoids within the 4 weeks before week 26 and week 52, respectively.METHODS: The Avacopan Development in Vasculitis to Obtain Corticosteroid elimination and Therapeutic Efficacy study is a randomized, double-blind, active-comparator (prednisone), 2-arm study evaluating the safety and efficacy of avacopan versus prednisone, administered in combination with "
}
] | 11
|
BioASQ-training11b
| null | null |
61f7c883882a024a10000026
| 4,699
|
factoid
|
What disease is also known as Bechterew's Disease?
|
['Ankylosing spondylitis']
|
[
"Ankylosing spondylitis",
"Bechterew's disease",
"Marie-Strümpell disease",
"AS"
] |
["Ankylosing spondylitis (Bechterew's disease) is the most typical form of axial SpA whereby sacroiliitis can be found on X-rays of the SI joints."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/6461592",
"http://www.ncbi.nlm.nih.gov/pubmed/6983935",
"http://www.ncbi.nlm.nih.gov/pubmed/25050151",
"http://www.ncbi.nlm.nih.gov/pubmed/11803718",
"http://www.ncbi.nlm.nih.gov/pubmed/22744304",
"http://www.ncbi.nlm.nih.gov/pubmed/18650743",
"http://www.ncbi.nlm.nih.gov/pubmed/32349490",
"http://www.ncbi.nlm.nih.gov/pubmed/3923615",
"http://www.ncbi.nlm.nih.gov/pubmed/29101454",
"http://www.ncbi.nlm.nih.gov/pubmed/2233790",
"http://www.ncbi.nlm.nih.gov/pubmed/22085520"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22085520",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 373,
"text": "Ankylosing spondylitis (Bechterew's disease) is the most typical form of axial SpA whereby sacroiliitis can be found on X-rays of the SI joints."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11803718",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "[Special considerations in therapy of injuries of the cervical spine in ankylosing spondylitis (Bechterew disease)]"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25050151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Ankylosing spondylitis (AS) or Bechterew disease is a chronic, usually progressive, systemic inflammatory joint disease, which predominantly affects the spine and sacroiliac joints. In "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22744304",
"endSection": "title",
"offsetInBeginSection": 2,
"offsetInEndSection": 106,
"text": "iagnosis and therapy of axial spondyloarthritis including ankylosing spondylitis (Bechterew's disease)]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18650743",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Hyperplasia of the coronoid process in patients with ankylosing spondylitis (Bechterew disease)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11803718",
"endSection": "title",
"offsetInBeginSection": 2,
"offsetInEndSection": 115,
"text": "pecial considerations in therapy of injuries of the cervical spine in ankylosing spondylitis (Bechterew disease)]"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2233790",
"endSection": "title",
"offsetInBeginSection": 2,
"offsetInEndSection": 113,
"text": "irected cloning of the HLA-B27 gene isolated from a patient with ankylosing spondylitis (Bechterew's disease)]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3923615",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "Bechterew's syndrome (ankylosing spondylitis)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25050151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "Ankylosing spondylitis (AS) or Bechterew disease is a chronic, usually progressive, systemic inflammatory joint disease, which predominantly affects the spine and sacroiliac joints."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6461592",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "[Ankylosing spondylitis (Bechterew's disease)--a current review (author's transl)]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6983935",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "The distribution of clinical findings in Bechterew's syndrome (ankylosing spondylitis) suggests distinct genetic subgroups."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18650743",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Hyperplasia of the coronoid process in patients with ankylosing spondylitis (Bechterew disease)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29101454",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "[Surgical management of ankylosing spondylitis (Bechterew's disease)]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22744304",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "[Diagnosis and therapy of axial spondyloarthritis including ankylosing spondylitis (Bechterew's disease)]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32349490",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "Ankylosing spondylitis (AS) or else Bechterews or Marie-Strümpells disease is a chronic inflammatory autoimmune disease affecting preferentially the spine in the form of sacroileitis and spondylitis [1,2]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18650743",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Although involvement of the temporomandibular joint in patients with ankylosing spondylitis (AS, Bechterew disease) has been described previously"
}
] | 11
|
BioASQ-training11b
| null | null |
622b9e743a8413c653000097
| 4,701
|
factoid
|
Through which pathway does epiregulin promote leptin secretion?
|
['EGFR/MAPK pathway']
|
[
"EGFR/MAPK pathway",
"Epidermal Growth Factor Receptor/Mitogen-Activated Protein Kinase pathway",
"EGFR signaling pathway",
"EGFR pathway",
"MAPK signaling pathway",
"Epidermal Growth Factor Receptor pathway"
] |
['EREG increased leptin production and secretion in a dose-dependent manner in iAb fat explants via the EGFR/MAPK pathway.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30400011"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30400011",
"endSection": "abstract",
"offsetInBeginSection": 724,
"offsetInEndSection": 845,
"text": "EREG increased leptin production and secretion in a dose-dependent manner in iAb fat explants via the EGFR/MAPK pathway. "
}
] | 11
|
BioASQ-training11b
| null | null |
6237ac143a8413c6530000b7
| 4,702
|
factoid
|
What is the target of Sotorasib?
|
['KRASG12C']
|
[
"KRASG12C",
"KRAS G12C",
"Kirsten rat sarcoma viral oncogene homolog G12C",
"Kirsten rat sarcoma viral oncogene",
"KRAS mutation G12C",
"KRAS mutant G12C"
] |
['Sotorasib is a KRASG12C inhibitor.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34553354",
"http://www.ncbi.nlm.nih.gov/pubmed/33547148",
"http://www.ncbi.nlm.nih.gov/pubmed/34800654",
"http://www.ncbi.nlm.nih.gov/pubmed/34504076",
"http://www.ncbi.nlm.nih.gov/pubmed/32955176",
"http://www.ncbi.nlm.nih.gov/pubmed/33466360",
"http://www.ncbi.nlm.nih.gov/pubmed/34520956",
"http://www.ncbi.nlm.nih.gov/pubmed/34004237",
"http://www.ncbi.nlm.nih.gov/pubmed/34776511",
"http://www.ncbi.nlm.nih.gov/pubmed/33004338",
"http://www.ncbi.nlm.nih.gov/pubmed/34607583",
"http://www.ncbi.nlm.nih.gov/pubmed/34200676",
"http://www.ncbi.nlm.nih.gov/pubmed/33971321",
"http://www.ncbi.nlm.nih.gov/pubmed/34158284",
"http://www.ncbi.nlm.nih.gov/pubmed/34715449",
"http://www.ncbi.nlm.nih.gov/pubmed/34838325",
"http://www.ncbi.nlm.nih.gov/pubmed/34607832",
"http://www.ncbi.nlm.nih.gov/pubmed/34590053",
"http://www.ncbi.nlm.nih.gov/pubmed/34558391",
"http://www.ncbi.nlm.nih.gov/pubmed/34675734",
"http://www.ncbi.nlm.nih.gov/pubmed/33097477",
"http://www.ncbi.nlm.nih.gov/pubmed/34137282"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34520956",
"endSection": "abstract",
"offsetInBeginSection": 425,
"offsetInEndSection": 622,
"text": "Encouragingly, the KRASG12C inhibitor AMG510 (sotorasib), which has been approved for treating NSCLC and CRC recently, makes directly targeting KRAS the most promising strategy for cancer therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34504076",
"endSection": "abstract",
"offsetInBeginSection": 705,
"offsetInEndSection": 881,
"text": "Finally, we show that a selective PI4KA inhibitor augments the antineoplastic activity of the KRASG12C inhibitor sotorasib, suggesting a clinical path to exploit this pathway. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34558391",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 811,
"text": "However, clinical candidates targeting the KRAS G12C protein have recently been developed. MRTX849 and recently approved Sotorasib are covalent binders targeting the mutated cysteine 12, occupying Switch II pocket."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34553354",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 736,
"text": "Sotorasib with efficacy in kRAS-G12C mutation of NSCLC"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34607583",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 954,
"text": "Two such inhibitors, sotorasib (AMG 510) and adagrasib (MRTX849), were recently evaluated in phase I-III trials for the treatment of non-small cell lung cancer with KRAS-G12C mutations, heralding a new era of precision oncology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34607832",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 616,
"text": "The findings, along with data on the KRASG12C inhibitor sotorasib, were presented at the 2021 European Society for Medical Oncology Congress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34158284",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "The FDA has approved the first KRAS-targeted therapy, sotorasib, for patients with previously treated non-small cell lung cancer with KRASG12C mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34800654",
"endSection": "abstract",
"offsetInBeginSection": 317,
"offsetInEndSection": 549,
"text": "In 2021, the Food and Drug Administration (FDA) approved the use of Sotorasib (Lumakras) for the treatment of adult patients with KRAS-G12C mutated locally advanced or metastatic NSCLC, following at least one prior systemic therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33547148",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 271,
"text": "The KRASG12C inhibitor sotorasib continues to impress in non-small cell lung cancer: In the phase II CodeBreak 100 trial, the agent elicited responses in more than a third of patients and led to a median progression-free survival of almost 7 months. Based on these result"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34590053",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Sotorasib is a first-in-class small molecule that irreversibly inhibits KRAS G12C, locking it in an inactive state, inhibiting oncogenic signaling, and inducing a proinflammatory microenvironment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34004237",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Sotorasib is a first-in class KRASG12C covalent inhibitor in clinical development for the treatment of tumors with the KRAS p.G12C mutation. In the nonclinical to"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33971321",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 247,
"text": "Recently, novel KRAS G12C inhibitors, such as sotorasib and adagrasib, are being developed in clinical trials and have revealed promising results in metastatic NSCLC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34838325",
"endSection": "abstract",
"offsetInBeginSection": 340,
"offsetInEndSection": 509,
"text": "We evaluated the clinical validity of Guardant360 CDx as a companion diagnostic for sotorasib for detection of KRAS p.G12C, an important oncogenic NSCLC driver mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34715449",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 379,
"text": "Until the recent approval of sotorasib, a KRAS G12C inhibitor, lack of targeted therapy for KRAS has resulted in poor prognosis of patients with tumors harboring KRAS mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34137282",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Sotorasib is a first-in-class KRASG12C covalent inhibitor in clinical development for the treatment of tumors with the KR"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34004237",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Sotorasib is a first-in class KRASG12C covalent inhibitor in clinical development for the treatment of tumors with the KRAS p.G12C mut"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34137282",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Nonclinical Safety Profile of Sotorasib, a KRASG12C-Specific Covalent Inhibitor for the Treatment of KRAS p.G12C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33466360",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 397,
"text": "t efforts to produce subtype specific inhibitors have been more successful, and several KRASG12C inhibitors have reached clinical trials, including adagrasib and sotorasib, which have shown early evidence of efficacy in patients. L"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34590053",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Sotorasib is a first-in-class small molecule that irreversibly inhibits KRAS G12C, locking it in an inactive state, inhibiting oncogenic signaling, and inducing a proinflammatory microenvironment. H"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33097477",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 290,
"text": "phase I trial, the KRASG12C inhibitor sotorasib elicited responses in about a third of patients with the disease and was generally well tolerated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34200676",
"endSection": "abstract",
"offsetInBeginSection": 533,
"offsetInEndSection": 658,
"text": "seven KRAS-G12C inhibitors are in clinical trials and sotorasib has become the first one to be granted FDA approval. Here, we"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34776511",
"endSection": "abstract",
"offsetInBeginSection": 560,
"offsetInEndSection": 800,
"text": "re have been surprising advances in directly targeted drugs for KRAS, especially in KRAS (G12C) inhibitors, such as AMG510 (sotorasib) and MRTX849 (adagrasib), which have obtained encouraging results in clinical trials. Excitingly, AMG510 w"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34520956",
"endSection": "abstract",
"offsetInBeginSection": 435,
"offsetInEndSection": 629,
"text": "gly, the KRASG12C inhibitor AMG510 (sotorasib), which has been approved for treating NSCLC and CRC recently, makes directly targeting KRAS the most promising strategy for cancer therapy. To bett"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32955176",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 367,
"text": "Sotorasib is a small molecule that selectively and irreversibly targets KRASG12C.METHODS: We conducted a phase 1 trial of sotorasib in patients with"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34137282",
"endSection": "abstract",
"offsetInBeginSection": 1642,
"offsetInEndSection": 1792,
"text": "esults of the nonclinical safety program support a high benefit/risk ratio of sotorasib for the treatment of patients with KRAS p.G12C-mutated tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34158284",
"endSection": "abstract",
"offsetInBeginSection": 16,
"offsetInEndSection": 166,
"text": "oved the first KRAS-targeted therapy, sotorasib, for patients with previously treated non-small cell lung cancer with KRASG12C mutations. In a phase I"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33004338",
"endSection": "abstract",
"offsetInBeginSection": 49,
"offsetInEndSection": 199,
"text": "ered an \"undruggable\" target, can be targeted successfully in non-small cell lung cancer. In a phase I trial, the KRASG12C inhibitor sotorasib elicite"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32955176",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 404,
"text": "er cancers. Sotorasib is a small molecule that selectively and irreversibly targets KRASG12C.METHODS: We conducted a phase 1 trial of sotorasib in patients with advanced solid tumors harboring the "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34137282",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Sotorasib is a first-in-class KRASG12C covalent inhibitor in clinical development for the treatment of tumors with the KRAS p.G12C mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34004237",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Sotorasib is a first-in class KRASG12C covalent inhibitor in clinical development for the treatment of tumors with the KRAS p.G12C mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34520956",
"endSection": "abstract",
"offsetInBeginSection": 425,
"offsetInEndSection": 621,
"text": "Encouragingly, the KRASG12C inhibitor AMG510 (sotorasib), which has been approved for treating NSCLC and CRC recently, makes directly targeting KRAS the most promising strategy for cancer therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34675734",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 513,
"text": "Based on promising results in both preclinical and clinical trials, sotorasib, a novel KRASG12C inhibitor, was given conditional approval by the FDA in May 2021."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34137282",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Nonclinical Safety Profile of Sotorasib, a KRASG12C-Specific Covalent Inhibitor for the Treatment of KRAS p.G12C-Mutated Cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33097477",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 290,
"text": "In a phase I trial, the KRASG12C inhibitor sotorasib elicited responses in about a third of patients with the disease and was generally well tolerated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34137282",
"endSection": "abstract",
"offsetInBeginSection": 1628,
"offsetInEndSection": 1792,
"text": "Overall, the results of the nonclinical safety program support a high benefit/risk ratio of sotorasib for the treatment of patients with KRAS p.G12C-mutated tumors."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32955176",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 60,
"text": "KRASG12C Inhibition with Sotorasib in Advanced Solid Tumors."
}
] | 11
|
BioASQ-training11b
| null | null |
61f7c60c882a024a10000025
| 4,709
|
factoid
|
What is Luteolin?
|
['flavonoid']
|
[
"flavonoid",
"flavonoids",
"bioflavonoid",
"polyphenol",
"plant pigment",
"flavonoid glycoside"
] |
['Luteolin has been reviewed as a flavonoid possessing potential cardioprotective, anti-inflammatory, anti-cancer activities.', 'Luteolin, a polyphenolic flavonoid, has potent anti-inflammatory properties.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18991571",
"http://www.ncbi.nlm.nih.gov/pubmed/21881237",
"http://www.ncbi.nlm.nih.gov/pubmed/34460026",
"http://www.ncbi.nlm.nih.gov/pubmed/32407927",
"http://www.ncbi.nlm.nih.gov/pubmed/30119240",
"http://www.ncbi.nlm.nih.gov/pubmed/29207088",
"http://www.ncbi.nlm.nih.gov/pubmed/33469821",
"http://www.ncbi.nlm.nih.gov/pubmed/23317200",
"http://www.ncbi.nlm.nih.gov/pubmed/29928143",
"http://www.ncbi.nlm.nih.gov/pubmed/24353826",
"http://www.ncbi.nlm.nih.gov/pubmed/34717250",
"http://www.ncbi.nlm.nih.gov/pubmed/20074346",
"http://www.ncbi.nlm.nih.gov/pubmed/22203870",
"http://www.ncbi.nlm.nih.gov/pubmed/22269172",
"http://www.ncbi.nlm.nih.gov/pubmed/28282295",
"http://www.ncbi.nlm.nih.gov/pubmed/10972088",
"http://www.ncbi.nlm.nih.gov/pubmed/24477342",
"http://www.ncbi.nlm.nih.gov/pubmed/26020516",
"http://www.ncbi.nlm.nih.gov/pubmed/18937165",
"http://www.ncbi.nlm.nih.gov/pubmed/27185356",
"http://www.ncbi.nlm.nih.gov/pubmed/27170112",
"http://www.ncbi.nlm.nih.gov/pubmed/27016074",
"http://www.ncbi.nlm.nih.gov/pubmed/32081041",
"http://www.ncbi.nlm.nih.gov/pubmed/12027807",
"http://www.ncbi.nlm.nih.gov/pubmed/30280574",
"http://www.ncbi.nlm.nih.gov/pubmed/16140950",
"http://www.ncbi.nlm.nih.gov/pubmed/32694396",
"http://www.ncbi.nlm.nih.gov/pubmed/26246742",
"http://www.ncbi.nlm.nih.gov/pubmed/31994822",
"http://www.ncbi.nlm.nih.gov/pubmed/31019613"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32081041",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Recently, many studies have reported the anticancer properties of flavonoid luteolin against a variety of tumors, but there is still a lack in the description of its mechanism of action"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32694396",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 319,
"text": "Luteolin, a polyphenolic flavonoid, has potent anti-inflammatory properties. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34460026",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 265,
"text": "Luteolin is a falconoid compound that has an antioxidant effect, but its mechanism in I/R injury in vivo and in vitro is still under explored."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27170112",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "Luteolin is a naturally occurring flavone that reportedly has anti-inflammatory effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30280574",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Luteolin is a flavonoid present in plants in the form of aglycone or glucosides."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24477342",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 294,
"text": "Luteolin, a naturally occurring flavonoid, possesses anti-cancer activities against several human cancers, but the exact molecular and biochemical mechanisms of above findings are not very clear, and its activity against head and neck squamous cell carcinoma (HNSCC) is seldom mentioned. In thi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33469821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "Luteolin is a flavonoid with antioxidant properties already demonstrated in studies related to inflammation, tumor, and cardiovascular processes; however, there are no available information regarding its antioxidant effects at the venous endothelial site. We "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32407927",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 258,
"text": "Luteolin (3',4',5,7-tetrahydroxyflavone) is a phytochemical found frequently in medicinal herbs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16140950",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 228,
"text": "Luteolin is a dietary flavonoid commonly found in some medicinal plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29928143",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 393,
"text": "Luteolin (2-[3,4-dihydroxyphenyl]-5,7-dihydroxy-4-chromenone), is a naturally occurring flavonoid found in fruits and vegetables that exhibits many anticancer properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18991571",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Luteolin, 3',4',5,7-tetrahydroxyflavone, is a common flavonoid that exists in many types of plants including fruits, vegetables, and medicinal herbs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27016074",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Luteolin is a common dietary flavonoid present in Chinese herbal medicines that has been reported to have important anti-inflammatory properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29207088",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Luteolin is a falconoid compound that is present in various types of plants and possesses remarkable potential as a chemopreventive agent."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30119240",
"endSection": "abstract",
"offsetInBeginSection": 75,
"offsetInEndSection": 166,
"text": "Luteolin is a natural flavonoid widely distributed in plants with anti-inflammatory effect."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23317200",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Luteolin is a plant flavonoid which exhibits anti-oxidative, anti-inflammatory and anti-tumor effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22203870",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 229,
"text": "Luteolin is an anti-inflammatory flavonoid and widely distributed in the plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27185356",
"endSection": "abstract",
"offsetInBeginSection": 34,
"offsetInEndSection": 184,
"text": "ucial in the pathogenesis of numerous brain disorders. Luteolin, a flavonoid compound, inhibits glutamate release, however, its ability to affect glut"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21881237",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 249,
"text": "depression and endoplasmic reticulum stress. Luteolin is a flavonoid contained in many plants and with a variety of known pharmacological properties s"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30119240",
"endSection": "abstract",
"offsetInBeginSection": 21,
"offsetInEndSection": 171,
"text": " common multiple infection disease under 2 years old. Luteolin is a natural flavonoid widely distributed in plants with anti-inflammatory effect. This"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28282295",
"endSection": "abstract",
"offsetInBeginSection": 222,
"offsetInEndSection": 360,
"text": "Luteolin is a naturally occurring flavonoid with diverse pharmacological properties such as anti-inflammatory, antioxidant and anticancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22269172",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "BACKGROUND: Luteolin is a 3',4',5,7-tetrahydroxyflavone found in various fruits and"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26246742",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Luteolin is a bioflavonoid that attenuates adipocyte-derived inflammatory responses via suppression of nuclear factor-κB/mitogen-activated protein kinases pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31019613",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Background: Luteolin (3',4',5,7-tetrahydroxyflavone) is a flavone with a yellow crystalline appearance present in numerous plants such as broccoli, green chili,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18937165",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Luteolin is a flavone which occurs in medicinal plants as well as in some vegetables and spices."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18991571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Luteolin, a flavonoid with potential for cancer prevention and therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26246742",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 563,
"text": "I diabetes. Luteolin is a bioflavonoid with many beneficial properties such as antioxidant, antiproliferative, and anti-cancer.OBJECTIVES: To elucidate the potential anti-inflammatory response and the underlying mechanism of luteolin in 3T3-L1 adipocytes.MATERIALS AND METHODS: We stimulated 3T3-L1 adipocytes with the mixture of tumor necrosis factor-α, lipopolysaccharide, and interferon-"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12027807",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Luteolin, an emerging anti-cancer flavonoid, poisons eukaryotic DNA topoisomerase I."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10972088",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 169,
"text": "Luteolin, an abundant dietary component is a potent anti-leishmanial agent that acts by inducing topoisomerase II-mediated kinetoplast DNA cleavage leading to apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31994822",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Luteolin is a natural flavonoid with strong anti-oxidative properties that is reported to have an anti-cancer effect in several malignancies other than bladder cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24353826",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Luteolin is a flavonoid found in abundance in celery, green pepper, and dandelions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20074346",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "BACKGROUND: Luteolin, a plant derived flavonoid, exerts a variety of pharmacological activities and anti-oxidant properties associated with its capacity to scavenge oxygen and nitro"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12027807",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Luteolin, a naturally occurring flavonoid, is abundant in our daily dietary intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26020516",
"endSection": "abstract",
"offsetInBeginSection": 714,
"offsetInEndSection": 809,
"text": "The flavonoid luteolin shows therapeutic potential with low incidence of unwanted side effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21881237",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 370,
"text": "Luteolin is a flavonoid contained in many plants and with a variety of known pharmacological properties such as anti-inflammatory, anti-anxiety, and memory-improving effects, suggesting that luteolin penetrates into the brain."
}
] | 11
|
BioASQ-training11b
| null | null |
6226335d3a8413c653000082
| 4,711
|
factoid
|
Which is the literature-based database of phenotypes?
|
['PheneBank']
|
[
"PheneBank",
"PhenomeBank",
"Phene Bank"
] |
['PheneBank is a Web-portal for retrieving human phenotype-disease associations that have been text-mined from the whole of Medline. This approach exploits state-of-the-art machine learning for concept identification by utilising an expert annotated rare disease corpus from the PMC Text Mining subset. Evaluation of the system for entities is conducted on a gold-standard corpus of rare disease sentences and for associations against the Monarch initiative data.', 'PheneBank is a Web-portal for retrieving human phenotype-disease associations that have been text-mined from the whole of Medline.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34788791"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34788791",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 53,
"text": "PheneBank: a literature-based database of phenotypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34788791",
"endSection": "abstract",
"offsetInBeginSection": 312,
"offsetInEndSection": 772,
"text": "PheneBank is a Web-portal for retrieving human phenotype-disease associations that have been text-mined from the whole of Medline. Our approach exploits state-of-the-art machine learning for concept identification by utilising an expert annotated rare disease corpus from the PMC Text Mining subset. Evaluation of the system for entities is conducted on a gold-standard corpus of rare disease sentences and for associations against the Monarch initiative data."
}
] | 11
|
BioASQ-training11b
| null | null |
621e63a43a8413c653000051
| 4,713
|
factoid
|
Idecabtagene vicleucel can be used for treatment of which disease?
|
['Multiple Myeloma']
|
[
"Multiple Myeloma",
"Plasma Cell Myeloma",
"Myeloma",
"Kahler's Disease",
"Myelomatosis"
] |
['Idecabtagene vicleucel was shown to be effective for Relapsed and Refractory Multiple Myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34461271",
"http://www.ncbi.nlm.nih.gov/pubmed/34256668",
"http://www.ncbi.nlm.nih.gov/pubmed/33896344",
"http://www.ncbi.nlm.nih.gov/pubmed/34527606",
"http://www.ncbi.nlm.nih.gov/pubmed/34625232",
"http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"http://www.ncbi.nlm.nih.gov/pubmed/33598857",
"http://www.ncbi.nlm.nih.gov/pubmed/34854741",
"http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"http://www.ncbi.nlm.nih.gov/pubmed/34145225"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34461271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 342,
"text": "B-cell maturation antigen (BCMA) has become a key target for antibody-drug conjugates, bispecific antibodies, chimeric antigen receptor T-cell therapies, and other immunotherapies in multiple myeloma. Some of these agents such as belantamab mafodotin and idecabtagene vicleucel have already received regulatory approval in the United States. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34527606",
"endSection": "abstract",
"offsetInBeginSection": 1113,
"offsetInEndSection": 1321,
"text": "These include isatuximab (also anti-CD38) and, in the past year, the antibody-drug conjugate (ADC) belantamab mafodotin and the chimeric antigen receptor (CAR) T-cell product idecabtagene vicleucel (ide-cel)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34256668",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Matching-adjusted indirect comparison of efficacy outcomes for ciltacabtagene autoleucel in CARTITUDE-1 versus idecabtagene vicleucel in KarMMa for the treatment of patients with relapsed or refractory multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34145225",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "KarMMa-RW: comparison of idecabtagene vicleucel with real-world outcomes in relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34145225",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 406,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a BCMA-directed CAR T-cell therapy, demonstrated efficacy in triple-class exposed RRMM patients in the KarMMa trial (NCT03361748). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Idecabtagene Vicleucel in Relapsed and Refractory Multiple Myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 1917,
"offsetInEndSection": 2100,
"text": "CONCLUSIONS: Ide-cel induced responses in a majority of heavily pretreated patients with refractory and relapsed myeloma; MRD-negative status was achieved in 26% of treated patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "abstract",
"offsetInBeginSection": 1633,
"offsetInEndSection": 1822,
"text": "Here, we will discuss the preclinical and clinical development of idecabtagene vicleucel and its future role in the changing treatment landscape of relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "abstract",
"offsetInBeginSection": 1207,
"offsetInEndSection": 1632,
"text": "After the recent publication of the results of a phase II trial confirming a notable efficacy and acceptable safety profile, idecabtagene vicleucel is the first CAR-T to gain regulatory US Food and Drug Administration approval to treat refractory multiple myeloma patients who have already been exposed to antibodies against CD38, proteasome inhibitors, and immunomodulatory agents and who are refractory to the last therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33598857",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 337,
"text": "BACKGROUND AND OBJECTIVE: Registrational trials for ciltacabtagene autoleucel [cilta-cel]) and idecabtagene vicleucel [ide-cel] chimeric antigen receptor T-cell (CAR-T) therapies were single-arm studies conducted with relapse refractory multiple myeloma (MM) patients who were triple-class-exposed (TCE) or triple-class-refractory (TCR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "BACKGROUND: Idecabtagene vicleucel (ide-cel, also called bb2121), a B-cell maturation antigen-directed chimeric antigen receptor (CAR) T-cell therapy, has shown clinical activity with expected CAR T-cell toxic effects in patients with relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33896344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a chimeric antigen receptor (CAR) T cell therapy, has been investigated in patients with relapsed and refractory multiple myeloma (RRMM) who have received an immunomodulatory drug, proteasome inhibitor, and anti-CD38 antibody in the single-arm phase 2 KarMMa clinical trial. Two ther"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "BACKGROUND: Idecabtagene vicleucel (ide-cel, also called bb2121), a B-cell maturation antigen-directed chimeric antigen receptor (CAR) T-cell therapy, has shown clinical activity with expected CAR T-cell toxic effects in patients with relapsed and refractory multiple m"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "The role of idecabtagene vicleucel in patients with heavily pretreated refractory multiple myeloma"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "The role of idecabtagene vicleucel in patients with heavily pretreated refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33896344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a chimeric antigen receptor (CAR) T cell therapy, has been investigated in patients with relapsed and refractory multiple myeloma (RRMM) who have received an immunomodulatory drug, proteasome inhibitor, and anti-CD38 antibody in the single-arm phase 2 KarMMa clinical trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34854741",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "Idecabtagene vicleucel (ide-cel), a novel chimeric antigen receptor (CAR) T-cell therapy targeting B-cell maturation antigen (BCMA), has recently gained approval by the US FDA for relapsed and refractory multiple myeloma (RRMM) after multicenter trials have demonstrated unprecedented results in this difficult-to-treat subgroup of patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34854741",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Idecabtagene vicleucel (ide-cel) CAR T-cell therapy for relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 392,
"text": "BACKGROUND: Idecabtagene vicleucel (ide-cel, also called bb2121), a B-cell maturation antigen-directed chimeric antigen receptor (CAR) T-cell therapy, has shown clinical activity with expected CAR T-cell toxic effects in patients with relapsed and refractory multiple myeloma.METHODS: In this phase 2 study, we sought to confirm the efficacy and safety of ide-cel in patients with relapsed an"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34625232",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 886,
"text": "The bulk of CAR T-cell constructs currently in clinical development target the B-cell maturation antigen (BCMA) and to date only idecabtagene vicleucel (ide-cel) is approved by the Food and Drug Administration (FDA) for commercial use in adult patients with relapsed or refractory MM based on the promising clinical responses and positive safety record shown in the pivotal KarMMa study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34145225",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 405,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a BCMA-directed CAR T-cell therapy, demonstrated efficacy in triple-class exposed RRMM patients in the KarMMa trial (NCT03361748)."
}
] | 11
|
BioASQ-training11b
| null | null |
61f7ce26882a024a1000002d
| 4,714
|
factoid
|
LINC00339 is a diagnostic, prognostic and treatment efficacy biomarker for what disease?
|
['cancer']
|
[
"cancer",
"malignancy",
"tumor",
"neoplasm",
"carcinoma",
"oncology",
"malignant growth",
"cancerous growth"
] |
['LINC00339 as a cancer diagnostic, prognostic and treatment efficacy biomarker.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31239716",
"http://www.ncbi.nlm.nih.gov/pubmed/31269584",
"http://www.ncbi.nlm.nih.gov/pubmed/28171565",
"http://www.ncbi.nlm.nih.gov/pubmed/34741346",
"http://www.ncbi.nlm.nih.gov/pubmed/31188482",
"http://www.ncbi.nlm.nih.gov/pubmed/31128030",
"http://www.ncbi.nlm.nih.gov/pubmed/34105151",
"http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"http://www.ncbi.nlm.nih.gov/pubmed/32991297",
"http://www.ncbi.nlm.nih.gov/pubmed/31081143",
"http://www.ncbi.nlm.nih.gov/pubmed/29499931",
"http://www.ncbi.nlm.nih.gov/pubmed/30485513",
"http://www.ncbi.nlm.nih.gov/pubmed/29906749",
"http://www.ncbi.nlm.nih.gov/pubmed/32308105",
"http://www.ncbi.nlm.nih.gov/pubmed/33235461",
"http://www.ncbi.nlm.nih.gov/pubmed/31781497"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Long noncoding RNA Linc00339 promotes triple-negative breast cancer progression through miR-377-3p/HOXC6 signaling pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 122,
"offsetInEndSection": 204,
"text": "Through microarray data, Linc00339 was identified as a candidate oncogenic lncRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31128030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "PURPOSE: To investigate the role and mechanism of long non-coding (lnc) RNA LINC00339 in pancreatic cancer (PANC), and provided a potential target for its biological diagnosis and trea"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29906749",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 417,
"text": " showed that LINC00339 was significantly up-regulated in NSCLC tissue and cells, which indicated the poor prognosis of NSCLC patients. Loss-o"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31239716",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 232,
"text": "(HCC). The lncRNA LINC00339 was reported to regulate the development of lung cancer or breast"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29499931",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 372,
"text": "we demonstrated that LINC00339 was upregulated in glioma tissue as well as in glioma cell lines. The e"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31128030",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "LINC00339 promotes cell proliferation and metastasis in pancreatic cancer via miR-497-5p/IGF1R axis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33235461",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "Introduction: Accumulating evidence has indicated that long noncoding RNAs (lncRNAs) are pivotal regulators involved in the pathogenesis of cancer; however, the molecular mechanism of LINC00339 in colorectal cancer (CRC) remain"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31239716",
"endSection": "abstract",
"offsetInBeginSection": 635,
"offsetInEndSection": 805,
"text": "vasion. Xenograft experiment was used to test tumor growth in vivo. Results: LINC00339 overexpression was correlated with an advanced stage, metastasis, and bad prognosis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28171565",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Endometriosis risk alleles at 1p36.12 act through inverse regulation of CDC42 and LINC00339"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31081143",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "LINC00339 regulates ROCK1 by miR-152 to promote cell proliferation and migration in hepatocellular carcinoma"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Long noncoding RNA Linc00339 promotes triple-negative breast cancer progression through miR-377-3p/HOXC6 signaling pathway"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 208,
"text": "ugh microarray data, Linc00339 was identified as a candidate oncogenic lncRNA. We "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 1063,
"offsetInEndSection": 1249,
"text": " in vivo experiments, Linc00339 overexpression promoted triple-negative breast cancer (TNBC) proliferation, inhibited cell cycle arrest, and suppressed apoptosis. Silencing of Linc00339 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 211,
"offsetInEndSection": 339,
"text": "pared the expression levels of Linc00339 in several breast cancer cell lines and normal mammary gland epithelial cell line. The "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32991297",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 700,
"text": "work identified a 5-lncRNA signature (ENSG00000206567, PCAT29, ENSG00000257989, LOC388282, and LINC00339) from TCGA training studies (n = 1,878). The identifie"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 341,
"offsetInEndSection": 426,
"text": "fects of Linc00339 on tumor progression were examined both in vitro and in vivo. 3-(4"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31269584",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 459,
"text": "LINC00339 expression in colorectal cancer tissues and adjacent colorectal sampleswas detected by Real-time PCR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31781497",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 628,
"text": "Linc00339 was then found to play a critical role in Huaier-mediated cancer suppression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31269584",
"endSection": "abstract",
"offsetInBeginSection": 2169,
"offsetInEndSection": 2306,
"text": "Conclusions: LINC00339 expression is upregulated in colorectal cancer tissues and correlated with patients' clinicopathological features."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31081143",
"endSection": "abstract",
"offsetInBeginSection": 839,
"offsetInEndSection": 937,
"text": "tween miR-152 and ROCK1. The role of LINC00339 in tumor formation and metastasis were explored thr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31128030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 327,
"text": "PURPOSE: To investigate the role and mechanism of long non-coding (lnc) RNA LINC00339 in pancreatic cancer (PANC), and provided a potential target for its biological diagnosis and treatment.METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of LINC00339 in PANC tissue specime"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31188482",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32308105",
"endSection": "abstract",
"offsetInBeginSection": 1486,
"offsetInEndSection": 1689,
"text": "Our findings highlight the importance of the LINC00339-miR-539-SOX9 pathway in gastric cancer pathogenesis and may point to novel targets for the diagnosis, prognosis, and/or treatment of gastric cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31128030",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "LINC00339 promotes cell proliferation and metastasis in pancreatic cancer via miR-497-5p/IGF1R axis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31188482",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 900,
"text": "In conclusion, LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31081143",
"endSection": "abstract",
"offsetInBeginSection": 1276,
"offsetInEndSection": 1514,
"text": "r transfected with miR-152 mimics. LINC00339 exerted oncogenesis effect on HCC progression by targeting miR-152/ROCK1, and the expression of LINC00339 was negatively correlated with miR-152 expression and positively correlated with ROCK1 "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32308105",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Long noncoding RNA LINC00339 promotes the oncogenicity of gastric cancer by regulating SRY-box 9 expression via sponging of microRNA-539."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30485513",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Long noncoding RNA LINC00339 promotes laryngeal squamous cell carcinoma cell proliferation and invasion via sponging miR-145."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 1762,
"offsetInEndSection": 1954,
"text": "In conclusion, our results illuminated that the novel Linc00339/miR-377-3p/HOXC6 axis played a critical role in TNBC progression and might be a promising therapeutic target for TNBC treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 1043,
"offsetInEndSection": 1225,
"text": "Through in vitro and in vivo experiments, Linc00339 overexpression promoted triple-negative breast cancer (TNBC) proliferation, inhibited cell cycle arrest, and suppressed apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 949,
"offsetInEndSection": 1042,
"text": "Linc00339 was increased in breast cancer cell lines compared with the normal epithelial cell."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 1609,
"offsetInEndSection": 1714,
"text": "And miR-377-3p was involved in Linc00339-mediated TNBC proliferation through regulating HOXC6 expression."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33235461",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "The SP1-Induced Long Noncoding RNA, LINC00339, Promotes Tumorigenesis in Colorectal Cancer via the miR-378a-3p/MED19 Axis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30618083",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 334,
"text": "We compared the expression levels of Linc00339 in several breast cancer cell lines and normal mammary gland epithelial cell line."
}
] | 11
|
BioASQ-training11b
| null | null |
623345bf3a8413c6530000ab
| 4,715
|
factoid
|
Which disease is caused by repeat expansion in VWA1?
|
['Recessive hereditary motor neuropathy']
|
[
"Recessive hereditary motor neuropathy",
"Hereditary motor neuropathy type 1A",
"HMN type 1A",
"Recessive hereditary motor neuron disease",
"Recessive hereditary motor neuronopathy"
] |
['An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33559681"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33559681",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33559681",
"endSection": "abstract",
"offsetInBeginSection": 2510,
"offsetInEndSection": 3068,
"text": "In summary, we estimate that biallelic variants in VWA1 may be responsible for up to 1% of unexplained hereditary motor neuropathy cases in Europeans. The detailed clinical characterization provided here will facilitate targeted testing on suitable patient cohorts. This novel disease gene may have previously evaded detection because of high GC content, consequential low coverage and computational difficulties associated with robustly detecting repeat-expansions. Reviewing previously unsolved exomes using lower QC filters may generate further diagnoses."
}
] | 11
|
BioASQ-training11b
| null | null |
61f86c03882a024a10000044
| 4,721
|
factoid
|
Is PPROM a condition that occurs in males or females?
|
['Females']
|
[
"Females",
"Female",
"Woman",
"Women",
"Girl",
"Daughter",
"Lady",
"Gals",
"Feminine"
] |
['Preterm premature rupture of fetal membranes (PPROM) occurs in pregnant females.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22506729",
"http://www.ncbi.nlm.nih.gov/pubmed/23179796",
"http://www.ncbi.nlm.nih.gov/pubmed/29727785",
"http://www.ncbi.nlm.nih.gov/pubmed/30957602",
"http://www.ncbi.nlm.nih.gov/pubmed/23599878",
"http://www.ncbi.nlm.nih.gov/pubmed/10838338",
"http://www.ncbi.nlm.nih.gov/pubmed/31018725",
"http://www.ncbi.nlm.nih.gov/pubmed/24304137",
"http://www.ncbi.nlm.nih.gov/pubmed/15703979",
"http://www.ncbi.nlm.nih.gov/pubmed/18301713",
"http://www.ncbi.nlm.nih.gov/pubmed/31272257",
"http://www.ncbi.nlm.nih.gov/pubmed/21749283",
"http://www.ncbi.nlm.nih.gov/pubmed/31402735",
"http://www.ncbi.nlm.nih.gov/pubmed/15329560",
"http://www.ncbi.nlm.nih.gov/pubmed/31372118",
"http://www.ncbi.nlm.nih.gov/pubmed/16118716",
"http://www.ncbi.nlm.nih.gov/pubmed/24840939",
"http://www.ncbi.nlm.nih.gov/pubmed/29373884",
"http://www.ncbi.nlm.nih.gov/pubmed/24175963",
"http://www.ncbi.nlm.nih.gov/pubmed/23573382",
"http://www.ncbi.nlm.nih.gov/pubmed/22706240"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30957602",
"endSection": "abstract",
"offsetInBeginSection": 104,
"offsetInEndSection": 156,
"text": "preterm premature rupture of fetal membranes (PPROM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31018725",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 301,
"text": "To examine the effect of aspirin, an anti-inflammatory agent, on the prevalence of preterm prelabor rupture of membranes (PPRoMs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31272257",
"endSection": "abstract",
"offsetInBeginSection": 228,
"offsetInEndSection": 276,
"text": " preterm prelabor rupture of membranes (PPROM). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31402735",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 215,
"text": "preterm premature rupture of membranes (PPROM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21749283",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 440,
"text": " focused on TTTS, preterm premature rupture of membranes (PPROM), pregnancy-induced hypertension (PIH), and fetal sex as possible causes of PTB.RE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31372118",
"endSection": "abstract",
"offsetInBeginSection": 910,
"offsetInEndSection": 1397,
"text": "lts: Patients with the pregnancy complicated by OHSS, had a considerably higher rate of preterm labor, whether this was labor before gestation week 37 (56.0% vs. 30.5%) or before gestation week 34 (34.0% vs. 6.8%); significantly lower weight of newborns, as in the newborns with low body weight <2500g (45.6% vs. 25.0%) and specially in the newborn with very low body weight <1500 grams (19.1% vs. 3.8%), as well as preterm premature rupture of membranes (PPROM), (11.76% vs. 1.59%).Conc"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23599878",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "OBJECTIVES: Preterm premature rupture of membranes (PPROM) is defined as a rupture of the amniotic membranes occurring before 37 weeks of gestation and before the onse"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24840939",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Preterm premature rupture of membranes (PPROM) occurs in 1% to 2% of births. Im"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24304137",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Preterm premature rupture of membranes (PPROM) is defined as rupture of membrane that happens before the onset of labor and 37 weeks. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23573382",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "OBJECTIVES: Preterm premature rupture of membranes (PPROM) is defined as the rupture of fetal membranes befor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10838338",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 188,
"text": "Objective: To show that infants delivered prematurely because of preterm premature rupture of the membranes (PPROM) show a tendency for asymmetric intrauterine growth retardation (IUGR). A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18301713",
"endSection": "abstract",
"offsetInBeginSection": 673,
"offsetInEndSection": 746,
"text": "ported among preterm prelabor rupture of membranes (PPROM). Educating the"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15703979",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 936,
"text": "ates with PC were significantly different from controls with regard to male prevalence ( P =0.002), rates of preterm premature rupture of membranes (PPROM) ( P =0.02), longer duration of antibiotic therapy ( P =0.01) and of ventilation ( P =0.02). The di"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22706240",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 162,
"text": "premature rupture of membranes (PPROM) is a common condition in pregnant women and is associated with significant maternal and perinatal morbidity. Mo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22506729",
"endSection": "abstract",
"offsetInBeginSection": 953,
"offsetInEndSection": 1137,
"text": "tory response to lipopolysaccharide (LPS). This heightened response could be a critical pathway in promoting premature rupture of membranes (PPROM) and may be associated with life long"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23599878",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "OBJECTIVES: Preterm premature rupture of membranes (PPROM) is defined as a rupture of the amniotic membranes occurring before 37 weeks of gestation and before the ons"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10838338",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Objective: To show that infants delivered prematurely because of preterm premature rupture of the membranes (PPROM) show a tendency for asymmetric intrauterine growth retardation (IUGR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24175963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 281,
"text": "AIM: To determine whether preterm premature rupture of membranes (PPROM) before 24 weeks is an independent risk factor for poor outcome in preterm neonates.METHODS: A retrospective comparative cohort study was conducted, including viable premature infants born between 25 and 34-we"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23179796",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 383,
"text": "PURPOSE: To assess prevalence and risk factors for posttraumatic stress disorder (PTSD) and depression in fathers after early preeclampsia (PE) or preterm premature rupture of membranes (PPROM).METHODS: Partners of patients hospitalized for PE or PPROM and partners of healthy controls completed PTSD (PSS-SR) and depression (BDI-II) questionnaires during pregnancy (t 1) and 6 weeks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29727785",
"endSection": "abstract",
"offsetInBeginSection": 1712,
"offsetInEndSection": 2081,
"text": "s and iatrogenic preterm delivery. In our high-risk cohort there was no gender difference for preeclampsia (RR 0.93, 95% CI 0.61 to 1.41, p = 0.725) or preterm premature rupture of membranes (PPROM) (RR 1.14, 95% CI 0.86 to 1.50, p = 0.384) CONCLUSIONS: In a high-risk cohort there was no significant increased risk of miscarriage, spontaneous or iatrogenic PTB, preecl"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29373884",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Preterm premature rupture of membranes (PPROM) is a condition leading to an increased risk of maternal and neonatal morbidity and mortality in pregnant women."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15329560",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "UNLABELLED: Preterm premature rupture of membranes (PPROM) occurs in 3% of pregnancies and is responsible for one third of all pre"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16118716",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Preterm premature rupture of the membranes (PPROM) occurs in approximately 3% of all pregnancies, and accounts for one third of all preterm births."
}
] | 11
|
BioASQ-training11b
| null | null |
622a5a7c3a8413c653000090
| 4,723
|
factoid
|
What is the target of Sutimlimab?
|
['C1s']
|
[
"C1s",
"Complement component 1 s",
"C1s protein",
"C1s serine protease"
] |
['Sutimlimab is a novel humanized monoclonal antibody directed against classical pathway complement factor C1s.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29737533",
"http://www.ncbi.nlm.nih.gov/pubmed/30635392",
"http://www.ncbi.nlm.nih.gov/pubmed/33261023",
"http://www.ncbi.nlm.nih.gov/pubmed/33512410",
"http://www.ncbi.nlm.nih.gov/pubmed/34482398",
"http://www.ncbi.nlm.nih.gov/pubmed/31114413",
"http://www.ncbi.nlm.nih.gov/pubmed/30559259",
"http://www.ncbi.nlm.nih.gov/pubmed/32176765",
"http://www.ncbi.nlm.nih.gov/pubmed/31523413",
"http://www.ncbi.nlm.nih.gov/pubmed/31229501",
"http://www.ncbi.nlm.nih.gov/pubmed/33826820"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34482398",
"endSection": "abstract",
"offsetInBeginSection": 805,
"offsetInEndSection": 1018,
"text": "Beyond PNH, complement inhibition has also shown efficacy and safety in cold agglutinin disease (CAD), primarily with the C1s inhibitor of the classical complement pathway, sutimlimab, but also with pegcetacoplan."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33512410",
"endSection": "abstract",
"offsetInBeginSection": 1218,
"offsetInEndSection": 1369,
"text": " The complement C1s inhibitor sutimlimab is an emerging option in the second line and may also find its place in the first line in specific situations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33826820",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 316,
"text": "Sutimlimab, a humanized monoclonal antibody, selectively targets the C1s protein, a C1 complex serine protease responsible for activating this pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32176765",
"endSection": "abstract",
"offsetInBeginSection": 113,
"offsetInEndSection": 223,
"text": "Sutimlimab is a novel humanized monoclonal antibody directed against classical pathway complement factor C1s. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29737533",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 494,
"text": "Therapeutic options for these complement-mediated disorders are limited and sutimlimab, a humanized monoclonal antibody directed against complement factor C1s, may be potentially useful for inhibition of the classical complement pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32176765",
"endSection": "abstract",
"offsetInBeginSection": 113,
"offsetInEndSection": 222,
"text": "Sutimlimab is a novel humanized monoclonal antibody directed against classical pathway complement factor C1s."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33826820",
"endSection": "abstract",
"offsetInBeginSection": 1975,
"offsetInEndSection": 2205,
"text": "SIONS: In patients with cold agglutinin disease who received sutimlimab, selective upstream inhibition of activity in the classic complement pathway rapidly halted hemolysis, increased hemoglobin levels, and reduced fatigue. (Fund"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33512410",
"endSection": "abstract",
"offsetInBeginSection": 1219,
"offsetInEndSection": 1369,
"text": "The complement C1s inhibitor sutimlimab is an emerging option in the second line and may also find its place in the first line in specific situations."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30635392",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "C1s Inhibition by BIVV009 (Sutimlimab) Prevents Complement-Enhanced Activation of Autoimmune Human B Cells In Vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30635392",
"endSection": "abstract",
"offsetInBeginSection": 471,
"offsetInEndSection": 730,
"text": "In this study, we use BIVV009 (Sutimlimab), a clinical stage, humanized mAb that specifically inhibits the CP-specific serine protease C1s to evaluate the impact of upstream CP antagonism on activation and proliferation of normal and autoimmune human B cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31114413",
"endSection": "abstract",
"offsetInBeginSection": 567,
"offsetInEndSection": 790,
"text": "Novel treatment options that target the classical complement pathway are under development and appear very promising, and the C1s inhibitor sutimlimab is currently being investigated in two clinical Phase II and III trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31523413",
"endSection": "abstract",
"offsetInBeginSection": 1087,
"offsetInEndSection": 1323,
"text": "Of these, the anti-C1s monoclonal antibody sutimlimab has shown favorable activity in CAD, while the anti-C3 cyclic peptide pegcetacoplan appears to be promising in PNH as well as CAD, and may also have a therapeutic potential in wAIHA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33826820",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 307,
"text": "t pathway. Sutimlimab, a humanized monoclonal antibody, selectively targets the C1s protein, a C1 complex serine protease responsible for activating this"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31114413",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 802,
"text": "ent options that target the classical complement pathway are under development and appear very promising, and the C1s inhibitor sutimlimab is currently being investigated in two clinical Phase II and III trials. These achie"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29737533",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 499,
"text": "apeutic options for these complement-mediated disorders are limited and sutimlimab, a humanized monoclonal antibody directed against complement factor C1s, may be potentially useful for inhibition of the classical complement pathway. A ph"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30559259",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 312,
"text": "is trial tested the hypothesis that the anti-C1s antibody sutimlimab would ameliorate hemolytic anemia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30635392",
"endSection": "abstract",
"offsetInBeginSection": 477,
"offsetInEndSection": 739,
"text": "s study, we use BIVV009 (Sutimlimab), a clinical stage, humanized mAb that specifically inhibits the CP-specific serine protease C1s to evaluate the impact of upstream CP antagonism on activation and proliferation of normal and autoimmune human B cells. We repor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31229501",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 526,
"text": "In this phase 1 trial, we evaluated the safety and activity of BIVV009 (sutimlimab, previously TNT009), a targeted C1s inhibitor, in 10 subjects with active or past bullous pemphigoid (NCT02502903)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31229501",
"endSection": "abstract",
"offsetInBeginSection": 374,
"offsetInEndSection": 524,
"text": " and activity of BIVV009 (sutimlimab, previously TNT009), a targeted C1s inhibitor, in 10 subjects with active or past bullous pemphigoid (NCT02502903"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29737533",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 479,
"text": "and sutimlimab, a humanized monoclonal antibody directed against complement factor C1s, may be potentially useful for inhibition of the classical comp"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33826820",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 313,
"text": ". Sutimlimab, a humanized monoclonal antibody, selectively targets the C1s protein, a C1 complex serine protease responsible for activating this pathw"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30559259",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 354,
"text": ". This trial tested the hypothesis that the anti-C1s antibody sutimlimab would ameliorate hemolytic anemia. Ten patients with cold agglutinin disease "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33261023",
"endSection": "abstract",
"offsetInBeginSection": 1257,
"offsetInEndSection": 1407,
"text": "cted therapies (ibrutinib, venetoclax, parsaclisib) and inhibitors of complement (sutimlimab, pegcetacoplan), spleen tyrosine kinases (fostamatinib), "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33826820",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 508,
"text": "nt pathway. Sutimlimab, a humanized monoclonal antibody, selectively targets the C1s protein, a C1 complex serine protease responsible for activating this pathway.METHODS: We conducted a 26-week multicenter, open-label, single-group study to assess the efficacy and safety of intravenous sutimlimab in patients with cold agglutinin disease and a recent hi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30559259",
"endSection": "abstract",
"offsetInBeginSection": 206,
"offsetInEndSection": 311,
"text": "This trial tested the hypothesis that the anti-C1s antibody sutimlimab would ameliorate hemolytic anemia."
}
] | 11
|
BioASQ-training11b
| null | null |
61f7cc0c882a024a1000002a
| 4,725
|
factoid
|
How many injections of CLS-TA did the patients participating in the PEACHTREE trial receive?
|
['two', '2']
|
[
"two",
"2"
] |
['The patients participating in the PEACHTREE trial received two suprachoroidal injections of CLS-TA at 0 and 12 weeks.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34322164"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34322164",
"endSection": "abstract",
"offsetInBeginSection": 711,
"offsetInEndSection": 1109,
"text": "Recent results from the PEACHTREE trial (ClinicalTrials.gov Identifier: NCT02595398), a phase III trial with two suprachoroidal injections of CLS-TA at 0 and 12 weeks with follow up lasting 24 weeks, showed the significant improvement in visual acuity and reduction in central subfield thickness, all without increasing the risk of elevated intraocular pressure or accelerated cataract progression."
}
] | 12
|
BioASQ-training12b
| null | null |
64403ab057b1c7a31500004d
| 4,736
|
factoid
|
is prosopagnosia inherited or acquired?
|
['both inherited and acquired']
|
[
"both inherited and acquired",
"inherited",
"acquired",
"hereditary",
"genetic",
"non-genetic"
] |
['Prosopagnosia can be inherited in an autosomal dominant mode of inheritance (congenital prosopagnosia) or acquired following a large unilateral right-hemispheric lesion in frontal (acquired prosopagnosia).', 'There is evidence that prosopagnosia can be inherited in an autosomal dominant mode of inheritance, suggesting that it is a genetic condition.', 'Prosopagnosia can be both inherited and acquired', 'Prosopagnosia can be both inherited (congenital) and acquired. Congenital prosopagnosia is a genetic condition present from birth, while acquired prosopagnosia occurs due to brain damage or injury.', 'Prosopagnosia is an acquired condition, usually caused by brain damage, although there is evidence of a genetic component in some cases.', 'Prosopagnosia can be inherited in an autosomal dominant mode of inheritance.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30389553",
"http://www.ncbi.nlm.nih.gov/pubmed/27115682",
"http://www.ncbi.nlm.nih.gov/pubmed/36202621",
"http://www.ncbi.nlm.nih.gov/pubmed/26933872",
"http://www.ncbi.nlm.nih.gov/pubmed/7091286",
"http://www.ncbi.nlm.nih.gov/pubmed/21366884",
"http://www.ncbi.nlm.nih.gov/pubmed/20689639",
"http://www.ncbi.nlm.nih.gov/pubmed/33392335",
"http://www.ncbi.nlm.nih.gov/pubmed/17981784",
"http://www.ncbi.nlm.nih.gov/pubmed/18523592",
"http://www.ncbi.nlm.nih.gov/pubmed/31740940",
"http://www.ncbi.nlm.nih.gov/pubmed/30947609",
"http://www.ncbi.nlm.nih.gov/pubmed/19334306",
"http://www.ncbi.nlm.nih.gov/pubmed/19823580",
"http://www.ncbi.nlm.nih.gov/pubmed/24389150",
"http://www.ncbi.nlm.nih.gov/pubmed/33832676",
"http://www.ncbi.nlm.nih.gov/pubmed/21414330",
"http://www.ncbi.nlm.nih.gov/pubmed/16767465",
"http://www.ncbi.nlm.nih.gov/pubmed/32648048",
"http://www.ncbi.nlm.nih.gov/pubmed/18374372",
"http://www.ncbi.nlm.nih.gov/pubmed/20657764",
"http://www.ncbi.nlm.nih.gov/pubmed/31231507",
"http://www.ncbi.nlm.nih.gov/pubmed/19429021",
"http://www.ncbi.nlm.nih.gov/pubmed/16817175"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16767465",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Prosopagnosia is the inability to recognize someone by the face alone in the absence of sensory or intellectual impairment. In contrast to the acquired form of prosopagnosia we studied the congenital form"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19429021",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "Congenital prosopagnosia (cPA) is a selective impairment in the visual learning and recognition of faces without detectable brain damage or malformation. There is evidence that it can be inherited in an autosomal dominant mode of inheritance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36202621",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 286,
"text": "Here we report a follow-up examination on M.T., suffering from acquired prosopagnosia following a large unilateral right-hemispheric lesion in frontal, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16767465",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 205,
"text": "In contrast to the acquired form of prosopagnosia we studied the congenital form."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19823580",
"endSection": "abstract",
"offsetInBeginSection": 67,
"offsetInEndSection": 257,
"text": "Acquired prosopagnosia results after brain damage, developmental or congenital prosopagnosia (CP) is not caused by brain lesion, but has presumably been present from early childhood onwards."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33832676",
"endSection": "abstract",
"offsetInBeginSection": 56,
"offsetInEndSection": 216,
"text": "Acquired prosopagnosia is the loss of familiarity for facial identity and has several functional variants, namely apperceptive, amnestic, and associative forms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19334306",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 478,
"text": "A selective deficit in the visual learning and recognition of faces is known as prosopagnosia, which can be found both in acquired and congenital form."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17981784",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Congenital prosopagnosia--a common hereditary cognitive dysfunction in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16767465",
"endSection": "abstract",
"offsetInBeginSection": 921,
"offsetInEndSection": 1029,
"text": "Thus, the face recognition impairment of the hereditary prosopagnosics is reflected in their gaze behaviour."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16767465",
"endSection": "abstract",
"offsetInBeginSection": 684,
"offsetInEndSection": 846,
"text": "Whereas the control participants focused their gaze on the central facial features, the hereditary prosopagnosics showed a significantly different gaze behaviour."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20657764",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "BACKGROUND: Prosopagnosia is a selective deficit in facial identification which can be either acquired, (e.g., after brain damage), or present from birth ("
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31231507",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Prosopagnosia is an impairment in the ability to recognize faces and can be acquired after a brain lesion or occur as a developmental variant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21366884",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Previous studies have shown that acquired prosopagnosia is characterized by impairment at holistic/configural processing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20689639",
"endSection": "abstract",
"offsetInBeginSection": 538,
"offsetInEndSection": 687,
"text": " This served to investigate whether congenital prosopagnosia results from process-specific deficiencies, or whether it is a face-specific impairment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30389553",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Prosopagnosia refers to an acquired or developmental deficit in face recognition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18523592",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "BACKGROUND: Congenital prosopagnosia is a severe face perception impairment which is not acquired by a brain lesion and is presumably present from birth"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7091286",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 225,
"text": "Three patients with prosopagnosia, and acquired inability to recognize familiar faces usually resulting from cerebrovascular insufficiency, had left-sided visual field defects and color vision abnormalities of central origin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16817175",
"endSection": "abstract",
"offsetInBeginSection": 1042,
"offsetInEndSection": 1161,
"text": "The segregation pattern of this hereditary prosopagnosia (HPA) is fully compatible with autosomal dominant inheritance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27115682",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "A Quick guide to developmental prosopagnosia, a condition definied by problems in recognising faces that, in contrast with acquired prosopagnosia, develop in the absence of manifest brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20657764",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "BACKGROUND: Prosopagnosia is a selective deficit in facial identification which can be either acquired, (e.g., after brain damage), or present from birth (congenital)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31740940",
"endSection": "abstract",
"offsetInBeginSection": 506,
"offsetInEndSection": 656,
"text": "ing clinically significant impairments in facial recognition. Cases of acquired prosopagnosia were identified through a systematic literature search a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24389150",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 326,
"text": "Reflecting this, acquired prosopagnosia is not a single entity but a family of disorders with different anatomic lesions and different functional deficits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33392335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "BACKGROUND: Acquired prosopagnosia is a rare condition characterized by the loss of familiarity with previously known faces and the inability to recognize new ones"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26933872",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 930,
"text": "Three key findings emerged: (a) Individuals with more severe prosopagnosia spent less time examining the internal facial region, (b) as observed in acquired prosopagnosia, some DPs spent less time examining the eyes and more time examining the mouth than controls, and (c) SRs spent more time examining the nose-a measure that also correlated with face recognition ability in controls."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32648048",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Acquired prosopagnosia is usually a consequence of bilateral or right hemisphere lesions and is often associated with topographical disorientation and dyschromatopsia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19823580",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Prosopagnosia is a deficit in recognizing people from their faces. Acquired prosopagnosia results after brain damage, developmental or congenital pros"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20689639",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 197,
"text": "Cases of acquired prosopagnosia have often been described over the last century."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18374372",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Acquired prosopagnosia is usually associated with bilateral or right-sided lesions of the occipital or temporal lobes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30947609",
"endSection": "abstract",
"offsetInBeginSection": 640,
"offsetInEndSection": 864,
"text": "Most subjects with developmental prosopagnosia were normal on the Old/New Tests: for acquired prosopagnosia, subjects with occipitotemporal lesions often showed impairments while those with anterior temporal lesions did not."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21414330",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "We studied a male with acquired prosopagnosia using a battery of Implicit Association Tests (IATs) to investigate whether observing faces varying by social category would activate the patient's implicit social biases."
}
] | 12
|
BioASQ-training12b
| null | null |
6411b678201352f04a000036
| 4,739
|
factoid
|
Where are promoters typically found in DNA?
|
['Upstream of the coding region', 'Directly upstream', "5' end of the transcription initiation site"]
|
[
"Upstream of the coding region",
"Directly upstream",
"5' end of the transcription initiation site",
"5' UTR",
"5' untranslated region",
"5' leader sequence",
"5' regulatory region"
] |
["Promoters are typically found in the 5' region of a gene, upstream of the transcription start site. They are DNA sequences that bind transcription factors and RNA polymerase, and are necessary for the initiation of transcription.", "A promoter is a short region of DNA (100-1,000 bp) where transcription of a gene by RNA polymerase begins. It is typically located directly upstream or at the 5' end of the transcription initiation site.", "A promoter is an important regulatory element which marks the region that transcription of a gene by RNA polymerase begins. It is typically located directly upstream or at the 5' end of the transcription initiation site."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34071849",
"http://www.ncbi.nlm.nih.gov/pubmed/19258451",
"http://www.ncbi.nlm.nih.gov/pubmed/30414142",
"http://www.ncbi.nlm.nih.gov/pubmed/15899964",
"http://www.ncbi.nlm.nih.gov/pubmed/36099980",
"http://www.ncbi.nlm.nih.gov/pubmed/33227813",
"http://www.ncbi.nlm.nih.gov/pubmed/25448745",
"http://www.ncbi.nlm.nih.gov/pubmed/24503515",
"http://www.ncbi.nlm.nih.gov/pubmed/31750297"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31750297",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "A promoter is a short region of DNA (100-1,000 bp) where transcription of a gene by RNA polymerase begins. It is typically located directly upstream or at the 5' end of the transcription initiation site. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15899964",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 369,
"text": "Promoters mark the start of every transcript and are an important class of regulatory elements."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33227813",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "A promoter is a region in the DNA sequence that defines where the transcription of a gene by RNA polymerase initiates, which is typically located proximal to the transcription start site (TSS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31750297",
"endSection": "abstract",
"offsetInBeginSection": 107,
"offsetInEndSection": 203,
"text": "It is typically located directly upstream or at the 5' end of the transcription initiation site."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36099980",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "A key step in the transcription of RNA is the binding of the RNA polymerase protein complex to a short promoter sequence that is typically upstream of the gene to be expressed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30414142",
"endSection": "abstract",
"offsetInBeginSection": 834,
"offsetInEndSection": 1023,
"text": "Promoter regions are located within ~2 kb upstream of the transcriptional start site, whereas enhancers may be located at some distance from promoter sequences and exert long-range effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19258451",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 245,
"text": "These sequences are typically located in promoters, which are regions of variable length upstream of the open reading frames of genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25448745",
"endSection": "abstract",
"offsetInBeginSection": 674,
"offsetInEndSection": 857,
"text": "Most of these promoters display the changes of DNA methylation in their Ups-regions, which are between +500 and +2000 bp upstream from the transcription start site (TSS) of the genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34071849",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Promoters are fundamental components of synthetic gene circuits. They are DNA segments where transcription initiation takes place."
}
] | 12
|
BioASQ-training12b
| null | null |
643bc8f957b1c7a31500002b
| 4,740
|
factoid
|
What was the duration of the follow-up period of patients in the PEACHTREE clinical trial?
|
['24 weeks', '6 months']
|
[
"24 weeks",
"6 months",
"half a year",
"six months",
"24 weeks gestation",
"24 weeks of pregnancy"
] |
['The patient follow-up period in the PEACHTREE trial lasted 24 weeks (6 months).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34322164"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34322164",
"endSection": "abstract",
"offsetInBeginSection": 711,
"offsetInEndSection": 1109,
"text": "Recent results from the PEACHTREE trial (ClinicalTrials.gov Identifier: NCT02595398), a phase III trial with two suprachoroidal injections of CLS-TA at 0 and 12 weeks with follow up lasting 24 weeks, showed the significant improvement in visual acuity and reduction in central subfield thickness, all without increasing the risk of elevated intraocular pressure or accelerated cataract progression."
}
] | 12
|
BioASQ-training12b
| null | null |
64403be357b1c7a31500004e
| 4,741
|
factoid
|
What is the mode of delivery of the drug XIPERE?
|
['microneedle-based delivery in the suprachoroidal space']
|
[
"microneedle-based delivery in the suprachoroidal space",
"microneedle delivery in the suprachoroidal space",
"microneedle-assisted delivery in the suprachoroidal space",
"microneedle technology for suprachoroidal delivery",
"suprachoroidal microneedle delivery",
"microneedle-mediated delivery in the suprachoroidal space"
] |
['XIPERE is administered via a microneedle-based device, the SCS Microinjector, in the suprachoroidal space.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35868358"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35868358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 513,
"text": "Drug delivery to the suprachoroidal space (SCS®) has become a clinical reality after the 2021 FDA approval of CLS-TA, a triamcinolone acetonide injectable suspension for suprachoroidal use (XIPERE®), administered via a microneedle-based device, the SCS Microinjector®. Suprachoroidal (SC) delivery facilitates targeting, compartmentalization, and durability of small molecule suspensions, thereby potentially addressing some of the efficacy, safety, and treatment burden limitations of current retinal therapies. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35868358",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Suprachoroidal delivery enables targeting, localization and durability of small molecule suspensions."
}
] | 12
|
BioASQ-training12b
| null | null |
6440396957b1c7a31500004b
| 4,746
|
factoid
|
Where does Brain (or B type) Natriuretic Protein, BNP usually originate from?
|
['heart', 'left atrium', 'right auricle', 'left ventricle']
|
[
"heart",
"left atrium",
"right auricle",
"left ventricle",
"cardiac muscle",
"myocardium",
"atria",
"ventricles",
"cardiac chambers",
"left atrial chamber",
"right atrial chamber",
"left ventricular chamber",
"right ventricular chamber"
] |
['Brain natriuretic peptide (BNP) is a cardiac hormone that is secreted from the heart. It is synthesized in the heart and circulates in the blood.', 'BNP usually originates from the ventricles of the heart.', 'The Brain or B Type Natriuretic Peptide, BNP is usually derived from neurons within the walls of the left atrium and right auricle.', 'Brain (or B type) Natriuretic Protein, BNP is produced mainly by the ventricles of the heart in response to increased wall stress.', 'BNP usually originates from the left ventricle of the heart in response to volume overload.', 'Stretching of cultured cardiomyocytes up-regulates the expression of brain natriuretic peptide (BNP).', 'BNP, or Brain (B-type) Natriuretic Protein, usually originates from the ventricles of the heart.', 'cardiomyocyte stress up-regulates the expression of brain natriuretic peptide (BNP).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/14574050",
"http://www.ncbi.nlm.nih.gov/pubmed/30135320",
"http://www.ncbi.nlm.nih.gov/pubmed/35693619",
"http://www.ncbi.nlm.nih.gov/pubmed/12084525",
"http://www.ncbi.nlm.nih.gov/pubmed/29859763",
"http://www.ncbi.nlm.nih.gov/pubmed/10519161",
"http://www.ncbi.nlm.nih.gov/pubmed/35741432",
"http://www.ncbi.nlm.nih.gov/pubmed/35882940",
"http://www.ncbi.nlm.nih.gov/pubmed/8100590",
"http://www.ncbi.nlm.nih.gov/pubmed/15478621",
"http://www.ncbi.nlm.nih.gov/pubmed/12732268",
"http://www.ncbi.nlm.nih.gov/pubmed/8025996",
"http://www.ncbi.nlm.nih.gov/pubmed/18706401",
"http://www.ncbi.nlm.nih.gov/pubmed/11558673",
"http://www.ncbi.nlm.nih.gov/pubmed/30120963",
"http://www.ncbi.nlm.nih.gov/pubmed/29978892",
"http://www.ncbi.nlm.nih.gov/pubmed/16689366",
"http://www.ncbi.nlm.nih.gov/pubmed/14987573"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35882940",
"endSection": "abstract",
"offsetInBeginSection": 203,
"offsetInEndSection": 365,
"text": "We explored the direct impact of T1AM on cardiomyocytes with a focus on the regulation of the intracellular temperature and natriuretic peptide (NP) expression. A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35693619",
"endSection": "abstract",
"offsetInBeginSection": 1458,
"offsetInEndSection": 1705,
"text": "In hypertrophic cardiomyocytes, after up-regulating the expression of miR-145, the relative messenger ribonucleic acid (mRNA) and protein expressions of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) induced by PE decreased."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12732268",
"endSection": "abstract",
"offsetInBeginSection": 401,
"offsetInEndSection": 579,
"text": "Stretching of cultured cardiomyocytes up-regulates the expression of brain natriuretic peptide (BNP). Intracellular calcium-elevating agents such as the calcium ionophore A23187,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14574050",
"endSection": "abstract",
"offsetInBeginSection": 460,
"offsetInEndSection": 571,
"text": "Atrial natriuretic peptide (ANP) and brain (or B-type) natriuretic peptide (BNP) are of myocardial cell origin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30135320",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Brain (or B-type) natriuretic peptide (BNP) is a cardiac hormone produced in the heart and an established biochemical marker for heart failure (HF) because the level in plasma increases in proportion to disease severity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14574050",
"endSection": "abstract",
"offsetInBeginSection": 572,
"offsetInEndSection": 768,
"text": "BNP is released mainly from the left ventricle in response to volume overload and has become the first biochemical marker for the identification of individuals with congestive heart failure (CHF)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8025996",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "BACKGROUND: B-type or brain natriuretic peptide (BNP) is a novel natriuretic peptide secreted from the heart that forms a peptide family with A-type or atrial natriuretic peptide (ANP), and its plasma level has been shown to be increased in patients with congestive he"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10519161",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 335,
"text": "Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are of myocardial cell origin and C-type natriuretic peptide (CNP) is of endothelial origin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8100590",
"endSection": "abstract",
"offsetInBeginSection": 496,
"offsetInEndSection": 620,
"text": " ANP and BNP are elucidated to be the cardiac hormone mainly secreted from the atrium, and from the ventricle, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14987573",
"endSection": "abstract",
"offsetInBeginSection": 659,
"offsetInEndSection": 830,
"text": " In contrast to atrial natriuretic peptides (ANP/NT-proANP), which originate mainly from atrial tissue, BNP related peptides are produced mainly from ventricular myocytes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29859763",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "Atrial and brain natriuretic peptides: Hormones secreted from the heart."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14574050",
"endSection": "abstract",
"offsetInBeginSection": 459,
"offsetInEndSection": 571,
"text": " Atrial natriuretic peptide (ANP) and brain (or B-type) natriuretic peptide (BNP) are of myocardial cell origin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15478621",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 309,
"text": "Atrial natriuretic peptide (ANP) and brain (or B-type) natriuretic peptide (BNP) are secreted from cardiomyocytes in response to atrial or ventricular wall stretch."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30120963",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 248,
"text": "riuretic peptide (BNP) are primarily produced by, and secreted from, heart tissue. They maintain cardiovascular homeostasis by binding to natriuretic "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14987573",
"endSection": "abstract",
"offsetInBeginSection": 744,
"offsetInEndSection": 894,
"text": "rom atrial tissue, BNP related peptides are produced mainly from ventricular myocytes. Ventricular (NT-pro)BNP production is strongly upregulated in c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29978892",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 271,
"text": ") and brain natriuretic peptide (BNP) are delivered predominantly by the heart. Two C-type natriuretic peptides (CNPs) are paracrine messengers, notab"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11558673",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 439,
"text": "tic and renin-angiotensin systems. Although originally isolated from porcine brain, the BNP gene is expressed in a specific manner in cardiac myocytes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35741432",
"endSection": "abstract",
"offsetInBeginSection": 88,
"offsetInEndSection": 366,
"text": "Unlike other members, i.e., atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which are cardiac hormones secreted from the atrium and ventricle of the heart, respectively, CNP is regarded as an autocrine/paracrine regulator with broad expression in the body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18706401",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 418,
"text": "However, there is an accumulating evidence that B-type natriuretic peptide (BNP) and its N-terminal fragment (NT-proBNP) may originate from right ventricle and their concentrations are elevated in patients with acute pulmonary embolism (APE) especially when resulting in right ventricular dysfunction (RVD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12084525",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "B-type natriuretic peptide (BNP) is a hormone mainly secreted by cardiac ventricle myocytes and which is increased in cardiac diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16689366",
"endSection": "abstract",
"offsetInBeginSection": 191,
"offsetInEndSection": 341,
"text": "vasoconstrictive molecules. The major source of plasma BNP is the cardiac ventricles. Elevated plasma BNP concentrations correlate with increased left"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14574050",
"endSection": "abstract",
"offsetInBeginSection": 484,
"offsetInEndSection": 634,
"text": "de (ANP) and brain (or B-type) natriuretic peptide (BNP) are of myocardial cell origin. BNP is released mainly from the left ventricle in response to "
}
] | 12
|
BioASQ-training12b
| null | null |
6431708a57b1c7a315000017
| 4,749
|
factoid
|
Where in the body would Schlemm's canal be found
|
['eye']
|
[
"eye",
"ocular organ",
"visual organ",
"sight organ",
"eyeball",
"optic organ"
] |
["Schlemm's canal can be found in the anterior chamber of the eye.", "Schlemm's canal is found in the eye.", "Schlemm's canal is in the eye", "Schlemm's canal is found in the eye, specifically in the trabecular meshwork of the anterior chamber of the eye."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28291197",
"http://www.ncbi.nlm.nih.gov/pubmed/25061871",
"http://www.ncbi.nlm.nih.gov/pubmed/1426078",
"http://www.ncbi.nlm.nih.gov/pubmed/25061877",
"http://www.ncbi.nlm.nih.gov/pubmed/729457",
"http://www.ncbi.nlm.nih.gov/pubmed/33488009",
"http://www.ncbi.nlm.nih.gov/pubmed/33613251",
"http://www.ncbi.nlm.nih.gov/pubmed/10581564",
"http://www.ncbi.nlm.nih.gov/pubmed/30242758",
"http://www.ncbi.nlm.nih.gov/pubmed/32672594"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33488009",
"endSection": "abstract",
"offsetInBeginSection": 184,
"offsetInEndSection": 402,
"text": " This retrospective case series included patients with PCG who underwent trabeculotomy using an illuminated microcatheter with the intent of catheterizing the full circumference of Schlemm's canal in a single procedure"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32672594",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 195,
"text": "To study the effect of 3 Schlemm's canal (SC) microinvasive glaucoma surgery (MIGS) devices on outflow facility.DESIGN: Paired comparisons, randomized design, baseline-controlled study.P"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32672594",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Outflow Facility Effects of 3 Schlemm's Canal Microinvasive Glaucoma Surgery Devices."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33613251",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 282,
"text": "Previously, blood reflux from Schlemm's canal (SC) after long-standing glaucoma surgery was reported in eyes treated with excisional LOT"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28291197",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "AIM: to comparatively evaluate the hypotensive effect of minimally invasive (type 1) and basic (type 2) subscleral removing of the external wall of Schlemm's canal with subsequent laser trabeculopuncture in patients with open-angle glaucoma "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30242758",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 397,
"text": "Schlemm's canal (SC) is a large, lymphatic-like vessel in the anterior chamber of the eye, which is essential for aqueous humor drainage required to maintain intraocular pressure and is sensitive to defects in blood and lymphatic vascular signaling pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25061877",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Schlemm's canal (SC) is a specialized vascular structure in the eye that functions to drain aqueous humor from the intraocular chamber into systemic circulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25061871",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Schlemm's canal (SC) is a unique vascular structure that functions to maintain fluid homeostasis by draining aqueous humor from the eye into the systemic circulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1426078",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 409,
"text": "We have tried to answer the question of whether the endothelium of Schlemm's canal is derived from and retains properties of blood vessels by studying: (1) the development of Schlemm's canal in human fetal eyes; (2) the existence of Weibel-Palade bodies in human neonatal, adult human and adult monkey eyes; and (3) the presence of blood coagulation Factor VIII-related antigen in adult human and monkey eyes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1426078",
"endSection": "abstract",
"offsetInBeginSection": 1450,
"offsetInEndSection": 1628,
"text": "Our results indicate that the endothelium of Schlemm's canal is derived from a vascular origin and that even in the adult eye it retains some of the properties of a blood vessel."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1426078",
"endSection": "abstract",
"offsetInBeginSection": 1258,
"offsetInEndSection": 1449,
"text": "(3) Blood coagulation Factor VIII-related antigen was detected in the endothelium of the collector channels and Schlemm's canal, as well as in the blood vessels of the other parts of the eye."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/729457",
"endSection": "abstract",
"offsetInBeginSection": 454,
"offsetInEndSection": 579,
"text": " Injecting fluorescein directly in Schlemm's canal proves that in cadaver eyes without glaucoma the lumen is open all around."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10581564",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Differences in parameters of ciliary body and Schlemm's canal in different meridians of the eyeball has been described using histotopographic methods on 20 eyeballs of human corpses."
}
] | 12
|
BioASQ-training12b
| null | null |
640f8641201352f04a00002c
| 4,754
|
factoid
|
What is the mode of inheritance of Friedreich’s ataxia?
|
['autosomal recessive']
|
[
"autosomal recessive",
"AR",
"autosomal recessive inheritance",
"autosomal recessive disorder",
"autosomal recessive trait"
] |
["Friedreich's Ataxia (FRDA) is an autosomal recessive neurodegenerative disorder."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30065630"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30065630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Friedreich's Ataxia (FRDA) is an autosomal recessive neurodegenerative disorder, affecting dorsal root ganglia (DRG), cerebellar dentate nuclei and heart. "
}
] | 12
|
BioASQ-training12b
| null | null |
644009c557b1c7a315000041
| 4,756
|
factoid
|
In prokaryotes, functionally related genes are sometimes positioned adjacent to each other in the genome and can be under the control of the same regulatory machinery. What are these called?
|
['Operons']
|
[
"Operons",
"Operon",
"Gene cluster",
"Transcriptional unit",
"Regulatory unit"
] |
['In prokaryotes, functionally related genes are often organized into operons. Operons are clusters of adjacent genes that are transcribed together under the control of a single promoter, allowing for coordinated gene expression and efficient co-translation of proteins involved in the same cellular pathway. This organization is a fundamental element of how genetic information is arranged in prokaryotes and ensures that coregulated gene expression occurs through co-transcription. The arrangement of functionally-related genes in operons provides spatiotemporal control over cellular processes, contributing to the overall regulation and efficiency of prokaryotic gene expression.', 'In prokaryotes, functionally related genes that are positioned adjacent to each other in the genome and under the control of the same regulatory machinery are called operons. Operons are a unique feature of prokaryotic gene organization, allowing for coordinated expression of multiple genes involved in a specific metabolic pathway or cellular process. An operon typically consists of a promoter region, an operator site, and a cluster of functionally related genes. The promoter region is where RNA polymerase binds to initiate transcription, while the operator site serves as a binding location for regulatory proteins called repressors or activators. These regulatory proteins modulate gene expression by either inhibiting or promoting transcription based on environmental conditions or cellular needs. One well-known example of an operon is the lac operon in Escherichia coli, which regulates lactose metabolism in response to glucose availability. Overall, operons provide an efficient mechanism for prokaryotes to regulate gene expression and adapt to changing environments.', 'In prokaryotes, functionally related genes are often arranged in operons, which are polycistronic messages transcribed from a single promoter. This organization allows for coordinated gene expression and efficient cotranslation of proteins involved in the same pathway. Operons can be regulated by the same regulatory machinery, ensuring that all genes within an operon are coregulated. The clustering of functionally related genes in operons is a fundamental element of how genetic information is organized in prokaryotes and plays a crucial role in their ability to adapt to changing environments. Overall, operons provide a mechanism for spatiotemporal control of cellular processes and allow prokaryotes to efficiently coordinate gene expression.', 'Prokaryotes often have functionally-related genes joined together under the direction of a single promoter. These structures are called operons. Clustering of functionally-related genes in operons allows for coordinated gene expression and spatiotemporal control of cellular processes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18269733",
"http://www.ncbi.nlm.nih.gov/pubmed/30635413",
"http://www.ncbi.nlm.nih.gov/pubmed/17671982",
"http://www.ncbi.nlm.nih.gov/pubmed/35934590",
"http://www.ncbi.nlm.nih.gov/pubmed/12220896",
"http://www.ncbi.nlm.nih.gov/pubmed/15487932",
"http://www.ncbi.nlm.nih.gov/pubmed/21690561",
"http://www.ncbi.nlm.nih.gov/pubmed/24012761",
"http://www.ncbi.nlm.nih.gov/pubmed/32209657",
"http://www.ncbi.nlm.nih.gov/pubmed/26543854",
"http://www.ncbi.nlm.nih.gov/pubmed/16755590",
"http://www.ncbi.nlm.nih.gov/pubmed/33483546"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35934590",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 336,
"text": "Coordinated gene expression allows spatiotemporal control of cellular processes and is achieved by the cotranscription/translation of functionally related genes/proteins. Prokaryotes evolved polycistronic messages (operons) to confer expression from a single promoter to efficiently cotranslate proteins functioning on the same pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32209657",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "The arrangement of functionally-related genes in operons is a fundamental element of how genetic information is organized in prokaryotes. This organization ensures coordinated gene expression by co-transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24012761",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Clustering of functionally related genes in operons allows for coregulated gene expression in prokaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16755590",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Operons are clusters of genes that are transcribed as a single message, and regulated by the same gene expression machinery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21690561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Bacterial genes are commonly encoded in clusters, known as operons, which share transcriptional regulatory control and often encode functionally related proteins that take part in certain biological pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15487932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "In prokaryotic genomes, related genes are frequently clustered in operons and higher-order arrangements that reflect functional context."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17671982",
"endSection": "abstract",
"offsetInBeginSection": 956,
"offsetInEndSection": 1213,
"text": " Genes in operons are located next to each other in the same DNA strand, and thus their presence should result in a higher proportion of predicted functional interactions among adjacent genes in the same strand than among adjacent genes in opposite strands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12220896",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Genes that are part of the same operon in prokaryotes, or have the same expression pattern in eukaryotes, are transcriptionally co-regulated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17671982",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 956,
"text": "The presence of operons (polycistronic transcription units formed of functionally related genes) in prokaryotic genomes offers such an alternative."
}
] | 12
|
BioASQ-training12b
| null | null |
64371a4257b1c7a315000029
| 4,760
|
factoid
|
What is the active ingredient of Xipere?
|
['triamcinolone acetonide']
|
[
"triamcinolone acetonide",
"triamcinolone",
"Kenalog",
"Aristocort",
"Nasacort",
"Trianex",
"Triderm"
] |
['The active ingredient of Xipere is triamcinolone acetonide.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35868358"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35868358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Drug delivery to the suprachoroidal space (SCS®) has become a clinical reality after the 2021 FDA approval of CLS-TA, a triamcinolone acetonide injectable suspension for suprachoroidal use (XIPERE®), administered via a microneedle-based device, the SCS Microinjector®. "
}
] | 12
|
BioASQ-training12b
| null | null |
6440377c57b1c7a315000049
| 4,761
|
factoid
|
What is the most commonly used pain scale for the measurement of pain in children?
|
['FLACC', 'Face, leg, activity, cry, and consolability', 'COMFORT Behavioural scale', 'Faces Pain Scale - Revised', 'FPS-R', 'FLACC-r']
|
[
"FLACC",
"Face, leg, activity, cry, and consolability",
"COMFORT Behavioural scale",
"Faces Pain Scale - Revised",
"FPS-R",
"FLACC-r",
"FLACC Scale",
"FLACC Pain Scale",
"FLACC Pain Assessment Tool"
] |
['The most pain scale used to measure pain in children is FLACC (Face, leg, activity, cry, and consolability) score.', 'The most commonly used pain scale for the measurement of pain in children is the Face, Legs, Activity, Cry, and Consolability (FLACC) scale.', 'The most commonly used pain scale for measuring pain in children is the Faces, Legs, Activity, Cry, Consolability (FLACC) scale.', 'The most commonly used pain scale for the measurement of pain in children is the Faces Pain Scale-Revised (FPS-R).', 'Face, leg, activity, cry, and consolability (FLACC) pain scale is used for postoperative pain assessment in children.', 'The most commonly used pain scale for the measurement of pain in children is the Face, Legs, Activity, Cry, and Consolability (FLACC) scale. This scale is reported to be used by 54% of pediatric intensive care units (PICUs) for daily assessment and documentation of pain.', 'The Faces Pain Scale (FPS) is one of the most commonly used scales for measuring pain in children.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33904220",
"http://www.ncbi.nlm.nih.gov/pubmed/35361254",
"http://www.ncbi.nlm.nih.gov/pubmed/35628840",
"http://www.ncbi.nlm.nih.gov/pubmed/34599744",
"http://www.ncbi.nlm.nih.gov/pubmed/35626783"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35626783",
"endSection": "abstract",
"offsetInBeginSection": 634,
"offsetInEndSection": 736,
"text": " Face, leg, activity, cry, and consolability (FLACC) scores for postoperative pain were also assessed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33904220",
"endSection": "abstract",
"offsetInBeginSection": 994,
"offsetInEndSection": 1051,
"text": "The FLACC and COMFORT scales were utilized to assess pain"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35628840",
"endSection": "abstract",
"offsetInBeginSection": 683,
"offsetInEndSection": 862,
"text": "Postoperative pain was assessed using the Visual Analogue Scale (VAS), the Wong-Baker Faces Pain Rating Scale, and the Face, Legs, Activity, Cry, and Consolability (FLACC) scale. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34599744",
"endSection": "abstract",
"offsetInBeginSection": 656,
"offsetInEndSection": 791,
"text": "The pain experience (intense, moderate, or mild) was evaluated by the Face, Legs, Activity, Cry, Consolability-revised scale (FLACC-r)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35361254",
"endSection": "abstract",
"offsetInBeginSection": 1301,
"offsetInEndSection": 1508,
"text": " Daily assessment and documentation for pain (81%) and sedation (87%) was reported by most of the PICUs, using the preferred validated FLACC scale (54%) and the COMFORT Behavioural scale (48%), respectively."
}
] | 12
|
BioASQ-training12b
| null | null |
6441057657b1c7a315000052
| 4,767
|
factoid
|
What is DILI-CAT used for?
|
['Drug induced hepatotoxicity scoring algorithm']
|
[
"Drug induced hepatotoxicity scoring algorithm",
"DILI scoring algorithm",
"Drug-induced liver injury scoring algorithm",
"Drug-induced hepatotoxicity assessment tool",
"Drug-induced liver injury assessment algorithm"
] |
["DILI-CAT, ia a clinically intuitive, data-driven, computer-assisted scoring algorithm and is a useful tool for early detection of drug's hepatotoxicity in clinical drug development.", "DILI-CAT, a novel phenotype-based drug-induced liver injury causality assessment tool, is a useful tool for early detection of drug's hepatotoxicity in clinical drug development.", "DILI-CAT, a clinically intuitive, data-driven, computer-assisted scoring algorithm, is a useful tool for early detection of drug's hepatotoxicity in clinical drug development.", "DILI-CAT is a clinically intuitive, data-driven, computer-assisted scoring algorithm used for early detection of drug's hepatotoxicity in clinical drug development. It is a novel phenotype-based drug-induced liver injury causality assessment tool that allows for signal confirmation in early drug development.", 'We utilised a novel DILI causality assessment tool (DILICAT) which uses drugspecific liver injury phenotypes to examine potential DILI in early phase ximelagatran clinical development.A novel p', 'DILI-CAT is a web-based tool used to assess the risk of drug-induced liver injury (DILI) in clinical trials. It uses a combination of clinical and laboratory parameters to predict the risk of DILI.', 'The DILI-CAT is a novel computer-assisted drug induced liver injury causality assessment tool designed to help differentiate drugs causing severe liver injuries from those causing mild or moderate liver damage.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36174069",
"http://www.ncbi.nlm.nih.gov/pubmed/35266155"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35266155",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 327,
"text": "We utilised a novel DILI causality assessment tool (DILI-CAT), which uses drug-specific liver injury phenotypes, to examine potential DILI in early phase ximelagatran clinical development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35266155",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "A novel phenotype-based drug-induced liver injury causality assessment tool (DILI-CAT) allows for signal confirmation in early drug development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35266155",
"endSection": "abstract",
"offsetInBeginSection": 1633,
"offsetInEndSection": 1808,
"text": "DILI-CAT, a clinically intuitive, data-driven, computer-assisted scoring algorithm, is a useful tool for early detection of drug's hepatotoxicity in clinical drug development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36174069",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "A novel quantitative computer-assisted drug-induced liver injury causality assessment tool (DILI-CAT)."
}
] | 12
|
BioASQ-training12b
| null | null |
64257c9c690f196b5100004b
| 4,769
|
factoid
|
What process involves metabolite-sensing mRNAs to control gene expression?
|
['Riboswitching', 'Riboswitch', 'Riboswitches']
|
[
"Riboswitching",
"Riboswitch",
"Riboswitches",
"Riboswitch RNA",
"Riboswitch element",
"Riboswitch motif"
] |
["The process involving metabolite-sensing mRNAs to control gene expression is known as riboswitch regulation. Riboswitches are structured RNA elements typically found in the 5' untranslated regions (UTRs) of mRNAs that can directly bind to small metabolites or ions. Upon binding, they undergo conformational changes that modulate gene expression by affecting transcription, translation, or mRNA stability. This mechanism allows cells to rapidly respond to fluctuations in the levels of specific metabolites, ensuring appropriate metabolic adaptation and homeostasis. Riboswitches have been identified in bacteria, archaea, and eukaryotes, with diverse ligands including purines, amino acids, coenzymes, and metal ions. They serve as an efficient means for cells to sense and regulate their internal environment without relying on protein factors such as transcription factors or regulatory enzymes.", 'Metabolite-sensing mRNAs are involved in a process known as riboswitch-mediated gene regulation. Riboswitches are RNA elements that can bind small molecules, such as metabolites, and change their conformation to regulate gene expression. Metabolite-sensing mRNAs contain riboswitches in their untranslated regions (UTRs), which allow them to sense changes in intracellular metabolite concentrations and modulate the translation or stability of the mRNA. This mechanism is particularly important for regulating metabolic pathways, where the availability of specific metabolites can affect the expression of genes involved in those pathways. For example, in bacteria, riboswitches have been identified that control the expression of genes involved in amino acid biosynthesis, vitamin biosynthesis, and sugar metabolism. The discovery of riboswitches has opened up new avenues for understanding how cells respond to changes in their environment and has potential applications for developing novel antibiotics and other therapeutics that target these regulatory elements.', 'Riboswitches are metabolite-sensing gene-control elements that are typically located in non-coding portions of mRNAs, where they selectively bind their target compound and subsequently modulate gene expression. In eukaryotes, a well-characterized riboswitch senses the vitamin B1 derivative TPP (thiamine pyro-phosphate).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22219369",
"http://www.ncbi.nlm.nih.gov/pubmed/36275359",
"http://www.ncbi.nlm.nih.gov/pubmed/17468745",
"http://www.ncbi.nlm.nih.gov/pubmed/15610857",
"http://www.ncbi.nlm.nih.gov/pubmed/32036061",
"http://www.ncbi.nlm.nih.gov/pubmed/24769284",
"http://www.ncbi.nlm.nih.gov/pubmed/12756322",
"http://www.ncbi.nlm.nih.gov/pubmed/19303767",
"http://www.ncbi.nlm.nih.gov/pubmed/12787499",
"http://www.ncbi.nlm.nih.gov/pubmed/25708284",
"http://www.ncbi.nlm.nih.gov/pubmed/15919195",
"http://www.ncbi.nlm.nih.gov/pubmed/27607554",
"http://www.ncbi.nlm.nih.gov/pubmed/16153177",
"http://www.ncbi.nlm.nih.gov/pubmed/20009507",
"http://www.ncbi.nlm.nih.gov/pubmed/19595806",
"http://www.ncbi.nlm.nih.gov/pubmed/17163768",
"http://www.ncbi.nlm.nih.gov/pubmed/23169642",
"http://www.ncbi.nlm.nih.gov/pubmed/19101979",
"http://www.ncbi.nlm.nih.gov/pubmed/17997835",
"http://www.ncbi.nlm.nih.gov/pubmed/20943759",
"http://www.ncbi.nlm.nih.gov/pubmed/18072940",
"http://www.ncbi.nlm.nih.gov/pubmed/16728979",
"http://www.ncbi.nlm.nih.gov/pubmed/24583553",
"http://www.ncbi.nlm.nih.gov/pubmed/17993623",
"http://www.ncbi.nlm.nih.gov/pubmed/12820954",
"http://www.ncbi.nlm.nih.gov/pubmed/36227561",
"http://www.ncbi.nlm.nih.gov/pubmed/34488573",
"http://www.ncbi.nlm.nih.gov/pubmed/27432066",
"http://www.ncbi.nlm.nih.gov/pubmed/14593443",
"http://www.ncbi.nlm.nih.gov/pubmed/20061809",
"http://www.ncbi.nlm.nih.gov/pubmed/26227035",
"http://www.ncbi.nlm.nih.gov/pubmed/26143008",
"http://www.ncbi.nlm.nih.gov/pubmed/34086280",
"http://www.ncbi.nlm.nih.gov/pubmed/18006684",
"http://www.ncbi.nlm.nih.gov/pubmed/31741723"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12756322",
"endSection": "abstract",
"offsetInBeginSection": 562,
"offsetInEndSection": 756,
"text": "These results suggest that metabolite-binding mRNAs are possibly involved in eukaryotic gene regulation and that some riboswitches might be representatives of an ancient form of genetic control."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12756322",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 399,
"text": "Genetic control by metabolite-binding mRNAs is widespread in prokaryotes. These riboswitches are typically located in noncoding regions of mRNA, where they selectively bind their target compound and subsequently modulate gene expression. We have identified mRNA elements in fungi and in plants that match the consensus sequence and structure of thiamine pyrophosphate-binding domains of prokaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15610857",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 311,
"text": "Metabolite-sensing mRNAs, or \"riboswitches,\" specifically interact with small ligands and direct expression of the genes involved in their metabolism. Riboswitches contain sensing \"aptamer\" modules, capable of ligand-induced structural changes, and downstream regions, harboring expression-controlling elements."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36227561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 291,
"text": "Riboswitches are a class of RNA motifs in the untranslated regions of bacterial messenger RNAs (mRNAs) that can adopt different conformations to regulate gene expression. The binding of specific small molecule or ion ligands, or other RNAs, influences the conformation the riboswitch adopts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15610857",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Metabolite-sensing mRNAs, or \"riboswitches,\" specifically interact with small ligands and direct expression of the genes involved in their metabolism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17468745",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Bacteria make extensive use of riboswitches to sense metabolites and control gene expression, and typically do so by modulating premature transcription termination or translation initiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36275359",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 384,
"text": "Riboswitches possess a metabolite-sensing system that controls gene regulation in a cis-acting fashion at the initiation of transcriptional/translational level by binding with a specific metabolite and controlling various biochemical pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15610857",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 311,
"text": "Riboswitches contain sensing \"aptamer\" modules, capable of ligand-induced structural changes, and downstream regions, harboring expression-controlling elements."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19303767",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Regulatory mRNA elements or riboswitches specifically control the expression of a large number of genes in response to various cellular metabolites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20009507",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "The discovery of metabolite-sensing RNA domains with gene regulatory functions, so-called riboswitches, has greatly expanded our view of the structural and functional complexity of RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16728979",
"endSection": "abstract",
"offsetInBeginSection": 435,
"offsetInEndSection": 760,
"text": "Organisms from all three domains of life, including bacteria, plants and fungi, use TPP-sensing riboswitches to control genes responsible for importing or synthesizing thiamine and its phosphorylated derivatives, making this riboswitch class the most widely distributed member of the metabolite-sensing RNA regulatory system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16728979",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Riboswitches are metabolite-sensing RNAs, typically located in the non-coding portions of messenger RNAs, that control the synthesis of metabolite-related proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18072940",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Structured mRNA elements called riboswitches control gene expression by binding to small metabolites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22219369",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Riboswitches are motifs in the untranslated regions (UTRs) of RNA transcripts that sense metabolite levels and modulate the expression of the corresponding genes for metabolite import, export, synthesis, or degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31741723",
"endSection": "abstract",
"offsetInBeginSection": 998,
"offsetInEndSection": 1221,
"text": " The discovery of a riboswitch in eukaryotes that is composed of a single class of thiamine pyrophosphate (TPP) suggests that additional ligand-sensing RNAs may be present to control eukaryotic or mammalian gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19101979",
"endSection": "abstract",
"offsetInBeginSection": 379,
"offsetInEndSection": 604,
"text": " Newly discovered metabolite-sensing riboswitches have revealed that cellular processes extensively make use of RNA structural modulation to regulate gene expression in response to subtle changes in metabolite concentrations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12756322",
"endSection": "abstract",
"offsetInBeginSection": 74,
"offsetInEndSection": 237,
"text": "These riboswitches are typically located in noncoding regions of mRNA, where they selectively bind their target compound and subsequently modulate gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23169642",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Riboswitches are mRNA regulatory elements that control gene expression by altering their structure in response to specific metabolite binding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20061809",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 225,
"text": "Riboswitches are gene control elements typically located in the 5' untranslated regions of bacterial mRNAs where they modulate the expression of associated genes in response to elevated concentrations of cellular metabolites."
}
] | 12
|
BioASQ-training12b
| null | null |
6429e85e57b1c7a315000009
| 4,775
|
factoid
|
Which year was XIPERE approved by the FDA?
|
['2021']
|
[
"2021",
"twenty twenty-one",
"two thousand twenty-one"
] |
['XIPERE was approved by the FDA in 2021.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35868358"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35868358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Drug delivery to the suprachoroidal space (SCS®) has become a clinical reality after the 2021 FDA approval of CLS-TA, a triamcinolone acetonide injectable suspension for suprachoroidal use (XIPERE®), administered via a microneedle-based device, the SCS Microinjector®. "
}
] | 12
|
BioASQ-training12b
| null | null |
6440393157b1c7a31500004a
| 4,781
|
factoid
|
What color light does the the inhibitory receptor halorhodopsin (eNpHR) respond to?
|
['yellow']
|
[
"yellow",
"amber",
"golden",
"canary",
"lemon",
"butter",
"dandelion",
"sunshine",
"mustard",
"banana"
] |
['The inhibitory receptor halorhodopsin (eNpHR) responds to yellow light.', 'Halorhodopsin (eNpHR) is an inhibitory receptor that responds to yellow-green light (wavelength of 590 nm).', 'Halorhodopsin responds to yellow light.', 'The eNpHR is sensitive to yellow light.', 'eNpHR responds to yellow light.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"http://www.ncbi.nlm.nih.gov/pubmed/23366158",
"http://www.ncbi.nlm.nih.gov/pubmed/22815873",
"http://www.ncbi.nlm.nih.gov/pubmed/27905012",
"http://www.ncbi.nlm.nih.gov/pubmed/23637949",
"http://www.ncbi.nlm.nih.gov/pubmed/17375185",
"http://www.ncbi.nlm.nih.gov/pubmed/28650460"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17375185",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 842,
"text": "Here we report that targeting the codon-optimized form of the light-driven chloride pump halorhodopsin from the archaebacterium Natronomas pharaonis (hereafter abbreviated Halo) to genetically-specified neurons enables them to be silenced reliably, and reversibly, by millisecond-timescale pulses of yellow light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28650460",
"endSection": "abstract",
"offsetInBeginSection": 661,
"offsetInEndSection": 891,
"text": "By using Cal-Light to drive expression of the inhibitory receptor halorhodopsin (eNpHR), which responds to yellow light, we temporarily inhibit the lever-pressing behavior, confirming that the labeled neurons mediate the behavior."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"endSection": "abstract",
"offsetInBeginSection": 465,
"offsetInEndSection": 723,
"text": "We introduced enhanced halorhodopsin (eNpHR), a yellow light-sensitive, membrane-targeting chloride pump, into mouse retinal ganglion cells (RGCs) by intravitreously injecting an adeno-associated virus serotype-2 vector carrying the CMV-eNpHR-EYFP construct."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23637949",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 912,
"text": "Hippocampal pyramidal neurons were transduced in vivo with a virus carrying an enhanced halorhodopsin (eNpHR), a yellow light activated chloride pump, and acute seizure progression was then monitored behaviorally and electrophysiologically in the presence and absence of illumination delivered via an optical fiber."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27905012",
"endSection": "abstract",
"offsetInBeginSection": 1223,
"offsetInEndSection": 1360,
"text": "Similarly, archaeon Natronomonas pharaonis (NpHR) expresses a monovalent Cl- channel protein halorhodopsin that responds to yellow light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23366158",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 380,
"text": "Towards achieving this goal, light-activated channelrhodopsin-2 (ChR2), a cation channel activated with 480 nm light, and a first generation halorhodopsin (NpHR1.0), an anion pump activated by 580 nm light, have been introduced into hiPSC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22815873",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 645,
"text": "In analogy, other excitable cells can be inhibited by expressing Halorhodopsin from Natronomonas pharaonis (NpHR) and subsequent illumination with yellow light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23366158",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 303,
"text": " Towards achieving this goal, light-activated channelrhodopsin-2 (ChR2), a cation channel activated with 480 nm light, and a first generation halorhodopsin (NpHR1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"endSection": "abstract",
"offsetInBeginSection": 441,
"offsetInEndSection": 591,
"text": " retino-tectal pathway. We introduced enhanced halorhodopsin (eNpHR), a yellow light-sensitive, membrane-targeting chloride pump, into mouse retinal g"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"endSection": "abstract",
"offsetInBeginSection": 724,
"offsetInEndSection": 1042,
"text": "Several weeks after the injection, whole-cell recordings made from sSC neurons in slice preparations revealed that yellow laser illumination of the eNpHR-expressing retino-tectal axons, putatively synapsing onto the recorded cells, effectively inhibited EPSCs evoked by electrical stimulation of the optic nerve layer."
}
] | 12
|
BioASQ-training12b
| null | null |
6415b3b4690f196b51000009
| 4,784
|
factoid
|
What regulatory element promotes RNA polymerase II binding as well as the binding of factors that facilitate the unwinding of DNA prior to translation?
|
['TATA box']
|
[
"TATA box",
"TATA element",
"TATA promoter",
"TATA sequence",
"TATA region"
] |
['Found in about 24% of human gene promoters, the TATA box is a critical regulatory element that is mostly found in genes transcribed by RNA polymerase II, and as such, recruits this enzyme to the promoter. Additionally, the TATA-binding protein aids in unwinding DNA.', 'The TATA box is a critical regulatory element found in many promoters transcribed by RNA polymerase II. Located 25-30 nucleotides upstream of the transcription initiation site, it promotes RNA polymerase II binding and facilitates the unwinding of DNA prior to translation. The TATA-binding protein (TBP), a major component of the human TFIID multiprotein complex, plays an essential role in directing the initiation of RNA transcription at a site immediately downstream of the TATA sequence. Approximately 24% of human genes have a TATA-like element with AT-rich promoters, but only around 10% contain the canonical TATA box (TATAWAWR).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/8502653",
"http://www.ncbi.nlm.nih.gov/pubmed/16522199",
"http://www.ncbi.nlm.nih.gov/pubmed/23801666",
"http://www.ncbi.nlm.nih.gov/pubmed/2197561",
"http://www.ncbi.nlm.nih.gov/pubmed/9618449",
"http://www.ncbi.nlm.nih.gov/pubmed/1736286",
"http://www.ncbi.nlm.nih.gov/pubmed/1409643",
"http://www.ncbi.nlm.nih.gov/pubmed/17123746",
"http://www.ncbi.nlm.nih.gov/pubmed/8507207",
"http://www.ncbi.nlm.nih.gov/pubmed/7729424",
"http://www.ncbi.nlm.nih.gov/pubmed/9383448"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1409643",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "A critical regulatory element in many promoters transcribed by RNA polymerase II is the \"TATA\" box, which is located 25-30 nucleotides upstream of the transcription initiation site."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17123746",
"endSection": "abstract",
"offsetInBeginSection": 722,
"offsetInEndSection": 921,
"text": "About 24% of human genes have a TATA-like element and their promoters are generally AT-rich; however, only approximately 10% of these TATA-containing promoters have the canonical TATA box (TATAWAWR)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9383448",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "TBP binding to the TATA box induces a specific downstream unwinding site that is targeted by pluramycin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9383448",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 281,
"text": "The TATA-binding protein (TBP) is one of the major components of the human TFIID multiprotein complex. It is important in directing the initiation of RNA transcription at a site immediately downstream of the TATA sequence (TATA box) found in many eukaryotic promoters. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1736286",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "The TATA box-binding factor TFIID plays a primary role in the process of transcription initiation by RNA polymerase II and its regulation by various gene-specific factors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16522199",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 211,
"text": "The canonical core promoter elements consist of the TATA box, initiator (Inr), downstream core promoter element (DPE), TFIIB recognition element (BRE) and the newly-discovered motif 10 element (MTE)."
}
] | 12
|
BioASQ-training12b
| null | null |
6429fad757b1c7a31500000e
| 4,785
|
factoid
|
How many patients with Friedreich's ataxia were included in each cohort of the phase I/II double-blind, comparator-controlled trial of RT001.
|
['Nine per cohort', '9/cohort', '18 in total']
|
[
"Nine per cohort",
"9/cohort",
"18 in total"
] |
["Each cohort of the phase I/II double-blind, comparator-controlled trial of RT001 involved 9 Friedreich's ataxia patients. In total nineteen patients enrolled in the trial, and 18 completed all safety and efficacy measurements."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29624723"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 498,
"text": "We conducted a phase I/II double-blind, comparator-controlled trial with 2 doses of RT001 in Friedreich's ataxia patients (9 subjects each cohort)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "abstract",
"offsetInBeginSection": 825,
"offsetInEndSection": 920,
"text": "Nineteen patients enrolled in the trial, and 18 completed all safety and efficacy measurements."
}
] | 12
|
BioASQ-training12b
| null | null |
64402e7757b1c7a315000044
| 4,786
|
factoid
|
What is the incidence of Facioscapulohumeral Muscular Dystrophy?
|
['1:8000 to 1:20000']
|
[
"1:8000 to 1:20000",
"1:8000-1:20000",
"1:8000-20000",
"1:8000 to 20000",
"1:8000 - 1:20000"
] |
['Facioscapulohumeral Muscular Dystrophy has and incidence of 1:8000 to 1:20000.', 'The incidence of Facioscapulohumeral Muscular Dystrophy (FSHD) is approximately 1 in 8000 individuals.', 'The incidence of Facioscapulohumeral Muscular Dystrophy is approximately 1 in 8,000.', 'The incidence of Facioscapulohumeral Muscular Dystrophy is approximately 1 in 8000 people.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34315378",
"http://www.ncbi.nlm.nih.gov/pubmed/21496633"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34315378",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Facioscapulohumeral Muscular Dystrophy (FSHD) is in the top three list of all dystrophies with an approximate 1:8000 incidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21496633",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 322,
"text": "It is present worldwide, with a prevalence of around 4 per 100000 and an incidence of about 1 in 20000. Overall lifespan is not affected significantly."
}
] | 12
|
BioASQ-training12b
| null | null |
64425ce357b1c7a315000059
| 4,787
|
factoid
|
Risdiplam is used for treatment of which disease?
|
['spinal muscular atrophy']
|
[
"spinal muscular atrophy",
"SMA",
"spinal muscular atrophy type 1",
"spinal muscular atrophy type 2",
"spinal muscular atrophy type 3",
"spinal muscular atrophy type 4",
"Werdnig-Hoffmann disease",
"Kugelberg-Welander disease"
] |
['Risdiplam is approved for treatment of spinal muscular atrophy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34620695",
"http://www.ncbi.nlm.nih.gov/pubmed/35614235",
"http://www.ncbi.nlm.nih.gov/pubmed/35567422"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34620695",
"endSection": "abstract",
"offsetInBeginSection": 513,
"offsetInEndSection": 781,
"text": "Risdiplam (Evrysdi)-an orally bioavailable, small molecule approved by the US Food and Drug Administration and more recently by the European Medicines Agency for the treatment of patients ≥2 months of age with spinal muscular atrophy-is presented here as a case study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35567422",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "An expanded access program of risdiplam for patients with Type 1 or 2 spinal muscular atrophy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35567422",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "OBJECTIVE: The US risdiplam expanded access program (EAP; NCT04256265) was opened to provide individuals with Type 1 or 2 spinal muscular atrophy (SMA) who had no satisfactory treatment options access to risdiplam prior to commercial availability. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35614235",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 560,
"text": "SMN1 produces SMN, a ubiquitously expressed protein, that is essential for the development and survival of motor neurons. Major advances and developments in SMA therapeutics are shifting the natural history of the disease. With three relatively new available therapies, nusinersen (Spinraza), onasemnogene abeparvovec (Zolgensma), and risdiplam (Evrysdi), patients survive longer and have improved outcomes. "
}
] | 12
|
BioASQ-training12b
| null | null |
63f581e933942b094c000007
| 4,788
|
factoid
|
What gene is mutated in Friedreich's ataxia?
|
['frataxin', 'FRDA']
|
[
"frataxin",
"FRDA",
"FXN",
"frataxin protein",
"frataxin gene"
] |
["Friedrich's ataxia is caused by mutations in the FXN gene.", "Friedreich's ataxia is caused by an intronic guanine-adenine-adenine (GAA) triplet expansion in the frataxin (FXN) gene.", "The gene mutated in Friedreich's ataxia is the frataxin (FXN) gene.", "Friedreich's ataxia is caused by a mutation in the FXN gene, which encodes the protein frataxin.", "The gene mutated in Friedreich's ataxia is frataxin (FXN).", "Friedreich's ataxia (FRDA) is an inherited, multisystemic disorder predominantly caused by GAA hyper expansion in intron 1 of the frataxin (FXN) gene", "The gene mutated in Friedreich's ataxia is called FXN (frataxin)", "The gene mutated in Friedreich's ataxia is FRDA (FXN)."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10982187",
"http://www.ncbi.nlm.nih.gov/pubmed/22798143",
"http://www.ncbi.nlm.nih.gov/pubmed/30624801",
"http://www.ncbi.nlm.nih.gov/pubmed/32582297",
"http://www.ncbi.nlm.nih.gov/pubmed/32291635",
"http://www.ncbi.nlm.nih.gov/pubmed/10633128",
"http://www.ncbi.nlm.nih.gov/pubmed/36107856",
"http://www.ncbi.nlm.nih.gov/pubmed/27343351",
"http://www.ncbi.nlm.nih.gov/pubmed/9241270",
"http://www.ncbi.nlm.nih.gov/pubmed/35573317",
"http://www.ncbi.nlm.nih.gov/pubmed/31020006",
"http://www.ncbi.nlm.nih.gov/pubmed/35038030",
"http://www.ncbi.nlm.nih.gov/pubmed/15340363",
"http://www.ncbi.nlm.nih.gov/pubmed/10686465",
"http://www.ncbi.nlm.nih.gov/pubmed/30159187",
"http://www.ncbi.nlm.nih.gov/pubmed/35663795"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35573317",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Friedreich's ataxia (FRDA) is an autosomal recessive disease caused by an intronic guanine-adenine-adenine (GAA) triplet expansion in the frataxin (FXN) gene, which leads to reduced expression of full-length frataxin (1-210) also known as isoform 1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35663795",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Friedreich's ataxia (FRDA) is an inherited, multisystemic disorder predominantly caused by GAA hyper expansion in intron 1 of frataxin (FXN) gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36107856",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "Friedreich ataxia, the most common hereditary ataxia, is a neuro- and cardio-degenerative disorder caused, in most cases, by decreased expression of the mitochondrial protein frataxin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35573317",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Simultaneous Quantification of Mitochondrial Mature Frataxin and Extra-Mitochondrial Frataxin Isoform E in Friedreich's Ataxia Blood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35573317",
"endSection": "abstract",
"offsetInBeginSection": 1338,
"offsetInEndSection": 1454,
"text": "We now report a quantitative assay for frataxin proteoforms in whole blood from healthy controls and FRDA patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35573317",
"endSection": "abstract",
"offsetInBeginSection": 1925,
"offsetInEndSection": 2122,
"text": "The mean levels of mature frataxin in whole blood from healthy controls and homozygous FRDA patients were significantly different (p < 0.0001) at 7.5 ± 1.5 ng/mL and 2.1 ± 1.2 ng/mL, respectively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35573317",
"endSection": "abstract",
"offsetInBeginSection": 2315,
"offsetInEndSection": 2511,
"text": "he mean levels of total frataxin in whole blood from healthy controls and homozygous FRDA patients were significantly different (p < 0.0001) at 34.2 ± 4.3 ng/mL and 6.8 ± 4.0 ng/mL, respectively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10982187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Friedreich's ataxia is caused by mutations in the FRDA gene that encodes frataxin, a nuclear-encoded mitochondrial protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32582297",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Friedreich's ataxia (FRDA) is a progressive neurodegenerative disorder caused by a homozygous GAA repeat expansion mutation in intron 1 of the frataxin gene (FXN), which instigates reduced transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35038030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Friedreich Ataxia (FA) is a rare neuro-cardiodegenerative disease caused by mutations in the frataxin (FXN) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31020006",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Friedreich's ataxia, characterized by decreased expression of frataxin protein, is caused by GAA trinucleotide repeats within intron 1 in 98% of patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30159187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Friedreich's ataxia is a neurodegenerative disorder associated with a GAA trinucleotide repeat expansion in intron 1 of the frataxin (FXN) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10982187",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 315,
"text": "Most patients are homozygous for the expansion of a GAA triplet repeat within the FRDA gene, but a few patients show compound heterozygosity for a point mutation and the GAA-repeat expansion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32291635",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Friedreich's ataxia (FRDA) is a genetic neurodegenerative disease that is caused by guanine-adenine-adenine (GAA) nucleotide repeat expansions in the first intron of the frataxin (FXN) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15340363",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Friedreich's ataxia (FRDA), the most common autosomal recessively inherited ataxia, is due to a homozygous GAA triplet repeat expansion in the first intron of the FRDA gene in about 96% of patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9241270",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Friedreich's ataxia is due to loss of function mutations in the gene encoding frataxin (FRDA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10633128",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Friedreich ataxia, an autosomal recessive neurodegenerative disease, is the most common of the inherited ataxias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27343351",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Mutations in Frataxin (FXN) cause Friedreich's ataxia (FRDA), a recessive neurodegenerative disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22798143",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "The genetic mutation in Friedreich ataxia (FRDA) is a hyperexpansion of the triplet-repeat sequence GAA·TTC within the first intron of the FXN gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10686465",
"endSection": "abstract",
"offsetInBeginSection": 415,
"offsetInEndSection": 575,
"text": "The expansion of a GAA triplet repeat within the first intron of the frataxin gene, which causes Friedreich's ataxia, was not identified in any of the patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30624801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "BACKGROUND: Friedreich's ataxia is an autosomal-recessive cerebellar ataxia caused by mutation of the frataxin gene, resulting in decreased frataxin expression, mitochondrial dysfunction, and oxidative stress"
}
] | 12
|
BioASQ-training12b
| null | null |
6431f7de57b1c7a31500001b
| 4,794
|
factoid
|
What is the incidence of Duchenne Muscular Dystrophy?
|
['1:5,000 live male births', '1 in 5076 live born males', '1:3500-1:5000', '1 per 3500-6000 males born', '1/3300', '1 in 3,500 to 5,000 male births']
|
[
"1:5,000 live male births",
"1 in 5076 live born males",
"1:3500-1:5000",
"1 per 3500-6000 males born",
"1/3300",
"1 in 3,500 to 5,000 male births"
] |
['The incidence of Duchenne Muscular Dystrophy is approximately 1:5,000 live male births', 'The overall incidence of Duchenne Muscular Dystrophy is 1:5,000 live male births.', 'The incidence of Duchenne Muscular Dystrophy (DMD) is estimated to be 1 in 3,500 to 5,000 male births.', 'The incidence of Duchenne Muscular Dystrophy (DMD) is estimated to be 1 in 3,500 to 5,000 male births worldwide.', 'The incidence of Duchenne Muscular Dystrophy is approximately 1 in 5,000 live male births.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16114258",
"http://www.ncbi.nlm.nih.gov/pubmed/20080524",
"http://www.ncbi.nlm.nih.gov/pubmed/35754057",
"http://www.ncbi.nlm.nih.gov/pubmed/36012442",
"http://www.ncbi.nlm.nih.gov/pubmed/28802771",
"http://www.ncbi.nlm.nih.gov/pubmed/31603849",
"http://www.ncbi.nlm.nih.gov/pubmed/1673177",
"http://www.ncbi.nlm.nih.gov/pubmed/7334342",
"http://www.ncbi.nlm.nih.gov/pubmed/29386334",
"http://www.ncbi.nlm.nih.gov/pubmed/8629099",
"http://www.ncbi.nlm.nih.gov/pubmed/18055393",
"http://www.ncbi.nlm.nih.gov/pubmed/25996334",
"http://www.ncbi.nlm.nih.gov/pubmed/35562557",
"http://www.ncbi.nlm.nih.gov/pubmed/7922631",
"http://www.ncbi.nlm.nih.gov/pubmed/7705851"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35562557",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 152,
"text": "Duchenne muscular dystrophy (DMD/Duchenne) is a progressive X-linked muscular disease with an overall incidence of 1:5,000 live male births."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35754057",
"endSection": "abstract",
"offsetInBeginSection": 966,
"offsetInEndSection": 1094,
"text": "The cumulative incidence of disease was 19.7 per 100,000 male live births and 1 in 5076 live born males were diagnosed with DMD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31603849",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "Duchenne muscular dystrophy is a genetically determined disease, linked to the X chromosome, c haracterized clinically by producing progressive muscle weakness, with an incidence of 1 per 3500-6000 males born."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29386334",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 218,
"text": "Duchenne muscular dystrophy (DMD) is a progressive wasting disease of skeletal and cardiac muscles, representing one of the most common recessive fatal inherited genetic diseases with 1:3500-1:5000 in yearly incidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25996334",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "INTRODUCTION: Duchenne muscular dystrophy is the most common form of muscular dystrophy, with an incidence of 1/3300 male live births and a prevalence rate in the total population of 3/10000"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18055393",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Duchenne/Becker muscular dystrophy is a severe, recessive, X-linked neuromuscular disease with an incidence of 1/3500 (Duchenne type) and 1/30,000 (Becker type) in newborn boys."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20080524",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 474,
"text": "Statistics Canada data on annual male births in Nova Scotia were obtained for each year.The overall incidence of 1 per 4700 male births remained stable during the 30-year period of the study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16114258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "Duchenne muscular dystrophy (DMD) is inherited in an X-linked recessive pattern and occurs at an incidence of 1 in 3500 male births, which means that it is a so-called \"orphan\" or rare disease (frequency < 1/2000)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36012442",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 244,
"text": "Duchenne muscular dystrophy (DMD) is the most common fatal muscle disease, with an estimated incidence of 1/3500-1/5000 male births, and it is associated with mutations in the X-linked DMD gene encoding dystrophin, the largest known human gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8629099",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Duchenne muscular dystrophy (DMD) is a common inherited disease with a worldwide incidence of 1 in 3,500 male births."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7705851",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Duchenne muscular dystrophy (DMD) is one of the most common and severe X-linked disorders with an incidence of approximately 1 in 3500 newborn males."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1673177",
"endSection": "abstract",
"offsetInBeginSection": 701,
"offsetInEndSection": 955,
"text": "The cumulative birth incidence of Becker muscular dystrophy (at least 1 in 18 450 male live births) was about one third that of Duchenne muscular dystrophy (1 in 5618 male live births), suggesting that the disorder is more common than previously thought."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28802771",
"endSection": "abstract",
"offsetInBeginSection": 57,
"offsetInEndSection": 207,
"text": "scular dystrophy in childhood, with a worldwide incidence of one in 5000 live male births. It is due to mutations in the dystrophin gene leading to ab"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25996334",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "INTRODUCTION: Duchenne muscular dystrophy is the most common form of muscular dystrophy, with an incidence of 1/3300 male live births and a prevalence rate in the total population of 3/100000 individuals"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7922631",
"endSection": "abstract",
"offsetInBeginSection": 577,
"offsetInEndSection": 727,
"text": "ur region too. The incidence of Duchenne muscular dystrophy was 1 in 4827 liveborn boys. The figure is in the range of the published data of the incid"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7334342",
"endSection": "abstract",
"offsetInBeginSection": 258,
"offsetInEndSection": 408,
"text": "ular dystrophies the authors estimate the incidence of DMD at 1/6500 living new born boys. The number of false positives (1,5 p. 1000) is little and, "
}
] | 12
|
BioASQ-training12b
| null | null |
643f9eeb57b1c7a31500003c
| 4,800
|
factoid
|
Which cancer is the BCG vaccine used for?
|
['Non-muscle Invasive Bladder Cancer']
|
[
"Non-muscle Invasive Bladder Cancer",
"NMIBC",
"Non-muscle invasive bladder carcinoma",
"Non-muscle invasive urothelial carcinoma",
"Non-invasive bladder cancer"
] |
['The Bacillus Calmette-Guerin vaccine is used for the teatment of non-muscle invasive bladder cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36274226"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36274226",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Bacillus Calmette-Guerin for the Treatment of Non-muscle Invasive Bladder Cancer: History and Current Status."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36274226",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 302,
"text": "In the past decades, the bacillus Calmette-Guerin (BCG) treatment for non-muscle invasive bladder cancer, especially for intermediate and high-risk groups, is increasingly accepted by multiple guidelines. Currently, the front-line setting for the high-risk group is still intravesical BCG instillation."
}
] | 12
|
BioASQ-training12b
| null | null |
6415c252690f196b51000011
| 4,803
|
factoid
|
What disease can be treated with Teclistamab?
|
['Multiple Myeloma']
|
[
"Multiple Myeloma",
"Plasma Cell Myeloma",
"Myeloma",
"Kahler's Disease",
"Myelomatosis"
] |
['Teclistamab can be used for Multiple Myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35749004",
"http://www.ncbi.nlm.nih.gov/pubmed/35661166"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35661166",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "Teclistamab in Relapsed or Refractory Multiple Myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35661166",
"endSection": "abstract",
"offsetInBeginSection": 199,
"offsetInEndSection": 345,
"text": "In the phase 1 dose-defining portion of the study, teclistamab showed promising efficacy in patients with relapsed or refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35661166",
"endSection": "abstract",
"offsetInBeginSection": 1946,
"offsetInEndSection": 2102,
"text": "CONCLUSIONS: Teclistamab resulted in a high rate of deep and durable response in patients with triple-class-exposed relapsed or refractory multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35749004",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Translational Modeling Predicts Efficacious Therapeutic Dosing Range of Teclistamab for Multiple Myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35749004",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "BACKGROUND: Teclistamab (JNJ-64007957), a B-cell maturation antigen × CD3 bispecific antibody, displayed potent T-cell-mediated cytotoxicity of multiple myeloma cells in preclinical studies."
}
] | 12
|
BioASQ-training12b
| null | null |
63eeed0af36125a426000007
| 4,805
|
factoid
|
SER-109 is developed for prevention of which disease?
|
['C. difficile']
|
[
"C. difficile",
"Clostridium difficile",
"C. diff",
"Clostridioides difficile"
] |
['SER-109 is an investigational microbiome therapeutic composed of purified Firmicutes spores for the treatment of recurrent C. difficile infection.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35789381",
"http://www.ncbi.nlm.nih.gov/pubmed/36158136",
"http://www.ncbi.nlm.nih.gov/pubmed/35045228"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35789381",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 279,
"text": "In ECOSPOR III, SER-109, an investigational oral microbiome therapeutic, was superior to placebo in reducing rCDI. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35045228",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "SER-109, an Oral Microbiome Therapy for Recurrent Clostridioides difficile Infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35045228",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 343,
"text": "SER-109 is an investigational microbiome therapeutic composed of purified Firmicutes spores for the treatment of recurrent C. difficile infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36158136",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 464,
"text": "We report that the manufacturing steps for SER-109, a purified investigational microbiome therapeutic developed to reduce risk of Clostridioides difficile recurrence, inactivate porcine epidemic diarrhea virus, a model coronavirus for SARS-CoV-2."
}
] | 12
|
BioASQ-training12b
| null | null |
63f03ea0f36125a426000020
| 4,809
|
factoid
|
Where is the DMD gene located?
|
['Xp21 chromosome locus', 'X-linked recessive disorders caused by mutations of the DMD gene located at Xp21', 'X chromosome (Xp21)']
|
[
"Xp21 chromosome locus",
"Xp21",
"X chromosome (Xp21)",
"X-linked recessive disorders caused by mutations of the DMD gene located at Xp21",
"Xp21.1",
"Xp21.2",
"Xp21.3",
"Duchenne muscular dystrophy locus",
"DMD gene locus"
] |
['The dystrophin gene (DMD) is located on the X chromosome (Xp21).', 'The dystrophin gene is located at chromosome Xp21.1, near the centromere.', 'The DMD gene is located on the X chromosome at Xp21.2.', 'The DMD gene is located on the X chromosome at the Xp21 locus.', 'The DMD gene is located on the X chromosome, on the Xp21 locus.', 'The DMD gene is located on the Xp21 chromosome locus on the X chromosome.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19078586",
"http://www.ncbi.nlm.nih.gov/pubmed/18471087",
"http://www.ncbi.nlm.nih.gov/pubmed/24014122",
"http://www.ncbi.nlm.nih.gov/pubmed/19461958",
"http://www.ncbi.nlm.nih.gov/pubmed/6655672",
"http://www.ncbi.nlm.nih.gov/pubmed/31661024",
"http://www.ncbi.nlm.nih.gov/pubmed/16936400",
"http://www.ncbi.nlm.nih.gov/pubmed/28247611",
"http://www.ncbi.nlm.nih.gov/pubmed/28028563",
"http://www.ncbi.nlm.nih.gov/pubmed/19837995",
"http://www.ncbi.nlm.nih.gov/pubmed/12488581",
"http://www.ncbi.nlm.nih.gov/pubmed/28867298",
"http://www.ncbi.nlm.nih.gov/pubmed/24274981",
"http://www.ncbi.nlm.nih.gov/pubmed/18935728",
"http://www.ncbi.nlm.nih.gov/pubmed/28740938",
"http://www.ncbi.nlm.nih.gov/pubmed/2889148",
"http://www.ncbi.nlm.nih.gov/pubmed/2541343",
"http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"http://www.ncbi.nlm.nih.gov/pubmed/12619170",
"http://www.ncbi.nlm.nih.gov/pubmed/24627880",
"http://www.ncbi.nlm.nih.gov/pubmed/33870095",
"http://www.ncbi.nlm.nih.gov/pubmed/36361862",
"http://www.ncbi.nlm.nih.gov/pubmed/3777020"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28867298",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "The dystrophin gene (DMD) is the largest gene in the human genome, mapping on the Xp21 chromosome locus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19461958",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are X-linked recessive disorders caused by mutations of the DMD gene located at Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18935728",
"endSection": "abstract",
"offsetInBeginSection": 130,
"offsetInEndSection": 255,
"text": "The disease is caused by deletion, duplication or point mutation of the dystrophin gene, located on the X chromosome (Xp21). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24274981",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "DMD gene which is composed of 79 exons is the largest known gene located on X chromosome (Xp21)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33870095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Dystrophinopathies are allelic conditions caused by deletions, duplications and point-mutations in the DMD gene, located on the X chromosome (Xp21.2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36361862",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 276,
"text": "The disease is caused by mutations in the DMD gene located on the X chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24627880",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "BACKGROUND: The Duchenne muscular dystrophy (DMD) gene is located in the short arm of the X chromo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18471087",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Duchenne muscular dystrophy (DMD) is an X-linked recessive neuromuscular disorder caused by mutations in the dystrophin DMD gene located at Xp21.1 region."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"endSection": "abstract",
"offsetInBeginSection": 401,
"offsetInEndSection": 678,
"text": "Because the DMD gene is located at Xp21.2, which is one breakpoint of the inv(X), and because its defects are rarely associated with severe mental retardation, the other clinical features of this patient were deemed likely to be associated with the opposite breakpoint at Xq22."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2889148",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 368,
"text": "Long-range physical mapping has shown that the DMD gene, localized in Xp21, is extremely large, exceeding 2 million base pairs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24014122",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 415,
"text": "The DMD gene, located on Xp21, is the largest human gene in the human genome (2.3 Mb)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2541343",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "The Duchenne muscular dystrophy (DMD) gene has been localized to chromosome Xp21 and codes for a 14-kilobase (kb) transcript and a protein called dystrophin, of relative molecular mass 427,000."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6655672",
"endSection": "abstract",
"offsetInBeginSection": 640,
"offsetInEndSection": 772,
"text": " The breakpoint in our patient is also located at Xp21, adding evidence for the assignment of this band as the site of the DMD gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24014122",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 409,
"text": " The DMD gene, located on Xp21, is the largest human gene in the human genome (2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3777020",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 381,
"text": " The present case supports the hypothesis that the DMD gene must be located at Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28247611",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 272,
"text": " The causal gene of DMD is the largest one in human that locates in the region of Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"endSection": "abstract",
"offsetInBeginSection": 400,
"offsetInEndSection": 441,
"text": " Because the DMD gene is located at Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28028563",
"endSection": "abstract",
"offsetInBeginSection": 39,
"offsetInEndSection": 189,
"text": "n coded by the Duchenne muscular dystrophy (DMD) gene located on the X-chromosome. Truncating mutations in the DMD gene cause loss of dystrophin and t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18471087",
"endSection": "abstract",
"offsetInBeginSection": 71,
"offsetInEndSection": 221,
"text": "r disorder caused by mutations in the dystrophin DMD gene located at Xp21.1 region. Up to 65% of the patients present dystrophin gene deletions. Mothe"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28740938",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "BACKGROUND: Duchenne muscular dystrophy (DMD) is caused by a defective gene located on the X-chromosome, responsible for the production of the dystrophin protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19837995",
"endSection": "abstract",
"offsetInBeginSection": 100,
"offsetInEndSection": 250,
"text": "l muscle disorders, caused by mutations in the dystrophin gene located in Xp21. DMD occurs with the incidence 1:3500, BMD with the incidence of 1:18,5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28867298",
"endSection": "abstract",
"offsetInBeginSection": 17,
"offsetInEndSection": 167,
"text": "ne (DMD) is the largest gene in the human genome, mapping on the Xp21 chromosome locus. It spans 2.2Mb and accounts for approximately 0,1% of the enti"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19078586",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 287,
"text": "Duchenne muscular dystrophy (DMD), glycerol kinase deficiency (GKD), and adrenal hypoplasia congenita (AHC) can occur together as part of a contiguous gene syndrome located at chromosome Xp21, GKD can manifest with recurrent episodes of vomiting, acidemia, mental retardation, or stupor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19461958",
"endSection": "abstract",
"offsetInBeginSection": 77,
"offsetInEndSection": 227,
"text": "inked recessive disorders caused by mutations of the DMD gene located at Xp21. In DMD patients, dystrophin is virtually absent; whereas BMD patients h"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12619170",
"endSection": "abstract",
"offsetInBeginSection": 22,
"offsetInEndSection": 172,
"text": "rophy (DMD) is a dystrophinopathy, and its associated gene is located on Xp21. Moreover, utrophin, a recently identified structural homologue of dystr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31661024",
"endSection": "abstract",
"offsetInBeginSection": 96,
"offsetInEndSection": 246,
"text": " disease in children, resulting from a defect in the DMD gene located on Xp21.2. The new emerging treatment using exon skipping strategy is tailored t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3777020",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 453,
"text": "resent case supports the hypothesis that the DMD gene must be located at Xp21. In this study, involvement of the father's chromosomes in the transloca"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 514,
"text": " only later was it diagnosed as DMD. Because the DMD gene is located at Xp21.2, which is one breakpoint of the inv(X), and because its defects are rar"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16936400",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 274,
"text": "letion, duplication or point mutation of the dystrophin gene located at Xp 21.2. In the present study DNA from seventy unrelated patients clinically d"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12488581",
"endSection": "abstract",
"offsetInBeginSection": 60,
"offsetInEndSection": 210,
"text": "inked diseases resulting from a defect in the dystrophin gene located on Xp21. DMD is the most frequent neuromuscular disease in humans (1/3500 male n"
}
] | 12
|
BioASQ-training12b
| null | null |
64179113690f196b5100002e
| 4,812
|
factoid
|
Which form of breast cancer has Keytruda been FDA approved for?
|
['triple-negative breast cancer']
|
[
"triple-negative breast cancer",
"TNBC",
"triple-negative tumor",
"triple-negative carcinoma",
"triple-negative breast carcinoma"
] |
['Keytruda has been FDA approved for use in combination with chemotherapy for treating PD-L1-positive mTNBC.', 'FDA has approved pembrolizumab (Keytruda) for the treatment of triple-negative breast cancer in combination with chemotherapy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33983696"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33983696",
"endSection": "abstract",
"offsetInBeginSection": 497,
"offsetInEndSection": 724,
"text": "The combination of chemotherapy and immunotherapy is a potential therapeutic option for PD-L1-positive mTNBC, as the FDA recently approved atezolizumab (Tecentriq) and pembrolizumab (Keytruda) in combination with chemotherapy. "
}
] | 12
|
BioASQ-training12b
| null | null |
6415c9e9690f196b51000018
| 4,815
|
factoid
|
Which gene is most frequently mutated in hereditary angioedema ?
|
['SERPING1', 'C1NH']
|
[
"SERPING1",
"C1NH",
"C1 inhibitor",
"serpin peptidase inhibitor, clade G (C1 inhibitor)",
"serpin G1",
"serpin 1",
"serpin C1 inhibitor"
] |
['Almost all cases of HAE are caused by mutations in the SERPING1 gene resulting in a deficiency in functional plasma C1 esterase inhibitor (C1EI), a serine protease inhibitor that normally inhibits proteases in the contact, complement, and fibrinolytic systems']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30059156"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30059156",
"endSection": "abstract",
"offsetInBeginSection": 232,
"offsetInEndSection": 491,
"text": "Almost all cases of HAE are caused by mutations in the SERPING1 gene resulting in a deficiency in functional plasma C1 esterase inhibitor (C1EI), a serine protease inhibitor that normally inhibits proteases in the contact, complement, and fibrinolytic systems"
}
] | 12
|
BioASQ-training12b
| null | null |
6432fc0457b1c7a31500001f
| 4,821
|
factoid
|
ZF2001 is used for which disease?
|
['COVID-19']
|
[
"COVID-19",
"Coronavirus Disease 2019",
"SARS-CoV-2 infection",
"2019-nCoV",
"Novel Coronavirus",
"Wuhan Coronavirus",
"COVID",
"Coronavirus"
] |
['ZF2001 is used for COVID-19.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35617368",
"http://www.ncbi.nlm.nih.gov/pubmed/35568034",
"http://www.ncbi.nlm.nih.gov/pubmed/35634276",
"http://www.ncbi.nlm.nih.gov/pubmed/35596222"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35617368",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "Safety and immunogenicity of heterologous boost immunization with an adenovirus type-5-vectored and protein-subunit-based COVID-19 vaccine (Convidecia/ZF2001): A randomized, observer-blinded, placebo-controlled trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35617368",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 420,
"text": "We assessed the safety and immunogenicity of heterologous immunization with a recombinant adenovirus type-5-vectored Coronavirus Disease 2019 (COVID-19) vaccine (Convidecia, hereafter referred to as CV) and a protein-subunit-based COVID-19 vaccine (ZF2001, hereafter referred to as ZF)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35617368",
"endSection": "abstract",
"offsetInBeginSection": 3124,
"offsetInEndSection": 3314,
"text": "CONCLUSIONS: Heterologous boosting with ZF2001 following primary vaccination with Convidecia is more immunogenic than a single dose of Convidecia and is not associated with safety concerns. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35634276",
"endSection": "abstract",
"offsetInBeginSection": 1434,
"offsetInEndSection": 1539,
"text": "Conclusion: SARS-CoV-2 vaccines (CoronaVac, BBIBP-CorV, and ZF2001) are safe in thyroid cancer patients. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35596222",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "Effective protection of ZF2001 against the SARS-CoV-2 Delta variant in lethal K18-hACE2 mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35596222",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 260,
"text": "To investigate the protective efficacy and mechanism of ZF2001 (a protein subunit vaccine with conditional approval in China) to SARS-CoV-2 Delta variant-induced severe pneumonia, the lethal challenge model of K18-hACE2 transgenic mice was used in this study. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35568034",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 233,
"text": "Previously, we developed the protein subunit vaccine ZF2001 based on the dimeric receptor-binding domain (RBD) of prototype SARS-CoV-2. "
}
] | 12
|
BioASQ-training12b
| null | null |
63f03c47f36125a42600001e
| 4,828
|
factoid
|
What mammal has the lowest known chromosome number?
|
['Indian muntjac']
|
[
"Indian muntjac",
"barking deer",
"Muntiacus muntjak",
"Muntjac",
"Indian barking deer"
] |
['The Indian muntjac, a placental mammal, has the lowest known chromosome number of 2n = 6 (or n = 3).', 'The mammal with the lowest known chromosome number is the Indian muntjac.', 'Here we used the unique cytological attributes of female Indian muntjac, the mammal with the lowest known chromosome number (2n = 6)', 'The Indian muntjac is the mammal with the lowest known chromosome number, with only 6 chromosomes.', 'The Etruscan Shrew (Suncus etruscus) has the lowest known chromosome number of any mammal, with only 2 pairs of chromosomes.', 'The mammal with the lowest known chromosome number is the Indian Muntjac.', 'The female Indian Muntjac is a placental mammal with only three chromosomes, the lowest known chromosome number of any mammal', 'The mammal with the lowest known chromosome number is the Etruscan shrew (Suncus etruscus), which has only 2 chromosomes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/5444269",
"http://www.ncbi.nlm.nih.gov/pubmed/8513693",
"http://www.ncbi.nlm.nih.gov/pubmed/16791631",
"http://www.ncbi.nlm.nih.gov/pubmed/35385739",
"http://www.ncbi.nlm.nih.gov/pubmed/31879909",
"http://www.ncbi.nlm.nih.gov/pubmed/8485991",
"http://www.ncbi.nlm.nih.gov/pubmed/29706521"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706521",
"endSection": "abstract",
"offsetInBeginSection": 615,
"offsetInEndSection": 748,
"text": "Here we used the unique cytological attributes of female Indian muntjac, the mammal with the lowest known chromosome number (2n = 6),"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31879909",
"endSection": "title",
"offsetInBeginSection": 73,
"offsetInEndSection": 136,
"text": "Indian Muntjac, a Placental Mammal with Only Three Chromosomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31879909",
"endSection": "abstract",
"offsetInBeginSection": 1373,
"offsetInEndSection": 1457,
"text": " Indian muntjac, a placental mammal with the lowest known chromosome number (n = 3)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706521",
"endSection": "abstract",
"offsetInBeginSection": 615,
"offsetInEndSection": 848,
"text": "Here we used the unique cytological attributes of female Indian muntjac, the mammal with the lowest known chromosome number (2n = 6), to characterize and track individual chromosomes with distinct kinetochore size throughout mitosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/5444269",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "The Indian muntjac (Muntiacus muntjak) has a diploid chromosome number of 7 in the male and 6 in the female, the lowest number yet described in a mammal."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8485991",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "The Indian muntjac is believed to have the lowest chromosome number in mammals (2n = 6 in females and 2n = 7 in males)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8513693",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "The Indian muntjac, an asiatic deer, has the lowest diploid chromosome number among mammals (female 2N = 6; male 2N = 7)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35385739",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 709,
"text": "By combining molecular perturbations and phenotypic analyses in Indian muntjac fibroblasts containing the lowest known diploid chromosome number in mammals (2N = 6) and distinctively large kinetochores, with fixed/live-cell super-resolution coherent-hybrid stimulated emission depletion (CH-STED) nanoscopy and laser microsurgery, we demonstrate a key role for augmin in kinetochore microtubule self-organization and maturation, regardless of pioneer centrosomal microtubules."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16791631",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "The karyotype of Indian muntjacs (Muntiacus muntjak vaginalis) has been greatly shaped by chromosomal fusion, which leads to its lowest diploid number among the extant known mammals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706521",
"endSection": "abstract",
"offsetInBeginSection": 614,
"offsetInEndSection": 848,
"text": " Here we used the unique cytological attributes of female Indian muntjac, the mammal with the lowest known chromosome number (2n = 6), to characterize and track individual chromosomes with distinct kinetochore size throughout mitosis."
}
] | 12
|
BioASQ-training12b
| null | null |
642c82c557b1c7a315000012
| 4,829
|
factoid
|
Which company produces Ruconest?
|
['Pharming']
|
[
"Pharming",
"Pharming technology",
"Pharming (pharmaceutical farming)",
"Pharming (genetic engineering)",
"Pharmaceutical farming"
] |
['Ruconest is produced by the company Pharming.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21426252"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21426252",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Recombinant human C1 esterase inhibitor (rhC1INH) (Ruconest(®), Pharming) is a new drug developed for the relief of symptoms occurring in patients with angioedema due to C1-inhibitor deficiency."
}
] | 12
|
BioASQ-training12b
| null | null |
643305b257b1c7a315000025
| 4,831
|
factoid
|
What is usually the age of diagnosis in Duchenne muscular dystrophy?
|
['4.43 years old', '4.9 years old', 'between 3 and 11 years of age', '4.9 years', '3 - 5 years']
|
[
"4.43 years old",
"4.9 years old",
"between 3 and 11 years of age",
"4.9 years",
"3 - 5 years",
"approximately 4 years",
"around 4 years",
"4 to 5 years",
"3 to 11 years",
"3 years to 11 years"
] |
['The usual age of diagnosis in Duchenne muscular dystrophy is around 4.9 years.', 'The mean age of diagnosis for Duchenne muscular dystrophy is around 4.5-5 years old.', 'The mean age of diagnosis is between 3 and 5 years, and the age of 4.9 years is most commonly reported.', 'The age of diagnosis in Duchenne muscular dystrophy usually ranges from 3 to 11 years, with a mean age of 4.43-4.9 years.', 'The mean age for DMD diagnosis was 4.9 years.', 'The age of diagnosis in Duchenne muscular dystrophy is usually between 1 and 6 years of age.', 'The mean age of onset of symptoms for 22 patients was 2.4 years. The mean age for DMD diagnosis was 4.9 years.', 'The average age of diagnosis for Duchenne muscular dystrophy is around 3-5 years old.', 'The average age of diagnosis for Duchenne muscular dystrophy is around 4-5 years old.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35312090",
"http://www.ncbi.nlm.nih.gov/pubmed/16322188",
"http://www.ncbi.nlm.nih.gov/pubmed/23494880",
"http://www.ncbi.nlm.nih.gov/pubmed/25996334",
"http://www.ncbi.nlm.nih.gov/pubmed/31573675",
"http://www.ncbi.nlm.nih.gov/pubmed/7557061"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35312090",
"endSection": "abstract",
"offsetInBeginSection": 1254,
"offsetInEndSection": 1482,
"text": "The mean [median] ages in years of diagnostic milestones were: first signs, 2.7 [2.0]; first creatine kinase (CK), 4.6 [4.6]; DNA/muscle biopsy testing, 4.9 [4.8]; and time from first signs to diagnostic confirmation, 2.2 [1.4]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31573675",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 547,
"text": "The mean age of diagnosis was 4.43 years. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7557061",
"endSection": "abstract",
"offsetInBeginSection": 646,
"offsetInEndSection": 693,
"text": " The mean age for DMD diagnosis was 4.9 years. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7557061",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 920,
"text": "In 10 cases of the group with locomotion problems (45.4%) the diagnosis was made between 3 and 11 years of age."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7557061",
"endSection": "abstract",
"offsetInBeginSection": 647,
"offsetInEndSection": 692,
"text": "The mean age for DMD diagnosis was 4.9 years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25996334",
"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 488,
"text": "lso frequent. The average age at diagnosis is 4.83 years but an early diagnosis is possible.CLINICAL CASE: An 18-month male infant in ambulatory study for failure to thrive and malnutrition was admitted in our hospi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16322188",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 298,
"text": "The disease is typically diagnosed between 3 and 7 years of age and follows a predictable clinical course marked by progressive skeletal muscle weakness with loss of ambulation by 12 years of age."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25996334",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 364,
"text": " The average age at diagnosis is 4.83 years but an early diagnosis is possible"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23494880",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 263,
"text": "ive loss of muscle function. Despite technological advances in diagnostic genetic testing, the mean age at diagnosis (4.7 years) has re"
}
] | 12
|
BioASQ-training12b
| null | null |
641635fa690f196b5100001c
| 4,832
|
factoid
|
Which drug was the first recombinant human C1 inhibitor protein (C1INH) for the treatment of acute attacks of hereditary angioedema (HAE)?
|
['Conestat alfa', 'Ruconest', 'rhC1INH']
|
[
"Conestat alfa",
"Ruconest",
"rhC1INH",
"C1 esterase inhibitor",
"C1 inhibitor",
"C1-INH",
"recombinant human C1 inhibitor"
] |
['Conestat alfa (Ruconest, rhC1INH) is the first recombinant human C1 inhibitor protein (C1INH) for the treatment of acute attacks of hereditary angioedema (HAE).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24556385"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24556385",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 172,
"text": "Conestat alfa (Ruconest, rhC1INH) is the first recombinant human C1 inhibitor protein (C1INH) for the treatment of acute attacks of hereditary angioedema (HAE)."
}
] | 12
|
BioASQ-training12b
| null | null |
6433050157b1c7a315000024
| 4,841
|
factoid
|
What type of DMD can viltolarsen be used for?
|
['exon 53']
|
[
"exon 53",
"exon 53 (human)",
"exon 53 (mouse)",
"exon 53 (rat)"
] |
['Viltolarsen can be used for the treatment of Duchenne muscular dystrophy (DMD) by skipping exon 53 of the DMD gene.', 'Viltolarsen is a targeted antisense oligonucleotide indicated for the treatment of Duchenne muscular dystrophy (DMD) caused by a confirmed mutation amenable to exon 53 skipping.', 'Viltolarsen is a phosphorodiamidate morpholino antisense oligonucleotide (PMO) designed to skip exon 53 of the DMD gene for the treatment of Duchenne muscular dystrophy (DMD)', 'Viltolarsen can be used for patients with Duchenne Muscular Dystrophy who are amenable to exon 53 skipping therapy.', 'Viltolarsen can be used for patients with DMD amenable to exon 53 skipping.', 'Viltolarsen can be used for the treatment of Duchenne muscular dystrophy (DMD) by restoring the reading frame of the DMD gene by skipping exon 53 and producing a truncated but functional form of dystrophin.', 'Viltolarsen be used for DMD patients that have mutations amenable to exon 53 skipping.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34938127",
"http://www.ncbi.nlm.nih.gov/pubmed/32519222",
"http://www.ncbi.nlm.nih.gov/pubmed/33285037",
"http://www.ncbi.nlm.nih.gov/pubmed/36401027",
"http://www.ncbi.nlm.nih.gov/pubmed/32453377",
"http://www.ncbi.nlm.nih.gov/pubmed/36401022",
"http://www.ncbi.nlm.nih.gov/pubmed/35634851",
"http://www.ncbi.nlm.nih.gov/pubmed/32483212",
"http://www.ncbi.nlm.nih.gov/pubmed/31720560",
"http://www.ncbi.nlm.nih.gov/pubmed/32947786"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401022",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Viltolarsen is a phosphorodiamidate morpholino antisense oligonucleotide (PMO) designed to skip exon 53 of the DMD gene for the treatment of Duchenne muscular dystrophy (DMD)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401022",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 829,
"text": "Viltolarsen restores the reading frame of the DMD gene by skipping exon 53 and produces a truncated but functional form of dystrophin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32519222",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 705,
"text": "In March 2020, intravenous viltolarsen received its first global approval in Japan for the treatment of DMD in patients with confirmed deletion of the dystrophin gene that is amenable to exon 53 skipping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401022",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 305,
"text": "Viltolarsen is a phosphorodiamidate morpholino antisense oligonucleotide (PMO) designed to skip exon 53 of the DMD gene for the treatment of Duchenne muscular dystrophy (DMD), one of the most common lethal genetic disorders characterized by progressive degeneration of skeletal muscles and cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31720560",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 762,
"text": "Viltolarsen, also known as NS-065/NCNP-01, is a PMO developed through comprehensive sequence optimization and is designed to skip exon 53 on the DMD primary transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33285037",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "OBJECTIVE: The novel morpholino antisense oligonucleotide viltolarsen targets exon 53 of the dystrophin gene, and could be an effective treatment for patients with Duchenne muscular dystr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32519222",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 500,
"text": "Viltolarsen binds to exon 53 of the dystrophin mRNA precursor and restores the amino acid open-reading frame by skipping exon 53, resulting in the production of a shortened dystrophin protein that contains essential functional portions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34938127",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 386,
"text": "Viltolarsen is a drug of phosphorodiamidate morpholino oligomer (PMO) chemistry, designed to skip exon 53 of the DMD gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32483212",
"endSection": "abstract",
"offsetInBeginSection": 482,
"offsetInEndSection": 569,
"text": " Viltolarsen, an AON for DMD exon 53 skipping, was approved in Japan earlier this year."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401027",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 506,
"text": " Two exon 53 skipping PMOs, golodirsen and viltolarsen, have received conditional approval for treating patients due to their ability to restore dystrophin protein expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32947786",
"endSection": "abstract",
"offsetInBeginSection": 420,
"offsetInEndSection": 570,
"text": "en for DMD exon 51 skipping and golodirsen and viltolarsen for DMD exon 53 skipping, have been approved in the last 4 years. We are witnessing the sta"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32453377",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 546,
"text": "Importance: An unmet need remains for safe and efficacious treatments for Duchenne muscular dystrophy (DMD). To date, there are limited agents available that address the underlying cause of the disease.Objective: To evaluate the safety, tolerability, and efficacy of viltolarsen, a novel antisense oligonucleotide, in participants with DMD amenable to exon 53 skipping.Design, Setting, and Participants: This phase 2 study was a 4-week randomized clinical trial for safety followed by a 20-week open-label treatment period of patients aged 4 to 9"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35634851",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 530,
"text": "BACKGROUND: Duchenne muscular dystrophy (DMD) is a rare, genetic disease caused by mutations in the DMD gene resulting in an absence of functional dystrophin protein. Viltolarsen, an exon 53 skipping therapy, has been shown to increase endogenous dystrophin levels. Herein, long-term (>2 years) functional outcomes in viltolarsen treated patients were compared to a matched historical control group.OBJECTIVE: To evaluate long-term efficacy and safety of the anti-sense oligonucleotide viltolarsen in the treatment of patients wit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32519222",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 705,
"text": "Viltolarsen (Viltepso® in Japan) is a phosphorodiamidate morpholino antisense oligonucleotide being developed by Nippon Shinyaku, in collaboration with the National Center of Neurology and Psychiatry (NCNP), for the treatment of Duchenne muscular dystrophy (DMD). Viltolarsen binds to exon 53 of the dystrophin mRNA precursor and restores the amino acid open-reading frame by skipping exon 53, resulting in the production of a shortened dystrophin protein that contains essential functional portions. In March 2020, intravenous viltolarsen received its first global approval in Japan for the treatment of DMD in patients with confirmed deletion of the dystrophin gene that is amenable to exon 53 skipping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401022",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Viltolarsen is a phosphorodiamidate morpholino antisense oligonucleotide (PMO) designed to skip exon 53 of the DMD gene for the treatment of Duchenne muscular dystrophy (DMD),"
}
] | 12
|
BioASQ-training12b
| null | null |
6417900b690f196b5100002a
| 4,842
|
factoid
|
What types of DMD can eteplirsen be used for?
|
['exon-51 amenable genetic mutations', 'exon 51-amenable patients']
|
[
"exon-51 amenable genetic mutations",
"exon 51-amenable patients",
"exon 51 mutations",
"exon 51 amenable",
"exon 51",
"exon 51 genetic mutations"
] |
['Eteplirsen can be used for patients with Duchenne muscular dystrophy (DMD) who have a mutation in exon 51.', 'Eteplirsen can be used for patients with Duchenne muscular dystrophy (DMD) who have a confirmed mutation of the DMD gene amenable to exon 51 skipping.', 'Eteplirsen is approved for the treatment of Duchenne muscular dystrophy (DMD) in patients who have a confirmed mutation of the DMD gene that is amenable to exon 51 skipping.', 'Eteplirsen can be used for treating Duchenne muscular dystrophy (DMD) in patients with confirmed exon-51 amenable genetic mutations.', 'Eteplirsen can only be used for patients with exon-51 amenable DMD.', 'Eteplirsen be used for DMD patients with mutations amenable to exon 51 skipping.', 'Eteplirsen can be used for patients with Duchenne Muscular Dystrophy who have a mutation in exon 51.', 'Eteplirsen can be used for the treatment of Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene amenable to exon 51 skipping.', 'Eteplirsen can be used for patients with Duchenne muscular dystrophy and confirmed exon-51 amenable genetic mutations.', 'Eteplirsen is approved for the treatment of Duchenne muscular dystrophy (DMD) caused by a specific genetic mutation known as a deletion of exon 51.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33523015",
"http://www.ncbi.nlm.nih.gov/pubmed/34420980"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34420980",
"endSection": "abstract",
"offsetInBeginSection": 53,
"offsetInEndSection": 192,
"text": "treatment effects of eteplirsen over 4 years in patients with Duchenne muscular dystrophy and confirmed exon-51 amenable genetic mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33523015",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 269,
"text": "A relationship between exon skipping and dystrophin production in exon 51-amenable patients treated with eteplirsen (EXONDYS 51®) "
}
] | 12
|
BioASQ-training12b
| null | null |
64178fea690f196b51000028
| 4,847
|
factoid
|
In what organ would you find the Ashwell receptor?
|
['liver']
|
[
"liver",
"hepatic",
"hepar",
"hepatocyte",
"liver organ",
"liver tissue"
] |
['The Ashwell receptor is found in the hepatocytes of the liver.', 'The Ashwell receptor is a cell-surface receptor found in the liver and intestine.', 'The Ashwell receptor is found in the liver, specifically on the surface of hepatocytes.', 'The Ashwell receptor would be found in the liver (specifically, on hepatocytes).', 'the Ashwell receptor is an asialoglycoprotein receptor (ASGPR) found on hepatocytes. It mediates removal of potentially hazardous glycoconjugates from blood in health and disease.', 'The Ashwell receptor is found in the liver, specifically on hepatocytes.', 'The Ashwell receptor is found in the liver.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/3089897",
"http://www.ncbi.nlm.nih.gov/pubmed/20816169",
"http://www.ncbi.nlm.nih.gov/pubmed/26185093",
"http://www.ncbi.nlm.nih.gov/pubmed/3610047",
"http://www.ncbi.nlm.nih.gov/pubmed/22919488",
"http://www.ncbi.nlm.nih.gov/pubmed/33762439",
"http://www.ncbi.nlm.nih.gov/pubmed/18488037",
"http://www.ncbi.nlm.nih.gov/pubmed/8702886",
"http://www.ncbi.nlm.nih.gov/pubmed/24284176"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3089897",
"endSection": "abstract",
"offsetInBeginSection": 612,
"offsetInEndSection": 781,
"text": "From these data, we inferred an additional hepatic uptake mechanism, competing with the Ashwell-receptor-mediated internalization of galactose-terminated glycoproteins. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3610047",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 522,
"text": " This study was designed to investigate several aspects of both models, using lactosylated albumin as a binding protein that can interact with the Ashwell receptor abundantly present on the hepatocyte."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22919488",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 172,
"text": "The asialoglycoprotein receptor (ASGPR) is a hepatic receptor that mediates removal of potentially hazardous glycoconjugates from blood in health and disease. T"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18488037",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "The Ashwell receptor, the major lectin of hepatocytes, rapidly clears from blood circulation glycoproteins bearing glycan ligands that include galactose and N-acetylgalactosamine"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20816169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 218,
"text": "The Ashwell-Morell receptor (AMR) of hepatocytes, originally termed the hepatic asialoglycoprotein receptor, was the first cellular receptor to be identified and isolated and the first lectin to be detected in mammals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18488037",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "The Ashwell receptor, the major lectin of hepatocytes, rapidly clears from blood circulation glycoproteins bearing glycan ligands that include galactose and N-acetylgalactosamine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24284176",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "The endocytic Ashwell-Morell receptor (AMR) of hepatocytes detects pathogen remodeling of host glycoproteins by neuraminidase in the bloodstream and mitigates the lethal coagulopathy of sepsis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33762439",
"endSection": "abstract",
"offsetInBeginSection": 293,
"offsetInEndSection": 581,
"text": "Platelet-derived antibacterial peptides are important in bloodstream defense against SA, but α-toxin decreased platelet viability, induced platelet sialidase to cause desialylation of platelet glycoproteins, and accelerated platelet clearance by the hepatic Ashwell-Morell receptor (AMR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3610047",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 522,
"text": "This study was designed to investigate several aspects of both models, using lactosylated albumin as a binding protein that can interact with the Ashwell receptor abundantly present on the hepatocyte."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26185093",
"endSection": "abstract",
"offsetInBeginSection": 765,
"offsetInEndSection": 946,
"text": "This leads to platelet clearance in the liver via hepatocyte Ashwell-Morell receptors, which is fundamentally different from the classical Fc-FcγR-dependent macrophage phagocytosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8702886",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 391,
"text": "The mammalian asialoglycoprotein receptor (ASGPR) is located on the sinusoidal membrane of hepatocytes where it binds and endocytoses galactose-terminated glycoproteins (asialoglycoproteins). ASGPR is composed of two highly homologous subunits, termed hepatic lectin 1 and 2. Despite numerous studies the contribution of both subunits to biosynthesis and functional activity of ASGPR in vivo"
}
] | 12
|
BioASQ-training12b
| null | null |
6426d131690f196b5100004e
| 4,849
|
factoid
|
What type of DMD can casimersen be used for?
|
['exon 45', 'confirmed mutation of the DMD gene that is amenable to exon 45 skipping', 'amenable to exon 45', 'amenable to exon 45 skipping']
|
[
"exon 45",
"exon 45 skipping",
"confirmed mutation of the DMD gene that is amenable to exon 45 skipping",
"amenable to exon 45",
"amenable to exon 45 skipping"
] |
['Casimersen can be used for the treatment of Duchenne muscular dystrophy (DMD) in patients who have a mutation in the DMD gene that is amenable to exon\xa045 skipping.', 'Casimersen can be used for treating Duchenne muscular dystrophy (DMD) in patients who have a confirmed mutation of the DMD gene that is amenable to exon 45 skipping.', 'Casimersen can be used for Duchenne muscular dystrophy (DMD) patients who have a mutation in the DMD gene that is amenable to exon 45 skipping.', 'Casimersen can be used for the treatment of DMD in patients who have a confirmed mutation of the DMD gene that is amenable to exon\xa045 skipping.', 'Casimersen can be used for Duchenne muscular dystrophy (DMD) in patients who have a mutation in the DMD gene that is amenable to exon 45 skipping.', 'Casimersen is approved for the treatment of Duchenne Muscular Dystrophy (DMD) in patients who have a confirmed mutation of the DMD gene that is amenable to exon 45 skipping.', 'Casimersen received its first approval on 25 February 2021, in the USA, for the treatment of DMD in patients who have a confirmed mutation of the DMD gene that is amenable to exon 45 skipping.', 'Casimersen can be used for the treatment of DMD in patients who have a confirmed mutation of the DMD gene that is amenable to exon 45 skipping.', 'Patients with a confirmed mutation of the DMD gene that is amenable to exon 45 skipping.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33861387"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33861387",
"endSection": "abstract",
"offsetInBeginSection": 568,
"offsetInEndSection": 760,
"text": "Casimersen received its first approval on 25 February 2021, in the USA, for the treatment of DMD in patients who have a confirmed mutation of the DMD gene that is amenable to exon 45 skipping."
}
] | 12
|
BioASQ-training12b
| null | null |
64178ffb690f196b51000029
| 4,852
|
factoid
|
What is targeted by CIS43LS?
|
['Plasmodium falciparum']
|
[
"Plasmodium falciparum",
"P. falciparum",
"malaria parasite",
"falciparum malaria",
"Plasmodium species",
"P. falciparum malaria"
] |
['CIS43LS is a monoclonal antibody that targets Plasmodium falciparum.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34379916",
"http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"http://www.ncbi.nlm.nih.gov/pubmed/33332286"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "BACKGROUND: CIS43LS is a monoclonal antibody that was shown to protect against controlled Plasmodium falciparum infection in a phase 1 clinical trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 485,
"text": "METHODS: We conducted a phase 2 trial to assess the safety and efficacy of a single intravenous infusion of CIS43LS against P. falciparum infection in healthy adults in Mali over a 6-month malaria season."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"endSection": "abstract",
"offsetInBeginSection": 1748,
"offsetInEndSection": 1887,
"text": "CONCLUSIONS: CIS43LS was protective against P. falciparum infection over a 6-month malaria season in Mali without evident safety concerns. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33332286",
"endSection": "abstract",
"offsetInBeginSection": 1150,
"offsetInEndSection": 1306,
"text": "Based on these data, CIS43LS has advanced to phase I clinical trials, and AAV delivery provides a potential next-generation approach for malaria prevention."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34379916",
"endSection": "abstract",
"offsetInBeginSection": 104,
"offsetInEndSection": 342,
"text": "METHODS: We conducted a two-part, phase 1 clinical trial to assess the safety and pharmacokinetics of CIS43LS, an antimalarial monoclonal antibody with an extended half-life, and its efficacy against infection with Plasmodium falciparum. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34379916",
"endSection": "abstract",
"offsetInBeginSection": 1910,
"offsetInEndSection": 2095,
"text": "CONCLUSIONS: Among adults who had never had malaria infection or vaccination, administration of the long-acting monoclonal antibody CIS43LS prevented malaria after controlled infection."
}
] | 12
|
BioASQ-training12b
| null | null |
63eeefc5f36125a426000009
| 4,853
|
factoid
|
To which region of a gene does an RNA polymerase bind to initiate transcription?
|
['Promoter', 'DNA sequences called promoters', 'Promoter region']
|
[
"Promoter",
"Promoter region",
"DNA sequences called promoters",
"Gene promoter",
"Transcriptional promoter",
"Regulatory region",
"Core promoter",
"Proximal promoter",
"Distal promoter"
] |
['RNA polymerases initiate transcription at DNA sequences called promoters. Polymerases are integral factors of gene expression and are essential for the maintenance and transmission of genetic information.', 'RNA polymerases bind to the upstream region of genes on their promoters to initiate the process of transcription.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18521075",
"http://www.ncbi.nlm.nih.gov/pubmed/2497942",
"http://www.ncbi.nlm.nih.gov/pubmed/3309340",
"http://www.ncbi.nlm.nih.gov/pubmed/32297955",
"http://www.ncbi.nlm.nih.gov/pubmed/6537904",
"http://www.ncbi.nlm.nih.gov/pubmed/9311784",
"http://www.ncbi.nlm.nih.gov/pubmed/1175600",
"http://www.ncbi.nlm.nih.gov/pubmed/24503515",
"http://www.ncbi.nlm.nih.gov/pubmed/11298753",
"http://www.ncbi.nlm.nih.gov/pubmed/11433282",
"http://www.ncbi.nlm.nih.gov/pubmed/17997859",
"http://www.ncbi.nlm.nih.gov/pubmed/25693126",
"http://www.ncbi.nlm.nih.gov/pubmed/2649403",
"http://www.ncbi.nlm.nih.gov/pubmed/11439189",
"http://www.ncbi.nlm.nih.gov/pubmed/31863129",
"http://www.ncbi.nlm.nih.gov/pubmed/23086998",
"http://www.ncbi.nlm.nih.gov/pubmed/3113736",
"http://www.ncbi.nlm.nih.gov/pubmed/29168694",
"http://www.ncbi.nlm.nih.gov/pubmed/18648001"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32297955",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "RNA polymerases initiate transcription at DNA sequences called promoters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31863129",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 363,
"text": "Polymerases are integral factors of gene expression and are essential for the maintenance and transmission of genetic information. RNA polymerases (RNAPs) differ from other polymerases in that they can bind promoter sequences and initiate transcription de novo and this promoter recognition requires the presence of specific DNA binding domains in the polymerase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18648001",
"endSection": "abstract",
"offsetInBeginSection": 258,
"offsetInEndSection": 392,
"text": "conventional transcription factors trigger transcription by the RNA polymerase II (pol II) paused within the proximal promoter region."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11298753",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 238,
"text": "RNA polymerase is known to bind and utilize the overlapping promoters P1 and P2 in Escherichia coli galactose operon. We have identified an additional specific site upstream of P2, where RNA polymerase binds in a heparin-resistant manner."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2497942",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 431,
"text": "The binding region of the RNA polymerase extends from 30 base pairs (bp) upstream (-30) to 20 bp downstream (+20) from the in vivo transcription start site."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1175600",
"endSection": "abstract",
"offsetInBeginSection": 724,
"offsetInEndSection": 921,
"text": "It is concluded that RNA polymerase binding site and initiation site are identical parts of a promoter region, and that no \"drift\" between these sites is required as a step in RNA chain initiation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3113736",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Eukaryotic RNA polymerase I promoter binding is directed by protein contacts with transcription initiation factor and is DNA sequence-independent."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6537904",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "A Drosophila RNA polymerase II transcription factor contains a promoter-region-specific DNA-binding activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3113736",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 667,
"text": "We infer that polymerase is directed to the promoter by a DNA sequence-independent mechanism, solely by protein-protein contacts with TIF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17997859",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "BACKGROUND: RNA Polymerase II (RNAP II) is recruited to core promoters by the pre-initiation complex (PIC) of general transcript"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31863129",
"endSection": "abstract",
"offsetInBeginSection": 130,
"offsetInEndSection": 363,
"text": " RNA polymerases (RNAPs) differ from other polymerases in that they can bind promoter sequences and initiate transcription de novo and this promoter recognition requires the presence of specific DNA binding domains in the polymerase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31863129",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 363,
"text": "RNA polymerases (RNAPs) differ from other polymerases in that they can bind promoter sequences and initiate transcription de novo and this promoter recognition requires the presence of specific DNA binding domains in the polymerase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24503515",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 706,
"text": "Regulatory information for transcription initiation is present in a stretch of genomic DNA, called the promoter region that is located upstream of the transcription start site (TSS) of the gene. The promoter region interacts with different transcription factors and RNA polymerase to initiate transcription and contains short stretches of transcription factor binding sites (TFBSs), as well as structurally unique elements. Recent experimental and computational analyses of promoter sequences show that they often have non-B-DNA structural motifs, as well as some conserved structural properties, such as stability, bendability, nucleosome positioning preference and curvature, across a class of organisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18521075",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 260,
"text": "Early work identified two promoter regions, the -10 and -35 elements, that interact sequence specifically with bacterial RNA polymerase (RNAP). However, we now know that several additional promoter elements contact RNAP and influence transcription initiation. "
}
] | 12
|
BioASQ-training12b
| null | null |
64172bb2690f196b5100001e
| 4,855
|
factoid
|
At what range of ages usually occurs the loss of independent ambulation in Duchenne muscular dystrophy?
|
['7-13 years of age', 'between 7-13 years of age']
|
[
"7-13 years of age",
"between 7-13 years of age",
"ages 7 to 13",
"age range 7-13",
"7 to 13 years",
"7-13 years",
"from 7 to 13 years old"
] |
['The loss of independent ambulation in Duchenne muscular dystrophy typically occurs between the ages of 7 and 13 years.', 'The age of loss of ambulation is between 7-13 years of age.', 'The loss of independent ambulation in Duchenne muscular dystrophy usually occurs between 7-13 years of age.', 'The loss of independent ambulation typically occurs between the ages of 8 and 12 in Duchenne muscular dystrophy.', 'The loss of independent ambulation in Duchenne muscular dystrophy usually occurs between the ages of 7-13 years.', 'The loss of independent ambulation usually occurs between 7-13 years of age in Duchenne muscular dystrophy.', 'The average age of loss of independent ambulation in Duchenne muscular dystrophy is 8-12 years.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12026233",
"http://www.ncbi.nlm.nih.gov/pubmed/23440719",
"http://www.ncbi.nlm.nih.gov/pubmed/21784636",
"http://www.ncbi.nlm.nih.gov/pubmed/12466073",
"http://www.ncbi.nlm.nih.gov/pubmed/33215271",
"http://www.ncbi.nlm.nih.gov/pubmed/26022172",
"http://www.ncbi.nlm.nih.gov/pubmed/10382913",
"http://www.ncbi.nlm.nih.gov/pubmed/34924398",
"http://www.ncbi.nlm.nih.gov/pubmed/17388226",
"http://www.ncbi.nlm.nih.gov/pubmed/16322188",
"http://www.ncbi.nlm.nih.gov/pubmed/27382620",
"http://www.ncbi.nlm.nih.gov/pubmed/8496368"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34924398",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 195,
"text": " Duchenne muscular dystrophy (DMD) is an X-linked recessive genetic disorder, that is characterized by progressive muscle degeneration and loss of ambulation between 7-13 years of age."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27382620",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 225,
"text": "Duchenne muscular dystrophy is a progressive disease with loss of ambulation at around 9-10 years of age, followed, if untreated, by development of scoliosis, respiratory insufficiency, and death in the second decade of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33215271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 369,
"text": "BACKGROUND: Duchenne muscular dystrophy (DMD) is the most frequent genetic neuromuscular disease in childhood with loss of ambulation usually occurring around the age of 9-11 years.OBJECTIVE, MATERIAL AND METHODS: Based on current guidelines and clinical trials, neuropediatric and neurological experts developed recommendations for the treatment of nonambulatory DMD p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21784636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Patients with Duchenne muscular dystrophy (DMD) lose ambulation by age 12."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12026233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Duchenne muscular dystrophy is the most common and most severe form of childhood muscular dystrophies, resulting in early loss of ambulation between the ages of 7 and 13 years and death in the teens and twenties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10382913",
"endSection": "abstract",
"offsetInBeginSection": 635,
"offsetInEndSection": 816,
"text": "Loss of walking ability occurred in the control group at an average of 9.29 years (5.85-13.63, SD 1.98) and in the operated group at an average of 10.55 years (8.17-14.39, SD 1.76)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26022172",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 303,
"text": " The more severe Duchenne muscular dystrophy typically presents around ages 2 to 5 with gait disturbance, and historically has led to the loss of ambulation by age 12."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26022172",
"endSection": "abstract",
"offsetInBeginSection": 226,
"offsetInEndSection": 376,
"text": "it disturbance, and historically has led to the loss of ambulation by age 12. It is important for the practicing pediatrician, however, to be aware of"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12026233",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 243,
"text": "trophies, resulting in early loss of ambulation between the ages of 7 and 13 years and death in the teens and twenties. Despite the phenomenal advance"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16322188",
"endSection": "abstract",
"offsetInBeginSection": 211,
"offsetInEndSection": 361,
"text": "ked by progressive skeletal muscle weakness with loss of ambulation by 12 years of age. Death occurs in early adulthood secondary to respiratory or ca"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12466073",
"endSection": "abstract",
"offsetInBeginSection": 971,
"offsetInEndSection": 1058,
"text": "Loss of independent gait occurred at similar ages in both groups (10.3 vs. 10.5 years)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17388226",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 414,
"text": "Subsequently, the disease immobilizes the patient (ages 9 to 14 years) and severe respiratory failure occurs due to chest and vertebral column deformity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33215271",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 249,
"text": " childhood with loss of ambulation usually occurring around the age of 9-11 years.OBJECTIVE, MATERIAL AND METHODS: Based on current guidelines and cli"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16322188",
"endSection": "abstract",
"offsetInBeginSection": 214,
"offsetInEndSection": 364,
"text": " by progressive skeletal muscle weakness with loss of ambulation by 12 years of age. Death occurs in early adulthood secondary to respiratory or cardi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8496368",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 458,
"text": "To assess the effect of subcutaneous (s.c.) lower limb tenotomies on the ambulatory ability of patients with Duchenne muscular dystrophy (DMD), 54 patients were followed. Twenty-nine patients underwent hip, knee, and ankle tenotomies at a mean age of 10 2/12 years and were followed postoperatively for an average of 3 9/12 years. These children continued ambulation in long-leg braces to a mean age of 12 8/12 years and stood to an average of 13 5/12 years."
}
] | 12
|
BioASQ-training12b
| null | null |
641790d6690f196b5100002d
| 4,857
|
factoid
|
What is the process that generates multiple transcripts from the same gene?
|
['Alternative splicing', 'Alternative splicing (AS)']
|
[
"Alternative splicing",
"Alternative splicing (AS)",
"AS",
"Alternative RNA splicing",
"Variable splicing",
"Differential splicing"
] |
['The process that generates multiple transcripts from the same gene is called alternative splicing (AS). AS is a post-transcriptional regulatory mechanism that allows for the production of different mRNA isoforms from a single gene. This process can increase proteome diversity and regulate mRNA levels, which is important for expanding proteomic complexity and functional diversity in higher eukaryotes. In plants, AS may also serve as a buffer against stress-responsive transcriptomes to reduce the metabolic cost of translating all AS transcripts. While the contribution of AS to proteome complexity remains elusive in plants, it is clear that this process plays an important role in regulating gene expression and generating protein isoforms with distinct functions.', 'Alternative splicing generates multiple transcripts and potentially more than one protein from the same gene. It markedly enhances the coding capacity of the genome and can increase protein diversity which plays a crucial role in controlling development and stress responses.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18369186",
"http://www.ncbi.nlm.nih.gov/pubmed/30014301",
"http://www.ncbi.nlm.nih.gov/pubmed/2788825",
"http://www.ncbi.nlm.nih.gov/pubmed/16611169",
"http://www.ncbi.nlm.nih.gov/pubmed/28064309",
"http://www.ncbi.nlm.nih.gov/pubmed/20815140",
"http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"http://www.ncbi.nlm.nih.gov/pubmed/33406240",
"http://www.ncbi.nlm.nih.gov/pubmed/34383135",
"http://www.ncbi.nlm.nih.gov/pubmed/35269461",
"http://www.ncbi.nlm.nih.gov/pubmed/26273603",
"http://www.ncbi.nlm.nih.gov/pubmed/21896509",
"http://www.ncbi.nlm.nih.gov/pubmed/18088312",
"http://www.ncbi.nlm.nih.gov/pubmed/16054339",
"http://www.ncbi.nlm.nih.gov/pubmed/24369421",
"http://www.ncbi.nlm.nih.gov/pubmed/32811430",
"http://www.ncbi.nlm.nih.gov/pubmed/22811948",
"http://www.ncbi.nlm.nih.gov/pubmed/22961303",
"http://www.ncbi.nlm.nih.gov/pubmed/18817741",
"http://www.ncbi.nlm.nih.gov/pubmed/31921258",
"http://www.ncbi.nlm.nih.gov/pubmed/35821097",
"http://www.ncbi.nlm.nih.gov/pubmed/26327458",
"http://www.ncbi.nlm.nih.gov/pubmed/32484809",
"http://www.ncbi.nlm.nih.gov/pubmed/34440445",
"http://www.ncbi.nlm.nih.gov/pubmed/33629774",
"http://www.ncbi.nlm.nih.gov/pubmed/28402429",
"http://www.ncbi.nlm.nih.gov/pubmed/25577379",
"http://www.ncbi.nlm.nih.gov/pubmed/25577391",
"http://www.ncbi.nlm.nih.gov/pubmed/29074233",
"http://www.ncbi.nlm.nih.gov/pubmed/35327956",
"http://www.ncbi.nlm.nih.gov/pubmed/28273663",
"http://www.ncbi.nlm.nih.gov/pubmed/35339647"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Alternative splicing (AS) generates multiple transcripts from the same gene, however, AS contribution to proteome complexity remains elusive in plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"endSection": "abstract",
"offsetInBeginSection": 306,
"offsetInEndSection": 522,
"text": "We propose that plants employ AS not only to potentially increasing proteomic complexity, but also to buffer against the stress-responsive transcriptome to reduce the metabolic cost of translating all AS transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29074233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Alternative splicing, which generates multiple transcripts from the same gene, is an important modulator of gene expression that can increase proteome diversity and regulate mRNA levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22961303",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Alternative splicing, which generates multiple transcripts from the same gene and potentially different protein isoforms, is a key posttranscriptional regulatory mechanism for expanding proteomic diversity and functional complexity in higher eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24369421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Alternative splicing (AS), in higher eukaryotes, is one of the mechanisms of post-transcriptional regulation that generate multiple transcripts from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26273603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 245,
"text": "Over the past decade, alternative splicing has been progressively recognized as a major mechanism regulating gene expression patterns in different tissues and disease states through the generation of multiple mRNAs from the same gene transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35269461",
"endSection": "abstract",
"offsetInBeginSection": 317,
"offsetInEndSection": 497,
"text": "Alternative splicing is a physiological process by which cells generate several transcripts from one single gene and may in turn give rise to different proteins from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16054339",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 490,
"text": "However, as well as conventional splicing, several genes have the inherent capacity to undergo alternative splicing, thus allowing synthesis of multiple gene transcripts, perhaps with different functional properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18088312",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Alternative splicing (AS) increases the proteomic and functional capacity of genomes through the generation of alternative mRNA transcripts from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25577391",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 226,
"text": "Indeed, through AS individual gene loci can generate multiple RNAs from the same pre-mRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26327458",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Alternative splicing is an important biological process in the generation of multiple functional transcripts from the same genomic sequences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33406240",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Alternative splicing generates multiple transcript and protein isoforms from a single gene and controls transcript intracellular localization and stability by coupling to mRNA export and nonsense-mediated mRNA decay (NMD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31921258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Alternative Splicing (AS) is a mechanism that generates different mature transcripts from precursor mRNAs (pre-mRNAs) of the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16611169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Alternative splicing is a widespread mechanism in mammals that generates several mRNAs from one gene, thereby creating genetic diversity of the genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34440445",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Alternative pre-mRNA splicing plays a very important role in expanding protein diversity as it generates numerous transcripts from a single protein-coding gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32484809",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 534,
"text": " This task is complicated due to the complexity of alternative splicing - a mechanism by which the same gene may generate multiple distinct RNA transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28064309",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Alternative splicing of pre-mRNA is one of the main mechanisms regulating gene expression that generates multiple transcripts from one gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28402429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Alternative splicing generates multiple transcript and protein isoforms from the same gene and thus is important in gene expression regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34383135",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Alternative splicing is a widespread phenomenon, which generates multiple isoforms of the gene product."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18817741",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Alternative splicing of messenger RNA (mRNA) precursors generates multiple transcripts from a single primary transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32811430",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 223,
"text": "Among eukaryotic organisms, alternative splicing is an important process that can generate multiple transcripts from one same precursor messenger RNA, which greatly increase transcriptome and proteome diversity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21896509",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 156,
"text": " Alternative splicing (AS) is a pre-mRNA maturation process leading to the expression of multiple mRNA variants from the same primary transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33629774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 375,
"text": "Alternative splicing (AS) is a process that produces various mRNA splicing isoforms via different splicing patterns of mRNA precursors (pre-mRNAs). AS is the primary mechanism for increasing the types and quantities of proteins to improve biodiversity and influence multiple biological processes, including chromatin modification, signal transduction, and protein expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35821097",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 274,
"text": "Alternative splicing generates multiple transcripts from a single gene, enriching the diversity of proteins and phenotypic traits."
}
] | 12
|
BioASQ-training12b
| null | null |
6428da74690f196b51000052
| 4,860
|
factoid
|
What is the life expectancy for Duchenne muscular dystrophy patients?
|
['28.1 years of age', '28.1 years (95% CI 25.1, 30.3)']
|
[
"28.1 years of age",
"28.1 years",
"28.1 years (95% CI 25.1, 30.3)",
"28.1 years old"
] |
['The life expectancy for Duchenne muscular dystrophy patients varies depending on the time period they were born in, but patients born after 1990 have a median life expectancy of 28.1 years.', 'The life expectancy for Duchenne muscular dystrophy patients is around 28.1 years.', 'The life expectancy for Duchenne muscular dystrophy patients is typically between the late teens and early 30s.', 'The median life expectancy for Duchenne muscular dystrophy patients born after 1990 is 28.1 years (95% CI 25.1, 30.3).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34645707",
"http://www.ncbi.nlm.nih.gov/pubmed/10193393",
"http://www.ncbi.nlm.nih.gov/pubmed/17939910",
"http://www.ncbi.nlm.nih.gov/pubmed/26153505",
"http://www.ncbi.nlm.nih.gov/pubmed/34802091",
"http://www.ncbi.nlm.nih.gov/pubmed/1450492"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34645707",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1315,
"text": "Analyses stratified by 3 time periods in which patients were born showed markedly increased life expectancy in more recent patient populations; patients born after 1990 have a median life expectancy of 28.1 years (95% CI 25.1, 30.3)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34645707",
"endSection": "abstract",
"offsetInBeginSection": 1038,
"offsetInEndSection": 1411,
"text": "s (95% confidence interval [CI] 21.2, 22.4). Analyses stratified by 3 time periods in which patients were born showed markedly increased life expectancy in more recent patient populations; patients born after 1990 have a median life expectancy of 28.1 years (95% CI 25.1, 30.3).DISCUSSION: This article presents a full overview of mortality across the lifetime of a patient"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26153505",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 246,
"text": "Over the course of the last century, the average life expectancy of these patients has doubled and now stands at ∼25 years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34802091",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Duchenne muscular dystrophy (DMD) is a severe neuromuscular disorder with increasing life expectancy from late teens to over 30 years of age."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1450492",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "The special medical care in the National Sanatorium prolonged the life span of the patients with progressive muscular dystrophy from 15.8 years to 20.4 years over the last 20 years."
}
] | 12
|
BioASQ-training12b
| null | null |
64179aac690f196b51000037
| 4,862
|
factoid
|
What cells produce erythroferrone?
|
['erythroid precursors', 'Erythroblasts']
|
[
"erythroid precursors",
"Erythroblasts",
"erythrocyte precursors",
"red blood cell precursors",
"proerythroblasts",
"normoblasts",
"immature red blood cells"
] |
['The cells that produce erythroferrone are erythroid cells or erythroblasts.', 'Erythroferrone is produced by erythroid cells, specifically erythroblasts.', 'Erythroferrone is produced by erythroid progenitor cells.', 'Erythroblasts produce erythroferrone.', '. Erythroferrone, a factor produced and secreted by erythroid precursors in response to erythropoietin, has been identified and characterized as a suppressor of hepcidin synthesis to allow iron mobilization and facilitate erythropoiesis.', 'Erythroferrone is a hormone produced by erythroid progenitor cells in response to erythropoietin.', 'The hormone erythroferrone (ERFE) is produced by erythroid precursor cells in response to hemorrhage, hypoxia, or other erythropoietic stimuli.', 'Erythroferrone is produced by erythroid precursors or erythroid cells in response to certain stimuli such as erythropoietin, hemorrhage or hypoxia.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35628152",
"http://www.ncbi.nlm.nih.gov/pubmed/31649559",
"http://www.ncbi.nlm.nih.gov/pubmed/34772005",
"http://www.ncbi.nlm.nih.gov/pubmed/31723763",
"http://www.ncbi.nlm.nih.gov/pubmed/34002695",
"http://www.ncbi.nlm.nih.gov/pubmed/28739636",
"http://www.ncbi.nlm.nih.gov/pubmed/30097509",
"http://www.ncbi.nlm.nih.gov/pubmed/35464433",
"http://www.ncbi.nlm.nih.gov/pubmed/34614145",
"http://www.ncbi.nlm.nih.gov/pubmed/24880340",
"http://www.ncbi.nlm.nih.gov/pubmed/31899794"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35628152",
"endSection": "abstract",
"offsetInBeginSection": 892,
"offsetInEndSection": 1129,
"text": ". Erythroferrone, a factor produced and secreted by erythroid precursors in response to erythropoietin, has been identified and characterized as a suppressor of hepcidin synthesis to allow iron mobilization and facilitate erythropoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34614145",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "The hormone erythroferrone (ERFE) is produced by erythroid cells in response to hemorrhage, hypoxia, or other erythropoietic stimuli, and it suppresses the hepatic production of the iron-regulatory hormone hepcidin"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34614145",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Erythroid overproduction of erythroferrone causes iron overload and developmental abnormalities in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31723763",
"endSection": "abstract",
"offsetInBeginSection": 825,
"offsetInEndSection": 1012,
"text": "Here the hormone erythroferrone, produced by erythroblasts, acts on hepatocytes to suppress hepcidin production, and thereby increase dietary iron absorption and mobilization from stores."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35464433",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Erythroferrone is a recently identified erythroid regulator produced by erythroblasts in the mammalian bone marrow and extramedullary sites, known to be induced in conditions of anemia or blood loss."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34614145",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "The hormone erythroferrone (ERFE) is produced by erythroid cells in response to hemorrhage, hypoxia, or other erythropoietic stimuli, and it suppresses the hepatic production of the iron-regulatory hormone hepcidin, thereby mobilizing iron for erythropoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31899794",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Erythroferrone (ERFE) is produced by erythroblasts in response to erythropoietin (EPO) and acts in the liver to prevent hepcidin stimulation by BMP6."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28739636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Erythroferrone (ERFE) is a glycoprotein hormone secreted by erythroblasts in response to stimulation by erythropoietin (EPO)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34772005",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 396,
"text": "Erythroferrone (ERFE) is an iron-regulatory hormone which is highly expressed in erythroblasts by erythropoietin (EPO) stimulation and osteoblasts independently of EPO by sequestering bone morphogenetic proteins and inhibiting hepatic hepcidin expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24880340",
"endSection": "abstract",
"offsetInBeginSection": 354,
"offsetInEndSection": 418,
"text": "ERFE is produced by erythroblasts in response to erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24880340",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 418,
"text": " ERFE is produced by erythroblasts in response to erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30097509",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 274,
"text": "Erythropoietin (EPO) enhances erythroferrone (ERFE) synthesis by erythroblasts, and ERFE suppresses hepatic hepcidin production through an unknown mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24880340",
"endSection": "abstract",
"offsetInBeginSection": 305,
"offsetInEndSection": 455,
"text": "pcidin suppression during stress erythropoiesis. ERFE is produced by erythroblasts in response to erythropoietin. ERFE-deficient mice fail to suppress"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35628152",
"endSection": "abstract",
"offsetInBeginSection": 894,
"offsetInEndSection": 1129,
"text": "Erythroferrone, a factor produced and secreted by erythroid precursors in response to erythropoietin, has been identified and characterized as a suppressor of hepcidin synthesis to allow iron mobilization and facilitate erythropoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31649559",
"endSection": "abstract",
"offsetInBeginSection": 1704,
"offsetInEndSection": 1964,
"text": "The paradigm is non-transfusion-dependent thalassemia where the release of erythroferrone from the expanded pool of immature erythroid cells results in hepcidin suppression and secondary iron overload that in turn worsens ineffective erythropoiesis and anemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30097509",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 437,
"text": "Decreased hepcidin mobilizes iron, which facilitates erythropoiesis, but excess iron is pathogenic in β-thalassemia. Erythropoietin (EPO) enhances erythroferrone (ERFE) synthesis by erythroblasts, and ERFE suppresses hepatic hepcidin production through an unknown mechanism. The BMP/SMAD pathway in the liver is critical for hepcidin control, and we show that EPO suppressed hepcidin and other BMP target genes in vivo in a partially ERF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34002695",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 421,
"text": "Background: Erythroblast erythroferrone (ERFE) secretion inhibits hepcidin expression by sequestering several bone morphogenetic protein (BMP) family members to increase iron availability for erythropoiesis.Methods: To address whether ERFE functions also in bone and whether the mechanism of ERFE action in bone involves BMPs, we utilize the Erfe-/- mouse model as well as β-thalassemic (Hbbth3/+) mice with systemic loss"
}
] | 12
|
BioASQ-training12b
| null | null |
6422ee03690f196b51000046
| 4,864
|
factoid
|
What does FBDD stand for?
|
['fragment-based drug discovery']
|
[
"fragment-based drug discovery",
"fragment-based lead discovery",
"fragment-based screening",
"fragment-based approach",
"fragment-based design"
] |
['FBDD stands for fragment-based drug discovery.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33226222"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33226222",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Fragment-based drug discovery (FBDD) has grown and matured to a point where it is valuable to keep track of its extent and details of application. "
}
] | 12
|
BioASQ-training12b
| null | null |
6415c0df690f196b51000010
| 4,866
|
factoid
|
What are PROTACs?
|
["bifunctional molecules that hijack the cell's ubiquitin-proteasome system (UPS)"]
|
[
"bifunctional molecules that hijack the cell's ubiquitin-proteasome system (UPS)",
"ubiquitin-proteasome system hijackers",
"UPS hijackers",
"ubiquitin-proteasome system modulators",
"bifunctional UPS inhibitors",
"ubiquitin-proteasome pathway disruptors"
] |
["Proteolysis-targeting chimeras (PROTACs) are bifunctional molecules that hijack the cell's ubiquitin-proteasome system (UPS)."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36255625"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255625",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 313,
"text": "Proteolysis-targeting chimeras (PROTACs) are bifunctional molecules that hijack the cell's ubiquitin-proteasome system (UPS)."
}
] | 12
|
BioASQ-training12b
| null | null |
6412331b201352f04a000038
| 4,874
|
factoid
|
Which form of cancer have paclitaxel, docetaxel, doxorubicin, and epirubicin been approved for?
|
['Triple negative breast cancer']
|
[
"Triple negative breast cancer",
"TNBC",
"Triple-negative breast carcinoma",
"Triple-negative breast neoplasm"
] |
['Paclitaxel, docetaxel, doxorubicin, and epirubicin have been longstanding, Food and Drug Administration (FDA)-approved therapies against \nTriple negative breast cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35976445"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35976445",
"endSection": "abstract",
"offsetInBeginSection": 631,
"offsetInEndSection": 773,
"text": "Paclitaxel, docetaxel, doxorubicin, and epirubicin have been longstanding, Food and Drug Administration (FDA)-approved therapies against TNBC."
}
] | 12
|
BioASQ-training12b
| null | null |
6415c8f1690f196b51000017
| 4,878
|
factoid
|
Talquetamab was developed for treatment of which disease?
|
['multiple myeloma']
|
[
"multiple myeloma",
"plasma cell myeloma",
"myeloma",
"Kahler's disease",
"myelomatosis"
] |
['Talquetamab was developed for treatment of multiple myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36352205",
"http://www.ncbi.nlm.nih.gov/pubmed/36006441"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36006441",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Effects of teclistamab and talquetamab on soluble BCMA levels in patients with relapsed/refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36006441",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 406,
"text": "The bispecific antibodies teclistamab (BCMA×CD3) and talquetamab (G protein-coupled receptor family C group 5 member D [GPRC5D]×CD3) are in clinical development as therapies for MM. "
}
] | 12
|
BioASQ-training12b
| null | null |
63eeec79f36125a426000006
| 4,879
|
factoid
|
What human cells are usually targeted with a Gal-Nac conjugated siRNA or ASO
|
['hepatocytes', 'liver cells']
|
[
"hepatocytes",
"liver cells",
"hepatic cells",
"liver parenchymal cells",
"hepatocyte",
"hepatocyte cells"
] |
['Gal-Nac conjugated siRNAs or ASOs are usually targeted to human hepatocytes, as they have a high affinity with the asialoglycoprotein receptor (ASGPR) on the surface of these cells.', 'GalNAc-conjugated siRNA or ASO typically target human liver cells, specifically hepatocytes, through the asialoglycoprotein receptor (ASGPR) mediated uptake.', 'Gal-Nac conjugated siRNA or ASO are usually targeted to human hepatocytes, which are the main target for gene therapy.', 'Gal-Nac conjugated siRNAs or ASOs are usually targeted to liver cells.', 'GalNAc conjugated siRNA or ASO are usually targeted towards liver hepatocytes.', 'N-acetylgalactosamine is a targeting moiety for liver hepatocytes,']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24992960",
"http://www.ncbi.nlm.nih.gov/pubmed/30576769",
"http://www.ncbi.nlm.nih.gov/pubmed/31303442",
"http://www.ncbi.nlm.nih.gov/pubmed/35819583",
"http://www.ncbi.nlm.nih.gov/pubmed/33928570",
"http://www.ncbi.nlm.nih.gov/pubmed/35997897",
"http://www.ncbi.nlm.nih.gov/pubmed/35251767",
"http://www.ncbi.nlm.nih.gov/pubmed/26907624"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33928570",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 672,
"text": "Most siRNA therapeutic efforts to date have focused on the treatment of liver diseases due to major breakthroughs in the development of efficient strategies for delivering siRNA drugs to the liver. Indeed, the development of lipid nanoparticle-formulated and GalNAc-conjugated siRNA therapeutics has resulted in recent FDA approvals of the first siRNA-based drugs, patisiran for the treatment of hereditary transthyretin amyloidosis and givosiran for the treatment of acute hepatic porphyria, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35997897",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 529,
"text": "the first siRNA drugs received approval for clinical use by the US Food and Drug Administration and the European Medicines Agency between 2018 and 2022. These are mainly based on an siRNA conjugation with a targeting moiety for liver hepatocytes, N-acetylgalactosamine,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35819583",
"endSection": "abstract",
"offsetInBeginSection": 343,
"offsetInEndSection": 476,
"text": "GalNAc-conjugated siRNAs rapidly distribute into the liver via asialoglycoprotein receptor (ASGPR) mediated uptake in the hepatocytes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35819583",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 342,
"text": "hree such products (givosiran, lumasiran and inclisiran) are liver-targeted, using tris N-acetylgalactosamine (GalNAc)3 as the targeting ligand. Upon subcutaneous administration,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35251767",
"endSection": "abstract",
"offsetInBeginSection": 550,
"offsetInEndSection": 726,
"text": "Beyond that, we show that GalNAc-conjugated siRNAs with bulges at certain positions of the guide strand repress transthyretin in murine primary hepatocytes and in vivo in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31303442",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 457,
"text": "One example is the targeted delivery of ASOs to hepatocytes, achieved with N-acetylgalactosamine (GalNAc) conjugation to ASO, which results in selective uptake by asialoglycoprotein receptor (ASGR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30576769",
"endSection": "abstract",
"offsetInBeginSection": 528,
"offsetInEndSection": 1289,
"text": "ng and NAFLD/NASH. Here, we studied the metabolic benefit of liver-specific STK25 inhibitors on NAFLD development and progression in a mouse model of diet-induced obesity.METHODS: We developed a hepatocyte-specific triantennary N-acetylgalactosamine (GalNAc)-conjugated antisense oligonucleotide (ASO) targeting Stk25 and evaluated its effect on NAFLD features in mice after chronic exposure to dietary lipids.RESULTS: We found that systemic administration of hepatocyte-targeting GalNAc-Stk25 ASO in obese mice effectively ameliorated steatosis, inflammatory infiltration, hepatic stellate cell activation, nutritional fibrosis, and hepatocellular damage in the liver compared with mice treated with GalNAc-conjugated nontargeting ASO, without any systemic tox"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24992960",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Triantennary N-acetyl galactosamine (GalNAc, GN3: ), a high-affinity ligand for the hepatocyte-specific asialoglycoprotein receptor (ASGPR), enhances the potency of second-generation gapmer antisense oligonucleotides (ASOs) 6-10-fold in mouse liver."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26907624",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "TriantennaryN-acetyl galactosamine (GalNAc, GN3) and lipophilic ligands such as cholesterol andα-tocopherol conjugations dramatically improve the distribution and efficacy of second-generation antisense oligonucleotides (ASOs) in the whole liver."
}
] | 12
|
BioASQ-training12b
| null | null |
6422e2f1690f196b51000043
| 4,884
|
factoid
|
The X-inactive specific transcript (Xist) gene is responsible for mediating the X-chromosome inactivation in females, where one X-chromosome is silenced and transcriptionally inactivated. What does Xist encode?
|
['Long non-coding RNA', 'lncRNA', 'long non-coding (lnc) RNA', 'long noncoding RNA']
|
[
"Long non-coding RNA",
"lncRNA",
"long non-coding (lnc) RNA",
"long noncoding RNA"
] |
['Xist is a gene that encodes a long noncoding RNA molecule, which plays a central role in inducing X-chromosome inactivation in female mammals. The Xist RNA has two major splicing variants: long and short isoforms. It is expressed exclusively from the inactive X chromosome and required for the silencing of most genes on that chromosome. The specific localization of Xist transcripts to the inactive X is important for silencing, but it is not known how these transcripts localize to the inactive X chromosome. Silencing on the inactive X chromosome coincides with the acquisition of chromatin modifications, resulting in the formation of extraordinarily stable facultative heterochromatin that is faithfully propagated through subsequent cell divisions. The integration of all these processes requires a region of the X chromosome known as the X-inactivation center, which contains the Xist gene and its cis-regulatory elements.', 'The Xist gene encodes a long non-coding (lnc) RNA that is expressed exclusively from the inactive X chromosome in female mammals and is required for the silencing of most of the genes on the chromosome.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16679409",
"http://www.ncbi.nlm.nih.gov/pubmed/28947655",
"http://www.ncbi.nlm.nih.gov/pubmed/29302591",
"http://www.ncbi.nlm.nih.gov/pubmed/20950563",
"http://www.ncbi.nlm.nih.gov/pubmed/33348832",
"http://www.ncbi.nlm.nih.gov/pubmed/30539545",
"http://www.ncbi.nlm.nih.gov/pubmed/23166390",
"http://www.ncbi.nlm.nih.gov/pubmed/26004255",
"http://www.ncbi.nlm.nih.gov/pubmed/28236732",
"http://www.ncbi.nlm.nih.gov/pubmed/21212949",
"http://www.ncbi.nlm.nih.gov/pubmed/30496473",
"http://www.ncbi.nlm.nih.gov/pubmed/30091314",
"http://www.ncbi.nlm.nih.gov/pubmed/12429693",
"http://www.ncbi.nlm.nih.gov/pubmed/26739568",
"http://www.ncbi.nlm.nih.gov/pubmed/14973270",
"http://www.ncbi.nlm.nih.gov/pubmed/30171939",
"http://www.ncbi.nlm.nih.gov/pubmed/26477563",
"http://www.ncbi.nlm.nih.gov/pubmed/25747039",
"http://www.ncbi.nlm.nih.gov/pubmed/29701779",
"http://www.ncbi.nlm.nih.gov/pubmed/26282267",
"http://www.ncbi.nlm.nih.gov/pubmed/25000994",
"http://www.ncbi.nlm.nih.gov/pubmed/17333537",
"http://www.ncbi.nlm.nih.gov/pubmed/12900550",
"http://www.ncbi.nlm.nih.gov/pubmed/28408975",
"http://www.ncbi.nlm.nih.gov/pubmed/25200388",
"http://www.ncbi.nlm.nih.gov/pubmed/31537017",
"http://www.ncbi.nlm.nih.gov/pubmed/20657585",
"http://www.ncbi.nlm.nih.gov/pubmed/32482714",
"http://www.ncbi.nlm.nih.gov/pubmed/29237010",
"http://www.ncbi.nlm.nih.gov/pubmed/12492109",
"http://www.ncbi.nlm.nih.gov/pubmed/29910081",
"http://www.ncbi.nlm.nih.gov/pubmed/23816838",
"http://www.ncbi.nlm.nih.gov/pubmed/21626138",
"http://www.ncbi.nlm.nih.gov/pubmed/32535328",
"http://www.ncbi.nlm.nih.gov/pubmed/34178980",
"http://www.ncbi.nlm.nih.gov/pubmed/22722828",
"http://www.ncbi.nlm.nih.gov/pubmed/26489649",
"http://www.ncbi.nlm.nih.gov/pubmed/11780141",
"http://www.ncbi.nlm.nih.gov/pubmed/25489864"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29237010",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 347,
"text": "Xist encodes a long noncoding RNA which is a central player to induce X-chromosome inactivation in female mammals and has two major splicing variants: long and short isoforms of Xist RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12492109",
"endSection": "abstract",
"offsetInBeginSection": 446,
"offsetInEndSection": 628,
"text": "XIST encodes a spliced noncoding polyadenylated transcript that is unique in being expressed exclusively from the inactive X chromosome and is involved in the X-inactivation process."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12900550",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 375,
"text": "XIST encodes a functional RNA that is expressed exclusively from the inactive X in female mammals and is required for the silencing of most of the genes on the chromosome. XIST transcripts remain in the nucleus, and their specific localization to the inactive X is important for silencing; however, it is not known how these transcripts localize to the inactive X chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12429693",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Dosage compensation in mammals is achieved by the transcriptional inactivation of one X chromosome in female cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12429693",
"endSection": "abstract",
"offsetInBeginSection": 516,
"offsetInEndSection": 1143,
"text": "Silencing on the inactive X chromosome coincides with the acquisition of a multitude of chromatin modifications, resulting in the formation of extraordinarily stable facultative heterochromatin that is faithfully propagated through subsequent cell divisions. The integration of all these processes requires a region of the X chromosome known as the X-inactivation center, which contains the Xist gene and its cis-regulatory elements. Xist encodes an RNA molecule that plays critical roles in the choice of which X chromosome remains active, and in the initial spread and establishment of silencing on the inactive X chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30496473",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "X-inactive-specific transcript (Xist) is a long noncoding RNA (lncRNA) essential for inactivating one of the two X chromosomes in mammalian females."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26739568",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "X-inactive specific transcript (Xist) long noncoding RNA (lncRNA) is thought to catalyze silencing of X-linked genes in cis during X-chromosome inactivation, which equalizes X-linked gene dosage between male and female mammals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17333537",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 360,
"text": "In eutherian mammals X inactivation is regulated by the X-inactive specific transcript (Xist), a cis-acting non-coding RNA that triggers silencing of the chromosome from which it is transcribed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26477563",
"endSection": "abstract",
"offsetInBeginSection": 246,
"offsetInEndSection": 451,
"text": " The X-linked Xist long non-coding RNA functions as an X inactivation master regulator; Xist is selectively upregulated from the prospective inactive X chromosome and is required in cis for X inactivation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26489649",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "The long noncoding X-inactivation-specific transcript (Xist gene) is responsible for mammalian X-chromosome dosage compensation between the sexes, the process by which one of the two X chromosomes is inactivated in the female soma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25747039",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "X chromosome inactivation (X-inactivation) is triggered by X-linked noncoding Xist RNA, which is expressed asymmetrically from one of the two X chromosomes in females and coats it in cis to induce chromosome-wide silencing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25489864",
"endSection": "abstract",
"offsetInBeginSection": 459,
"offsetInEndSection": 651,
"text": " X-inactive specific transcript (Xist) lncRNA accumulation (called an Xist cloud) on one of the two X-chromosomes in mammalian females is a critical step to initiate X-chromosome inactivation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30539545",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "X-inactive specific transcript (Xist) is a long noncoding RNA that is essential for initiating and maintaining epigenetic silencing of one copy of the X chromosome in mammalian females."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20657585",
"endSection": "abstract",
"offsetInBeginSection": 81,
"offsetInEndSection": 192,
"text": "Xist encodes a noncoding RNA that influences the probability that the cis-linked X chromosome will be silenced."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21626138",
"endSection": "abstract",
"offsetInBeginSection": 187,
"offsetInEndSection": 309,
"text": "Central to XCI is the long non-coding RNA Xist, which is highly and specifically expressed from the inactive X chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25200388",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 406,
"text": "While most genes are silenced on the inactive X chromosome, the gene for the long non-coding RNA XIST is silenced on the active X chromosome and expressed from the inactive X chromosome with which the XIST RNA associates, triggering silencing of the chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25000994",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 330,
"text": "In mammals, the process of X-chromosome inactivation ensures equivalent levels of X-linked gene expression between males and females through the silencing of one of the two X chromosomes in female cells. The process is established early in development and is initiated by a unique locus, which produces a long noncoding RNA, Xist."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32482714",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 323,
"text": "The X inactive-specific transcript (Xist) gene is the master regulator of X chromosome inactivation in mammals. Xist produces a long noncoding (lnc)RNA that accumulates over the entire length of the chromosome from which it is transcribed, recruiting factors to modify underlying chromatin and silence X-linked genes in cis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20950563",
"endSection": "abstract",
"offsetInBeginSection": 118,
"offsetInEndSection": 341,
"text": "This process, known as X-chromosome inactivation, relies on monoallelic activation of the Xist gene. Xist produces a non-coding RNA that can coat the chromosome from which it is transcribed in cis and trigger its silencing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29701779",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 568,
"text": "The process of inactivation is initiated by the long non-coding RNA X-inactive specific transcript (XIST) and achieved through interaction with multiple synergistic silencing pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23166390",
"endSection": "abstract",
"offsetInBeginSection": 470,
"offsetInEndSection": 628,
"text": "The Xist gene produces a non-coding RNA that functions as the primary switch for X-inactivation, coating the X chromosome from which it is transcribed in cis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14973270",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Xist (X-inactive specific transcript) plays a crucial role in X-inactivation. This non-coding RNA becomes upregulated on the X chromosome that is to be inactivated upon differentiation."
}
] | 12
|
BioASQ-training12b
| null | null |
6429ad3857b1c7a315000003
| 4,889
|
factoid
|
Which amino acid in implicated in the Blue diaper syndrome?
|
['tryptophan']
|
[
"tryptophan",
"L-tryptophan",
"α-amino-β-(3-indolyl)propionic acid",
"indole-3-amino acid",
"Trp"
] |
['Blue diaper syndrome is an extremely rare disorder with characteristic finding is a bluish discoloration of urine spots in the diapers of affected infants. An intestinal defect of tryptophan absorption was postulated as the underlying pathology.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29610180",
"http://www.ncbi.nlm.nih.gov/pubmed/1818237"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29610180",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 477,
"text": "Blue diaper syndrome (BDS) (Online Mendelian Inheritance in Man number 211000) is an extremely rare disorder that was first described in 1964. The characteristic finding is a bluish discoloration of urine spots in the diapers of affected infants. Additional clinical features of the first described patients included diarrhea, inadequate weight gain, hypercalcemia, and nephrocalcinosis. An intestinal defect of tryptophan absorption was postulated as the underlying pathology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1818237",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "We describe the ocular abnormalities seen in a new metabolic disease which is deficient in the transport of tryptophan. "
}
] | 12
|
BioASQ-training12b
| null | null |
63f57d9b33942b094c000004
| 4,893
|
factoid
|
What is the cause of Friedreich's Ataxia (FA)?
|
['triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene', 'triplet repeat in the FXN gene', 'GAA repeat expansion', 'GAA repeat expansion in intron 1 of the FXN gene', 'FXN Gene Mutation', 'riplet guanine-adenine-adenine (gaa) repeat expansion in intron 1 of the fxn gene', 'frataxin deficiency']
|
[
"triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene",
"triplet repeat in the FXN gene",
"GAA repeat expansion",
"GAA repeat expansion in intron 1 of the FXN gene",
"FXN Gene Mutation",
"triplet guanine-adenine-adenine (gaa) repeat expansion in intron 1 of the fxn gene",
"frataxin deficiency",
"GAA repeat",
"FXN mutation",
"frataxin gene mutation",
"frataxin",
"FXN"
] |
["Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disorder caused by a triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene, which leads to decreased levels of the frataxin protein.", "Friedreich's Ataxia is caused by a triplet GAA repeat expansion in the FXN gene.", "Friedreich's ataxia (FA) is an autosomal recessive neurodegenerative disorder caused by a triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene, which leads to decreased levels of the frataxin protein.", "Friedreich's Ataxia (FA) is caused by a triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene, leading to decreased levels of the frataxin protein.", "Friedreich's Ataxia (FA) is caused by an autosomal recessive inheritance of a GAA repeat expansion in the FXN gene. This results in decreased levels of the frataxin protein, leading to the disorder.", "Friedreich's Ataxia (FA) is an autosomal recessive neurodegenerative disorder caused by a triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene, which leads to decreased levels of the frataxin protein.", "Friedreich's Ataxia (FA) is caused by a triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene, which leads to decreased levels of the frataxin protein.", "Friedreich's Ataxia is caused by a triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene.", "Friedreich's Ataxia is an autosomal recessive neurodegenerative disorder caused by a GAA repeat expansion in the FXN gene. This results in decreased levels of the frataxin protein."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35289725",
"http://www.ncbi.nlm.nih.gov/pubmed/9630233",
"http://www.ncbi.nlm.nih.gov/pubmed/35850241",
"http://www.ncbi.nlm.nih.gov/pubmed/16344344",
"http://www.ncbi.nlm.nih.gov/pubmed/16581313",
"http://www.ncbi.nlm.nih.gov/pubmed/24152405",
"http://www.ncbi.nlm.nih.gov/pubmed/35038030",
"http://www.ncbi.nlm.nih.gov/pubmed/25831023"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35850241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disorder caused by a triplet guanine-adenine-adenine (GAA) repeat expansion in intron 1 of the FXN gene, which leads to decreased levels of the frataxin protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9630233",
"endSection": "abstract",
"offsetInBeginSection": 225,
"offsetInEndSection": 403,
"text": "The classic form of autosomal recessive ataxia, Friedreich's ataxia (FA), is now known to be due to an intronic expansion of a guanine-adenine-adenine (GAA)-trinucleotide repeat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16581313",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Friedreich's Ataxia (FA) is the commonest genetic cause of ataxia and is associated with the expansion of a GAA repeat in intron 1 of the frataxin gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25831023",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Reduced expression of the mitochondrial protein Frataxin (FXN) is the underlying cause of Friedreich's ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24152405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Friedreich Ataxia (FA) is the most common hereditary ataxia, caused by abnormal expansion of the GAA triplet of the first intron of the X25 gene on chromosome 9."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16344344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "BACKGROUND: Friedreich ataxia (FA), the most common hereditary ataxia, is caused by pathological expansion of GAA repeats in the first intron of the X25 gene on c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35038030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Friedreich Ataxia (FA) is a rare neuro-cardiodegenerative disease caused by mutations in the frataxin (FXN) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35289725",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Friedreich's ataxia (FA) is an inherited neurodegenerative disorder caused by decreased expression of frataxin (FXN) protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16344344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "BACKGROUND: Friedreich ataxia (FA), the most common hereditary ataxia, is caused by pathological expansion of GAA repeats in the first intron of the X25 gene on chromosome 9"
}
] | 12
|
BioASQ-training12b
| null | null |
6450ec0c57b1c7a31500008f
| 4,897
|
factoid
|
What are positive cell-cycle regulators that can cause cancer when mutated called?
|
['Proto-oncogenes']
|
[
"Proto-oncogenes",
"Proto-oncogene",
"Oncogenes",
"Oncogene",
"Cancer genes",
"Tumorigenic genes"
] |
['Proto-oncogenes are normal regulatory genes that can be transformed - by gain-of-function mutations - to oncogenes which are important contributors to human carcinogenesis.', 'Positive cell-cycle regulators that can cause cancer when mutated are called oncogenes. These genes are gain-of-function mutations of normal regulatory genes or proto-oncogenes, which are altered by point mutation, amplification or rearrangement. Oncogenes were originally discovered in retroviruses initiating a variety of animal and avian cancers, and they are believed to be important contributors to human carcinogenesis. When activated, oncogenes promote cell proliferation and inhibit apoptosis, leading to uncontrolled growth and tumor formation. Some examples of well-known oncogenes include HER2/neu, KRAS, BRAF, and MYC. Mutations in these genes have been implicated in various types of cancer such as breast cancer, lung cancer, melanoma, and leukemia. Understanding the role of oncogenes in cancer development is crucial for the development of targeted therapies aimed at inhibiting their activity and preventing tumor growth.', 'Oncogenes are gain-of-function mutations of normal regulatory genes or proto-oncogenes. Originally discovered in retroviruses initiating a variety of animal and avian cancers, oncogenes are believed to be important contributors to human carcinogenesis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12665054",
"http://www.ncbi.nlm.nih.gov/pubmed/1546217",
"http://www.ncbi.nlm.nih.gov/pubmed/8143345",
"http://www.ncbi.nlm.nih.gov/pubmed/10697588"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10697588",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 331,
"text": "Oncogenes are gain-of-function mutations of normal regulatory genes or proto-oncogenes. Originally discovered in retroviruses initiating a variety of animal and avian cancers, oncogenes are believed to be important contributors to human carcinogenesis. Proto-oncogenes are altered by point mutation, amplification or rearrangement."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12665054",
"endSection": "abstract",
"offsetInBeginSection": 340,
"offsetInEndSection": 599,
"text": "Aberrant proteolysis with oncogenic potential is elicited by two major mechanisms: defective degradation of positive cell cycle regulators (i.e., proto-oncoproteins) and enhanced degradation of negative cell cycle regulators (i.e., tumor suppressor proteins)."
}
] | 12
|
BioASQ-training12b
| null | null |
644ef46557b1c7a315000083
| 4,900
|
factoid
|
What is the inheritance pattern of hereditary angioedema?
|
['autosomal dominant']
|
[
"autosomal dominant",
"AD",
"autosomal dominant inheritance",
"dominant inheritance",
"dominant trait"
] |
['Hereditary angioedema (HAE) is an autosomal dominant disorder.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27965672"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27965672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Hereditary angioedema (HAE) is a rare autosomal dominant disorder caused by mutations of the SERPING1 or the Factor 12 genes."
}
] | 12
|
BioASQ-training12b
| null | null |
6432fdd857b1c7a315000020
| 4,901
|
factoid
|
What is usually the onset age of Friedreich's Ataxia?
|
['first or second decade', 'before age 25', 'the first or second decade']
|
[
"first or second decade",
"before age 25",
"the first or second decade",
"first decade",
"second decade",
"teenage years",
"young adulthood"
] |
["The onset of Friedreich's Ataxia is usually in the first or second decade.", "Friedreich's Ataxia typically has an onset age in the first or second decade.", "Friedreich's ataxia typically has an onset age in the first or second decade of life.", "The usual onset age of Friedreich's Ataxia is before the age of 25.", "The onset age of Friedreich's Ataxia is typically in the first or second decade of a person's life.", "During the first or second decade is usually the onset age of Friedreich's Ataxia.", 'The classical form of FRDA typically presents between 10 to 20 years of age. \nHowever, it can also present much later than this, including into adulthood.', "Friedreich's ataxia is classically considered a disease with onset in the first or second decade.", "The onset age of Friedreich's Ataxia is typically in the first or second decade of life.", "the onset age of friedreich's ataxia is classically considered to be in the first or second decade.", "Friedreich's ataxia is usually considered a disease with onset in the first or second decade."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26388117",
"http://www.ncbi.nlm.nih.gov/pubmed/11586299",
"http://www.ncbi.nlm.nih.gov/pubmed/9553847",
"http://www.ncbi.nlm.nih.gov/pubmed/31467149",
"http://www.ncbi.nlm.nih.gov/pubmed/16092110",
"http://www.ncbi.nlm.nih.gov/pubmed/8677022",
"http://www.ncbi.nlm.nih.gov/pubmed/25566998",
"http://www.ncbi.nlm.nih.gov/pubmed/25685137",
"http://www.ncbi.nlm.nih.gov/pubmed/26754264"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31467149",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Friedreich's ataxia is classically considered a disease with onset in the first or second decade."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26388117",
"endSection": "abstract",
"offsetInBeginSection": 57,
"offsetInEndSection": 218,
"text": " age of 25. Rare variants have been described, such as late-onset Friedreich's ataxia and very-late-onset Friedreich's ataxia, occurring after 25 and 40 years, r"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8677022",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "The onset of Friedreich ataxia (FA) was before 10 years of age in 36 out of 95 personally observed patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11586299",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 299,
"text": "Friedreich ataxia (FRDA), the most common autosomal recessive neurodegenerative disease among Europeans and people of European descent, is characterized by an early onset (usually before the age of 25), progressive ataxia, sensory loss, absence of tendon reflexes and pyramidal weakness of the legs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16092110",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Very late-onset Friedreich's ataxia (VLOFA) is characterized by symptomatic onset after 40 years of age and, usually, a benign phenotype."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25685137",
"endSection": "abstract",
"offsetInBeginSection": 394,
"offsetInEndSection": 634,
"text": "Onset is usually in the first or second decade of life; however, late-onset cases of Freidreich ataxia (LOFA), after the age of 25 years, and very late-onset cases of Freidreich ataxia (VLOFA), after the age of 40 years, have been reported."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26754264",
"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 369,
"text": "Disease begins after the age of 25 in occasional patients (late-onset Friedreich ataxia (LOFA))."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25566998",
"endSection": "abstract",
"offsetInBeginSection": 871,
"offsetInEndSection": 1101,
"text": "ing Scale and EQ-5D. The Friedreich's ataxia cohort was subdivided into three groups: early disease onset (≤14 years), intermediate onset (15-24 years), and late onset (≥25 years), which were compared for clinical characteristics "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26754264",
"endSection": "abstract",
"offsetInBeginSection": 272,
"offsetInEndSection": 369,
"text": " Disease begins after the age of 25 in occasional patients (late-onset Friedreich ataxia (LOFA))."
}
] | 12
|
BioASQ-training12b
| null | null |
6450ede757b1c7a315000090
| 4,902
|
factoid
|
What disease was the topic of the World Hip Trauma Evaluation (WHiTE) trial?
|
['hip fracture']
|
[
"hip fracture",
"femoral neck fracture",
"proximal femur fracture",
"hip joint fracture",
"intracapsular hip fracture",
"extracapsular hip fracture",
"intertrochanteric fracture",
"subcapital fracture"
] |
['The World Hip Trauma Evaluation (WHiTE) was set up to measure outcome of patients with hip fracture.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33630700",
"http://www.ncbi.nlm.nih.gov/pubmed/35909375",
"http://www.ncbi.nlm.nih.gov/pubmed/26825319",
"http://www.ncbi.nlm.nih.gov/pubmed/27797994"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35909375",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Cost-utility analysis of cemented hemiarthroplasty versus hydroxyapatite-coated uncemented hemiarthroplasty for the treatment of displaced intracapsular hip fractures : the World Hip Trauma Evaluation 5 (WHiTE 5) trial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33630700",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "A randomized clinical trial of low dose single antibiotic-loaded cement versus high dose dual antibiotic-loaded cement in patients receiving a hip hemiarthroplasty after fracture: A protocol for the WHiTE 8 COPAL study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26825319",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "The World Hip Trauma Evaluation Study 3: Hemiarthroplasty Evaluation by Multicentre Investigation - WHITE 3: HEMI - An Abridged Protocol."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27797994",
"endSection": "abstract",
"offsetInBeginSection": 253,
"offsetInEndSection": 405,
"text": "METHODS AND ANALYSIS: The World Hip Trauma Evaluation (WHiTE) was set up to measure outcome in a comprehensive cohort of UK patients with hip fracture. "
}
] | 12
|
BioASQ-training12b
| null | null |
63f03d58f36125a42600001f
| 4,903
|
factoid
|
What is the alternative name of RTA 408?
|
['Omaveloxolone']
|
[
"Omaveloxolone",
"RTA 408",
"Omav",
"Omaveloxolone (RTA 408)"
] |
['RTA 408 is also known as omaveloxolone.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34573098"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34573098",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 854,
"text": "Omaveloxolone (RTA 408) is an activator of Nrf2 and an inhibitor of NFκB, possessing antioxidative and anti-inflammatory activities in mitochondrial bioenergetics. "
}
] | 12
|
BioASQ-training12b
| null | null |
644008a657b1c7a31500003f
| 4,906
|
factoid
|
What is the cause of Spinal Muscular Atrophy (SMA)?
|
['mutations in SMN1 (encoding survival motor neuron protein (SMN))', 'Reduced expression of SMN', 'Loss or deletion of survival motor neuron 1 gene (SMN1)', 'defects in the survival motor neuron 1 (SMN1) gene', 'loss of the SMN1 gene', 'loss of the SMN1 gene in most cases or mutations in rare cases']
|
[
"mutations in SMN1 (encoding survival motor neuron protein (SMN))",
"Reduced expression of SMN",
"Loss or deletion of survival motor neuron 1 gene (SMN1)",
"defects in the survival motor neuron 1 (SMN1) gene",
"loss of the SMN1 gene",
"loss of the SMN1 gene in most cases or mutations in rare cases",
"survival motor neuron 1",
"SMN1",
"SMN"
] |
['Spinal muscular atrophy (SMA) is a neurodegenerative disease caused by mutations in the survival motor neuron 1 (SMN1) gene.', 'Spinal Muscular Atrophy (SMA) is caused by loss or deletion of survival motor neuron 1 gene (SMN) 1 or mutations in rare cases.', 'Spinal muscular atrophy (SMA) is an autosomal recessive neurodegenerative disorder caused by defects in the survival motor neuron 1 (SMN1) gene.', 'Spinal Muscular Atrophy (SMA) is caused by loss or deletion of the survival motor neuron 1 (SMN1) gene.', 'Spinal Muscular Atrophy (SMA) is an autosomal recessive neurodegenerative disorder caused by defects in the survival motor neuron 1 (SMN1) gene, which encodes survival motor neuron protein (SMN).', 'Spinal muscular atrophy (SMA) is a neurodegenerative disorder caused by mutations in SMN1 (encoding survival motor neuron protein (SMN)).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/11528396",
"http://www.ncbi.nlm.nih.gov/pubmed/9225684",
"http://www.ncbi.nlm.nih.gov/pubmed/34217376",
"http://www.ncbi.nlm.nih.gov/pubmed/30065610",
"http://www.ncbi.nlm.nih.gov/pubmed/28811488",
"http://www.ncbi.nlm.nih.gov/pubmed/29799103",
"http://www.ncbi.nlm.nih.gov/pubmed/35643151",
"http://www.ncbi.nlm.nih.gov/pubmed/35927425",
"http://www.ncbi.nlm.nih.gov/pubmed/19535574",
"http://www.ncbi.nlm.nih.gov/pubmed/35126465",
"http://www.ncbi.nlm.nih.gov/pubmed/27299569",
"http://www.ncbi.nlm.nih.gov/pubmed/36375840",
"http://www.ncbi.nlm.nih.gov/pubmed/31371553",
"http://www.ncbi.nlm.nih.gov/pubmed/36142791",
"http://www.ncbi.nlm.nih.gov/pubmed/31127156",
"http://www.ncbi.nlm.nih.gov/pubmed/12427909",
"http://www.ncbi.nlm.nih.gov/pubmed/20392710",
"http://www.ncbi.nlm.nih.gov/pubmed/30010942",
"http://www.ncbi.nlm.nih.gov/pubmed/30368521",
"http://www.ncbi.nlm.nih.gov/pubmed/35614235"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36375840",
"endSection": "abstract",
"offsetInBeginSection": 167,
"offsetInEndSection": 285,
"text": "SMA is a monogenic pathology that originates from the loss of the SMN1 gene in most cases or mutations in rare cases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35643151",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 156,
"text": "Spinal muscular atrophy (SMA) is an autosomal recessive neurodegenerative disorder caused by defects in the survival motor neuron 1 (SMN1) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35614235",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Loss or deletion of survival motor neuron 1 gene (SMN1) is causative for a severe and devastating neuromuscular disease, Spinal Muscular Atrophy (SMA). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35927425",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "Spinal muscular atrophy (SMA) is a neurodegenerative disorder caused by mutations in SMN1 (encoding survival motor neuron protein (SMN)). Reduced expression of SMN leads to loss of α-motor neurons, severe muscle weakness and often early death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9225684",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 299,
"text": "The primary cause of most, if not all, forms of childhood-onset spinal muscular atrophy appears to be the homozygous loss of the telomeric copy of the survival motor neuron (SMNT) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31127156",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Spinal muscular atrophy (SMA) is caused by loss-of-function mutations in the survival of motoneuron gene 1 (SMN1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28811488",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Spinal muscular atrophy (SMA) is caused by the low levels of survival motor neuron (SMN) protein and is characterized by motor neuron degeneration and muscle atrophy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35126465",
"endSection": "abstract",
"offsetInBeginSection": 196,
"offsetInEndSection": 424,
"text": "Although the major cause of SMA is autosomal recessive exon deletions or loss-of-function mutations of survival motor neuron 1 (SMN1) gene, next generation sequencing technologies are increasing the genetic heterogeneity of SMA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31371553",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disease caused by deletions or mutations in the survival motor neuron (SMN1) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19535574",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Spinal muscular atrophy (SMA) is caused by homozygous mutation or deletion of the SMN1 gene encoding survival of motor neuron (SMN) protein, resulting in the selective loss of alpha-motor neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30010942",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Chronic low levels of survival motor neuron (SMN) protein cause spinal muscular atrophy (SMA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27299569",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "The underlying cause of spinal muscular atrophy (SMA) is a deficiency of the survival motor neuron (SMN) protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35927425",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Spinal muscular atrophy (SMA) is a neurodegenerative disorder caused by mutations in SMN1 (encoding survival motor neuron protein (SMN))."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29799103",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Spinal muscular atrophy (SMA) is an autosomal recessive genetic disorder caused by survival motor neuron (SMN) protein deficiency leading the loss of motor neurons in the anterior horns of the spinal cord and brainstem."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12427909",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Spinal muscular atrophy (SMA) is caused by SMN1 gene deletions or mutations, and ALS is the most frequent motor neuron condition in adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30368521",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Spinal Muscular Atrophy (SMA) is caused by genetic mutations in the SMN1 gene, resulting in drastically reduced levels of Survival of Motor Neuron (SMN) protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36142791",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Spinal muscular atrophy (SMA) is a devastating neuromuscular disorder caused by recessive mutations in the SMN1 gene, globally affecting ~8-14 newborns per 100,000."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30065610",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Spinal Muscular Atrophy (SMA) is a neuromuscular disorder caused by mutations in the SMN1 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34217376",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Spinal muscular atrophy (SMA) is a neuromuscular genetic disease caused by reduced survival motor neuron (SMN) protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11528396",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Classic spinal muscular atrophy (SMA) is caused by mutations in the telomeric copy of SMN1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20392710",
"endSection": "abstract",
"offsetInBeginSection": 104,
"offsetInEndSection": 254,
"text": " cause of infantile mortality. SMA is caused by mutation or deletion of Survival Motor Neuron-1 (SMN1). The clinical features of the disease are cause"
}
] | 12
|
BioASQ-training12b
| null | null |
644640de57b1c7a31500006b
| 4,907
|
factoid
|
What was the phase of the clinical trial PEACHTREE?
|
['three', 'III']
|
[
"three",
"III"
] |
['The PEACHTREE trial was a phase III clinical trial.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34322164"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34322164",
"endSection": "abstract",
"offsetInBeginSection": 711,
"offsetInEndSection": 1109,
"text": "Recent results from the PEACHTREE trial (ClinicalTrials.gov Identifier: NCT02595398), a phase III trial with two suprachoroidal injections of CLS-TA at 0 and 12 weeks with follow up lasting 24 weeks, showed the significant improvement in visual acuity and reduction in central subfield thickness, all without increasing the risk of elevated intraocular pressure or accelerated cataract progression."
}
] | 12
|
BioASQ-training12b
| null | null |
64403a5857b1c7a31500004c
| 4,911
|
factoid
|
In what type of clinical trial has RT001 been evaluated against Friedreich's ataxia?
|
['phase I/II double-blind, randomized, comparator-controlled trial']
|
[
"phase I/II double-blind, randomized, comparator-controlled trial",
"phase I/II trial",
"phase I/II clinical trial",
"phase I/II study",
"double-blind phase I/II trial",
"randomized phase I/II trial",
"comparator-controlled phase I/II trial",
"phase I/II randomized controlled trial",
"phase I/II double-blind study",
"phase I/II randomized study"
] |
["RT001 was evaluatd in a phase I/II double-blind, randomized, comparator-controlled trial in Friedreich's ataxia patients."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29624723"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Randomized, clinical trial of RT001: Early signals of efficacy in Friedreich's ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 500,
"text": "We conducted a phase I/II double-blind, comparator-controlled trial with 2 doses of RT001 in Friedreich's ataxia patients (9 subjects each cohort). "
}
] | 12
|
BioASQ-training12b
| null | null |
64402bb057b1c7a315000043
| 4,916
|
factoid
|
L9LS was developed for which disease?
|
['malaria']
|
[
"malaria",
"Plasmodium infection",
"malarial infection",
"malarial disease",
"malarial fever",
"tertian fever",
"quartan fever"
] |
['L9LS was developed for malaria.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36260982",
"http://www.ncbi.nlm.nih.gov/pubmed/35921449"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35921449",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 464,
"text": "METHODS: We conducted a phase 1 clinical trial to assess the safety and pharmacokinetics of L9LS, a next-generation antimalarial monoclonal antibody, and its protective efficacy against controlled human malaria infection in healthy adults who had never had malaria or received a vaccine for malaria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35921449",
"endSection": "abstract",
"offsetInBeginSection": 2119,
"offsetInEndSection": 2300,
"text": "CONCLUSIONS: In this small trial, L9LS administered intravenously or subcutaneously protected recipients against malaria after controlled infection, without evident safety concerns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36260982",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "L9LS, a potent and safe antimalarial monoclonal antibody, demonstrated 88% protective efficacy against infection in a phase 1 trial in healthy adults.1 "
}
] | 12
|
BioASQ-training12b
| null | null |
63eef8d6f36125a42600000f
| 4,918
|
factoid
|
What does PROTACs stand for?
|
['proteolysis targeting chimeras']
|
[
"proteolysis targeting chimeras",
"PROTACs",
"proteolysis-targeting chimeras",
"proteolysis-targeting chimera",
"protein degradation targeting chimeras"
] |
['PROTACs are proteolysis targeting chimeras.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35594654"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35594654",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Design and synthesis of proteolysis targeting chimeras (PROTACs) as an EGFR degrader based on CO-1686."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35594654",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 365,
"text": "The emerging technology proteolysis targeting chimera (PROTAC) could be an alternative strategy to overcome these problems. "
}
] | 12
|
BioASQ-training12b
| null | null |
64121f44201352f04a000037
| 4,921
|
factoid
|
What is the incidence of Leigh syndrome?
|
['1:40,000 - 1:77,000 liveborn infants a year']
|
[
"1:40,000 - 1:77,000 liveborn infants a year",
"1 in 40,000 to 1 in 77,000 liveborn infants annually",
"40,000 to 77,000 live births per year",
"40,000 to 77,000 liveborn infants each year"
] |
['The incidence of Leigh syndrome ranges from 1:40,000 to 1:77,000 liveborn infants annually.', 'The incidence of Leigh syndrome is 1:40,000 - 1:77,000 liveborn infants a year.', 'The estimated incidence of Leigh syndrome is 1:40,000 - 1:77,000 liveborn infants a year.', 'Leigh syndrome has an estimated incidence of 1:40,000 to 1:77,000 liveborn infants per year.', 'the estimated incidence of leigh syndrome is 1:40,000 - 1:77,000 liveborn infants per year.', 'Leigh syndrome has an estimated incidence of approximately 1:40,000 to 1:77,000 liveborn infants per year.', 'Leigh syndrome affects 1 in 40,000 to 1 in 77,000 liveborn infants annually.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34868319",
"http://www.ncbi.nlm.nih.gov/pubmed/24299589",
"http://www.ncbi.nlm.nih.gov/pubmed/18651330",
"http://www.ncbi.nlm.nih.gov/pubmed/26725255",
"http://www.ncbi.nlm.nih.gov/pubmed/30392038"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24299589",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Leigh syndrome (LS), or subacute necrotizing encephalomyelopathy, is the most common childhood mitochondrial encephalopathy, accounting for more than 50% of cases in this age group. Its estimated incidence is 1:40,000 - 1:77,000 liveborn infants a year."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24299589",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 253,
"text": "Its estimated incidence is 1:40,000 - 1:77,000 liveborn infants a year."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18651330",
"endSection": "abstract",
"offsetInBeginSection": 834,
"offsetInEndSection": 917,
"text": "Leigh syndrome occurs with an estimated frequency of 1:77,000-1:34,000 live births."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34868319",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Leigh syndrome is a neurodegenerative disorder with an incidence of 1 : 40,000 live births."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26725255",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Leigh syndrome is a progressive neurodegenerative disorder, affecting 1 in 40,000 live births."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30392038",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 210,
"text": "It has an incidence of 1 in 77,000 live births worldwide with poor prognosis."
}
] | 12
|
BioASQ-training12b
| null | null |
6451029f57b1c7a315000094
| 4,922
|
factoid
|
What does Zanubrutinib inhibit?
|
['Bruton tyrosine kinase']
|
[
"Bruton tyrosine kinase",
"BTK",
"Bruton's tyrosine kinase",
"Bruton’s tyrosine kinase"
] |
['Zanubrutinib is a Bruton tyrosine kinase inhibitor.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35651781"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35651781",
"endSection": "abstract",
"offsetInBeginSection": 543,
"offsetInEndSection": 892,
"text": "In the United States, zanubrutinib, a next-generation BTK inhibitor, has been approved for treating adults with mantle cell lymphoma who have received at least one prior therapy, for adults with Waldenström macroglobulinemia, and for adults with relapsed or refractory marginal zone lymphoma who have received at least one anti-CD20-based therapy. B"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35651781",
"endSection": "abstract",
"offsetInBeginSection": 2451,
"offsetInEndSection": 2587,
"text": "To reduce these side effects, zanubrutinib, a next-generation BTK inhibitor, was designed to block BTK more specifically than ibrutinib."
}
] | 12
|
BioASQ-training12b
| null | null |
6432f5f257b1c7a31500001c
| 4,926
|
factoid
|
What is Apretude used for?
|
['HIV-1 pre-exposure prophylaxis']
|
[
"HIV-1 pre-exposure prophylaxis",
"PrEP",
"HIV pre-exposure prophylaxis",
"HIV pre-exposure prophylaxis medication",
"HIV prevention pill"
] |
['Cabotegravir extended-release (ER) injectable suspension (Apretude™) is the first long-acting injectable option to be approved for HIV-1 pre-exposure prophylaxis (PrEP).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36255686"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Cabotegravir Extended-Release Injectable Suspension: A Review in HIV-1 Pre-Exposure Prophylaxis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Cabotegravir extended-release (ER) injectable suspension (Apretude™) is the first long-acting injectable option to be approved for HIV-1 pre-exposure prophylaxis (PrEP). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "abstract",
"offsetInBeginSection": 465,
"offsetInEndSection": 694,
"text": "Cabotegravir ER injectable suspension is indicated in the USA for PrEP to reduce the risk of sexually acquired HIV-1 infection in at-risk adults and adolescents weighing ≥ 35 kg who have a negative HIV-1 test prior to initiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36255686",
"endSection": "abstract",
"offsetInBeginSection": 1086,
"offsetInEndSection": 1312,
"text": "With its convenient, less-frequent dosing schedule and its long-acting formulation enabling intramuscular administration, cabotegravir ER injectable suspension represents a novel and efficacious alternative to daily oral PrEP."
}
] | 12
|
BioASQ-training12b
| null | null |
6440420857b1c7a315000050
| 4,931
|
factoid
|
What disease is treated with Ublituximab?
|
['multiple sclerosis']
|
[
"multiple sclerosis",
"MS",
"sclerosis multiplex",
"disseminated sclerosis"
] |
['Ublituximab is being tested for multiple sclerosis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35779372",
"http://www.ncbi.nlm.nih.gov/pubmed/35570581",
"http://www.ncbi.nlm.nih.gov/pubmed/35869335",
"http://www.ncbi.nlm.nih.gov/pubmed/36001711",
"http://www.ncbi.nlm.nih.gov/pubmed/35378683"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35779372",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Outcomes of Ublituximab compared to Teriflunomide for relapsing multiple sclerosis: A meta-analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35779372",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Ublituximab is an anti-CD20 antibody that immunomodulates B-cells for relapsing multiple sclerosis (MS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35570581",
"endSection": "abstract",
"offsetInBeginSection": 826,
"offsetInEndSection": 1348,
"text": " In the second part of the review, we summarize medications that have targeted B cells in patients with MS and their current position in the therapeutic armamentarium based on clinical trials and real-world data. Covered therapeutic strategies include the targeting of surface molecules such as CD20 (rituximab, ocrelizumab, ofatumumab, ublituximab) and CD19 (inebilizumab), and molecules necessary for B-cell activation such as B cell activating factor (BAFF) (belimumab) and Bruton's Tyrosine Kinase (BTK) (evobrutinib)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36001711",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Ublituximab versus Teriflunomide in Relapsing Multiple Sclerosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36001711",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 207,
"text": "Ublituximab is being evaluated for the treatment of relapsing multiple sclerosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36001711",
"endSection": "abstract",
"offsetInBeginSection": 1973,
"offsetInEndSection": 2248,
"text": "CONCLUSIONS: Among participants with relapsing multiple sclerosis, ublituximab resulted in lower annualized relapse rates and fewer brain lesions on MRI than teriflunomide over a period of 96 weeks but did not result in a significantly lower risk of worsening of disability. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35869335",
"endSection": "abstract",
"offsetInBeginSection": 815,
"offsetInEndSection": 908,
"text": "The glycoengineered antibody ublituximab is the next anti-CD20 therapy about to be approved. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35378683",
"endSection": "abstract",
"offsetInBeginSection": 707,
"offsetInEndSection": 923,
"text": "On the other hand, the anti-CD52 monoclonal antibody alemtuzumab and the anti-CD20 monoclonal antibodies rituximab, ocrelizumab, ofatumumab, and ublituximab work via eliminating selected pathogenic cell populations. "
}
] | 12
|
BioASQ-training12b
| null | null |
63eef4f5f36125a42600000b
| 4,933
|
factoid
|
What is Palmar Erythema?
|
['redness of the palms', 'liver palms']
|
[
"redness of the palms",
"liver palms",
"palmar erythema"
] |
["Palmar erythema refers to symmetrical, reddish discoloration on the palms of the hands, often accompanied by slight warmth but no scaling or thickening of the skin. It can be caused by various conditions including autoimmune diseases such as Graves' disease.", 'Palmar erythema is a skin condition characterized by redness of the palms of the hands. It is commonly seen in patients with rheumatoid arthritis and other internal diseases.', 'Palmar Erythema also known as liver palms is redness of the palms', "Palmar erythema, also known as 'liver palms,' is a reddening of the palms, usually linked to several conditions like rheumatoid arthritis and liver diseases. It is characterized by redness on the palms and may be caused due to increased blood flow to the area.", 'Palmar erythema, also known as "liver palms," is a condition characterized by redness or flushing of the skin on the palm of the hand. It has been observed in some individuals with rheumatoid arthritis, but its exact cause and significance are still unclear.', 'Palmar erythema is a skin condition characterized by redness of the palms.', "Palmar Erythema, also known as 'liver palms', is a reddening of the palms, usually on the thenar and hypothenar eminences. It can be associated with various conditions, including rheumatoid arthritis, liver diseases, and other internal disorders.", 'Palmar erythema is a skin condition characterized by redness of the palms of the hands. It is seen more commonly in patients with classical rheumatoid arthritis than in patients with other internal diseases.', 'Palmar erythema, also known as redness of the palms, is a medical condition characterized by redness of the palms of the hands.', 'Palmar erythema is a redness on the palms of the hands caused by inflammation or injury to the skin. It can be associated with several conditions such as rheumatoid arthritis, infections, drug reactions, etc.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/3830522",
"http://www.ncbi.nlm.nih.gov/pubmed/22474732"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3830522",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Palmar erythema (\"liver palms\") was seen in 32/100 consecutive patients with classical rheumatoid arthritis and in 10/100 patients with various other internal diseases (p less than 0.001"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22474732",
"endSection": "abstract",
"offsetInBeginSection": 193,
"offsetInEndSection": 373,
"text": "Palmar erythema commonly presents as symmetric, blanchable, slightly warm, nonscaling erythema, most frequently involving the thenar and hypothenar eminences of the palmar surface."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3830522",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 188,
"text": "Palmar erythema (\"liver palms\") was seen in 32/100 consecutive patients with classical rheumatoid arthritis and in 10/100 patients with various other internal diseases (p less than 0.001)."
}
] | 12
|
BioASQ-training12b
| null | null |
640c842f201352f04a000025
| 4,934
|
factoid
|
What is the cause of Oculopharyngeal Muscular Dystrophy (OPMD)?
|
['expansion of the alanine-encoding (GCN)n trinucleotide repeat in the exon 1 of the polyadenosine (poly[A]) binding protein nuclear 1 gene', 'abnormal expansion of GCN repeat in PABPN1 gene', 'abnormal expansion of the GCN repeat in the polyadenosine binding protein nuclear 1 gene', 'GCA trinucleotide repeat in PABPN1 gene', 'short expansion of a GCG or GCA trinucleotide repeat in PABPN1 gene']
|
[
"expansion of the alanine-encoding (GCN)n trinucleotide repeat in the exon 1 of the polyadenosine (poly[A]) binding protein nuclear 1 gene",
"abnormal expansion of GCN repeat in PABPN1 gene",
"abnormal expansion of the GCN repeat in the polyadenosine binding protein nuclear 1 gene",
"GCA trinucleotide repeat in PABPN1 gene",
"short expansion of a GCG or GCA trinucleotide repeat in PABPN1 gene",
"GCN repeat expansion in PABPN1",
"PABPN1 GCN repeat expansion",
"PABPN1 gene GCN repeat",
"poly(A) binding protein nuclear 1 GCN repeat expansion"
] |
['The cause of Oculopharyngeal Muscular Dystrophy (OPMD) is an abnormal expansion of the alanine-encoding (GCN)n trinucleotide repeat in the exon 1 of the polyadenosine (poly[A]) binding protein nuclear 1 gene (11-18 repeats in OPMD instead of the normal 10 repeats).', 'Oculopharyngeal Muscular Dystrophy (OPMD) is caused by the abnormal expansion of the alanine-encoding (GCN)n trinucleotide repeat in the exon 1 of the polyadenosine (poly[A]) binding protein nuclear 1 gene (PABPN1).', 'The most common cause of Oculopharyngeal Muscular Dystrophy (OPMD) is an expansion of a GCG/GCA trinucleotide repeat in the PABPN1 gene. However, some cases may also be caused by a single nucleotide point mutation, such as the PABPN1 c.35G > C mutation described in the report.', 'The most common cause of Oculopharyngeal Muscular Dystrophy (OPMD) is an expansion of a GCG/GCA trinucleotide repeat in the PABPN1 gene. However, some cases may be caused by a single nucleotide point mutation, such as the PABPN1 c.35G > C mutation described in the report.', 'Oculopharyngeal Muscular Dystrophy (OPMD) is caused by an abnormal expansion of a trinucleotide repeat in the poly(A) binding protein nuclear 1 (PABPN1) gene.', 'The cause of Oculopharyngeal Muscular Dystrophy (OPMD) is the short expansion of a GCG or GCA trinucleotide repeat in the PABPN1 gene.', 'Oculopharyngeal muscular dystrophy (OPMD) is caused by the abnormal expansion of the alanine-encoding (GCN)n trinucleotide repeat in the exon 1 of the polyadenosine (poly[A]) binding protein nuclear 1 gene (11-18 repeats in OPMD instead of the normal 10 repeats).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33805441",
"http://www.ncbi.nlm.nih.gov/pubmed/34225694"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33805441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 387,
"text": "Oculopharyngeal muscular dystrophy (OPMD) is a late-onset intractable myopathy, characterized by slowly progressive ptosis, dysphagia, and proximal limb weakness. It is caused by the abnormal expansion of the alanine-encoding (GCN)n trinucleotide repeat in the exon 1 of the polyadenosine (poly[A]) binding protein nuclear 1 gene (11-18 repeats in OPMD instead of the normal 10 repeats)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34225694",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 277,
"text": "A common cause of OPMD is the short expansion of a GCG or GCA trinucleotide repeat in PABPN1 gene."
}
] | 12
|
BioASQ-training12b
| null | null |
64468b0757b1c7a315000070
| 4,937
|
factoid
|
Which viral disease can be treated with EDP-938?
|
['Respiratory Syncytial Virus']
|
[
"Respiratory Syncytial Virus",
"RSV",
"Human Respiratory Syncytial Virus",
"HRSV",
"Respiratory Syncytial Virus A",
"Respiratory Syncytial Virus B"
] |
['Respiratory Syncytial Virus can be treated with EDP-938.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33720995",
"http://www.ncbi.nlm.nih.gov/pubmed/35172056",
"http://www.ncbi.nlm.nih.gov/pubmed/36401806"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35172056",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "EDP-938, a Respiratory Syncytial Virus Inhibitor, in a Human Virus Challenge."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35172056",
"endSection": "abstract",
"offsetInBeginSection": 158,
"offsetInEndSection": 252,
"text": "EDP-938, a nonfusion replication inhibitor of RSV, acts by modulating the viral nucleoprotein."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401806",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "EDP-938, a new antiviral with inhibitory activity against the nucleoprotein of the respiratory syncytial virus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401806",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 586,
"text": "EDP-938 has shown high efficacy against RSV. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33720995",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "EDP-938, a novel nucleoprotein inhibitor of respiratory syncytial virus, demonstrates potent antiviral activities in vitro and in a non-human primate model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33720995",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "EDP-938 is a novel non-fusion replication inhibitor of respiratory syncytial virus (RSV). "
}
] | 12
|
BioASQ-training12b
| null | null |
63f0494cf36125a426000028
| 4,938
|
factoid
|
What is the generic name for Imfinzi?
|
['Durvalumab']
|
[
"Durvalumab",
"MEDI4736",
"Imfinzi"
] |
['Durvalumab (Imfinzi) is used to treat locally advanced or metastatic cancer.', 'the generic name for imfinzi is durvalumab.', 'The generic name for Imfinzi is durvalumab.', 'durvalumab (Imfinzi®)']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30917623",
"http://www.ncbi.nlm.nih.gov/pubmed/32727810",
"http://www.ncbi.nlm.nih.gov/pubmed/34731446",
"http://www.ncbi.nlm.nih.gov/pubmed/29571563",
"http://www.ncbi.nlm.nih.gov/pubmed/28643244"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28643244",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 168,
"text": "durvalumab (Imfinzi™; AstraZeneca) is a fully human monoclonal antibody that blocks programmed cell death ligand-1 binding to its receptors (PD-1 and CD80),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29571563",
"endSection": "abstract",
"offsetInBeginSection": 369,
"offsetInEndSection": 403,
"text": "durvalumab (IMFINZI®, Astra-Zeneca"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30917623",
"endSection": "abstract",
"offsetInBeginSection": 375,
"offsetInEndSection": 396,
"text": "durvalumab (Imfinzi®)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28643244",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 229,
"text": "Intravenous durvalumab (Imfinzi™; AstraZeneca) is a fully human monoclonal antibody that blocks programmed cell death ligand-1 binding to its receptors (PD-1 and CD80), resulting in enhanced T-cell responses against cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34731446",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 286,
"text": "Durvalumab (IMFINZI®), a fully human monoclonal antibody against programmed cell death-ligand 1 (PD-L1), is approved for use in combination with etoposide and either carboplatin or cisplatin for the first-line treatment of patients with extensive-stage small cell lung cancer (ES-SCLC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30917623",
"endSection": "abstract",
"offsetInBeginSection": 211,
"offsetInEndSection": 608,
"text": "Since 2011, the FDA-approved antibody drugs ipilimumab (Yervoy®), nivolumab (Opdivo®), pembrolizumab (Keytruda®), cemiplimab (Libtayo®), atezolizumab (Tecentriq®), durvalumab (Imfinzi®), and avelumab (Bavencio®), which block the immune checkpoint proteins, have brought about a significant breakthrough in the treatment of a wide range of cancers, as they can induce durable therapeutic responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29571563",
"endSection": "abstract",
"offsetInBeginSection": 113,
"offsetInEndSection": 443,
"text": "Nevertheless, new therapies have emerged recently, among which PD1 immune checkpoint inhibitors (ICI), such as nivolumab (OPDIVO®, Bristol-Myers Squibb) and pembrolizumab (KEYTRUDA®, Merck & Co), or PD-L1 ICI, such as atezolizumab (TECENTRIQ®, Genentech), durvalumab (IMFINZI®, Astra-Zeneca), and avelumab (BAVENCIO®, EMD Serono)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32727810",
"endSection": "abstract",
"offsetInBeginSection": 2406,
"offsetInEndSection": 2741,
"text": "titumor immunity. This unique mechanism of action in CD103+ DCs may contribute to clinical responses as AZD4635 is being evaluated in clinical trials with IMFINZI (durvalumab, αPD-L1) in patients with solid malignancies.CONCLUSION: We provide evidence implicating suppression of adaptive and innate immunity by adenosine as a mechanism"
}
] | 12
|
BioASQ-training12b
| null | null |
640ddbe9201352f04a000027
| 4,939
|
factoid
|
What are negative cell-cycle regulators that can cause cancer when mutated called?
|
['Tumor suppressor genes', 'Tumor-suppressor genes', 'tumor suppressors', 'antioncogenes', 'anti-oncogenes']
|
[
"Tumor suppressor genes",
"Tumor-suppressor genes",
"tumor suppressors",
"antioncogenes",
"anti-oncogenes",
"tumor suppressor",
"tumor suppressor gene"
] |
["Negative cell-cycle regulators that can cause cancer when mutated are commonly referred to as tumor suppressor genes. These genes play a crucial role in controlling cell division and preventing uncontrolled proliferation, which could lead to the formation of tumors. Tumor suppressor genes function by inhibiting cell cycle progression, promoting DNA repair, and inducing apoptosis in response to cellular stress or damage. Some well-known examples of tumor suppressor genes include TP53 (p53), RB1 (retinoblastoma protein), and CDKN2A (p16INK4a). Mutations or loss of function in these genes can disrupt their ability to regulate the cell cycle, thereby contributing to the development of cancer. In many cases, both copies of a tumor suppressor gene must be inactivated for a complete loss of function, following Knudson's two-hit hypothesis. The identification and study of tumor suppressor genes have significantly advanced our understanding of cancer biology and provided potential targets for therapeutic interventions.", 'The cell cycle is a series of events that take place in a cell, leading to its division and duplication. Cell division requires cell cycle checkpoints that are used by the cell to both monitor and regulate the progress of the cell cycle. Deregulation of the cell cycle underlies the aberrant cell proliferation that characterizes cancer and loss of cell cycle checkpoint control promotes genetic instability.\n\nTumor suppressor genes are genes that protect the cell from a single event or multiple events leading to cancer. When these genes mutate, the cell can progress to a cancerous state. We now recognize that tumor suppressor genes regulate diverse cellular activities, including cell cycle checkpoint responses, detection and repair of DNA damage, protein ubiquitination and degradation, mitogenic signaling, cell specification, differentiation and migration, and tumor angiogenesis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26573797",
"http://www.ncbi.nlm.nih.gov/pubmed/21990031",
"http://www.ncbi.nlm.nih.gov/pubmed/1399577",
"http://www.ncbi.nlm.nih.gov/pubmed/20492666",
"http://www.ncbi.nlm.nih.gov/pubmed/2140509",
"http://www.ncbi.nlm.nih.gov/pubmed/2046748",
"http://www.ncbi.nlm.nih.gov/pubmed/14744434",
"http://www.ncbi.nlm.nih.gov/pubmed/12665054",
"http://www.ncbi.nlm.nih.gov/pubmed/33682629",
"http://www.ncbi.nlm.nih.gov/pubmed/11327114",
"http://www.ncbi.nlm.nih.gov/pubmed/26110128",
"http://www.ncbi.nlm.nih.gov/pubmed/9179973",
"http://www.ncbi.nlm.nih.gov/pubmed/8652807",
"http://www.ncbi.nlm.nih.gov/pubmed/9815577",
"http://www.ncbi.nlm.nih.gov/pubmed/32359398",
"http://www.ncbi.nlm.nih.gov/pubmed/12542976",
"http://www.ncbi.nlm.nih.gov/pubmed/16150895",
"http://www.ncbi.nlm.nih.gov/pubmed/10854145"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26110128",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 474,
"text": "The cell cycle (or cell-division cycle) is a series of events that take place in a cell, leading to its division and duplication. Cell division requires cell cycle checkpoints (CPs) that are used by the cell to both monitor and regulate the progress of the cell cycle. Tumor-suppressor genes (TSGs) or antioncogenes are genes that protect the cell from a single event or multiple events leading to cancer. When these genes mutate, the cell can progress to a cancerous state."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21990031",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 378,
"text": "Deregulation of the cell cycle underlies the aberrant cell proliferation that characterizes cancer and loss of cell cycle checkpoint control promotes genetic instability. During the past two decades, cancer genetics has shown that hyperactivating mutations in growth signalling networks, coupled to loss of function of tumour suppressor proteins, drives oncogenic proliferation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14744434",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 737,
"text": " We now recognize that tumor suppressor genes regulate diverse cellular activities, including cell cycle checkpoint responses, detection and repair of DNA damage, protein ubiquitination and degradation, mitogenic signaling, cell specification, differentiation and migration, and tumor angiogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32359398",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "p53 is a critical tumor-suppressor protein that guards the human genome against mutations by inducing cell-cycle arrest or apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10854145",
"endSection": "abstract",
"offsetInBeginSection": 1238,
"offsetInEndSection": 1405,
"text": "Tumor-suppressor gene p16 is an important negative cell-cycle regulator whose functional loss may significantly contribute to malignant transformation and progression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1399577",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Tumor suppressor genes are negative regulators of cell growth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12665054",
"endSection": "abstract",
"offsetInBeginSection": 340,
"offsetInEndSection": 599,
"text": "Aberrant proteolysis with oncogenic potential is elicited by two major mechanisms: defective degradation of positive cell cycle regulators (i.e., proto-oncoproteins) and enhanced degradation of negative cell cycle regulators (i.e., tumor suppressor proteins)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11327114",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 738,
"text": " Genes positively controlling cell cycle checkpoints can be targets for oncogenic activation in cancer, whereas negative regulators, such as tumour suppressor genes, are targeted for inactivation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9815577",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 345,
"text": "The p27(Kip1) protein belongs to a family of cyclin-dependent kinase-inhibitory proteins that are negative regulators of cell cycle progression and have been proposed as candidate tumor suppressor genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33682629",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 463,
"text": "Retinoblastoma 1 (RB1) is the first discovered tumor suppressor gene and recognized as the simple model system whose encoded defective protein can cause a pediatric cancer retinoblastoma. It functions as a negative regulator of the cell cycle through the interactions with members of the E2F transcription factors family. The protein of the RB1 gene (pRB) is engaged in various cell cycle processes including apoptosis, cell cycle arrest and chromatin remodeling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2046748",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "The cell cycle is composed of a series of steps which can be negatively or positively regulated by various factors. Chief among the negative regulators is the p53 protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20492666",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 111,
"text": "p27Kip1 (p27) is an important negative regulator of the cell cycle and a putative tumor suppressor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8652807",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 438,
"text": "It is now evident that the cell cycle machinery has a variety of elements negatively regulating cell cycle progression. However, among these negative regulators in cell cycle control, only 4 have been shown to be consistently involved in the development of human cancers as tumor suppressors: Rb (Retinoblastoma susceptibility protein), p53, and two recently identified cyclin-dependent kinase inhibitors, p16INK4A/MTS1 and p15INK4B/MTS2."
}
] | 12
|
BioASQ-training12b
| null | null |
644e81fa57b1c7a315000079
| 4,940
|
factoid
|
When was Keytruda approved for the treatment of melanoma?
|
['September 4, 2014']
|
[
"September 4, 2014",
"9/4/2014",
"4th September 2014",
"September 4th, 2014",
"09-04-2014"
] |
['On September 4, 2014, the FDA approved pembrolizumab (KEYTRUDA) for the treatment of patients with unresectable or metastatic melanoma who have progressed following treatment with ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28235882"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28235882",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 346,
"text": "On September 4, 2014, the FDA approved pembrolizumab (KEYTRUDA; Merck Sharp & Dohme Corp.) with a recommended dose of 2 mg/kg every 3 weeks by intravenous infusion for the treatment of patients with unresectable or metastatic melanoma who have progressed following treatment with ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. "
}
] | 12
|
BioASQ-training12b
| null | null |
6415c7fb690f196b51000016
| 4,941
|
factoid
|
What is the incidence of Oculopharyngeal Muscular Dystrophy (OPMD)?
|
['1:600 to 1:80,000']
|
[
"1:600 to 1:80,000",
"1:600-1:80,000",
"1 in 600 to 1 in 80,000",
"1 in 600-1 in 80,000",
"1:600 to 80000",
"1:600-80000",
"1 in 600 to 80000",
"1 in 600-80000"
] |
['OPMD affects approximately 1 in 80,000 individuals worldwide. However, in some populations, it can affect as much as 1 in 600 individuals due to a strong founder effect.', 'Oculopharyngeal muscular dystrophy (OPMD) is a late-onset rare muscle disease affecting approximately 1 in 80,000 individuals worldwide. However, it can affect as much as 1:600 individuals in some populations due to a strong founder effect.', 'The incidence of Oculopharyngeal Muscular Dystrophy (OPMD) is approximately 1 in 80,000 individuals worldwide. However, in some populations with a strong founder effect, it can affect as much as 1 in 600 individuals.', 'The incidence of Oculopharyngeal Muscular Dystrophy (OPMD) is approximately 1 in 80,000 individuals worldwide, but it can affect as much as 1:600 individuals in some populations due to a strong founder effect.', 'The incidence of Oculopharyngeal Muscular Dystrophy (OPMD) is approximately 1 in 80,000 individuals worldwide, but can affect as much as 1:600 individuals in some populations due to a strong founder effect.', 'The incidence of Oculopharyngeal Muscular Dystrophy (OPMD) is approximately 1 in 80,000 individuals worldwide, but can be as high as 1:600 individuals in some populations due to a strong founder effect.', 'OPMD has an incidence of approximately 1 in 80,000 individuals worldwide, although in some populations it can affect as much as 1:600 individuals due to a strong founder effect.', 'The incidence of Oculopharyngeal Muscular Dystrophy (OPMD) is 1:600 to 1:80,000.', 'The incidence of Oculopharyngeal Muscular Dystrophy (OPMD) varies depending on population, but globally it affects approximately 1 in 80,000 individuals. In certain populations, the prevalence can be as high as 1 in 600 individuals.', 'The incidence of Oculopharyngeal Muscular Dystrophy (OPMD) is approximately 1 in 80,000 individuals worldwide. However, in some populations, it can affect as many as 1 in 600 individuals due to a strong founder effect.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36401050"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "Oculopharyngeal muscular dystrophy (OPMD) is a late-onset rare muscle disease affecting approximately 1 in 80,000 individuals worldwide. However, it can affect as much as 1:600 individuals in some populations due to a strong founder effect. "
}
] | 12
|
BioASQ-training12b
| null | null |
64468e0d57b1c7a315000071
| 4,942
|
factoid
|
Donidalorsen was tested for which disease?
|
['hereditary angioedema']
|
[
"hereditary angioedema",
"HAE",
"hereditary angioedema type I",
"hereditary angioedema type II",
"C1 inhibitor deficiency",
"C1 esterase inhibitor deficiency"
] |
['Donidalorsen is tested for hereditary angioedema.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36172291",
"http://www.ncbi.nlm.nih.gov/pubmed/35294812"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35294812",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 306,
"text": "BACKGROUND: Hereditary angioedema is characterized by recurrent and unpredictable swellings that are disabling and potentially fatal. Selective inhibition of plasma prekallikrein production by antisense oligonucleotide treatment (donidalorsen) may reduce the frequency of attacks and the burden of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35294812",
"endSection": "abstract",
"offsetInBeginSection": 1698,
"offsetInEndSection": 1880,
"text": "CONCLUSIONS: Among patients with hereditary angioedema, donidalorsen treatment resulted in a significantly lower rate of angioedema attacks than placebo in this small, phase 2 trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36172291",
"endSection": "abstract",
"offsetInBeginSection": 2231,
"offsetInEndSection": 2610,
"text": "Investigational therapies, including the activated factor XII inhibitor garadacimab and an antisense oligonucleotide targeting plasma prekallikrein messenger RNA (donidalorsen), have shown promise as long-term prophylaxis. Given the requirement of lifelong management for HAE, further research is needed to determine how best to individualize optimal treatments for each patient."
}
] | 12
|
BioASQ-training12b
| null | null |
63f04716f36125a426000025
| 4,948
|
factoid
|
What are the proteins that are necessary for the use of lactose in E. coli collectively called?
|
['Lac operon']
|
[
"Lac operon",
"lactose operon",
"lactose operon system",
"lacZYA operon",
"lac operon system"
] |
['The proteins necessary for the use of lactose in E. coli are collectively called the lac operon. This gene regulatory circuit controls the transcription of genes involved in lactose metabolism and is nearly ubiquitous in E. coli strains, making it a useful phenotype for species identification. The activity of the lac operon is controlled by both cis- and trans-acting regulators, which integrate environmental signals such as glucose and lactose availability to fine-tune gene expression. While most studies of lac operon regulation have focused on a few closely related strains, this system remains an important model for understanding how bacteria adapt their metabolism to changing nutritional conditions.', 'Transcription of bacterial genes is controlled by the coordinated action of cis- and trans-acting regulators. The activity and mode of action of these regulators can reflect different requirements for gene products in different environments. The lac operon is one of the best-known gene regulatory circuits and constitutes a landmark example of how bacteria tune their metabolism to nutritional conditions. It is nearly ubiquitous in Escherichia coli strains justifying the use of its phenotype, the ability to consume lactose, for species identification.', 'The proteins necessary for the use of lactose in Escherichia coli (E. coli) are collectively referred to as the lac operon. The lac operon is a well-known gene regulatory circuit that serves as a landmark example of how bacteria adjust their metabolism according to nutritional conditions. It is nearly ubiquitous in E. coli strains, and its phenotype, the ability to consume lactose, is used for species identification. The transcription of bacterial genes within the lac operon is controlled by the coordinated action of cis- and trans-acting regulators, which integrate environmental availability of glucose and lactose to regulate gene expression. Most studies on lac operon regulation have focused on a few closely related strains of E. coli.', 'The proteins necessary for the use of lactose in Escherichia coli (E. coli) are collectively called the lac operon. The lac operon is a set of genes that encode proteins involved in the transport and metabolism of lactose, allowing E. coli to utilize this sugar as an energy source when glucose is scarce. The primary components of the lac operon include three structural genes: lacZ, lacY, and lacA. The lacZ gene encodes β-galactosidase, an enzyme responsible for cleaving lactose into glucose and galactose. The lacY gene encodes lactose permease, a membrane protein that facilitates the transport of lactose into the cell. Lastly, the lacA gene encodes thiogalactoside transacetylase, which detoxifies certain byproducts generated during lactose metabolism. Additionally, regulatory elements such as the promoter region (lacP), operator region (lacO), and repressor protein (LacI) play crucial roles in controlling the expression of these genes in response to environmental conditions like lactose availability and glucose levels.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31719176",
"http://www.ncbi.nlm.nih.gov/pubmed/34367115",
"http://www.ncbi.nlm.nih.gov/pubmed/34891476",
"http://www.ncbi.nlm.nih.gov/pubmed/34953812",
"http://www.ncbi.nlm.nih.gov/pubmed/26415599"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34367115",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 313,
"text": "The lac operon is one of the best known gene regulatory circuits and constitutes a landmark example of how bacteria tune their metabolism to nutritional conditions. It is nearly ubiquitous in Escherichia coli strains justifying the use of its phenotype, the ability to consume lactose, for species identification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31719176",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 489,
"text": "Transcription of bacterial genes is controlled by the coordinated action of cis- and trans-acting regulators. The activity and mode of action of these regulators can reflect different requirements for gene products in different environments. A well-studied example is the regulatory function that integrates the environmental availability of glucose and lactose to control the Escherichia colilac operon. Most studies of lac operon regulation have focused on a few closely related strains."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34953812",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 278,
"text": "In the induced state of the lac pathway, the genes comprising the lac operon are transcribed, leading to the production of proteins that import and metabolize lactose."
}
] | 12
|
BioASQ-training12b
| null | null |
644ec7fe57b1c7a315000082
| 4,950
|
factoid
|
Alternative microexon splicing is associated with metastasis in which cancer?
|
['Colorectal cancer']
|
[
"Colorectal cancer",
"Colon cancer",
"Rectal cancer",
"Bowel cancer",
"Large intestine cancer",
"Colon carcinoma",
"Rectal carcinoma",
"Colorectal carcinoma"
] |
['Alternative microexon splicing by RBFOX2 and PTBP1 is associated with metastasis in colorectal cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34346508"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34346508",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Alternative microexon splicing by RBFOX2 and PTBP1 is associated with metastasis in colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34346508",
"endSection": "abstract",
"offsetInBeginSection": 1073,
"offsetInEndSection": 1320,
"text": "Finally, we found that changes in the pattern of microexon splicing were associated with CRC metastasis. Our data thus suggest that altered expression of RBFOX2 and PTBP1 might influence CRC metastasis through the regulation of microexon splicing."
}
] | 12
|
BioASQ-training12b
| null | null |
63fa16d8201352f04a000002
| 4,951
|
factoid
|
What is the cause of spinal-bulbar muscular atrophy?
|
['mutations in the androgen receptor encoding gene (AR)', 'CAG repeat expansion mutation', 'CAG trinucleotide repeat expansion in the androgen receptor (AR) gene', 'a CAG trinucleotide repeat expansion', 'Androgen receptor gene mutations']
|
[
"mutations in the androgen receptor encoding gene (AR)",
"CAG repeat expansion mutation",
"CAG trinucleotide repeat expansion in the androgen receptor (AR) gene",
"a CAG trinucleotide repeat expansion",
"Androgen receptor gene mutations",
"androgen receptor mutations",
"AR mutations",
"androgen receptor encoding gene mutations",
"CAG repeat mutations",
"CAG repeat expansions"
] |
['Spinal bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene.', 'Spinal-bulbar muscular atrophy is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene. This genetic mutation leads to the neuromuscular disorder.', 'Spinal-bulbar muscular atrophy is caused by mutations, i.e., a CAG trinucleotide repeat expansion, in the androgen receptor encoding gene (AR).', 'Spinal-bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene.', 'Spinal-bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene. Mutant AR is presumed to act in motoneurons to cause SBMA.', 'spinal bulbar muscular atrophy is caused by a cag repeat expansion mutation in the androgen receptor (ar) gene.', 'Spinal-bulbar muscular atrophy is caused by a CAG trinucleotide repeat expansion in the androgen receptor gene.', 'Spinal-bulbar muscular atrophy is caused by a CAG trinucleotide repeat expansion in the androgen receptor (AR) gene.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20689246",
"http://www.ncbi.nlm.nih.gov/pubmed/35996994",
"http://www.ncbi.nlm.nih.gov/pubmed/32773451"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35996994",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 213,
"text": "Kennedy's disease is nearly exclusively caused by mutations in the androgen receptor encoding gene (AR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20689246",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 193,
"text": "Spinal bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene, and mutant AR is presumed to act in motoneurons to cause SBMA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32773451",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 286,
"text": "spinal and bulbar muscular atrophy (SBMA), an inherited neuromuscular disorder caused by a CAG trinucleotide repeat expansion in the androgen receptor (AR) gene."
}
] | 12
|
BioASQ-training12b
| null | null |
6451060c57b1c7a315000096
| 4,956
|
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