tbuckley/cabot-search huggingface dataset:
Change in body weight and longevity
Authors: I. M. Lee
Journal: JAMA (1992)

<h3>Objective.</h3> —To investigate the effect of body weight change on longevity. <h3>Design.</h3> —Cohort analytic study, following men from 1977 through 1988. <h3>Setting.</h3> —The study was conducted among Harvard University alumni with mean age of 58 years. <h3>Patients.</h3> —Alumni, free of cardiovascular disease and cancer, completed questionnaires on weight, height, cigarette habit, and physical activities in 1962 or 1966 and in 1977 (n=11 703). We assessed weight change between questionnaires, based on self-reported weights. <h3>Main Outcome Measure.</h3> —Mortality from all causes (n=1441), coronary heart disease (n=345), and cancer (n=459), determined from death certificates. <h3>Results.</h3> —Lowest all-cause mortality was among alumni maintaining stable weight (±1 kg). With this category as referent (relative risk=1.00), relative risks of death associated with losing more than 5 kg, losing between 1 and 5 kg, (more than 1 kg and up to 5 kg) gaining between 1 and 5 kg (more than 1 kg and up to 5 kg), and gaining more than 5 kg were 1.57 (95% confidence interval, 1.34 to 1.84), 1.26 (1.10 to 1.46), 1.06 (0.90 to 1.24), and 1.36 (1.11 to 1.66), respectively. For coronary heart disease mortality, relative risks were 1.75 (1.26 to 2.43), 1.43 (1.05 to 1.93), 1.28 (0.91 to 1.80), and 2.01 (1.36 to 2.97), respectively. Weight change did not predict cancer mortality. Findings were not explained by cigarette habit, physical activity, or body mass index. We observed similar trends for follow-up between 1977 and 1982 and between 1983 and 1988. Those losing or gaining more weight also reported greater total lifetime weight loss, which may indicate weight cycling. <h3>Conclusions.</h3> —Both body weight loss and weight gain are associated with significantly increased mortality from all causes and from coronary heart disease but not from cancer. (<i>JAMA</i>. 1992;268:2045-2049)
The role of cytomegalovirus in inflammatory bowel disease: a systematic review
Authors: P. Henderson, D. C. Wilson
Journal: Gut (2011)

<h3>Introduction</h3> Cytomegalovirus (CMV) has been widely implicated in the aetiopathogenesis, exacerbation and treatment-refractoriness of inflammatory bowel disease (IBD). In addition, recent research showing that NOD2 and TLR2 (genes in which germline mutations give rise to increased IBD susceptibility) both act as viral pattern recognition receptors has stimulated a renewed interest in the role of this common virus in IBD. <h3>Methods</h3> To study the evidence for the role of CMV in IBD by formal systematic review. An electronic database search of the Cochrane Library, Medline, Embase and the British Nursing Index and Archive was performed with keywords related to IBD and cytomegalovirus in addition to searches on PubMed, other online indexes and foreign language periodical databases. A hand search of reference lists of articles was also performed along with reviews of major gastroenterology journals and meeting abstracts. The papers identified were then reviewed and the level of evidence (EL) was assessed using the Scottish Intercollegiate Guidelines Network (SIGN) methodology (http://www.sign.ac.uk). <h3>Results</h3> The initial database searches produced 264 hits and after review of their abstracts a total of 69 papers were identified; a further 77 papers were sourced from their reference lists. A total of 108 were included and comprised 3 systematic reviews, 12 case–control studies (EL 2-), 5 cohort studies (EL 2-), 20 case series (EL 3) and 68 case reports. The literature search in the only methodological robust systematic review (EL 1+) ended in 2002 with the two subsequent systematic reviews demonstrating major weaknesses (EL 1-). The remaining studies varied widely with regard to the population studied, the method of CMV detection and the clinical details presented. Analysing the case–control studies that tested biopsy or surgical specimens the overall incidence of CMV detection was 32/100 in IBD and 12/100 in controls (p=0.001). There was some consensus that CMV contributed to steroid-refractory disease and anecdotal evidence that the treatment of CMV-related relapses with antiviral therapy may be beneficial. <h3>Conclusion</h3> The evidence surrounding the role of CMV in IBD is poor. Few studies have been of sufficient quality to provide convincing evidence of CMV as an aetiopathological factor in active IBD or that the use of antivirals should be routinely used in those in which CMV disease is suspected. A prospective randomised controlled trial of antiviral therapy for those found to have active CMV, by a variety of accurate investigations, should be considered to ascertain the benefits of treating this prevalent pathogen.
Incorrect Terminology
Journal: JAMA (1990)

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
Candida Endophthalmitis Complicating Candidemia.
Authors: Burt R. Meyers
Journal: Annals of Internal Medicine (1973)

Meeting Abstracts1 May 1973Candida Endophthalmitis Complicating Candidemia.Burt R. Meyers, M.D., F.A.C.P., Theodore Leiberman, M.D., Andrew P. Ferry, M.D., Shalom Z. Hirschman, M.D., F.A.C.P.Burt R. Meyers, M.D., F.A.C.P.Search for more papers by this author, Theodore Leiberman, M.D.Search for more papers by this author, Andrew P. Ferry, M.D.Search for more papers by this author, Shalom Z. Hirschman, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-5-826_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSix patients withCandida albicansendophthalmitis complicating candidemia had complicated medical or surgical problems; all had a history of multiple antibiotic therapy, and some received corticosteroids. Candidemia was present in four of the six patients; in three patients extraocular sites of Candida infection were noted. The presenting signs of redness and irritation of the eye, which suggested simple conjunctivitis to the internist, appeared 3 to 7 days after candidemia. Ophthalmological examination showed marked iritis in five patients, chorioretinal involvement in two patients, and an iris abscess in one patient. Specimens of the eye for pathological examination were available from four... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, New York. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByTHE INFLUENCE OF PORTOSYSTEMIC SHUNT OPERATION ON IMMUNOGLOBULINS AND ESCHERICHIA COLI ANTIBODIES IN PATIENTS WITH CIRRHOSIS OF THE LIVER 1 May 1973Volume 78, Issue 5Page: 826-826KeywordsAbscessesAntibioticsCandidaCandida albicansConjunctivitisCorticosteroid therapy Issue Published: 1 May 1973 PDF DownloadLoading ...
SLEEP
Journal: JAMA (1968)

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
GOOD JOURNALS REPAY.
Journal: JAMA (1895)

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 SY44-02: Aberrant polycomb repression in midline and hindbrain tumors
Authors: Peter W. Lewis
Journal: Cancer Research (2019)

Abstract The discovery of high-frequency histone H3 missense mutations (‘oncohistones’) in pediatric gliomas was the first time that histone mutations were linked to any disease. Since the original discovery, monoallelic missense mutations in genes encoding histone H3 have been found in a variety of cancer types. Previous studies have led to mechanistic insights into how one class of oncohistones promotes tumorigenesis by demonstrating that lysine-to-methionine (K-to-M) substitutions transform histones from serving as substrates into specific and potent inhibitors of lysine methyltransferases. Approximately 84% of diffuse intrinsic pontine glioma (DIPG) and 60% of high-grade non-brainstem pediatric midline gliomas contain a lysine 27-methionine (K27M) mutation. DIPG and other midline tumors have extremely low H3K27me3 levels caused by the action of the H3 K27M oncohistone. The H3 K27M protein binds to and inhibits the catalytic subunit (EZH2) of the Polycomb Repressive Complex 2 (PRC2), a conserved protein complex involved in gene silencing. Polycomb group (PcG) proteins are essential for development and are frequently misregulated in human cancers. Polycomb Repressive Complexes (PRC1, PRC2) function in a collaborative epigenetic cross-talk with H3K27me3 to initiate and maintain transcriptional silencing. Posterior fossa type A (PFA) ependymomas also exhibit very low H3K27 methylation but lack the K27M oncohistone. Instead, PFA tumors express high levels of KIP75 (K27M-like inhibitor of PRC2, 75kDa, also termed CXORF67). We find that a highly conserved sequence within the C-terminus of KIP75 is necessary and sufficient to inhibit the catalytic activity of PRC2 in vitro and in vivo. Our biochemical experiments indicate that KIP75 directly interacts with the active site of the EZH2 subunit in a mechanism that is remarkably similar to the K27M oncohistone. Furthermore, expression of H3 K27M or KIP75 promote similar chromatin landscapes and gene expression profiles in cell culture. Our data indicate that PFA ependymoma and DIPG tumors are driven in part by the action of peptidyl PRC2 inhibitors that dysregulate gene silencing to promote tumorigenesis. Citation Format: Peter W. Lewis. Aberrant polycomb repression in midline and hindbrain tumors [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 SY44-02.
"GROUP PRACTICE; DIAGNOSTIC AND PAY CLINICS"
Journal: JAMA (1921)

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
LIABILITY OF DRUGGIST TO PHYSICIAN.
Journal: JAMA (1894)

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
Abstracts
Journal: Annals of the Rheumatic Diseases (1948)

Streptococci and staphylococci alter extracts of certain tissues so that they become antigenic to animals of the same species-that is, become auto-or iso-antigens according as they act in the same individual or in another animal of the same species.The antibodies produced by injecting simple mixtures of killed organisms and tissue extracts into animals of the same species react with the microbe and also separately Iand specifically with the tissue-extract.The author demonstrates the development of antibodies against iso-antigens obtained from rat muscle and connective tissue (he used the celloidin particle agglutination technique).He describes lesions in the heart valves of the injected rats which he regards as due to damage by the anti-connective-tissue antibodies.They have some resemblance to rheumatic lesions, and the author considers that damage by antibodies to con- nective-tissue auto-antigens plays a part in the patho- genesis of rheumatic carditis in man.He also claims that glomerular nephritis produced in earlier experiments by the simultaneous injection of killed streptococci and kidney extract was due to the development of antibodies against kidney autoantigens.
Nonsurgical inferior vena cava obstruction for prevention of pulmonary emboli
Authors: B. M. Beller
Journal: JAMA (1972)

Four acutely ill patients with multiple, recurrent pulmonary emboli, despite adequate anticoagulation therapy, have had the Mobin-Uddin inferior vena cava filter implanted at the time of diagnostic cardiac catheterization. In each patient, clinical improvement has occurred without significant morbidity, and there has been no instance of repeated major pulmonary embolization. This new device can be inserted quickly and safely in acutely ill patients without need for extensive surgery or general anesthesia. This report documents the clinical course of the patients, and the potential advantages of the method.
Genetic damage from diagnostic radiation
Authors: Theodore R. Bledsoe
Journal: JAMA (1977)

<h3>To the Editor.—</h3> Among the highly questionable theses and assertions in the article by Bross and Natarajan is the following: "These findings refute a dogma that is often cited by radiologists who claim that diagnostic radiation is harmless." No responsible radiologist is "dogmatic" regarding the hazards of diagnostic procedures. While most of us feel that the margin of safety in these procedures is comfortable, we constantly strive to reduce further the already very low levels of radiation involved. After all, we have the enduring examples of the x-ray pioneers in the early years of this century who died because of their complete ignorance of radiation safety. In conjunction with our scientific and engineering colleagues, we are responsible for the many innovations in equipment and techniques that have resulted in the present low levels of exposure and attendant vanishingly small risks. I might also point out that while we radiologists as
Massachusetts Department of Mental Health
Authors: Jack R. Ewalt
Journal: New England Journal of Medicine (1954)

FURTHER INFORMATION ON MENTAL HOSPITALSMental hospitals, and general hospitals, are special environments constructed and maintained to care for people whose homes cannot supply the health resources they need at the particular moment. For example, if appendectomy is necessary the patient goes to a hospital that has the special facilities and personnel necessary for surgery. Mental hospitals as special environments offering health resources not available elsewhere in the community must be planned and operated around this concept. The following circumstances are essential:Facilities to segregate the patient from the general public that he may be relieved of the demands made . . .
Chemical Structure and Properties of Selected Benzene Compounds in Relation to Biological Activity
Authors: V. H. Freed, R. Haque
Journal: Environmental Health Perspectives (1976)

Four fundamental physical parameters of series of benzene derivatives were studied to ascertain correlations with biological activity. These included octanol/water coefficient, vapor pressure, infrared absorption (out-of-plane C-H vibration), and the pi values. Each physicochemical constant exhibited a partial correlation with biological activity suggesting that each played a role. It was presumed that more precise and specific data on the biological activity would have permitted a better correlation. It is postulated that the biological activity of a compound is due to the sum of such physicochemical factors as: partition coefficient, molecular geometry and spatial orientation, electronic characteristics of the molecular orbitals, and vibrational-rotational frequencies of constituent groups.
Proposal of a Twin Aarginine Translocator System-Mediated Constraint against Loss of ATP Synthase Genes from Nonphotosynthetic Plastid Genomes
Authors: Ryoma Kamikawa, Goro Tanifuji, Sohta A. Ishikawa, Ken-Ichiro Ishii, Yusei Matsuno, Naoko T. Onodera, Ken-Ichiro Ishida, Tetsuo Hashimoto, Hideaki Miyashita, Shigeki Mayama, Yuji Inagaki
Journal: Molecular Biology and Evolution (2015)

Organisms with nonphotosynthetic plastids often retain genomes; their gene contents provide clues as to the functions of these organelles. Yet the functional roles of some retained genes—such as those coding for ATP synthase—remain mysterious. In this study, we report the complete plastid genome and transcriptome data of a nonphotosynthetic diatom and propose that its ATP synthase genes may function in ATP hydrolysis to maintain a proton gradient between thylakoids and stroma, required by the twin arginine translocator (Tat) system for translocation of particular proteins into thylakoids. Given the correlated retention of ATP synthase genes and genes for the Tat system in distantly related nonphotosynthetic plastids, we suggest that this Tat-related role for ATP synthase was a key constraint during parallel loss of photosynthesis in multiple independent lineages of algae/plants.
"THE TREATMENT OF AMERICAN MEDICAL WRITERS BY A CONTEMPORARY."
Journal: JAMA (1900)

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
Fatal complement-induced leukostasis after diatrizoate injection. Principles of clinicopathologic diagnosis
Authors: H. Schneiderman
Journal: JAMA (1983)

A case of fatal radiographic contrast medium (RCM)-induced pulmonary granulocyte aggregation (leukostasis) showed massive elevation of the postmortem histamine level. Suspicion of this phenomenon in diverse clinical settings permits clinical and pathological documentation via increased plasma levels of C3a and other means. The existence of effective prophylaxis stimulates a search for predictive tests. (<i>JAMA</i>1983;250:2340-2342)