tbuckley/cabot-search huggingface dataset:
Association of tuberculosis infection with increased time in or admission to the New York City jail system
Authors: E. Y. Bellin
Journal: JAMA (1993)

<h3>Objective.</h3> —To establish the association between time spent in jail or number of jail admissions and development of tuberculosis in a cohort of inmates incarcerated without evidence of tuberculosis infection on entry. <h3>Design.</h3> —Nested case-control design within a prospective cohort. A cohort of 2636 tuberculin skin test—negative inmates incarcerated in 1985 was matched against the Tuberculosis Registry of New York City. Each case of tuberculosis reported prior to May 15,1992, was assigned to three randomly selected controls from the cohort. We determined time spent in jail by reviewing the computer records of the New York City Inmate Information System. Conditional logistic regression modeling was performed to establish the association of jail time with the development of tuberculosis. <h3>Setting.</h3> —New York City Jail. <h3>Results.</h3> —Sixty inmates developed tuberculosis by May 15, 1992. Eighty-five percent of these had pulmonary tuberculosis. Univariate analysis identified the number of jail admissions (<i>P</i>=.02), age greater than or equal to 30 years (<i>P</i>=.001), and assignment to a methadone detoxification unit (<i>P</i>=.001) as significant in predicting tuberculosis. Multivariate modeling identified these same variables and jail time as significant. One year of jail time increased the odds of tuberculosis to 2.2 (95% confidence interval, 1.1 to 4.4). <h3>Conclusion.</h3> —The demonstrated association between jail time or jail admissions and development of tuberculosis suggests that the New York City jail system may be an important amplification point in the ongoing tuberculosis epidemic, deserving significant public health attention. (<i>JAMA</i>. 1993;269:2228-2231)
THE VIABILITY OF RED BLOOD CELLS
Journal: JAMA (1920)

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
Certification of Poliomyelitis Eradication— the Americas, 1994
Journal: JAMA (1994)

In May 1985, the Pan American Health Organization (PAHO) proposed the goal of interruption of wild poliovirus transmission in the Western Hemisphere by 1990 (1). This proposal was endorsed by all member governments and was supported by several agencies and organizations, including Rotary International, the U.S. Agency for International Development, the United Nations Children's Fund, the Inter-American Development Bank, and the Canadian Public Health Association. On August 20, 1994, PAHO reported that 3 years had passed since the occurrence of the last case of poliomyelitis associated with wild poliovirus isolation in the Americas (Peru, August 1991) (2). This report summarizes the steps to certify eradication of polio in the Americas.
Erratum
Authors: ! Yi', Sheila Annie, R Campbell, F Carlton, Mary Cuthbert, J Irvine, J Kinnear, A Macgillivray, Flora Macdonald, D.-W Hudson, Fifteen Years, ' Standitg, ).-J Arkle, E Down, B Anv, -P Anderson, G Clark, W Duncan, E Dunlop, C Hunter, H Irwin, Freda Marriott, T Newman, Abdel Shaw, -W Shelhid
Journal: BMJ (1917)
THE NEW OPHTHALMOLOGYAND ITS RELATION TO GENERAL MEDICINE, BIOLOGY AND SOCIOLOGY.
Authors: GEORGE M. GOULD
Journal: JAMA (1904)

Again the critic may justly ask: "Have none, then, recognized and spoken out this much unrecognized truth?" Oh, yes, many and good men have done so. There is a vast quantity of literature produced by clinicians of the best character and professional standing, and it is astonishingly convincing and cogent. It is unfortunately scattered, and hence, in part ignored by too many physicians. The last weighty utterances are Dr. Zimmerman's study,<sup>6</sup>and especially since they are from England, the excellent reports of Dr. Snell,<sup>7</sup>and Dr. Pronger.<sup>8</sup>Hundreds of others might be cited, the testimonies,<i>e. g.,</i>of such good professional journals as the<i>Cleveland Medical Journal</i>, the<i>St. Paul Medical Journal,</i>the<i>Lancet,</i>the<i>Pacific Medical Journal, American Medicine,</i>the<i>Maryland Medical Journal, Colorado Medicine, Science, Mind,</i>the<i>Harvard Graduates' Magazine, Bulletin of the American</i>
Protective effect of fruits and vegetables on development of stroke in men
Authors: M. W. Gillman
Journal: JAMA (1995)

<h3>Objective.</h3> —To examine the effect of fruit and vegetable intake on risk of stroke among middle-aged men over 20 years of follow-up. <h3>Design.</h3> —Cohort. <h3>Setting.</h3> —The Framingham Study, a population-based longitudinal study. <h3>Participants.</h3> —All 832 men, aged 45 through 65 years, who were free of cardiovascular disease at baseline (1966 through 1969). <h3>Measurements and Data Analysis.</h3> —The diet of each subject was assessed at baseline by a single 24-hour recall. The estimated total number of servings per day of fruits and vegetables was the exposure variable for this analysis. Using Kaplan-Meier survival analysis, we examined age-adjusted cumulative incidence of stroke by quintile of servings per day. To adjust for multiple covariates, we used proportional hazards regression to calculate the relative risk (RR) of stroke for each increment of three servings per day. <h3>Main Outcome Measure.</h3> —Incidence of completed strokes and transient ischemic attacks. <h3>Results.</h3> —At baseline, the mean (±SD) number of fruit and vegetable servings per day was 5.1 (±2.8). During follow-up there were 97 incident strokes, including 73 completed strokes and 24 transient ischemic attacks. Age-adjusted risk of stroke decreased across increasing quintile of servings per day (log rank<i>P</i>for trend,.01). Age-adjusted RR for all stroke, including transient ischemic attack, was 0.78 (95% confidence interval [CI], 0.62 to 0.98) for each increase of three servings per day. For completed stroke the RR was 0.74 (95% CI, 0.57 to 0.96); for completed stroke of ischemic origin the RR was 0.76 (95% CI, 0.57 to 1.02); and for completed stroke of hemorrhagic origin, 0.49 (95% CI, 0.25 to 0.95). Adjustment for body mass index, cigarette smoking, glucose intolerance, physical activity, blood pressure, serum cholesterol, and intake of energy, ethanol, and fat did not materially change the results. <h3>Conclusion.</h3> —Intake of fruits and vegetables may protect against development of stroke in men. (<i>JAMA</i>. 1995;273:1113-1117)
RTOG 0525: Molecular correlates from randomized phase III trial of newly diagnosed glioblastoma (GBM).
Authors: K. D. Aldape, M. Wang, E. P. Sulman, D. P. Cahill, M. Hegi, H. Colman, G. Jones, A. Chakravarti, M. P. Mehta, D. W. Andrews, L. Long, K. Diefes, L. Heathcock, R. Jenkins, C. J. Schultz, M. R. Gilbert
Journal: Journal of Clinical Oncology (2011)

LBA2000 The full, final text of this abstract will be available in Part II of the 2011 Annual Meeting Proceedings, distributed onsite at the Meeting on June 4, 2011, and as a supplement to the June 20, 2011, issue of Journal of Clinical Oncology.
RECOVERY ALLOWED FOR INJURIES SUSTAINED BEFORE BIRTH.
Journal: JAMA (1997)

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
Human vaccines and vaccination By M. Mackett and J. D. Williamson, 215 pp. Oxford: BIOS Scientific Publishers, 1995. $37.95
Authors: R KOFF
Journal: Hepatology (1995)

Chronic liver diseases (CLD) are common, and are therefore mainly managed by non-hepatologists. These physicians lack access to the best non-invasive tests of liver fibrosis, and consequently cannot accurately determine the disease severity. Referral to a hepatologist is then needed. We aimed to implement an algorithm, comprising a new first-line test usable by all physicians, for the detection of advanced liver fibrosis in all CLD patients.Diagnostic study: 3754 CLD patients with liver biopsy were 2:1 randomized into derivation and validation sets. Prognostic study: longitudinal follow-up of 1275 CLD patients with baseline fibrosis tests.Diagnostic study: the easy liver fibrosis test (eLIFT), an “at-a-glance” sum of points attributed to age, gender, gamma-glutamyl transferase, aspartate aminotransferase (AST), platelets and prothrombin time, was developed for the diagnosis of advanced fibrosis. In the validation set, eLIFT and fibrosis-4 (FIB4) had the same sensitivity (78.0% vs. 76.6%, p = 0.470) but eLIFT gave fewer false positive results, especially in patients ≥60 years old (53.8% vs. 82.0%, p <0.001), and was thus more suitable as screening test. FibroMeter with vibration controlled transient elastography (VCTE) was the most accurate among the eight fibrosis tests evaluated. The sensitivity of the eLIFT-FMVCTE algorithm (first-line eLIFT, second-line FibroMeterVCTE) was 76.1% for advanced fibrosis and 92.1% for cirrhosis. Prognostic study: patients diagnosed as having “no/mild fibrosis” by the algorithm had excellent liver-related prognosis with thus no need for referral to a hepatologist.The eLIFT-FMVCTE algorithm extends the detection of advanced liver fibrosis to all CLD patients and reduces unnecessary referrals of patients without significant CLD to hepatologists.Blood fibrosis tests and transient elastography accurately diagnose advanced liver fibrosis in the large population of patients having chronic liver disease, but these non-invasive tests are only currently available in specialized centers. We have developed an algorithm including the easy liver fibrosis test (eLIFT), a new simple and widely available blood test. It is used as a first-line procedure that selects at-risk patients who need further evaluation with the FibroMeterVCTE, an accurate fibrosis test combining blood markers and transient elastography result. This new algorithm, called the eLIFT-FMVCTE, accurately identifies the patients with advanced chronic liver disease who need referral to a specialist, and those with no or mild liver lesions who can remain under the care of their usual physician.No registration (analysis of pooled data from previously published diagnostic studies).
Salvageable
Authors: Susan A. Glod
Journal: Annals of Internal Medicine (2012)

Ad Libitum16 October 2012SalvageableSusan A. Glod, MDSusan A. Glod, MDFrom Penn State Milton S. Hershey Medical Center, Hershey, PA 17033-0850.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-157-8-201210160-00012 Audio Reading - “Salvageable” Audio. Listen to a reading of "Salvageable" by Susan A. Glod, MD. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Old armchairs are salvageable,and decrepit lawn mowers,and crumbling architecture.Even your lemon pie, from which you, halfway between sigh and giggle,would scrape the sagging meringue into the sink,was salvageable.It's been months since we've had pie together, andThat Term no longer applies to you, they tell me.Who will tell you?Susan A. Glod, MDPenn State Milton S. Hershey Medical CenterHershey, PA 17033-0850 Author, Article, and Disclosure InformationAffiliations: From Penn State Milton S. Hershey Medical Center, Hershey, PA 17033-0850.Current Author Address: Susan A. Glod, MD, Division of General Internal Medicine, Penn State Milton S. Hershey Medical Center, Mail Code H106, 500 University Drive, PO Box 850, Hershey, PA 17033-0850; e-mail, [email protected]. PreviousarticleNextarticle Advertisement Audio Reading - “Salvageable” Audio. Listen to a reading of "Salvageable" by Susan A. Glod, MD. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics 16 October 2012Volume 157, Issue 8Page: 579 ePublished: 16 October 2012 Issue Published: 16 October 2012 Copyright & PermissionsCopyright © 2012 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Orthopedics
Journal: JAMA (1999)

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
Glutathione-S-Transferase M1 (GSTM1) and T1 (GSTT1) Deletion Polymorphisms Predict Regimen-Related Toxicity after Autologous and Allogeneic Blood and Marrow Transplantation (BMT).
Authors: Theresa Hahn, Eugenia Zhelnova, Irina Demidova, Valery Savchenko, Christine B. Ambrosone, Philip L. McCarthy
Journal: Blood (2007)
Pathology
Authors: Dennis W. Ross
Journal: JAMA (1990)

In keeping with the inevitable wave of changes experienced by medicine each year, several developing technologies in the field of pathology are particularly noteworthy. In hematopathology, recombinant DNA technology has provided a tool that increases our understanding of disease and enhances diagnostic capabilities. The rearrangement of the immunoglobulin genes and T-cell receptor genes by differentiating lymphocytes reveals an intricate process that is helping us understand neoplasia.<sup>1</sup>Early hematopoietic progenitor cells begin lymphoid differentiation by rearranging the δ-chain gene of the T-cell receptor. If this rearrangement produces a DNA sequence without a triplet stop codon for termination of transcription through the gene (a so-called open reading frame), the cell will bear γ/δ-chain dimers and become a CD3<sup>+</sup>CD4- CD8- natural killer/cytotoxic lymphocyte. δ-Chain rearrangement usually fails; then the lymphocyte attempts an α-chain rearrangement. The α-chain gene surrounds the δ-chain DNA sequences and an α-chain rearrangement results in permanent deletion of
AB0078 Effect of Mpges-1 Targeting on Lipid Metabolism in Human Cells
Authors: M. Korotkova, H. Idborg, J. Raouf, E. Ossipova, A. Checa, P. Olsson, P. Leclerc, G. Oliynyk, C. Wheelock, P.-J. Jakobsson
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme in the induced PGE2 production and well-recognized target for the development of novel anti-inflammatory drugs. Genetic deletion and inhibition of mPGES-1 appears to be protective in experimental models of arthritis. Targeting mPGES-1 alters eicosanoid profiles and may potentially affect the metabolism of other lipids. Fatty acids (FA) play essential roles as energy substrates, membrane structural components, second messengers and precursors of lipid mediators. Genetic deletion of mPGES-1 resulted in reduced levels of MUFA in the mouse spleen suggesting a decreased activity/expression of stearoyl-CoA-desaturase (SCD). SCD has been implicated in modulation of inflammation. However whether mPGES-1 inhibition affects lipid metabolism in human cells is not known. <h3>Objectives</h3> To investigate the effect of mPGES-1 inhibition on lipid metabolism in human cells. <h3>Methods</h3> A549 cells were induced with IL-1b and treated with mPGES-1 inhibitor (compound III) or COX-2 inhibitor (NS398). Eicosanoid profiles were analyzed using LC-MS/MS and protein profiles were analyzed using mass spectrometry based proteomics. FA composition of total lipids was determined using gas chromatography with flame ionization detector and sphingolipids were analysed by LC-MS/MS. <h3>Results</h3> Prostanoid profiles in supernatants from the IL-1b-induced cells treated with the COX-2 or mPGES-1 inhibitors were significantly different suggesting diverse effects of the inhibitors on down-stream pathways. Proteomic analysis of A549 cells identified the reduction of SCD levels in response to treatment with mPGES-1 or COX-2 inhibitors, as well as the suppression of the levels of a number of proteins involved in metabolism of fatty acids and sphingolipids. <h3>Conclusions</h3> The results suggest that down-regulation of COX-2/mPGES-1/PGE2 axis affects the lipid metabolism in A549 cells. These effects have important implications regarding potential consequences of pharmacologic mPGES-1 inhibition. <h3>Acknowledgements</h3> The Swedish Research Council, The Swedish Rheumatism Association, King Gustaf V 80 years Foundation, The Swedish Society of Medicine, Karolinska Institutet Foundation, The Swedish County Council and Marianne and Marcus Wallenberg foundation. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5002
Sarcoma Complicating Paget's Disease of Bone
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
Saddle Nose
Authors: Guido Valesini, Roberta Priori, Fabrizio Conti
Journal: New England Journal of Medicine (1995)

To the Editor: The study by Perriëns et al. (March 23 issue) 1 demonstrates that extending antituberculous treatment from 6 to 12 months reduces the rate of relapse in patients infected with the human immunodeficiency virus (HIV) who have pulmonary tuberculosis.In spite of this, the authors considered the six-month program to be an acceptable alternative because the longer-term therapy did not prolong survival.We question the validity of their survival analysis and therefore their recommendations for treatment.The short follow-up after treatment (1 year for patients in the 12-month treatment group) along with the unacceptable percentage of patients lost to follow-up (34 percent) lessens the statistical power of the study to reach that conclusion.The authors argue that most relapses could be successfully retreated.As shown in Table 2 of the article, only 20 of 335 patients (6 percent) died of tuberculosis in the first episode, as compared with 3 of 9 patients (33 percent) who relapsed (P ϭ 0.01 by Fisher's exact test).We also doubt that the patients who were lost to follow-up and those who are not enrolled in carefully controlled studies have the same opportunities for diagnosis and treatment as the patients who completed follow-up in the study by Perriëns et al.This point is even more important if patients are treated for only six months, because such patients have a greater risk of relapse.The theoretical savings afforded by a shorter course of thera-py may be counteracted by the need for closer follow-up.Furthermore, close follow-up is not an easy matter in HIV-infected patients, as reflected by the 34 percent rate of loss to follow-up.We believe that treatment of tuberculosis in HIV-infected patients must be continued for at least 9 months 2 as long as subsequent studies confirm that regimens lasting 6 months or 9 to 12 months are associated with the same rates of survival.