tbuckley/cabot-search huggingface dataset:
Eye Hazards in Industry: Extent, Cause, and Means of Prevention
Journal: JAMA (1942)

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Efficacy Data and HPV Vaccination Studies
Authors: Norman W. Baylor
Journal: JAMA (2009)

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BBS volume 6 issue 3 Cover and Front matter
Authors: Daniel Dennett, J Beatty, J Bennett, A Danto, R Dawkins, N Eldredge, ; Mt, G Graham, ; Dr, J Heil, R Lewontin, D Lloyd, Maynard Smith, Millikan Rg, Rachlin Ca, Ristau Hl, A Rosenberg, B Skinner, H Terrace, Edward Stabler, R Berwick, ; Rp, M Davis, W Demopoulos, R Matthews, M Gross, G Harman, R Harnish, ; Mr, J Marshall, J Morton, T Roeper, J Samet, H Thompson, R Wilensky, John Campion, Richard Latto, Y Smith, P Bach-Y-Rita, J Barbur, Ruddock Kh, B Bridgeman, A Cowey, J Economos, ; Rn, C Legg, T Pasik, M Jeannerod, E Poppel, R Puccetti, ; Richards
Journal: Behavioral and Brain Sciences (1983)

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Ethical issues in informed consent. Research on medical cost containment
Authors: D. M. Mahler
Journal: JAMA (1982)

The decision to contain medical costs, which is a political and social decision, entails restriction of medical services. To guide public policy, research on the impact of such restriction must be carried out, but this type of research differs significantly from most other medical research. Difficult issues concerning informed consent arise, with potential conflicts among principles of maximization of good and minimization of harm to the patient, the patient's right to self-determination, and the utilitarian goal of maximization of collective welfare. We have discussed these principles in the context of relationships between patient and physician and between subject and investigator. Approaches considered include emphasis on retrospective studies, use of statistical techniques to formulate clinical decision-making rules on the basis of available data, three-celled randomization designs, and the role of the primary-care physician in maximizing patient autonomy and minimizing the potentially threatening aspects of informed consent for such studies. (<i>JAMA</i>1982;247:481-485)
Dietary salt intake and blood pressure
Authors: Norman M. Kaplan
Journal: JAMA (1984)

<h3>To the Editor.—</h3> The two articles and accompanying editorials in the July 15, 1983, issue ofThe Journalpoint out the great contrasts in the strength of the current evidence on the question about dietary sodium in the pathogenesis of hypertension. The article by Holden et al purports to show no association, concluding that "it does not appear justifiable or appropriate to undertake large-scale salt restriction in the general population to prevent hypertension." The basis for this statement is their failure to find any difference in blood pressures between persons who said they ate different amounts of salty foods. Despite their sophisticated analyses and statistical methods, their data are likely worthless since such crude estimates are so inaccurate.<sup>1</sup> Dr Scribner's<sup>2</sup>editorial on this article presents a much more sensible view, although I believe his diagram of the "saturation effect" can be better drawn (Figure). Most studies show little
Table of Contents
Authors: Peter Harris, Radhika Narla, Susan Ott, Takehiro Suzuki, Takaaki Abe, Sagar Nigwekar, Rosalynn Nazarian, Peter Blake, Federica Barutta, Graziella Bruno, Raffaella Mastrocola, Stefania Bellini, Gabriella Gruden, Edward Grimley, Gregory Dressler
Journal: Kidney International (2018)
New England Journal of Medicine, Boston
Journal: JAMA (1967)

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THE WRONG AND RIGHT WAY OF PROSECUTING ILLEGAL PRACTITIONERS.
Journal: JAMA (1901)

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
THE PRECIPITIN TEST FOR HUMAN BLOOD.
Journal: JAMA (1905)

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
MEDICAL POLITICAL CLUBS.
Journal: JAMA (1899)

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The Cover
Authors: M. Therese Southgate
Journal: JAMA (1990)

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PROTOZOA AND MAN
Journal: JAMA (1926)

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
Pictorial Atlas of Skin Diseases and Syphilitic Affections.
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 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
Gulstonian Lectures: On Diabetes and Saccharine Conditions of the Urine
Authors: A. B. Garrod
Journal: BMJ (1857)

PRESIDENT AND GENTLEM3EN,-Towards the close of my last lecture, I endeavoured to bring under your notice the principal theories which liave been advanced in explanation of the real nature of sacchlarine diabetes, and gave the various arguments which have been employed in support of and in opposition to each.I likewise endeavoured to present a short sketch of the important researches of M. Bernard upon the subject of glycogenesis: I showed you that sugar was constantly generated in the animal economy, and that the liver was the organ destined to perform this function; that this sugar-form-
IMMU-54. THE ONCOMETABOLITE R-2-HYDROXYGLUTARATE SUPPRESSES THE INNATE IMMUNE MICROENVIRONMENT OF IDH1-MUTATED GLIOMAS VIA ARYL HYDROCARBON RECEPTOR SIGNALING
Authors: Mirco Friedrich, Lukas Bunse, Theresa Bunse, Edward Green, Tobias Kessler, Stefan Pusch, Rafael Carretero, Andreas von Deimling, Francisco J Quintana, Wolfgang Wick, Michael Platten
Journal: Neuro-Oncology (2018)

IDH1-mutated gliomas are associated with less abundant and phenotypically skewed innate and adaptive immune cell infiltrates compared to IDH1 wild-type tumors. Despite this, the most frequent mutation, IDHR132H, represents a clonal shared neoantigen and mutations in IDH are associated with a more favorable prognosis. While the tumor cell-intrinsic consequences of the oncometabolite R-2-hydroxyglutarate (R-2-HG) accumulating in IDH1-mutated gliomas as a result of a neomorphic enzymatic function, are well-characterized, potential direct paracrine effects of R-2-HG influencing the glioma immune microenvironment remain incompletely understood. METHODS AND By means of comprehensive analyses of expression datasets from human gliomas and syngeneic murine tumor models as well as transporter studies we demonstrate that R-2-HG is imported by both microglia and macrophages via SLC family transporters and suppresses their function in a paracrine manner. Functional analyses of microglia and macrophages indicate an R-2-HG-driven induction of tolerogenicity as evidenced by accumulation of IL10 and TGFβ and suppression of MHC-II expression, which results in impaired activation of antigen-specific T cells and activation of immune checkpoint molecules. Multi-level signature profiling of human tumor-infiltrating as well as primary immune cells was complemented by reporter gene assays and pathway analyses and revealed that R-2-HG activates the cytosolic transcription factor aryl hydrocarbon receptor (AHR), a key immunomodulatory target of immunosuppressive tryptophan metabolism. Functional relevance of R-2-HG-mediated, AHR-driven impairment of myeloid cell immunity was demonstrated in vivo by pharmacological AHR inhibition, increasing the efficacy of checkpoint blockade. R-2-HG impairs antitumor immunity in IDH1-mutated gliomas by activating the AHR in innate immune cells, thus suppressing the innate immune microenvironment by compromising antigen presentation and activation of antigen-specific T cells. This, together with recent findings on inhibitory effects on T cell immunity, represents a novel mechanism of immune evasion of an immunogenic driver mutation and opens a novel therapeutic approach to IDH1-mutated gliomas.
8. Clindamycin and Lincomycin: Oral and Parenteral Therapy
Journal: JAMA (1977)

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
A new high-potency glycine-precipitated antihemophilic factor (AHF) concentrate. Treatment of classical hemophilia and hemophilia with inhibitors
Authors: K. M. Brinkhous
Journal: JAMA (1968)

A new, high-potency, glycine-precipitated antihemophilic factor (AHF, factor VIII) concentrate, from 100 to 400 times purified, can be administered to patients in solutions 100 times more concentrated than plasma. The product appears to be stable and causes no immediate untoward side reactions. The plasma AHF levels of patients with classical hemophilia can be normalized with small volumes of the glycine-precipitated material given by syringe. Surgery can be performed safely under cover of this fraction. Two patients with classical hemophilia complicated by a circulating inhibitor to AHF were treated with large amounts of the high-potency fraction; partial to complete neutralization of the inhibitor occurred with clinical improvement.
Abstract P183: Visit to Visit Variability in Diastolic Blood Pressure Predicts Incident Cardiovascular Disease Events in Middle-aged Adults
Authors: Shih-Jen Hwang, Martin G Larson, Chunyu Liu, Ramachandran S Vasan, Daniel Levy
Journal: Circulation (2016)

Introduction: visit-to-visit variability (VVV) in blood pressure (BP) relates to risk for cardiovascular disease (CVD) in clinical studies. It is unknown if VVV in systolic or in diastolic BP predicts incidents CVD in community-based middle-aged adults. Methods: The study sample comprised 1817 Framingham Heart Study (FHS) offspring cohort participants free of clinical CVD at the sixth examination (1995-1998) cycle who had attended examination cycles three, four and five at four year intervals. Exclusion criteria include medication treatment for elevated BP at any of the four examinations. We defined VVV in systolic and diastolic BP as the standard deviation of BP values across the four examinations. Incident CVD events were identified through physician panel review of medical records with follow-up through December 31, 2013. We used proportional hazards regression models to test associations of between VVV in systolic and diastolic BP and CVD risk adjusting for age, sex, body-mass-index, mean systolic and diastolic BP, total cholesterol, HDL cholesterol, medication treatment for hyperlipidemia, fasting blood sugar, diabetes, and cigarette smoking. Results: During follow up (average 16.2 years), 276 (15.2%) participants developed CVD. Mean and standard deviation values of VVV in systolic and diastolic BP were 8.09±4.48 and 5.38±2.5, respectively. Each standard deviation increase in diastolic BP VVV was associated with a hazards ratio (HR) of 1.08 (95% confidence interval [CI] 1.03-1.14) for incident CVD. The HR of systolic BP VVV was 1.03 (95% CI 1.00-1.06). Including both variables gave an HR of 1.01 (95% CI 0.98-1.04) for VVV in systolic BP and 1.08 (95% CI 1.03-1.13) for VVV in diastolic BP. There were significant linear trends in CVD risk according to quartiles of VVV in systolic and diastolic BP. Participants in the highest quartile of VVV in systolic BP had a HR of 1.68 (95% CI 1.13-2.50) for incident CVD; those with highest quartile of VVV in diastolic BP had a HR of 1.66 (95% CI 1.17--2.35). Conclusion: Visit-to-visit variability in BP predicts CVD risk in middle-aged adults.