tbuckley/cabot-search huggingface dataset:
Abstract 2599: Pleiotropic effects of PPARD accelerate colorectal tumorigenesis progression and invasion
Authors: Yi Liu, Yasunori Deguchi, Rui Tian, Daoyan Wei, Ling Wu, Weidong Chen, Weiguo Xu, Min Xu, Fuyao Liu, Shen Gao, Jonathan C. Jaoude, Sarah P. Chrieki, Micheline J. Moussalli, Mihai Gagea, Jeffrey S. Morris, Russell Broaddus, Xiangsheng Zuo, Imad Shureiqi
Journal: Cancer Research (2019)

Abstract APC mutations activate aberrant β-catenin signaling to drive colorectal cancer (CRC) initiation. CRC progression however requires additional molecular mechanisms. PPAR-delta (PPARD) is a downstream target of β-catenin and upregulated in CRC. PPARD germline genetic deletion has however been reported to promote intestinal tumorigenesis in Apcmin mice, which has questioned PPARD effects on β-catenin aberrant activation and CRC. Addressing this knowledge gap is important because PPARD is a druggable protein. Mice with targeted PPARD overexpression/deletion into intestinal epithelial cells (IECs) were bred with mice with intestinally targeted ApcΔ580 mutation via CDX2-cre (ApcΔ580) or CDX2-cre-ERT2 (ApcΔ580-TMX). APCΔ580 mice treated with PPARD agonist (GW501516) or antagonist (GSK3787), and human CRC organoid cells were also tested. PPARD expression was examined in human CRC invasive fronts and their paired colorectal adenomas and cancer centers. PPARD’s mechanisms to promote CRC were screened by Functional Proteomics Reverse Phase Protein Assay (RPPA) and subsequently validated in in-vitro and in-vivo studies. PPARD overexpression/deletion in IECs in mice augmented/suppressed β-catenin activation via upregulation/downregulation of BMP7/TAK1 signaling and strongly promoted/suppressed CRC .PPARD downregulation by siRNA in human CRC organoid cells inhibited BMP7/β-catenin signaling and suppressed organoid self-renewals. GW501516 enhanced while GSK3787 suppressed CRC tumorigenesis in ApcΔ580 mice. PPARD expression was significantly higher in human CRC invasive fronts versus their paired invasive tumor centers and adenomas. RPPA and validation studies identified PPARD upregulation of multiple other pro-invasive pathways: PDGFRβ, connexin 43, AKT1, EIF4G1 and CDK1, Our data demonstrate that PPARD strongly potentiates multiple pro-tumorigenic pathways to promote CRC progression and invasiveness. Citation Format: Yi Liu, Yasunori Deguchi, Rui Tian, Daoyan Wei, Ling Wu, Weidong Chen, Weiguo Xu, Min Xu, Fuyao Liu, Shen Gao, Jonathan C. Jaoude, Sarah P. Chrieki, Micheline J. Moussalli, Mihai Gagea, Jeffrey S. Morris, Russell Broaddus, Xiangsheng Zuo, Imad Shureiqi. Pleiotropic effects of PPARD accelerate colorectal tumorigenesis progression and invasion [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 2599.
Klinische Wochenschrift, Berlin
Journal: JAMA (1967)

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
Incorrect Journal Name.
Journal: JAMA (1991)

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
Missing Decimal
Journal: JAMA (1981)

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
Pseudohypophosphatasia
Authors: Charles R. Scriver, Dorothy Cameron
Journal: New England Journal of Medicine (1969)

WE report herewith a condition, presumably hereditary, that resembles classic hypophosphatasia.1 The new trait is characterized by an osteopathy of skull and long bones resembling that of typical hypophosphatasia, muscular hypotonia, hypercalcemia and phosphoethanolaminuria. One important feature distinguishes the new trait from the old, and that is the consistently normal total alkaline phosphatase activity in plasma; because of this, we have called it "pseudohypophosphatasia."2 Clinical FeaturesL.W., a 3-month-old girl, born on April 20, 1964, attracted attention because of her irritable temperament, widened skull sutures, bulging anterior fontanelle and hypotonia. Investigation showed her to be below the 3d percentile for . . .
The Chronic Fatigue Syndrome
Authors: Keiji Fukuda
Journal: Annals of Internal Medicine (1995)

Letters1 July 1995The Chronic Fatigue SyndromeKeiji Fukuda, MD, MPH, William C. Reeves, MD, and Stephen E. Strauss, MDKeiji Fukuda, MD, MPHCenters for Disease Control and Prevention; Atlanta, GA 30333National Institutes of Health; Bethesda, MD 20892Search for more papers by this author, William C. Reeves, MDCenters for Disease Control and Prevention; Atlanta, GA 30333National Institutes of Health; Bethesda, MD 20892Search for more papers by this author, and Stephen E. Strauss, MDCenters for Disease Control and Prevention; Atlanta, GA 30333National Institutes of Health; Bethesda, MD 20892Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-1-199507010-00019 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:The remarks from Dr. Rest, coauthor of the recent guidelines on chronic fatigue syndrome [1], bear careful reflection because they touch on important and complex issues that are easily misunderstood.The 1988 chronic fatigue syndrome working case definition [2] was revised to mitigate ambiguities and deficiencies that became apparent after field testing. The revised case definition remains a work in progress and not a “definitive” diagnostic tool. Thus, until an independent way to identify the syndrome is found, the validity of this or any similar case definition cannot be definitively established. Do these considerations negate the clinical value ...References1. Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A, and the International Chronic Fatigue Syndrome Study Group. The chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann Intern Med. 1994; 121:953-9. Google Scholar2. Holmes GP, Kaplan JE, Gantz NM, Komaroff AL, Schonberger LB, Straus SE, et al. Chronic fatigue syndrome: a working case definition. Ann Intern Med. 1988; 108:387-9. Google Scholar Author, Article, and Disclosure InformationAffiliations: Centers for Disease Control and Prevention; Atlanta, GA 30333National Institutes of Health; Bethesda, MD 20892 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byEicosapentaenoic acid-rich essential fatty acid supplementation in chronic fatigue syndrome associated with symptom remission and structural brain changesVoluntary motor function in patients with chronic fatigue syndromeLaborchemische, neurohormonelle und immunologische Befunde beim Fibromyalgie- und chronischen Müdigkeitssyndrom und ihre klinische RelevanzMitochondrial Dysfunction in Chronic Fatigue Syndrome 1 July 1995Volume 123, Issue 1Page: 74-76KeywordsBehaviorChronic fatigue syndromeDisabilitiesFatigueNauseaTouch ePublished: 15 August 2000 Issue Published: 1 July 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Aldicarb Poisoning
Authors: James M. Witt
Journal: JAMA (1986)

<h3>To the Editor.—</h3> The article entitled "Aldicarb Food Poisoning From Contaminated Melons—California"<sup>1</sup>reports that illnesses occurred that were compatible with carbamate poisoning, although laboratory tests disclosed no aldicarb. The implication was that laboratory analyses are too insensitive to detect aldicarb at levels that can cause human illness. Although no attempt was made to test this hypothesis, information is already available. Since the news media and policymakers may attribute illness to undetectable levels of aldicarb or any other environmental chemical, we felt that a quantitative evaluation of the likelihood of this occurring should be attempted. The relevant limits of sensitivity for the different laboratories involved in these analyses for aldicarb ranged from 0.01 to 0.20 parts per million (ppm). Assuming a worst-case scenario, ie, that the highest limit of detection was 0.20 ppm and that the individual had a large appetite for melon (1.35 kg) and a small body weight
The Dangers of "Safe" Solvents
Journal: JAMA (1969)

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
Publication of Death Investigation Practices
Journal: JAMA (1993)

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
Reply to Bingzhi Wang, Huan Deng, and Lan Cao's Letter to the Editor re: Hojjat Ahmadzadehfar, Markus Essler. Prostate-specific Membrane Antigen Imaging: A Game Changer in Prostate Cancer Diagnosis and Therapy Planning. Eur Urol. In press. https://doi.org/10.1016/j.eururo.2019.02.028
Authors: Hojjat Ahmadzadehfar, Markus Essler
Journal: European Urology (2019)
Adverse Outcomes Associated With Use of Proton Pump Inhibitors and Clopidogrel
Authors: Stephen Hayes
Journal: JAMA (2009)

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
Preventing the Last Epidemic: II
Authors: Howard H. Hiatt
Journal: JAMA (1981)

A RECENT report to the US Congress by the Federal Trade Commission indicates that as many as 80% of Americans now know that cigarette smoking causes lung cancer. Two out of three are aware of the connection between smoking and heart disease. How have they come to know this? Who told them? Since the release in 1965 of the Surgeon General's report on the health hazards of cigarettes, physicians have taken the lead in spreading the message. They have done this both in their role as personal physicians, talking to individual patients about the possible medical consequences of their actions, and in campaigns of public education that are sometimes complemented by government intervention. For example, in its recently expressed opposition to federal tobacco subsidies, the House of Delegates of the American Medical Association took another important step in its efforts to prevent contemporary epidemics of cigarette-associated diseases. In the last
Massachusetts Medical Society
Authors: Eliot Hubbard
Journal: New England Journal of Medicine (1956)

CHARITABLE AND EDUCATIONAL FUNDAt the October, 1955, meeting of the Council a charitable and educational fund was established with the following provisions:The principal of the Fund shall never be used for any purpose other than charitable and educational ones.The income from the Fund, when not added to the principal, shall be used exclusively for such purposes.The Fund is to be administered by a board of directors, five in number, all members of the Massachusetts Medical Society, appointed by the president, and approved by the Council, for terms of one, two, three, four and five years initially . . .
August 16, 2000
Journal: JAMA (2000)

Elliott M. Antman, MD; Marc Cohen, MD; Peter J. L. M. Bernink, MD; Carolyn H. McCabe, BS; Thomas Horacek, MD; Gary Papuchis, MD; Branco Mautner, MD; Ramon Corbalan, MD; David Radley, MS; Eugene Braunwald, MD
Medical injury compensation. A time for testing new approaches
Authors: W. Wadlington
Journal: JAMA (1991)

Despite an improved climate for professional liability insurance, medical injury compensation remains a subject of serious concern. The current tort system has been assailed as too slow, too costly, too complicated, and inconsistent in awards. Some critics assert that it induces overutilization through "defensive" medicine while limiting access by influencing physicians to forgo high-risk procedures or to shift to specialties with less liability exposure. Many medical practitioners also contend that it often stigmatizes physicians unfairly. Legislative reform in the 1970s and 1980s produced changes in the tort system in response to perceived crises arising from the increasing cost and diminishing availability of professional liability insurance. Because of limited understanding about the nature and dimensions of the problems at which they were directed, it was highly conjectural whether those remedies would effect anything close to a cure. Today's situation differs significantly. We now have a significant body of research, and such
Neurotoxicity and Behavioral Effects of Thiram in Rats
Authors: Cheng-Chun Lee, Paul J. Peters
Journal: Environmental Health Perspectives (1976)

Eight of 24 female rats fed 66.9 mg/kg-day of thiram developed neurotoxicity. The neurotoxic effects were characterized by ataxia and paralysis of the hind legs. There were demyelination, degeneration of the axis cylinders, and presence of macrophages in the nerve bundle of the sciatic nerve. Degeneration in the ventral horn of the lower lumbar region of the spinal cord was evidenced by chromatolysis of motorneurons, pyknosis, and satellitosis. During a second experiment, 4 of 24 females fed 65.8 mg/kg--day also developed ataxia and paralysis. An additional 9 females showed clasping of the hind feet when picked up by the tail. Nerve conduction could not be measured for one severely ataxic rat and the electromyogram indicated a loss of motor unit function. Histopathology of this rat, along with the others, suggests the peripheral nerve as the primary site of the lesion. Thiram also caused behavioral changes in apparently normal rats. The walking pattern of the hind legs was altered with decreases in stride width and the angle between contralateral steps. These rats required significantly more shock-motivations and cleared a lower height in a jump/climb ability test. An open-field study indicated that thiram caused hyperactivity in the nonataxic rats of both sexes. Three of 24 rats fed 95.8 mg/kg-day of ferbam also developed ataxia or paralysis.
Deciding against resuscitation: encouraging signs and potential dangers
Authors: R. M. Veatch
Journal: JAMA (1985)

One of the most important developments in medical ethics of the last decade has been the increasing recognition that there are times when it is unnecessary, even wrong, to resuscitate seriously ill patients. The American Medical Association's Judicial Council makes clear that this is its view when it says that "with informed consent a physician may do what is medically necessary to alleviate severe pain, or cease or omit treatment to let a terminally ill patient die, but he should not intentionally cause death."<sup>1(p9)</sup>The lay population seems to agree. Both secular philosophers and spokespersons for most of the major religious traditions now agree with the recent report of the President's Commission on Ethical Problems in Medicine that states that "a competent and informed patient or an incompetent patient's surrogate is entitled to decide with the attending physician that an order against resuscitation should be written in the chart."
Abstract 5135: Genome-wide CRISPR-based screening reveals ABCG2 as a novel drug resistance gene in pancreatic cancer
Authors: Ryne C. Ramaker, Andrew A. Hardigan, Emily R. Gordon, Richard M. Myers, Sara J. Cooper
Journal: Cancer Research (2019)

Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most deadly cancers and incidence is increasing due to the increase in risk factors such as diabetes and obesity. One reason for the high mortality rate associated with this cancer is the high rate of resistance to commonly used chemotherapies. Our previous work showed a link between patient survival and expression of drug resistance genes, thus we undertook genome-wide CRISPR knockout and activation screens to identify genes conferring resistance to cytotoxic chemotherapies in two pancreatic cancer cell lines. Our screen revealed hundreds of genes with potential roles in drug resistance, many of which have expression levels that correlate with patient survival. We have validated our top candidates by stably expressing individual guide RNAs in each of three pancreatic cell lines, Panc-1, BxPC-3 and MiaPaCa-2 and screening for viability following treatment with three chemotherapeutic agents, oxaliplatin, gemcitabine, and irinotecan. ABCG2, an ABC transporter, was revealed as our top hit, conferring resistance to multiple drugs in multiple cell lines. Our results would suggest that repression of ABCG2 might improve sensitivity to cytotoxic chemotherapies. We test this hypothesis using an ABCG2 inhibitor and demonstrate the effect of this inhibitor on cell viability, drug sensitivity and transcriptomic profiles in the context of cell lines with variable ABCG2 expression. Note: This abstract was not presented at the meeting. Citation Format: Ryne C. Ramaker, Andrew A. Hardigan, Emily R. Gordon, Richard M. Myers, Sara J. Cooper. Genome-wide CRISPR-based screening reveals ABCG2 as a novel drug resistance gene in pancreatic cancer [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 5135.