tbuckley/cabot-search huggingface dataset:
Radiologic Notes in Cardiology
Authors: MURRAY G. BARON
Journal: Circulation (1971)

The anatomic hallmark of a double-outlet right ventricle is the separation of the mitral and aortic valves by a band of myocardium. The two valves remain in contact with each other in tetralogy of Fallot no matter how far anteriorly the aorta is displaced. The mitral-aortic relationship can usually be well demonstrated in both anomalies by selective right ventricular angiocardiography.
Hope and Humility for Azithromycin
Authors: Naor Bar-Zeev, William J. Moss
Journal: New England Journal of Medicine (2019)

Azithromycin, which was discovered by Croatian scientists in 1980, has broad antimicrobial activity. Its seeming broad-spectrum activity led its discoverers to name it Sumamed, invoking the summum bonum — the ultimate good. But is azithromycin the elixir of life, capable of reducing mortality? The results, published in 2009, of the Trachoma Amelioration in Northern Amhara (TANA) trial, conducted near Lake Tana in Ethiopia, were stunning. Mass administration of azithromycin for trachoma halved all-cause mortality among children 1 to 9 years of age in communities that received azithromycin.1 Mass administration of azithromycin had previously been shown to reduce morbidity associated with . . .
From Policy to Patient Care—The Cycle of Health Policy Research
Authors: Nader N. Massarweh, Rachel R. Kelz
Journal: JAMA Surgery (2019)

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 Surgery 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 Surgery journal
Abstract 5109: National cyberinfrastructure and bioinformatic analysis support available to the cancer research community
Authors: Bhavya Papudeshi, Carrie Ganote, Sheri Sanders, Thomas G. Doak
Journal: Cancer Research (2019)

Abstract National Center for Genomic Analysis Support (NCGAS) is an NSF-funded center whose goal is to help biologists optimize their bioinformatic pipelines to best address their research questions. To help reach these goals, NCGAS provides a range of services based on the researchers needs. We currently host gateways, Trinity Galaxy and Genepattern, with built-in workflows to support cancer researchers who have little background in command line work. Both these gateways are projects funded by the Information Technologies in Cancer Research (ITCR) program of NIH, NCI, to aid in the genomic and transcriptomic characterization of cancers. NSF-funded researchers comfortable in command line can gain access to IU cyberinfrastructure (HIPAA compliant), to run or develop bioinformatic workflows. Bioinformatic packages are already installed system wide, with reference databases, and new programs are always added upon user’s request. NCGAS is also an ambassador of Extreme Science and Engineering Discovery Environment (XSEDE) resources, providing access to other HIPAA compliant national cyberinfrastructure (Texas Advanced Computing Center, Pittsburgh Supercomputing Center, etc.), available to the entire research community. XSEDE resources include the Jetstream cloud, based at IU and TACC, allowing researchers to use preconfigured virtual machines (VMs) already setup, create custom VM environments for their own work, and to share with classes and collaborators. Data can be transferred and managed between all of these resources securely with already available Globus endpoints which allows transfer for terabytes of data quickly. Additionally, NCGAS hosts workshops to help researchers get started. These training events can be scheduled online or at your local university upon request. NCGAS currently supports projects working on transcriptome, genome-level assembly, phylogenetics, metagenomics, and meta-transcriptomics analysis through providing a range of compute resources that best serve the research project. Citation Format: Bhavya Papudeshi, Carrie Ganote, Sheri Sanders, Thomas G. Doak. National cyberinfrastructure and bioinformatic analysis support available to the cancer research community [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 5109.
Pre-treated anti-PD-1 refractory Merkel cell carcinoma successfully treated with the combination of PD-1/PD-L1 axis inhibitors and TVEC: a report of two cases
Authors: R. Knackstedt, T.A. Sussman, L. McCahon, J.-M. Song, P. Funchain, B. Gastman
Journal: Annals of Oncology (2019)
Implications of Changing Public Charge Immigration Rules for Children Who Need Medical Care
Authors: Leah Zallman, Karen E. Finnegan, David U. Himmelstein, Sharon Touw, Steffie Woolhandler
Journal: JAMA Pediatrics (2019)

In October 2018, the Trump administration published a proposed rule change that would increase the chance of an immigrant being deemed a "public charge" and thereby denied legal permanent residency or entry to the United States. The proposed changes are expected to cause many immigrant parents to disenroll their families from safety-net programs, in large part because of fear and confusion about the rule, even among families to whom the rule does not technically apply.To simulate the potential harms of the rule change by estimating the number, medical conditions, and care needs of children who are at risk of losing their current benefits, including Medicaid and Children's Health Insurance Program (CHIP) and Supplemental Nutrition Assistance Program (SNAP).A cross-sectional study used nationally representative data from 4007 children 17 years of age or younger who participated in the 2015 Medical Expenditure Panel Survey to assess their potential risk of losing benefits because they live with a noncitizen adult. Statistical analysis was conducted from January 3 to April 8, 2019.The number of children at risk of losing benefits; the number of children with medical need, defined as having a potentially serious medical diagnosis; being disabled (or functionally limited); or having received any specific treatment in the past year. The numbers of children who would be disenrolled under likely disenrollment scenarios drawn from research on immigrants before and after the 1996 welfare reform were estimated.A total of 8.3 million children who are currently enrolled in Medicaid and CHIP or receiving SNAP benefits are potentially at risk of disenrollment, of whom 5.5 million have specific medical needs, including 615 842 children with asthma, 53 728 children with epilepsy, 3658 children with cancer, and 583 700 children with disabilities or functional limitations. Nonetheless, among the population potentially at risk of disenrollment, medical need was less common than among other children receiving Medicaid and CHIP or SNAP (64.5%; 95% CI, 61.5%-67.4%; vs 76.0%; 95% CI, 73.9%-78.4%; P < .001). The proposed rule is likely to cause parents to disenroll between 0.8 million and 1.9 million children with specific medical needs from health and nutrition benefits.The proposed public charge rule would likely cause millions of children to lose health and nutrition benefits, including many with specific medical needs that, if left untreated, may contribute to child deaths and future disability.
Abstract 725: Anticancer effect and mechanism of exosomes mediated microRNA let-7b in breast cancer cells
Authors: Xu Biantiao
Journal: Cancer Research (2019)

Abstract Exosome is referred as membrane-bound nano-vesicles secreted by various mammalian cells. It can be found in different body fluids, such as plasma, saliva, urine, latex, cerebrospinal fluid, ascites, and cell supernatant, which contains a large number of proteins, miRNAs, mRNAs, lipids, nucleic acids, peptides and other substances. Exosome plays a pivotal role in the information transmission signals between cells and the diagnosis and prognosis of diseases as well as drug evaluation. It has become an emerging field in cancer research recently. Therefore, we separated exosomes from human kidney embryo cell (HEK-293) by ultra high speed centrifugation. To identify exosomes from their surface specific proteins by Western blotting analysis. We found enrichment of exosome markers CD63 and TSG101 without Calnexin protein in the exosoms so confirmed that exosome was successfully isolated. Then, we transfered mRNA let-7b into the exosomes by electric transfection further evaluated the effects of cytotoxicity and apoptosis induction on human breast cancer MCF-7 cells by CCK 8 assay Hochest 33342-PI and AnnexinV-PI dual staining analysis, respectively. The results showed that exosome mediated microRNA let-7b exhibited significant anticancer activity and apoptosis induction in a concentration-dependent manner in MCF-7 cells. Moreover, exosome mediated let-7b significantly up-regulated the expression levels of apoptosis related proteins casepase 3, casepase 9, and PARP determined by Western blotting analysis. Our results indicate that the exosomes mediated microRNA such as let-7b can effectively inhibit cell growth and induce apoptosis against breast cancer cells and it may be developed as a novel anticancer agent in the treatment of cancer clinically. Citation Format: Xu Biantiao. Anticancer effect and mechanism of exosomes mediated microRNA let-7b in breast cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 725.
Building toolkits for COPD exacerbations: lessons from the past and present
Authors: Elizabeth Sapey, Mona Bafadhel, Charlotte E Bolton, Thomas Wilkinson, John R Hurst, Jennifer K Quint
Journal: Thorax (2019)

In the nineteenth century, it was recognised that acute attacks of chronic bronchitis were harmful. 140 years later, it is clearer than ever that exacerbations of chronic obstructive pulmonary disease (ECOPD) are important events. They are associated with significant mortality, morbidity, a reduced quality of life and an increasing reliance on social care. ECOPD are common and are increasing in prevalence. Exacerbations beget exacerbations, with up to a quarter of in-patient episodes ending with readmission to hospital within 30 days. The healthcare costs are immense. Yet despite this, the tools available to diagnose and treat ECOPD are essentially unchanged, with the last new intervention (non-invasive ventilation) introduced over 25 years ago. An ECOPD is ‘an acute worsening of respiratory symptoms that results in additional therapy’. This symptom and healthcare utility-based definition does not describe pathology and is unable to differentiate from other causes of an acute deterioration in breathlessness with or without a cough and sputum. There is limited understanding of the host immune response during an acute event and no reliable and readily available means to identify aetiology or direct treatment at the point of care (POC). Corticosteroids, short acting bronchodilators with or without antibiotics have been the mainstay of treatment for over 30 years. This is in stark contrast to many other acute presentations of chronic illness, where specific biomarkers and mechanistic understanding has revolutionised care pathways. So why has progress been so slow in ECOPD? This review examines the history of diagnosing and treating ECOPD. It suggests that to move forward, there needs to be an acceptance that not all exacerbations are alike (just as not all COPD is alike) and that clinical presentation alone cannot identify aetiology or stratify treatment.
A 15 Mg/M2/d Dose of Decitabine Confers Comparable Responses and Better Tolerance Than the Standard Regimen in MDS patients—results of a Multicenter Prospective Cohort Study
Authors: Xiao Li, Qiang Song, Yu Chen, Chunkang Chang, Dong Wu, Lingyun Wu, Jiying Su, Luxi Song, Zheng Zhang, Feng Xu, Ming Hou
Journal: Blood (2012)
Abstract 19168: Effect of Endurance Exercise on Transgenic Arrhythomeginc Right Ventricular Cardiomyopathy Mice
Authors: Rahul Jain, Ruben Martherus, Ken Takagi, Jeanne James, Kristen Kramer, Enkhsaikhan Purevjav, Jeffrey A Towbin
Journal: Circulation (2012)

Introduction: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disorder that causes sudden death and right ventricular heart failure in the young. Clinically, it has been suggested that competitive sports may accelerate ARVC pathogenesis in susceptible persons. The goal of this study was to investigate the cause and effect of exercise stress in the development of ARVC using a transgenic (Tg) mouse model with cardiac-restricted overexpression of human mutant R2834H desmoplakin (DSP). Methods: DSP R2834H Tg (Tg-mut), non-transgenic human wild type DSP WT (Tg-wt) and control non-transgenic (Ntg) mice were divided into groups, sedentary and exercise. Mice in the exercise group were subjected to graded increase in intensity of exercise on a treadmill from the age of 4 weeks. Every 4 weeks, echocardiograms (echo) and ECGs (single lead) were recorded. Mice were dissected for tissue sampling and gross morphology. Results: Initial echo data results are as shown in Table 1. When adjusted for age, number of days exercised, gender, interaction of genotype and exercise status, Tg-mut RV was bigger than Ntg mice (P=0.0005). Within the Tg-mut group, the RV diameter was not statistically significantly different between exercise and sedentary mice when adjusted for same variables. Heart weight/body weight ratio was higher in Tg-mut as compared to Ntg &amp; lcub;sedentary (= 0.001) and exercise group (P = 0.0060&amp;rcub; and Tg-wt. Tissue staining showed early development of fibrosis and fat in Tg-mut mice. The only significant ECG finding occurred in the exercise group: Tg-muthadincreased P wave amplitude and decreased R wave amplitude (P = 0.02 and P =0.001, respectively) compared to Ntg mice. Conclusions: We report significant early histopathologic, and ECG changes with exercise in mutant DSP R2834H Tg mice compared to Ntg and Tg-wt mice.
Abstract 13982: Impact of Persistent Smoking on Long-Term Outcomes Including Bleeding Events in Patients with Nonvalvular Atrial Fibrillation
Authors: Keiko Nakagawa, Tadakazu Hirai, Kazumasa Ohara, Nobuyuki Fukuda, Satoshi Numa, Shutaro Takashima, Takashi Nozawa, Kortaro Tanaka, Hiroshi Inoue
Journal: Circulation (2012)

Background: Although smoking is a risk factor for cardiovascular (CV) disease, little is known about the impact of smoking status on long-term outcomes including bleeding events in patients with at...
Abstract 4654: Hotspot mutations in the core spliceosomal protein SF3B1 promote breast tumorigenesis
Authors: Bo Liu, Michelle Ki, Omar Abdel-Wahab, Sarat Chandarlapaty
Journal: Cancer Research (2019)

Abstract The core RNA splicing factor SF3B1 is targeted by recurrent hotspot mutations in leukemias and solid tumors with the K700E substitution observed in 2% of unselected breast cancer patients. These mutations promote usage of aberrant intron proximal 3’ splice sites. In breast cancer, the links between these aberrant splicing events and the transformed phenotype are not well understood. Here, we integrated findings from multiple genetically modified model systems and human tumor specimens to understand the contributions of mutant SF3B1 to breast cancer pathogenesis. To identify the aberrant splicing events in breast cancers specifically, we first performed RNA-seq analyses of MCF10A breast epithelial cells with CRISPR knock-in of the K700E mutation. Dysregulation of splicing at over 1,000 splice junctions was discovered, most of which involve the use of alternative 3’ splice sites. Gene expression analysis revealed upregulation of expression of NFκB pathway genes in the SF3B1 mutant cells. SF3B1 mutant cells showed higher phosphorylation of RelA (p65) and, accordingly, greater migration in wound-healing assays. Mis-splicing of exon 5 in MAP3K7, a gene encoding a central regulator of NFκB pathway, significantly reduced MAP3K7 protein expression in SF3B1 K700E mutant cells. Consistent with these data, pharmacologic MAP3K7 inhibition in SF3B1 wild-type breast cells increased phosphorylation of RelA. To further understand the effects of the K700E mutation on breast cancer development and progression, we generated a conditional knock-in mouse model, in which Sf3b1 K700E mutant allele was activated through MMTV promoter-controlled expression of Cre recombinase in mammary epithelium. Accelerated tumor formation was not identified in the mammary gland of these mice. However, RNA-seq analysis of mammary epithelial cells from the Sf3b1 K700E mutant mice revealed dysregulation of alternative splicing including Map3k7. As we found the majority of SF3B1 k700E mutations to co-occur with activating mutations in the PI3K pathway, we additionally introduced the Pik3ca H1047R mutant allele, by mating the MMTV-Cre Sf3b1 K700E mice with Rosa26-Pik3ca H1047R knock-in line. Markedly decreased survival was observed in double mutant animals, which developed mammary tumors faster, compared with single mutant controls. Overall, these data reveal that breast cancer-associated Sf3b1 mutations induce the NFkB pathway to promote invasion and cooperate with the PI3K pathway to accelerate mammary tumor development. Citation Format: Bo Liu, Michelle Ki, Omar Abdel-Wahab, Sarat Chandarlapaty. Hotspot mutations in the core spliceosomal protein SF3B1 promote breast tumorigenesis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4654.
Abstract 811: Multi-targeted inhibitors of mitochondrial one-carbon metabolism and cytosolic <i>de novo</i> purine synthesis enzymes as anti-tumor agents
Authors: Md Junayed Nayeen, Khushbu Shah, Aamod Dekhne, Changwon Ning, Carrie O'Connor, Jade M. Katinas, Jennifer Wong, Zhanjun Hou, Charles E. Dann, Larry H. Matherly, Aleem Gangjee
Journal: Cancer Research (2019)

Abstract Targeting cellular one-carbon (1C) metabolism in cancer cells with pyrrolo[3,2-d]pyrimidine analogs provides in vivo antitumor efficacy. We discovered a first-in-class series of 5-substituted pyrrolo[3,2-d]pyrimidine analogs (AGF291, AGF320, AGF347) with inhibition of serine hydroxymethyltransferase 2 (SHMT2), a key enzyme in mitochondrial 1C metabolism and a reported oncodriver. In addition, AGF291, AGF320 and AGF347 inhibited de novo purine nucleotide biosynthesis at glycinamide ribonucleotide formyltransferase (GARFTase) and 5-aminoimidazole-4-carboxamide (AICA) ribonucleotide formyltransferase (AICARFTase), and serine hydroxymethyltransferase 1 (SHMT1). In vivo studies demonstrated excellent antitumor efficacy for AGF347 against MIA PaCa-2 pancreatic adenocarcinoma xenografts in SCID mice with a median tumor growth delay (T-C) of &amp;gt;38 days for 4 mice, and 1 of 5 mice tumor-free 122 days post-treatment. AGF359, a new analog in this series, was a potent inhibitor of KB human tumor cell proliferation in vitro. AGF359 inhibition of KB human tumor cells was reversed with glycine and adenosine, establishing mitochondrial 1C metabolism and de novo purine biosynthesis as the targeted pathways; AICA plus glycine was incompletely protective, implicating AICARFTase as a direct cellular target. AGF359, like AGF291, AGF320, and AGF347, inhibited purified human SHMT2 (Ki = 0.399 ± 0.174 µM), SHMT1 (Ki = 0.70 ± 0.088 µM) and AICARFTase (Ki = 8.86 ± 2.83 µM). There was no inhibition of 5,10-methylene tetrahydrofolate dehydrogenase 2 (MTHFD2). Further structural modifications of these multi-targeted agents afforded pyrrolo[3,2-d]pyrimidine analogs AGF307 and AGF312. Cell-based glycine/nucleotide rescue experiments in KB tumor cells established that, as with AGF359, AGF307 and AGF312 were dual inhibitors of the mitochondrial 1C metabolism (AGF307) and de novo purine biosynthesis (AGF307, AGF312). These compounds are currently in further preclinical evaluation as a prelude to possible clinical development as antitumor agents. Citation Format: Md Junayed Nayeen, Khushbu Shah, Aamod Dekhne, Changwon Ning, Carrie O'Connor, Jade M. Katinas, Jennifer Wong, Zhanjun Hou, Charles E. Dann III, Larry H. Matherly, Aleem Gangjee. Multi-targeted inhibitors of mitochondrial one-carbon metabolism and cytosolic de novo purine synthesis enzymes as anti-tumor agents [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 811.
Abstract 18546: Transcriptome Profiling Identifies Nrf2 And Let-7 As Upstream Regulators of Mechanical Stretch Induced Hypertrophic Gene Response in Cardiac Myocytes
Authors: Heikki Tokola, Heikki Ruskoaho, Jaana Rysä
Journal: Circulation (2017)

Background: Mechanical forces are critically important for the hypertrophic growth in the overloaded myocardium. Hypertrophic response of cardiac myocytes is characterized by an increase in cell si...
Cytosponge™ for post‐chemoradiation surveillance of oesophageal cancer: a feasibility study
Authors: S. Levy, J. Moschandreas, I. Debiram-Beecham, M. O’Donovan, C. Brooks, A. Bailey, M. Hawkins, S. Kadri, J. de Caestecker, T. Crosby, R. Fitzgerald, S. Mukherjee
Journal: Annals of Oncology (2019)
Evidence-Based Medicine and the American Thoracic Society Guidelines—Reply
Authors: Ross C. Schumacher, Oanh Kieu Nguyen, Anil N. Makam
Journal: JAMA Internal Medicine (2019)

In Reply We are encouraged by the commitment of Myers and Bates and Dweik and colleagues, members of the American Thoracic Society’s (ATS) guideline community, to develop robust clinical practice guidelines (CPGs).