tbuckley/cabot-search huggingface dataset:
Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part VI. Pediatric advanced life support
Journal: JAMA (1992)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Ensuring Access to Injectable Generic Drugs — The Case of Intravesical BCG for Bladder Cancer
Authors: Benjamin J. Davies, Thomas J. Hwang, Aaron S. Kesselheim
Journal: New England Journal of Medicine (2017)

Limits on access to injectable generic drugs force providers to use potentially less effective alternatives, current patients to discontinue therapy, and some new patients to receive more invasive interventions. Yet shortages of important generic drugs remain frequent.
Decision Making in Adrenoleukodystrophy
Authors: Keith Van Haren, Marc Engelen
Journal: JAMA Neurology (2017)

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 Neurology HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Neurology journal
Population- and individual-specific regulatory variation in Sardinia
Authors: Mauro Pala, Zachary Zappala, Mara Marongiu, Xin Li, Joe R Davis, Roberto Cusano, Francesca Crobu, Kimberly R Kukurba, Michael J Gloudemans, Frederic Reinier, Riccardo Berutti, Maria G Piras, Antonella Mulas, Magdalena Zoledziewska, Michele Marongiu, Elena P Sorokin, Gaelen T Hess, Kevin S Smith, Fabio Busonero, Andrea Maschio, Maristella Steri, Carlo Sidore, Serena Sanna, Edoardo Fiorillo, Michael C Bassik, Stephen J Sawcer, Alexis Battle, John Novembre, Chris Jones, Andrea Angius, Gonçalo R Abecasis, David Schlessinger, Francesco Cucca, Stephen B Montgomery
Journal: Nature Genetics (2017)
Abstract 71: Soy Isoflavone Protects Myocardial Ischemia/reperfusion Injury Through Increasing Endothelial Nitric Oxide Synthase and Decreasing Oxidative Stress in Ovariectomized Rats
Authors: Liping Xie, Guoliang Meng, Yong Ji
Journal: Circulation Research (2015)

Rationale: There is a special role for estrogens in preventing and curing cardiovascular disease in women. Soy isoflavone (SI), a soy-derived phytoestrogen, is a group of biologically active plant substances with chemical structures which are similar to that of an endogenous estrogen-estradiol. Objective: We ought to elucidate possible mechanism of SI to improve myocardial ischemia/reperfusion (MI/R) injury in ovariectomized rats. Methods and Results: Female SD rats were underwent bilateral ovariectomy or sham ovariectomy. One week later, rats were randomly divided into several groups and began to feed soy-free chow: sham ovariectomy operation (control group), ovariectomy with MI/R or ovariectomy with sham MI/R. Other ovariectomy rats were given different doses of SI dissolved in 0.5% carboxymethycellulose (CMC-Na) by gavage. Additional ovariectomy rats were administrated with the same volume of CMC-Na by gavage or 50 μg/kg·d of 17β-estradiol (E 2 ) by subcutaneous injection. After four-week treatment, they were exposed to 30 minutes of left coronary artery occlusion followed by 6 or 24 hours of reperfusion. SI treatment decreased body weight, increased estradiol level and uterus weight. Isoflavone administration significantly reduced myocardial infarct size, improved left ventricle function and restored endothelium-dependent relaxation function of thoracic aortas after MI/R in ovariectomized rats. SI also decreased creatine kinase and malonaldehyde in plasma and attenuated oxidative stress in the myocardium. Meanwhile, SI increased phosphatidylinositol 3 kinase (PI3K) / Akt/ endothelial nitric oxide synthase (eNOS) signal pathway. Conclusion: Soy isoflavone protects myocardial ischemia/reperfusion injurys in ovariectomized rats through increasing PI3K/Akt/eNOS signal pathway and decreasing oxidative stress.
Distinct Serum Sphingolipid Profiles among School-aged Children with Exercise-induced Wheeze and Asthma Persistence
Authors: Matthew S. Perzanowski, Jennie G. Ono, Luis M. Acosta, Benjamin I. Kim, Adnan Divjan, Rachel Miller, Andrew Rundle, Stefan Worgall, Tilla S. Worgall
Journal: American Journal of Respiratory and Critical Care Medicine (2017)
DNA methylome analysis reveals distinct epigenetic patterns of ascending aortic dissection and bicuspid aortic valve
Authors: Sun Pan, Hao Lai, Yiru Shen, Charles Breeze, Stephan Beck, Tao Hong, Chunsheng Wang, Andrew E. Teschendorff
Journal: Cardiovascular Research (2017)

Epigenetics may mediate the effects of environmental risk factors on disease, including heart disease. Thus, measuring the DNA methylome offers the opportunity to identify novel disease biomarkers and novel insights into disease mechanisms. The DNA methylation landscape of ascending aortic dissection (AD) and bicuspid aortic valve (BAV) with aortic aneurysmal dilatation remain uncharacterized. The present study aimed to explore the genome-wide DNA methylation landscape underpinning these two diseases.We used Illumina 450k DNA methylation beadarrays to analyse 21 ascending aorta samples, including 10 cases with AD, 5 with BAV and 6 healthy controls. We adjusted for intra-sample cellular heterogeneity, providing the first unbiased genome-wide exploration of the DNA methylation landscape underpinning these two diseases. We discover that both diseases are characterized by loss of DNA methylation at non-CpG sites. We validate this non-CpG hypomethylation signature with pyrosequencing. In contrast to non-CpGs, AD and BAV exhibit distinct DNA methylation landscapes at CpG sites, with BAV characterized mainly by hypermethylation of EZH2 targets. In the case of AD, integrative DNA methylation gene expression analysis reveals that AD is characterized by a dedifferentiated smooth muscle cell phenotype. Our integrative analysis further reveals hypomethylation associated overexpression of RARA in AD, a pattern which is also seen in cells exposed to smoke toxins.Our data supports a model in which increased cellular proliferation in AD and BAV underpins loss of methylation at non-CpG sites. Our data further supports a model, in which AD is associated with an inflammatory vascular remodeling process, possibly mediated by the epigenome and linked to environmental risk factors such as smoking.
Terence J Wilkin
Authors: John Carter
Journal: BMJ (2017)

Terence J Wilkin (“Terry”) graduated from St Andrews University Medical School, where he met Linda Voss, who was to be his professional colleague (and collaborator in more than three dozen of his 200 publications) as well as his spouse for nearly 50 years. He received his MD (commended) on thyroid autoimmunity from Dundee University and spent the next 15 years with the Wellcome Trust, first as European travelling fellow at the University of Montpellier (where he …
Mitochondrial Recombination and Introgression during Speciation by Hybridization
Authors: Jean-Baptiste Leducq, Mathieu Henault, Guillaume Charron, Lou Nielly-Thibault, Yves Terrat, Heather L. Fiumera, B. Jesse Shapiro, Christian R. Landry
Journal: Molecular Biology and Evolution (2017)

Abstract Genome recombination is a major source of genotypic diversity and contributes to adaptation and speciation following interspecies hybridization. The contribution of recombination in these processes has been thought to be largely limited to the nuclear genome because organelles are mostly uniparentally inherited in animals and plants, which prevents recombination. Unicellular eukaryotes such as budding yeasts do, however, transmit mitochondria biparentally, suggesting that during hybridization, both parents could provide alleles that contribute to mitochondrial functions such as respiration and metabolism in hybrid populations or hybrid species. We examined the dynamics of mitochondrial genome transmission and evolution during speciation by hybridization in the natural budding yeast Saccharomyces paradoxus. Using population-scale mitochondrial genome sequencing in two endemic North American incipient species SpB and SpC and their hybrid species SpC*, we found that both parental species contributed to the hybrid mitochondrial genome through recombination. We support our findings by showing that mitochondrial recombination between parental types is frequent in experimental crosses that recreate the early step of this speciation event. In these artificial hybrids, we observed that mitochondrial genome recombination enhances phenotypic variation among diploid hybrids, suggesting that it could play a role in the phenotypic differentiation of hybrid species. Like the nuclear genome, the mitochondrial genome can, therefore, also play a role in hybrid speciation.
Current and potential imaging applications of ferumoxytol for magnetic resonance imaging
Authors: Gerda B. Toth, Csanad G. Varallyay, Andrea Horvath, Mustafa R. Bashir, Peter L. Choyke, Heike E. Daldrup-Link, Edit Dosa, John Paul Finn, Seymur Gahramanov, Mukesh Harisinghani, Iain Macdougall, Alexander Neuwelt, Shreyas S. Vasanawala, Prakash Ambady, Ramon Barajas, Justin S. Cetas, Jeremy Ciporen, Thomas J. DeLoughery, Nancy D. Doolittle, Rongwei Fu, John Grinstead, Alexander R. Guimaraes, Bronwyn E. Hamilton, Xin Li, Heather L. McConnell, Leslie L. Muldoon, Gary Nesbit, Joao P. Netto, David Petterson, William D. Rooney, Daniel Schwartz, Laszlo Szidonya, Edward A. Neuwelt
Journal: Kidney International (2017)
Expanding access to healthcare in South Asia
Authors: Shehla Zaidi, Prasanna Saligram, Syed Ahmed, Egbert Sonderp, Kabir Sheikh
Journal: BMJ (2017)

Policy initiatives aiming to improve access to healthcare in South Asia have proliferated in recent years, but are they enough to address widespread health inequity in the region, ask <b>Shehla Zaidi and colleagues</b>?
Development And Evaluation Of A Quantitative Lateral Flow Immunoassay For The Detection Of Ferritin As Point-of-care Testing
Authors: Fumiaki Kimura, Sanami Miyoshi, Yasuo Mishima, Nobuyuki Shigeto, Tomoko Fukuda, Shigehiro Yamahara, Tadashi Matsumura, Shinji Fujii, Mitsune Tanimoto
Journal: American Journal of Hematology (2013)
The within-host population dynamics of Mycobacterium tuberculosis vary with treatment efficacy
Authors: Andrej Trauner, Qingyun Liu, Laura E. Via, Xin Liu, Xianglin Ruan, Lili Liang, Huimin Shi, Ying Chen, Ziling Wang, Ruixia Liang, Wei Zhang, Wang Wei, Jingcai Gao, Gang Sun, Daniela Brites, Kathleen England, Guolong Zhang, Sebastien Gagneux, Clifton E. Barry, Qian Gao
Journal: Genome biology (2017)

Combination therapy is one of the most effective tools for limiting the emergence of drug resistance in pathogens. Despite the widespread adoption of combination therapy across diseases, drug resistance rates continue to rise, leading to failing treatment regimens. The mechanisms underlying treatment failure are well studied, but the processes governing successful combination therapy are poorly understood. We address this question by studying the population dynamics of Mycobacterium tuberculosis within tuberculosis patients undergoing treatment with different combinations of antibiotics. By combining very deep whole genome sequencing (~1000-fold genome-wide coverage) with sequential sputum sampling, we were able to detect transient genetic diversity driven by the apparently continuous turnover of minor alleles, which could serve as the source of drug-resistant bacteria. However, we report that treatment efficacy has a clear impact on the population dynamics: sufficient drug pressure bears a clear signature of purifying selection leading to apparent genetic stability. In contrast, M. tuberculosis populations subject to less drug pressure show markedly different dynamics, including cases of acquisition of additional drug resistance. Our findings show that for a pathogen like M. tuberculosis, which is well adapted to the human host, purifying selection constrains the evolutionary trajectory to resistance in effectively treated individuals. Nonetheless, we also report a continuous turnover of minor variants, which could give rise to the emergence of drug resistance in cases of drug pressure weakening. Monitoring bacterial population dynamics could therefore provide an informative metric for assessing the efficacy of novel drug combinations.
EGFR Mediates Responses to Small-Molecule Drugs Targeting Oncogenic Fusion Kinases
Authors: Aria Vaishnavi, Laura Schubert, Uwe Rix, Lindsay A. Marek, Anh T. Le, Stephen B. Keysar, Magdalena J. Glogowska, Matthew A. Smith, Severine Kako, Natalia J. Sumi, Kurtis D. Davies, Kathryn E. Ware, Marileila Varella-Garcia, Eric B. Haura, Antonio Jimeno, Lynn E. Heasley, Dara L. Aisner, Robert C. Doebele
Journal: Cancer Research (2017)

Oncogenic kinase fusions of ALK, ROS1, RET, and NTRK1 act as drivers in human lung and other cancers. Residual tumor burden following treatment of ALK or ROS1+ lung cancer patients with oncogene-targeted therapy ultimately enables the emergence of drug-resistant clones, limiting the long-term effectiveness of these therapies. To determine the signaling mechanisms underlying incomplete tumor cell killing in oncogene-addicted cancer cells, we investigated the role of EGFR signaling in drug-naïve cancer cells harboring these oncogene fusions. We defined three distinct roles for EGFR in the response to oncogene-specific therapies. First, EGF-mediated activation of EGFR blunted fusion kinase inhibitor binding and restored fusion kinase signaling complexes. Second, fusion kinase inhibition shifted adaptor protein binding from the fusion oncoprotein to EGFR. Third, EGFR enabled bypass signaling to critical downstream pathways such as MAPK. While evidence of EGFR-mediated bypass signaling has been reported after ALK and ROS1 blockade, our results extended this effect to RET and NTRK1 blockade and uncovered the other additional mechanisms in gene fusion-positive lung cancer cells, mouse models, and human clinical specimens before the onset of acquired drug resistance. Collectively, our findings show how EGFR signaling can provide a critical adaptive survival mechanism that allows cancer cells to evade oncogene-specific inhibitors, providing a rationale to cotarget EGFR to reduce the risks of developing drug resistance. Cancer Res; 77(13); 3551-63. ©2017 AACR.
United States Population-Based Estimates of Patient-Reported Outcomes Measurement Information System Symptom and Functional Status Reference Values for Individuals With Cancer
Authors: Roxanne E. Jensen, Arnold L. Potosky, Carol M. Moinpour, Tania Lobo, David Cella, Elizabeth A. Hahn, David Thissen, Ashley Wilder Smith, Jaeil Ahn, George Luta, Bryce B. Reeve
Journal: Journal of Clinical Oncology (2017)

Purpose To estimate cancer population-based reference values in the United States for eight PROMIS (Patient-Reported Outcomes Measurement Information System) domains by age and stage of disease. Patients and Methods For the Measuring Your Health (MY-Health) study, persons newly diagnosed with cancer (prostate, colorectal, non-small-cell lung, non-Hodgkin lymphoma, breast, uterine, or cervical) from 2010 to 2012 (N = 5,284) were recruited through the National Cancer Institute's SEER Program. Participants were mailed surveys 6 to 13 months after diagnosis. Raking by race/ethnicity, age, and stage generated weighted average PROMIS scores for pain interference, fatigue, anxiety, depression, sleep disturbance, physical function, ability to participate in social roles, and cognitive function. PROMIS measures are standardized to a T-score metric, with a score of 50 representing the general US population mean. Clinically meaningful differences were defined as a 3-point difference in scores. Results Several reference values (means) for patients with cancer were worse than the general United States population norms of 50. These include pain interference (52.4), fatigue (52.2), and physical function (44.1). Reference values were highest (ie, showed greatest symptom burden) in lung cancer (pain interference, 55.5; fatigue, 57.3; depression, 51.4) and cervical cancer (anxiety, 53.2; sleep disturbance, 53.4). Reference values for patients age 65 to 84 years reported lower sleep disturbance, anxiety, and depression, and better cognitive function than younger patients. Cancer reference values were poorer among those with advanced disease compared with patients with limited or no evidence of disease, specifically physical function (41.1 v 46.6, respectively), fatigue (55.8 v 50.2, respectively), and pain interference (55.2 v 50.9, respectively). Conclusion In a large, population-based sample of patients with recently diagnosed cancer, we observed symptom severity and functional deficits by age, stage, and cancer type consistent with the expected impact of cancer diagnosis and treatment. These United States cancer reference values can help facilitate interpretation of the PROMIS domain scores in research studies or in clinical applications that measure and evaluate the symptom and functional burden patients with cancer experience after initial treatment.
Lymphocyte migratory genes may program tumor metastasis
Authors: To-Yu Huang, Valerie N. Montel, Kersi Pestonjamasp, Luminita Castillos, David Tarin
Journal: Cancer Research (2004)

1750   Metastasizing tumor cells leave their assigned positional addresses in the body and travel via circulatory channels to distant organs that they colonize. The only other adult cell lineages which make similar journeys are members of the leukocytic series, particularly lymphocytes. In this study we tested whether human breast cancer cells may utilize the same molecular machinery to migrate to the lymph nodes and lungs. We examined primary tumors resulting from orthotopic injections of non-metastatic (NM2C5) or metastatic (M4A4) sublines, both derived from the MDA-MB-435 parental cell line and the lung metastases from M4A4 tumors. Screening of gene expression levels was first performed with Affymetrix Genechip U133A microarrays that interrogate more than 22,000 human genes. Expression of genes of interest was further examined by real-time PCR, using human-specific primers and by immunofluorescence imaging of corresponding proteins, to independently validate observations. Analysis of microarray data revealed distinctive expression patterns of integrins (ITGs) and cell adhesion molecules (CAMs). Previous work in this laboratory identified VLA-4 (ITGα4β1) as being differentially expressed in primary tumors of opposite metastatic behaviors, giving some support to this hypothesis. In this study, we examined the expression of additional ITGs and CAMs, including those that were recently implicated in directing lymphocytes to bronchus-associated lymphoid tissues (BALT). Among all integrins, ITGβ1 and ITGα6 were the most highly expressed, followed by ITGαE, αV, α2 and α5 at medium levels. ITGα4 was elevated in metastatic primary tumors and lung metastases compared to their non-metastatic counterparts. This was demonstrated by real-time PCR, consistent with our previous observations on VLA-4 and its functional role recently established in lymphocyte homing to BALT. Similar patterns were also observed for ITGαL, which comprises the α subunit of LFA-1, and its cognate receptors, intercellular cell adhesion molecule (ICAM) 1 and ICAM2. The real-time PCR data suggested that ICAM1 expression is elevated in M4A4 tumors relative to NMC5 tumors, and further elevated in M4A4 lung metastases. In addition, we have observed that the protein levels of ICAM1 by immunofluorescence imaging concur with the increase of ICAM1 transcripts in metastatic cell lines. In contrast, no expression signal above the noise levels was detectable for ITGα1, α7, α8, αX and ITGβ3, β4 and β7. Hence, by high-throughput screening of gene expression and subsequent validation, we have identified a group of candidate genes whose biological functions are potentially shared by trafficking lymphocyte and metastatic tumor cells. Further experiments to assess the effects of manipulating the expression of these genes on metastasis are in progress.