tbuckley/cabot-search huggingface dataset:
From the Centers for Disease Control and Prevention. Chaparral-induced toxic hepatitis--California and Texas, 1992
Journal: JAMA (1992)

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THE INDEX MEDICUS.
Journal: JAMA (1906)

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SWOG S0925: A randomized phase 2 study of androgen deprivation combined with cixutumumab versus androgen deprivation alone in patients with new metastatic hormone-sensitive prostate cancer.
Authors: Evan Y. Yu, Catherine M. Tangen, Celestia S. Higano, Neeraj Agarwal, Sumanta Kumar Pal, Ajjai Shivaram Alva, Elisabeth I. Heath, Elaine Tat Lam, Shilpa Gupta, Michael B. Lilly, Yoshio Inoue, Kim N. Chi, Nicholas J. Vogelzang, David I. Quinn, Hongli Li, Heather H. Cheng, Stephen R Plymate, Maha Hussain, Ian Murchie Thompson
Journal: Journal of Clinical Oncology (2014)

5006 Background: Cixutumumab (CIX), formerly IMC-A12, is a fully recombinant human monoclonal IgG1antibody that specifically targets insulin-like growth factor 1 receptor (IGF-IR). Pre-clinical studies have shown interaction between IGF-IR and the androgen receptor, with greatest anti-tumor activity in castration-sensitive xenografts. Methods: Patients with new metastatic prostate cancer were randomized within 30 days of initiation of LHRH agonist plus bicalutamide (AD) to CIX with AD versus AD alone. With 180 eligible patients randomized and one-sided alpha=0.10 there would be 90% power to detect an absolute difference of 20% in the primary endpoint, undetectable PSA (≤0.2 ng/mL) rate at 28 weeks (relative risk (RR)=1.44) using an intent-to-treat analysis; this endpoint was previously shown to be strongly correlated with survival. Secondary endpoints included the proportion of patients with 0.3 ≤ PSA ≤4.0 ng/mL, safety and tolerability, circulating tumor cell levels (CTCs) and multiple plasma IGF biomarkers. Fisher’s exact test was used for the primary endpoint, and extended MH chi-square was used for 3 PSA response categories. Results: The trial accrued 210 eligible patients (105 randomized to each arm). Patient characteristics were similar in both arms. The undetectable PSA rate was 42/105 (40.0%) for CIX with AD and 34/105 (32.3%) for AD alone (RR=1.24, one-sided p=0.16). When separating out the PSA ≤4.0 ng/mL rate (see Table), there was no significant difference in PSA response rates between arms (p=0.17). CTCs were obtained at baseline prior to AD for 39 patients. Lower CTC (<5 vs. ≥ 5/7.5 mL whole blood) levels were associated with higher rate of PSA response (3 categories) (p=0.03). IGF-associated biomarkers will be reported at the meeting. Conclusions: CIX with AD did not significantly increase the proportion of men with an undetectable PSA in men with new metastatic hormone-sensitive prostate cancer. CTCs at baseline may carry prognostic value for this population. Clinical trial information: NCT01120236. PSA response Total PSA<=0.2 0.2<PSA<=4.0 PSA>4.0 n % n % n % n % Treatment CIX + AD 42 40.0% 17 16.1% 46 43.8% 105 100.0% AD 34 32.3% 15 14.2% 56 53.3% 105 100.0%
EDITORIAL
Journal: British Journal of Sports Medicine (1984)

This Olympic year of 1984 has started well, even for Britain who does not always do very well in the Winter Olympics, though we must not forget skating medals won by Cousins and Currie in previous Olympics, nor a good performance by our bob-sleigh teams in past years.The well deserved Gold Medal won by Torville and Deane on St. Valentine's Day displayed not only a superb artistic performance but also all the physical attributes needed for any top class sport - health, physique, strength, power, cardio-respiratory and muscle endurance, flexibility, and above all the acme of neuro- muscular co-ordination between two people, making the fullest use of proprioceptive feedback from their skates, the ice, the environment and especially the movements of the partner.Can we hope to see a similar degree of excellence in the Summer Olympics in California later this year?Without time and facilities for training, this could be a forlorn hope.The City of Nottingham sponsored Torville and Deane for the past four years and by the kudos gained by this pair the City regards their grant as a sound investment.
Genetic Testing of Families With Hereditary Diseases
Authors: Theodore F. Thurmon
Journal: JAMA (1996)

<h3>To the Editor.</h3> —Studies dating from 20 years ago<sup>1</sup>bear on utilization of clinical genetics services that were alluded to in the article about testing for hereditary breast cancer by Dr Lerman and colleagues.<sup>2</sup>The medical problem evaluated in our study<sup>1</sup>was mental retardation risk in future progeny. After informed consent was obtained from responsible family members, we applied all available diagnostic modalities to 1000 institutionalized probands to estimate the risk of mental retardation in future progeny of their parents and siblings. After the evaluations, families were notified by registered mail of the results in general terms (heritable or nonheritable, high or low risk to progeny), and free genetic counseling was offered. A randomized sample of 100 probands was selected for study of utilization of clinical genetics services. Families could not be located in 17 cases. A genetic counselor interviewed the remainder by telephone or during a home visit. Of
A BILL to Establish a Department of Public Health and to Define its Duties.
Journal: JAMA (1897)

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
ESGE News and Upcoming Events July 2019
Journal: Endoscopy (2019)

It is an honour to serve as the ESGE President for 2019 – 2021! Together with the governing board, I hope to continue the success of ESGE as the leader in Europe in the field of endoscopy. Following the landmarks of my predecessors, our aim will be to continue to strengthen the society in synergy with our individual members, national societies and other societies in Europe and worldwide.
THE TECHNICAL EXPOSITION
Journal: JAMA (1931)

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
Abstract 2988: International cancer genome consortium (ICGC)
Authors: Jennifer L. Jennings, Thomas J. Hudson
Journal: Cancer Research (2015)

Abstract The International Cancer Genome Consortium (ICGC) was established to bring together researchers from around the globe to comprehensively analyze the genomic, transcriptomic, and epigenomic changes in 50 different tumour types or subtypes that are of clinical and societal importance across the globe (International network of cancer genome projects. Nature 464, 993-998 (15 April 2010)). As of December 2014, the ICGC has received commitments from researchers and funding organizations in Asia, Australia, Europe, North America and South America for 77 project teams in 17 jurisdictions to study more than 25,000 tumour genomes. More than 27,000 tumours that meet ICGC requirements for consent have been obtained and research pathologists have approved over 27,000 samples as meeting ICGC standards. Processed data is available via the Data Coordination Centre (http://dcc.icgc.org) based at the Ontario Institute for Cancer Research and is updated quarterly. The data release (Version 17) in October 2014 included datasets from 42 ICGC members. The ICGC Data Portal has been improved to provide enhanced support to the research community browsing this vast dataset. The ICGC and The Cancer Genome Atlas (TCGA) PanCancer Analysis of Whole Genomes (PCAWG) project is committing more than 2,500 tumour-normal whole genome pairs from 23 different tumour types to uniform alignment and variant calling. More than 600 researchers will contribute to the interpretation of the data and writing of papers that will focus on specific analyses covering: Identification of driver mutations outside coding regions, including those that affect cis-regulatory regions and non-coding RNAs; and identification of gene regulatory pathways altered by non-coding mutations. Because the projected size of the pan-cancer dataset for 5,000 WGS is very large, PCAWG is using a distributed compute cloud environment (at different computing centres in the USA, Europe and Asia) that meet technical requirements of the project and the bioethical framework of ICGC and its member projects. More information can be found on www.icgc.org. Citation Format: Jennifer L. Jennings, Thomas J. Hudson. International cancer genome consortium (ICGC). [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2988. doi:10.1158/1538-7445.AM2015-2988
JAMA reference directories
Journal: JAMA (1977)

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Discussion
Journal: British Journal of Sports Medicine (1976)

methylsilylation, 25 JAI of N,N-dimethylhydrazine are added and heating is continued for 30 min.This reaction mixture may be used directly for GC or MS studies.For biological samples, especially when the advantageous detection by the N-FID is intended, a partition step is necessary to remove the nitrogen containing silylating reagents.Iso-octane (3 ml) and water (1 ml) are added and the sample is shaken and centrifuged.The organic phase is dried in vacuo and the residue dissolved in n-hexane for GC with the N-F ID.For GC-MS-analysis, the residue is taken up in a mixture of MSTFA, v:v:v) to protect the O-TMS-functions for longer periods of time.The fragmenta- tion pattern under electron impact of the 0-TMS-dimethylhydrazones of the anabolic steroids is the most favourable of all derivatives we have hitherto investigated (Donike & Strat- mann, 1976).
VIEWS IN THE STUDY OF CANCER
Journal: JAMA (1925)

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
<i>Erratum:</i> Vol. 70, No. 3
Journal: MMWR Morbidity and Mortality Weekly Report (2021)

In the report "The Advisory Committee on Immunization Practices' Interim Recommendation for Use of Pfizer-BioNTech COVID-19 Vaccine -United States, December 2020," on page 1922, in the third paragraph, the third and fourth sentences should have read Consistent high efficacy (≥92%) was observed across age, sex, race, and ethnicity categories and among persons with underlying medical conditions.Efficacy was similarly high in a secondary analysis including participants both with or without evidence of previous SARS-CoV-2 infection.Although numbers of observed hospitalizations and deaths were low, the available data were consistent with reduced risk for these severe outcomes among vaccinated persons compared with that among placebo recipients.
Chronic alcohol intoxication induces hepatic injury through enhanced macrophage inflammatory protein-2 production and intercellular adhesion molecule-1 expression in the liver
Authors: A Bautista
Journal: Hepatology (1997)

This study tested the hypothesis that prolonged consumption of alcohol directly or indirectly, through endotoxin influx in the circulation, stimulates the Kupffer cells to produce macrophage inflammatory protein-2 (MIP2) and up-regulates the expression of adhesion molecules, i.e., CD18 on PMNs and its counter-receptor, intercellular adhesion molecule-1 (ICAM-1), on hepatic cells. As a result, enhanced sequestration and cell-cell interaction among these cell types may occur in the liver, which in turn could result in altered hepatic function and hepatotoxicity. This hypothesis was tested in alcohol-fed, specific pathogen-free, male Sprague-Dawley rats. After 16 weeks of feeding, endotoxin (0.2 ± 0.043 EU/mL) and MIP2 (625 ± 100 pg/mL) were detected in the sera of alcoholic rats but not in the pair-fed rats. Concomitantly, serum aspartate transaminase (AST) activity was significantly increased. Small lipid deposition and inflammatory-like changes in the liver were also observed. Isolated Kupffer cells from alcohol-fed rats released large amount of MIP2 (> 600 pg/106 Kupffer cells/24 hr) in vitro compared with Kupffer cells from pair-fed rats (< 150 pg/106 Kupffer cells/24 hr). At the same time, the expression of CD18 and ICAM-1 on polymorphonuclear neutrophils (PMNs) and hepatic cells was increased more than twofold. Monoclonal antibody 1F12, an anti-CD18 antibody, attenuated hepatic injury in vivo, and in PMN-hepatocyte coculture in vitro in the alcohol-fed group. Another factor that could contribute to hepatic injury was MIP2, which was cytotoxic to alcoholic hepatocytes in vitro. This was reversed by cycloheximide, thus suggesting the indirect hepatotoxic effect of MIP2. In addition, isolated PMNs and Kupffer cells from alcohol-fed rats released large amounts of superoxide, which may also play a role in hepatic injury. These results demonstrate that MIP2 and adhesion molecules may contribute, at least in part, in the initiation of hepatic injury during alcohol intoxication.
The role of cerebral amyloid accumulation in common forms of Alzheimer disease
Authors: S. Gandy
Journal: Journal of Clinical Investigation (2005)

For approximately 80 years following Alzheimer's description of the disease that bears his name, a gulf divided researchers who believed that extracellular deposits of the amyloid β (Aβ) peptide were pathogenic from those who believed that the deposits were secondary detritus. Since 1990, the discoveries of missense mutations in the Aβ peptide precursor (APP) and the APP-cleaving enzyme presenilin 1 (PS1) have enabled much progress in understanding the molecular, cellular, and tissue pathology of the aggregates that accumulate in the interstices of the brains of patients with autosomal dominant familial Alzheimer disease (AD). Clarification of the molecular basis of common forms of AD has been more elusive. The central questions in common AD focus on whether cerebral and cerebrovascular Aβ accumulation is (a) a final neurotoxic pathway, common to all forms of AD; (b) a toxic by-product of an independent primary metabolic lesion that, by itself, is also neurotoxic; or (c) an inert by-product of an independent primary neurotoxic reaction. Antiamyloid medications are entering clinical trials so that researchers can evaluate whether abolition of cerebral amyloidosis can mitigate, treat, or prevent the dementia associated with common forms of AD. Successful development of antiamyloid medications is critical for elucidating the role of Aβ in common AD.
PTU-153 The Timing Of Oncogenic Events In The Evolution Of The Oesophageal Adenocarcinoma Genome And Implications For Clinical Diagnostics
Authors: J Weaver, C Ross-Innes, N Shannon, A Lynch, M Murtaza, T Forshew, M Dunning, T Underwood, R Hardwick, M Eldridge, P Edwards, N Rosenfeld, S Tavare, R Fitzgerald
Journal: Gut (2014)

<h3>Introduction</h3> A series of clonal expansions are thought to underlie the progression of Barrett’s oesophagus (BE) to oesophageal adenocarcinoma (OAC). Each expansion carries with it somatic driver mutation (s) fixing it within a larger population and therefore increasing the likelihood of acquiring a second mutation. However, the precise order in which somatic variants occur remains unknown. <h3>Methods</h3> We performed whole genome sequencing in 25 cases of OAC and 3 matched cases of BE. Findings were validated in a larger cohort of OACs (n = 90), metaplastic never-dysplastic BE (NDBE, n = 66 with a median follow-up of 58 months) and high-grade dysplasia (n = 43) using amplicon resequencing. Mutational signatures and gene-centric somatic mutations were determined using an in-house pipeline incorporating standard statistical methods and the publically available EMu pipeline. <h3>Results</h3> There were 7 distinct mutational signatures present in both early (BE) and late disease (OAC). Fifteen genes were determined to be potential novel drivers of OAC development. Surprisingly in 53% of NDBE tissue samples we identified clonal expansion of cells (&gt;10% mutant fraction) harbouring mutations in one or more of 13/15 of these putative driver genes. No difference in the frequency of mutation of these genes was observed between any of the disease stages studied. <i>TP53</i> mutations clearly delineate between HGD/OAC and benign NDBE (p &lt; 0.001). Whilst <i>SMAD4 </i>mutations are only observed in OAC (p &lt; 0.001) demonstrating for the first time a clear genetic difference between the two. <h3>Conclusion</h3> Mutagenic processes active in OAC are also active in the earliest stages of BE. Recurrent driver mutations identified in cancer may be acquired very early in the disease and may provide little or no progression advantage. Molecular diagnostic approaches must account for this. <h3>Disclosure of Interest</h3> None Declared.
Emission Control Devices, Fuel Additive, and Fuel Composition Changes
Authors: Warren T. Piver
Journal: Environmental Health Perspectives (1977)

Emission control devices are installed to meet the exhaust standards of the Clean Air Act for carbon monoxide and hydrocarbons, and it is necessary to know, from a public health point of view, how exhaust emissions may be affected by changes in fuel additives and fuel composition. Since these topics are concerned with developing technologies, the available literature on exhaust emission characteristics and the limited information on health effects, is reviewed.