tbuckley/cabot-search huggingface dataset:
No Mortality Benefit Found From Intensive Glucose Control
Journal: JAMA (2014)

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
Male Circumcision for the Prevention of HSV-2 and HPV Infections and Syphilis
Authors: Anthony Gill, Nicholas Pachter, Adele Clarkson, Katherine Tucker, Ingrid Winship, Diana Benn, Bruce Robinson, J Roderick
Journal: New England Journal of Medicine (2011)

correctionsfor SDHB indicates the need for genetic testing for SDHB, SDHC, and SDHD in patients who present with pheochromocytoma-paraganglioma. 3,4 As of this writing, a single SDHB-negative renalcell carcinoma in a patient with PGL4 has been reported. 3 We performed immunohistochemical analysis to detect SDHB in renal-cell carcinoma specimens obtained from three kindreds who were subsequently shown to harbor a germline SDHB mutation (Fig. 1). 3,4SDHB was completely negative in all three specimens of SDHB mutation-related renal-cell carcinoma, but it was positive in nonneoplastic cells obtained from these patients and in 70 unselected renal tumors used as controls.The unselected renal tumors included 45 conventional clear-cell renal carcinomas (including 3 associated with the von Hippel-Lindau syndrome), 10 papillary renal carcinomas, 9 chromophobe carcinomas, 5 oncocytomas, and 1 hereditary leiomyomatosis renal-cell carcinoma-related tumor.Details of the kindreds, tumor morphologic characteristics, and results of further immunohistochemical analyses are available in the Supplementary Appendix, available with the full text of this letter at NEJM.org.Given the parallels with pheochromocytomaparaganglioma, it is possible that negative staining for SDHB may accompany SDHD-mutated renal-cell carcinoma.Negative SDHB staining also occurs in a distinct subgroup of gastrointestinal stromal tumors (pediatric wild-type gastrointestinal stromal tumors, the gastrointestinal stromal tumors of the Carney triad, and the subgroup of adult gastrointestinal stromal tumors that these tumors resemble clinically and pathologically). 5Not all of these gastrointestinal stromal tumors will be associated with identifiable mitochondrial complex II mutations.Therefore, it is likely that there are other as-yet-undescribed mechanisms of mitochondrial complex II instability and tumorigenesis that are also associated with negative staining for SDHB.Immunohistochemical analysis to detect SDHB can be used to screen patients with renal tumors for underlying SDHB germline mutations (and possibly other mitochondrial complex II-related syndromes) at a fraction of the time and cost of formal genetic testing.
Specifically PNPLA3-Mediated Accumulation of Liver Fat in Obese Patients with Type 2 Diabetes
Authors: Jean Michel Petit, Boris Guiu, David Masson, Laurence Duvillard, Valerie Jooste, Perrine Buffier, Beatrice Terriat, Benjamin Bouillet, Marie-Claude Brindisi, Romaric Loffroy, Isabelle Robin, Patrick Hillon, Jean-Pierre Cercueil, Bruno Verges
Journal: Endocrine Reviews (2010)

Recently, it has been shown in the general population that an allele in the adiponutrin (PNPLA3) gene was strongly associated with increased liver fat content (LFC), independently of visceral adiposity and insulin resistance. In this study, we set out to determine whether LFC, evaluated using 1H-MR spectroscopy, was associated with PNPLA3 rs738409 polymorphism in people with type 2 diabetes. We also evaluated the influence of this polymorphism on the relationship between LFC and either visceral adiposity or carotid intima media thickness (CIMT). A total of 218 type 2 diabetic patients were included in this study. LFC, area of visceral fat, and CIMT were measured. A total of 139 (63.7%) patients had steatosis. The rs738409 minor G allele was associated with LFC. The number of patients with steatosis was significantly higher among minor G allele carriers in comparison to C allele homozygote carriers (70.3 vs. 57.2%; P = 0.04). In the subgroup of C allele homozygote carriers, LFC correlated with body mass index (r = 0.27; P = 0.003) and visceral fat area (r = 0.30; P = 0.002), but not with CIMT. In the subgroup of minor G allele carriers, LFC correlated inversely with CIMT (r = −0.23; P = 0.03), but not with body mass index or with visceral fat area. In multivariate logistic regression, the relationship between the highest quartile of CIMT and steatosis was different according to adiponutrin polymorphism. This study confirms that in people with type 2 diabetes, LFC is related to rs738409 polymorphism. The lack of a relationship with visceral obesity and the inverse correlation with CIMT suggest that fatty liver associated with the minor G allele of the PNPLA3 rs738409 polymorphism may not be linked to metabolic disorders.
Infant Feeding in its Relation to Health and Disease. A Modern Book on All Methods of Feeding. For Students, Practitioners and Nurses.
Journal: JAMA (1904)

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
Electroencephalographic Findings in Chronic Acetophenetidine Abusers
Journal: JAMA (1963)

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
Methadone-induced pulmonary edema
Authors: J. M. Kjeldgaard
Journal: JAMA (1971)

A 19-year-old former heroin addict developed pulmonary edema within six hours after the oral ingestion of 80 mg of methadone hydrochloride and recovered rapidly and without sequalae, with vigorous ventilatory support. This complication has been observed following intravenous overdosage with morphine and heroin, but has not previously been recorded after methadone ingestion.
Bronchial Asthma
Authors: J. J. Robbins
Journal: JAMA (1963)

<h3>To the Editor:—</h3> In reply to Dr. Rebhun's letter about bronchial asthma (<i>JAMA</i><b>184</b>:601 [May 18] 1963) may I say that simplicity is no stranger to truth. Pharmacology has an old law which states that the number of remedies employed in the treatment of any disease is inversely proportional to their effectiveness. I have readily available for anyone interested the names and full addresses of the last more-than-300 patients whom I have treated for bronchial asthma, chronic bronchitis, and pulmonary emphysema. For every one who so much as intimates that he feels unlucky in having been treated by me I will contribute the sum of $100 to any charity Dr. Rebhun wishes to designate.
Left ventricular hypertrophy and hypertension
Authors: R. C. Tarazi
Journal: JAMA (1983)

Elsewhere in this issue (p 1285), Sparrow et al report that ECG signs suggestive of left ventricular hypertrophy (LVH) might serve as predictors of subsequent hypertension. These epidemiologic observations raise new questions regarding cardiac involvement in hypertension; the latter has recently been a rapidly evolving field. The relationship between hypertension and LVH was usually thought of as a direct response of the heart to a pressure overload. Apparently supporting that viewpoint was the high incidence of LVH in hypertensive patients both at autopsy and in epidemiologic studies,<sup>1</sup>as well as the close correlation found in some models of experimental hypertension between BP level and ventricular weight. More recently, however, evidence has been accumulating, again from both experimental and clinical studies, to the effect that the cardiac response to hypertension was more complex than originally surmised,<sup>2</sup>that it developed early in the evolution of the disease,<sup>3</sup>and that
Leukocyte engagement of fibrin(ogen) via the integrin receptor αMβ2/Mac-1 is critical for host inflammatory response in vivo
Authors: Matthew J. Flick, XinLi Du, David P. Witte, Markéta Jiroušková, Dmitry A. Soloviev, Steven J. Busuttil, Edward F. Plow, Jay L. Degen
Journal: Journal of Clinical Investigation (2004)

The leukocyte integrin αMβ2/Mac-1 appears to support the inflammatory response through multiple ligands, but local engagement of fibrin(ogen) may be particularly important for leukocyte function. To define the biological significance of fibrin(ogen)-αMβ2 interaction in vivo, gene-targeted mice were generated in which the αMβ2-binding motif within the fibrinogen γ chain (N390RLSIGE396) was converted to a series of alanine residues. Mice carrying the Fibγ390–396A allele maintained normal levels of fibrinogen, retained normal clotting function, supported platelet aggregation, and never developed spontaneous hemorrhagic events. However, the mutant fibrinogen failed to support αMβ2-mediated adhesion of primary neutrophils, macrophages, and αMβ2-expressing cell lines. The elimination of the αMβ2-binding motif on fibrin(ogen) severely compromised the inflammatory response in vivo as evidenced by a dramatic impediment in leukocyte clearance of Staphylococcus aureus inoculated into the peritoneal cavity. This defect in bacterial clearance was due not to diminished leukocyte trafficking but rather to a failure to fully implement antimicrobial functions. These studies definitively demonstrate that fibrin(ogen) is a physiologically relevant ligand for αMβ2, integrin engagement of fibrin(ogen) is critical to leukocyte function and innate immunity in vivo, and the biological importance of fibrinogen in regulating the inflammatory response can be appreciated outside of any alteration in clotting function.
A PECULIAR TYPHOID SEQUEL.
Journal: JAMA (1906)

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
Canine Hemophilia
Journal: JAMA (1963)

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
Committee on Foods
Journal: JAMA (1934)

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
Copyright law undergoes major face-lift
Authors: D. S. Dobkin
Journal: JAMA (1979)

ON JAN 1,1978, the first major statutory revision of US copyright law in almost 70 years became effective. The new law, embodying the efforts of many years of compromise between the interests of publishers and authors, contains wide-sweeping changes. While the enactment of the new law has thrust copyright into greater public focus of late, copyright law in this country is not a recent phenomenon. The earliest origins of copyright in the United States stem from a 1710 English statute known as the Statute of Anne. Following the American Revolution, most of the states enacted copyright laws generally patterned after the English act. The need for federal legislation, however, was soon recognized, and when the US Constitution was drafted, copyright was included. Article I, Section 8 of the Constitution granted Congress the power "to promote the progress of science and useful acts by securing for limited times to authors and
Sports Medicine: Fitness, Training, Injuries
Authors: Bruno Balke
Journal: JAMA (1984)

The editors of this book (second edition) have set out to offer a "text" on sports medicine that would be useful for teaching a structured course on the broad areas of fitness, training, and sports injuries. They have succeeded in presenting essential parts of medical specialties related to sports and physical activities. The potential student of sports medicine is expertly introduced to many problems he will be facing in a practice dedicated to the examination, treatment, and consultation of persons who engage in competitive, preventive, rehabilitative, or recreational activities. The potential value of this book as a basic text for the teaching and understanding of sports medicine problems is somewhat dwarfed by the multiple authorship of the 22 chapters. A greater effort could have been made to coordinate the contributions more effectively. As it is, there is a great deal of overlapping that might be acceptable in an actual lecture
Drug Identification
Authors: William O. Robertson
Journal: JAMA (1972)

<h3>To the Editor.—</h3> Two weeks ago a young boy appeared at our hospital from a distant community, because of an uncertainty as to his problem, a drug ingestion, a head injury, or something else. He had been found surrounded by capsules from a bottle labelled "estrogens" but was becoming progressively obtunded. The underlying problem was that no one had verified, by use of the available coded imprint, what the medication actually was. A 40-second search of the<i>Physicians Desk Reference</i>showed it to have been a barbiturate, and all concern about encephalitis and battered babies evaporated. Simple barbiturate poisoning management was effective. At least 29 manufacturers now utilize coded imprints on some or all their solid medication forms; legislation has been introduced into Congress to make this mandatory for all solid medication forms. Studies at our Poison Control Center attest to the fact that rapid, accurate identification (that is, in
Abstract P192: Metabolomic Profiles Associated with Total and CVD Mortality in Women
Authors: Kathryn M Rexrode, Raji Balasubramanian, Nina Paynter, Franco Giulianini, JC Chen, JoAnn E Manson, Mara Vitolins, Christine M Albert, Clary Clish
Journal: Circulation (2017)

Background: Using novel metabolomic markers to identify individuals at increased risk for total and cardiovascular mortality may help inform therapeutic or prevention strategies. Methods: A total of 2306 women in the Women’s Health Initiative (WHI) Observational Study (WHI-OS) and Hormone Trials (WHI-HT) had 370 plasma metabolites measured at baseline by liquid chromatography tandem mass spectroscopy. The analysis cohort included 2298 women (943 WHI-OS; 1355 WHI-HT) with complete covariate data. Multivariate cox proportional hazards models were constructed to examine the association of metabolites with mortality, adjusting for age, body mass index, systolic blood pressure, hypertension treatment, diabetes, smoking, total and HDL cholesterol. The WHI-OS data were used for discovery analyses; metabolites with a multivariate-adjusted false discovery rate (FDR) adjusted p value &lt;0.05 were considered significant. These candidate metabolites were included for backwards selection (p for exclusion &gt; 0.05) to identify independent metabolites for inclusion in a composite score. The score of these significant mutually-adjusted metabolites was created based on the quartile score for each metabolite, with higher values indicating higher likelihood of all cause mortality and was tested in the WHI-HT cohort. Results: During a median follow-up of 16.7 years, 1,102 women died (417 WHI-OS; 685 WHI-HT), with 601 cardiovascular deaths. At baseline, the median age was 68 years (interquartile range 62-72) and median time to death was 9.9 years. In the WHI-OS discovery cohort, 56 metabolites were significantly associated with multivariate-adjusted total mortality (FDR p&lt; 0.05). When all 56 metabolites were mutually adjusted in the same model and subjected to backwards selection, 15 metabolites remained significantly associated with total mortality after multivariate adjustment and were used to create a composite score. In the separate WHI-HT validation cohort, women in the highest score quartile had a hazards ratio (HR) of 2.36 (95% CI: 1.88-3.21) for death. The mortality score was also associated with CVD death (HR 3.27 [2.54-4.22] highest vs. lowest quartile) for the combined WHI-OS and WHI-HT sample. Six metabolites were significantly associated with mortality in both samples with multivariate mutual adjustment; docosatrienoic acid an omega-3 fatty acid, histamine a pro-inflammatory compound , and the alpha-amino acids histidine and tryptophan were protective while 3-ureidopropionic acid an intermediate in the metabolism of uracil, and 18:1 cholesterol ester were associated with increased risk. Conclusions: Using a robust discovery and validation design, metabolite profiles were associated with significantly increased total and CVD mortality, even after adjustment for traditional risk factors.