tbuckley/cabot-search huggingface dataset:
Drowsy Driving—19 States and the District of Columbia, 2009-2010
Authors: Anne G Wheaton, Daniel P Chapman, Letitia R Presley-Cantrell, Janet B Croft, Douglas R Roehler
Journal: JAMA (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Fusion of TEL, the ETS-Variant Gene 6 (ETV6), to the Receptor-Associated Kinase JAK2 as a Result of t(9; 12) in a Lymphoid and t(9; 15; 12) in a Myeloid Leukemia
Authors: Pieter Peeters, Sophie D. Raynaud, Jan Cools, Iwona Wlodarska, Josiane Grosgeorge, Patrick Philip, Fabrice Monpoux, Luc Van Rompaey, Mathijs Baens, Herman Van den Berghe, Peter Marynen
Journal: Blood (1997)
Toward standard practices for sharing computer code and programs in neuroscience
Authors: Stephen J Eglen, Ben Marwick, Yaroslav O Halchenko, Michael Hanke, Shoaib Sufi, Padraig Gleeson, R Angus Silver, Andrew P Davison, Linda Lanyon, Mathew Abrams, Thomas Wachtler, David J Willshaw, Christophe Pouzat, Jean-Baptiste Poline
Journal: Nature Neuroscience (2017)
Management of Severe Acute Colitis in District Hospitals
Authors: Jean K Ritchie, Sheila M Ritchie, P B McIntyre, C G Marks
Journal: Journal of the Royal Society of Medicine (1984)

Among 10 hospitals of the North East Thames Region, 84 patients were operated on for inflammatory bowel disease in the years 1977-81. There was one death in the 51 patients treated electively. The postoperative mortality was 24% in 33 patients coming to urgent surgery. The factors leading to this continuing high mortality are analysed as a contribution to an improvement in management.
Concur: a Randomized, Placebo-Controlled Phase 3 Study of Regorafenib (Reg) Monotherapy in Asian Patients with Previously Treated Metastatic Colorectal Cancer (Mcrc)
Authors: T.W. Kim, R. Xu, T.C.C. Yau, B. Ma, H. Pan, J. Xu, Y. Bai, Y. Chi, L. Wang, K. Yeh, F. Bi, Y. Cheng, A.T. Le, J. Lin, T. Liu, D. Ma, J. Shapiro, J. Kalmus, S. Qin, J. Li
Journal: Annals of Oncology (2014)
Tumor Regression and Allograft Rejection after Administration of Anti–PD-1
Authors: Evan J Lipson, Serena M Bagnasco, Jack Moore, Sekwon Jang, Manisha J Patel, Andrea A Zachary, Drew M Pardoll, Janis M Taube, Charles G Drake
Journal: New England Journal of Medicine (2016)

Cancers, especially skin cancers, may develop in patients undergoing solid-organ transplantation who receive long-term immunosuppression. The use of anti–PD-1 in one such patient produced an antitumor response but led to rejection of the transplanted kidney.
Host-directed therapies for infectious diseases: current status, recent progress, and future prospects
Authors: Alimuddin Zumla, Martin Rao, Robert S Wallis, Stefan H E Kaufmann, Roxana Rustomjee, Peter Mwaba, Cris Vilaplana, Dorothy Yeboah-Manu, Jeremiah Chakaya, Giuseppe Ippolito, Esam Azhar, Michael Hoelscher, Markus Maeurer
Journal: The Lancet Infectious Diseases (2016)

Despite extensive global efforts in the fight against killer infectious diseases, they still cause one in four deaths worldwide and are important causes of long-term functional disability arising from tissue damage. The continuing epidemics of tuberculosis, HIV, malaria, and influenza, and the emergence of novel zoonotic pathogens represent major clinical management challenges worldwide. Newer approaches to improving treatment outcomes are needed to reduce the high morbidity and mortality caused by infectious diseases. Recent insights into pathogen-host interactions, pathogenesis, inflammatory pathways, and the host's innate and acquired immune responses are leading to identification and development of a wide range of host-directed therapies with different mechanisms of action. Host-directed therapeutic strategies are now becoming viable adjuncts to standard antimicrobial treatment. Host-directed therapies include commonly used drugs for non-communicable diseases with good safety profiles, immunomodulatory agents, biologics (eg monoclonal antibodies), nutritional products, and cellular therapy using the patient's own immune or bone marrow mesenchymal stromal cells. We discuss clinically relevant examples of progress in identifying host-directed therapies as adjunct treatment options for bacterial, viral, and parasitic infectious diseases.
Long-Term Effects of Acute and Chronic Irradiation in Mice. I. Survival and Tumor Incidence Following Chronic Irradiation of 0.11 r Per Day
Authors: E LORENZ, J W HOLLCROFT, E MILLER, C C CONGDON, R SCHWEISTHAL
Journal: JNCI Journal of the National Cancer Institute (1955)

Journal Article Long-Term Effects of Acute and Chronic Irradiation in Mice. I. Survival and Tumor Incidence Following Chronic Irradiation of 0.11 r Per Day Get access Egon Lorenz, Egon Lorenz Search for other works by this author on: Oxford Academic PubMed Google Scholar Joanne Weikel Hollcroft, Joanne Weikel Hollcroft Search for other works by this author on: Oxford Academic PubMed Google Scholar Eliza Miller, Eliza Miller Search for other works by this author on: Oxford Academic PubMed Google Scholar Charles C. Congdon, Charles C. Congdon Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert Schweisthal Robert Schweisthal Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 15, Issue 4, February 1955, Pages 1049–1058, https://doi.org/10.1093/jnci/15.4.1049 Published: 01 February 1955 Article history Received: 22 October 1954 Published: 01 February 1955
A randomized, double-blind, placebo-controlled phase II study to assess the efficacy and safety of mapatumumab with sorafenib in patients with advanced hepatocellular carcinoma
Authors: T. Ciuleanu, I. Bazin, D. Lungulescu, L. Miron, I. Bondarenko, A. Deptala, M. Rodriguez-Torres, B. Giantonio, N.L. Fox, P. Wissel, J. Egger, M. Ding, R.N. Kalyani, R. Humphreys, M. Gribbin, W. Sun
Journal: Annals of Oncology (2016)
A novel form of congenital dyserythropoietic anemia associated with deficiency of erythroid CD44 and a unique blood group phenotype [In(a-b- ), Co(a-b-)]
Authors: SF Parsons, J Jones, DJ Anstee, PA Judson, B Gardner, E Wiener, J Poole, N Illum, SN Wickramasinghe
Journal: Blood (1994)
Pomalidomide Augments Fetal Hemoglobin Production In Primary Erythroid Cells By a Novel Mechanism Modulating BCL11A But Not KLF-1
Authors: Abena O. Appiah-Kubi, Lionel Blanc, Sharon A. Singh, Sebastien Didier, Sehba Dsilva, Kyle W.H. Chan, Jeffrey Michael Lipton, Johnson M. Liu
Journal: Blood (2013)
Qingfei Xiaoyan Wan, a traditional Chinese medicine formula, ameliorates Pseudomonas aeruginosa–induced acute lung inflammation by regulation of PI3K/AKT and Ras/MAPK pathways
Authors: Yuanyuan Hou, Yan Nie, Binfeng Cheng, Jin Tao, Xiaoyao Ma, Min Jiang, Jie Gao, Gang Bai
Journal: Acta Pharmaceutica Sinica B (2016)

Gram-negative pathogen–induced nosocomial infections and resistance are a most serious menace to global public health. Qingfei Xiaoyan Wan (QF), a traditional Chinese medicine (TCM) formula, has been used clinically in China for the treatment of upper respiratory tract infections, acute or chronic bronchitis and pulmonary infection. In this study, the effects of QF on Pseudomonas aeruginosa–induced acute pneumonia in mice were evaluated. The mechanisms by which four typical anti-inflammatory ingredients from QF, arctigenin (ATG), cholic acid (CLA), chlorogenic acid (CGA) and sinapic acid (SPA), regulate anti-inflammatory signaling pathways and related targets were investigated using molecular biology and molecular docking techniques. The results showed that pretreatment with QF significantly inhibits the release of cytokines (TNF-α and IL-6) and chemokines (IL-8 and RANTES), reduces leukocytes recruitment into inflamed tissues and ameliorates pulmonary edema and necrosis. In addition, ATG was identified as the primary anti-inflammatory agent with action on the PI3K/AKT and Ras/MAPK pathways. CLA and CGA enhanced the actions of ATG and exhibited synergistic NF-κB inactivation effects possibly via the Ras/MAPK signaling pathway. Moreover, CLA is speculated to target FGFR and MEK firstly. Overall, QF regulated the PI3K/AKT and Ras/MAPK pathways to inhibit pathogenic bacterial infections effectively.
Aspirin Suppresses the Acquisition of Chemoresistance in Breast Cancer by Disrupting an NFκB–IL6 Signaling Axis Responsible for the Generation of Cancer Stem Cells
Authors: Shilpi Saha, Shravanti Mukherjee, Poulami Khan, Kirti Kajal, Minakshi Mazumdar, Argha Manna, Sanhita Mukherjee, Sunanda De, Debarshi Jana, Diptendra K. Sarkar, Tanya Das
Journal: Cancer Research (2016)

Acquired chemoresistance has curtailed cancer survival since the dawn of chemotherapy. Accumulating evidence suggests a major role for cancer stem cells (CSC) in chemoresistance, although their involvement in acquired resistance is still unknown. The use of aspirin has been associated with reduced cancer risk and recurrence, suggesting that the anti-inflammatory drug may exert effects on CSCs. In this study, we investigated the contribution of CSCs to acquired chemoresistance of breast cancer and the avenues for reversing such effects with aspirin. We observed that the residual risk of recurrence was higher in breast cancer patients who had acquired chemoresistance. Treatment of preexisting CSCs with a genotoxic drug combination (5-fluorouracil, doxorubicin, and cyclophosphamide) generated an NFκB-IL6-dependent inflammatory environment that imparted stemness to nonstem cancer cells, induced multidrug resistance, and enhanced the migration potential of CSCs. Treatment with aspirin prior to chemotherapy suppressed the acquisition of chemoresistance by perturbing the nuclear translocation of NFκB in preexisting CSCs. Therefore, disruptions to the NFκB-IL6 feedback loop prevented CSC induction and sensitized preexisting CSCs to chemotherapy. Collectively, our findings suggest that combining aspirin and conventional chemotherapy may offer a new treatment strategy to improve recurrence-free survival of breast cancer patients. Cancer Res; 76(7); 2000-12. ©2016 AACR.
Abstract 16081: A Familial Hypertrophic Cardiomyopathy is Caused by a Mutation in Elp2, Encoding One of Subunits of Elongator Acetyltransferase Complex
Authors: Ryuji Okamoto, Itaru Goto, Issei Kobayashi, Ryotaro Hashizume, Naoshi Shimojo, Kaoru Dohi, Mashio Nakamura, Masaaki Ito
Journal: Circulation (2014)

Introduction: Elongator protein 2 (ELP2) is known as a STAT3-interacting protein and one of subunits of elongator, which can regulate RNA elongation via its histone acetyltransferase activity. It remains unknown whether ELP2 plays an important role in cardiac hypertrophy. Aim: Our aim is to identify new gene mutations that cause familial HCM, which can progresses into dilated-phase HCM (d-HCM). Methods: We examined a patient and her elder brother who both presented with complicated severe HCM and whose parents are married cousins. The elder brother had died suddenly as a child; the autopsy revealed that he had developed HCM. The patient was diagnosed with HCM, and HCM progressed to d-HCM during the 20-year follow-up. The patient received a left ventricular-assist device implant, and the patient is currently on a waiting list for cardiac transplantation. The parents are healthy. We hypothesized that a causative allele was transmitted to both the patient and the elder brother as an autosomal recessive mutation that caused familial HCM. The genome analysis and whole-exome sequencing was performed with samples from each of the three participants. Sarcomere organization in H9C2 cells overexpressed with ELP2 and localization of ELP2 in biopsy samples were examined. Results: The gene exome analysis showed 340 single nucleotide polymorphisms (SNPs) that caused amino acid change for which the patient was homozygous and both parents were heterozygous. After excluding all known common (&gt;10%) SNP gene mutations in the SNP Database (dbSNP), ELP2 was the only identified gene that is possibly associated with cardiac muscle. The identified missense mutation was a 2385 G&gt;A nucleotide transition in ELP2 isoform 2. The resultant E795G substitution replaces a polar carboxylic glutamate with a nonpolar glycine. The H9C2 overexpressed with mutant ELP2 showed a distinct sarcomere organization compared with cells overexpressed with intact ELP2. Immunohistochemistry studies showed the localization of ELP2 in the patient’s endomyocardial biopsy sample was different from in control samples. Conclusions: These results indicate both that mutations in ELP2 can cause a familial form of HCM and that ELP2 may be a new target for treatment of cardiac hypertrophy.
Abstract 1121: Ca2+ Influx through T-type Ca2+ Channels Is Necessary for Differentiation of Cardiac Stem Cells into Functional Cardiac Myocytes
Authors: Hajime Kubo, Remus M Berretta, Scott MacDonnell, Naser Jaleel, Micheal P Quaile, Abby Dean, Xiongwen Chen, Rachel Wilson, David Angert, George Bratinov, Xiaoyin Shan, Kenneth B Margulies, Patrycja Galazka, Leanne L Cribbs, Claudia Bearzi, Stefano Cascapera, Jan Kajstura, Annarosa Leri, Piero Anversa, Steven R Houser
Journal: Circulation (2007)

Recent reports have shown that the heart contains a population of resident cardiac stem cells (CSCs) with the capacity to form new cardiac myocytes. The present study explored the hypothesis that C...
Abstract 12855: Added Value of Pharmacogenetic Factors to a Clinical Risk Score for Prediction f oThrombotic Events After ST-Segment Elevation Myocardial Infarction
Authors: Jeffrey J Verschuren, Helen Boden, Georgette E Hoogslag, Matthijs A Velders, Stella Trompet, Bas L van der Hoeven, Henk-Jan Guchelaar, Hein Putter, Martin J Schalij, J. Wouter Jukema
Journal: Circulation (2012)

Introduction: Several single nucleotide polymorphisms (SNPs), related to antiplatelet drug efficacy, are known to be associated with adverse events during antiplatelet therapy. However, their added...
The live attenuated dengue vaccine TV003 elicits complete protection against dengue in a human challenge model
Authors: Beth D. Kirkpatrick, Stephen S. Whitehead, Kristen K. Pierce, Cecilia M. Tibery, Palmtama L. Grier, Noreen A. Hynes, Catherine J. Larsson, Beulah P. Sabundayo, Kawsar R. Talaat, Anna Janiak, Marya P. Carmolli, Catherine J. Luke, Sean A. Diehl, Anna P. Durbin
Journal: Science Translational Medicine (2016)

A controlled dengue human challenge model may determine whether to evaluate candidate dengue vaccines in large efficacy trials.
Conservation of a long open reading frame in two Neurospora mitochondrial plasmids.
Authors: F E Nargang
Journal: Molecular Biology and Evolution (1986)

The nucleotide sequence of a specific region of the mitochondrial plasmid from the Neurospora intermedia Varkud-lc strain was determined. Analysis of the sequence revealed the presence of a long (up to 710 amino acids) ORF. This ORF is almost identical to a previously characterized ORF in the mitochondrial plasmid from the Neurospora crassa Mauriceville-lc strain. When the ORFs from the two plasmids are compared over their entire length of 2,133 bp, only 34 nucleotide substitutions are found (greater than 98% identity). These substitutions result in only nine amino acid replacements in the protein sequences predicted from the two ORFs. Though no function can be assigned to the putative products of these ORFs, their high conservation of nucleotide and deduced amino acid sequence suggest that they are under selective pressure, presumably to preserve the function of some protein.
Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport
Authors: Andrew S. Terker, Bethzaida Yarbrough, Mohammed Z. Ferdaus, Rebecca A. Lazelle, Kayla J. Erspamer, Nicholas P. Meermeier, Hae J. Park, James A. McCormick, Chao-Ling Yang, David H. Ellison
Journal: Journal of the American Society of Nephrology (2015)

Excess aldosterone is an important contributor to hypertension and cardiovascular disease. Conversely, low circulating aldosterone causes salt wasting and hypotension. Aldosterone activates mineralocorticoid receptors (MRs) to increase epithelial sodium channel (ENaC) activity. However, aldosterone may also stimulate the thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC). Here, we generated mice in which MRs could be deleted along the nephron to test this hypothesis. These kidney-specific MR-knockout mice exhibited salt wasting, low BP, and hyperkalemia. Notably, we found evidence of deficient apical orientation and cleavage of ENaC, despite the salt wasting. Although these mice also exhibited deficient NCC activity, NCC could be stimulated by restricting dietary potassium, which also returned BP to control levels. Together, these results indicate that MRs regulate ENaC directly, but modulation of NCC is mediated by secondary changes in plasma potassium concentration. Electrolyte balance and BP seem to be determined, therefore, by a delicate interplay between direct and indirect mineralocorticoid actions in the distal nephron.
Tumor marker guidelines.
Authors: R B Sklaroff
Journal: Journal of Clinical Oncology (1997)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1997.15.5.2175 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 9164236 Tumor marker guidelines. R B SklaroffxR B SklaroffSearch for articles by this author https://doi.org/10.1200/JCO.1997.15.5.2175 PDF "Tumor marker guidelines.." Journal of Clinical Oncology, 15(5), pp. 2175–2176© 1997 by American Society of Clinical Oncology
Fucosyltransferase Activity in Metastasizing and Nonmetastasizing Rat Mammary Carcinomas2
Authors: Sunil K. Chatterjee, Untae Kim
Journal: JNCI Journal of the National Cancer Institute (1978)

Fucosyltransferase levels in 6 established strains of spontaneously metastasizing rat mammary tumors (STMT-058, MT-449, DMBA-4, SMT-077, TMT-081, and SMT-2A) were compared with 4 nonmetastasizing strains (MT-W9B, MT-W9A, MT-100, and MT-66) as controls. Two acceptors were prepared from fetuin for the assay, one by acid hydrolysis of N-acetylneuraminic acid and the other by the stepwise removal of N-acetylneuraminic acid and penultimate galactose by Smith degradation. The enzyme that transfers fucose to the first acceptor was designated fucosyltransferase A, whereas the one that uses the second acceptor was designated fucosyltransferase B. Both types of fucosyltransferases were found in this rat mammary tumor system. Whereas the levels of fucosyltransferase A in the 2 tumor groups were comparable, those of fucosyltransferase B were sixfold to sevenfold higher in the metastasizing tumors. This difference in the level of fucosyltransferase B was not caused either by differential hydrolysis of GDP-fucose by pyrophosphatase in the 2 groups or by hydrolysis of the product by fucosidases. Presence of any other inhibitor(s) or activator(s) of fucosyltransferase was excluded by mixing experiments. Optimal conditions for the assay of this enzyme were determined in a representative strain from each group. Under all circumstances, the activity of fucosyltransferase B was higher in the metastasizing tumors. The enzyme was inhibited by nucleoside diphosphates and triphosphates, and guanosine nucleotides were the most efficient inhibitors. Sub-cellular distributions of the two fucosyltransferases were similar, 35–50% of the enzyme activity being present in the crude microsomes. When plasma membrane fractions were prepared from the microsomes, the major part (50–70%) of the enzyme was associated with the light and heavy plasma membrane fractions. Increased activity of fucosyltransferase B in the group of metastasizing tumors may have reflected faster synthesis and shedding of fucose-containing glycoprotein antigens. Similar molecules possibly were also synthesized in the nonmetastasizing cells but at a much slower rate, because the antigen is not easily lost from the cell surface. Any alteration of the specificity of this fucosyltransferase in the metastasizing tumors, in addition, may have caused antigen modulation.
Improved Risk Assessment by Integrating Molecular and Clinicopathological Factors in Early-stage Endometrial Cancer—Combined Analysis of the PORTEC Cohorts
Authors: Ellen Stelloo, Remi A. Nout, Elisabeth M. Osse, Ina J. Jürgenliemk-Schulz, Jan J. Jobsen, Ludy C. Lutgens, Elzbieta M. van der Steen-Banasik, Hans W. Nijman, Hein Putter, Tjalling Bosse, Carien L. Creutzberg, Vincent T.H.B.M. Smit
Journal: Clinical Cancer Research (2016)

Recommendations for adjuvant treatment for women with early-stage endometrial carcinoma are based on clinicopathologic features. Comprehensive genomic characterization defined four subgroups: p53-mutant, microsatellite instability (MSI), POLE-mutant, and no specific molecular profile (NSMP). We aimed to confirm the prognostic capacity of these subgroups in large randomized trial populations, investigate potential other prognostic classifiers, and integrate these into an integrated molecular risk assessment guiding adjuvant therapy.Analysis of MSI, hotspot mutations in 14 genes including POLE, protein expression of p53, ARID1a, β-catenin, L1CAM, PTEN, ER, and PR was undertaken on 947 available early-stage endometrioid endometrial carcinomas from the PORTEC-1 and -2 trials, mostly high-intermediate risk (n = 614). Prognostic value was determined using univariable and multivariable Cox proportional hazard models. AUCs of different risk stratification models were compared.Molecular analyses were feasible in >96% of the patients and confirmed the four molecular subgroups: p53-mutant (9%), MSI (26%), POLE-mutant (6%), and NSMP (59%). Integration of prognostic molecular alterations with established clinicopathologic factors resulted in a stronger model with improved risk prognostication. Approximately 15% of high-intermediate risk patients had unfavorable features (substantial lymphovascular space invasion, p53-mutant, and/or >10% L1CAM), 50% favorable features (POLE-mutant, NSMP being microsatellite stable, and CTNNB1 wild-type), and 35% intermediate features (MSI or CTNNB1-mutant).Integrating clinicopathologic and molecular factors improves the risk assessment of patients with early-stage endometrial carcinoma. Assessment of this integrated risk profile is feasible in daily practice, and holds promise to reduce both overtreatment and undertreatment. Clin Cancer Res; 22(16); 4215-24. ©2016 AACR.