tbuckley/cabot-search huggingface dataset:
Beating the heat: development and evaluation of a Canadian hot weather health-response plan.
Authors: K E Smoyer-Tomic, D G Rainham
Journal: Environmental Health Perspectives (2001)

An increasing number of cities subject to hazardous summer weather in the United States and Canada have begun to develop and implement hot weather response plans to prevent heat-related illnesses and deaths. In this study we focus on heat-mortality relationships in Toronto, Ontario, between 1980 and 1996 and evaluate the potential effectiveness of the city's interim hot weather-health response plan. Using two heat stress indexes--humidex and apparent temperature--we identified excess mortality associated with hot and humid weather and then estimated excess deaths for hot and cool summers. Mortality rates for all ages and for > 64 years age groups rose with increasing humidex and apparent temperature, with no significant increase for the population < 65 years. Excess mortality occurred as low as the 30-35 degrees C humidex range, which is below the 40 degrees C humidex used to issue a heat warning under Toronto's interim hot weather response plan. During a hot summer (such as 1988 or 1995), 32 excess deaths would be expected, whereas 34 fewer deaths than baseline levels would be expected during a cool summer like 1982 or 1992. Days with high humidex levels occur infrequently in Toronto, and thus exposure is limited under current climatic conditions. In the event of a warming climate, more days with dangerously high humidex levels are likely to occur, and summer deaths are expected to increase. Toronto's hot weather health-response plan is an important early step for adaptation to climate change.
Immunologic Responsiveness of Man to Penicillin
Authors: Robert H. Schwartz, John H. Vaughan
Journal: JAMA (1963)

OBSERVATIONS of patients have repeatedly indicated that man may develop an immunologic response to penicillin that can cause hypersensitivity symptoms. Many antibiotics appear to be allergenic, but by no means to the same degree. Today penicillin heads the list of medicinal agents in the frequency, diversity, and severity of hypersensitivities which it induces,<sup>1</sup>and it probably has replaced foreign sera as the most common cause of anaphylactic shock. In 1958, Ley and collaborators<sup>2</sup>reported that penicillin-sensitized erythrocytes were agglutinated by the sera of some individuals who have been treated with penicillin. He presented evidence that the agglutination was not due to skin-sensitizing antibody, but to another antibody which seemed not to be implicated in hypersensitivity reactions. In his study, only 25 of 2,000 random sera investigated had factors capable of agglutinating penicillin-sensitized cells. Investigation of the case histories of 30 of these patients revealed a past exposure to
Abstract 3522: Vincristine activates c-Jun N-terminal kinase in chronic lymphocytic leukemia <i>in vivo</i>.
Authors: Darcy JP Bates, Alexey V. Danilov, Bernard B. Beaulieu, Lionel D. Lewis, Alan Eastman
Journal: Cancer Research (2013)

Abstract Chronic lymphocytic leukemia (CLL) is a cancer of B cell lymphocytes whose survival depends on the anti-apoptotic activity of Bcl-2 family proteins. Due to the low growth fraction of CLL cells, drugs that kill during mitosis, such as the microtubule-targeting vinca alkaloids, are not expected to be effective. However, we have found that vincristine and vinblastine can act independently of mitosis and induce acute apoptosis in freshly isolated CLL cells. The mechanism of this effect still depends on destabilization of microtubules as similar events occur with combretastatin A4 which destabilizes microtubules through binding to a different site on tubulin. Vinca-mediated apoptosis in CLL cells can be enhanced by addition of the cyclin-dependent kinase (CDK) inhibitor dinaciclib, killing cells acutely within 6 h. Dinaciclib functions by inhibiting CDK9, suppressing transcription and preventing expression of Mcl-1. The combination of dinaciclib and vinca alkaloids depends on vinca-induced phosphorylation of c-Jun N-terminal kinase (JNK). Therefore, we investigated whether JNK phosphorylation occurs in peripheral blood CLL cells in patients receiving vincristine. Patients received 2 mg vincristine intravenously by infusion over 5 minutes. Venous blood samples were obtained at time zero (pre-treatment) and post drug administration for up to 6 h. Patients then continued to receive chemotherapy treatment as prescribed by their primary oncologist. Pre-treatment CLL cells were studied ex vivo for JNK phosphorylation on exposure to vincristine. These studies showed that CLL cells phosphorylated JNK in response to clinically relevant concentrations of vincristine (10-50 nM). In the CLL cells from all 4 patients studied thus far, vincristine led to rapid (≤ 1 h) JNK phosphorylation which was sustained for 4-6 h post vincristine administration. These proof-of-principle study results provide justification for the development of a Phase I study to define the effect of the combination of vinca alkaloids and dinaciclib in patients with CLL. Citation Format: Darcy JP Bates, Alexey V. Danilov, Bernard B. Beaulieu, Lionel D. Lewis, Alan Eastman. Vincristine activates c-Jun N-terminal kinase in chronic lymphocytic leukemia in vivo. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3522. doi:10.1158/1538-7445.AM2013-3522
MPD-RC 101 prospective study of reduced-intensity allogeneic hematopoietic stem cell transplantation in patients with myelofibrosis
Authors: Damiano Rondelli, Judith D. Goldberg, Luis Isola, Leah S. Price, Tsiporah B. Shore, Michael Boyer, Andrea Bacigalupo, Alessandro Rambaldi, Marco Scarano, Rebecca B. Klisovic, Vikas Gupta, Bjorn Andreasson, John Mascarenhas, Meir Wetzler, Alessandro M. Vannucchi, Josef T. Prchal, Vesna Najfeld, Attilio Orazi, Rona S. Weinberg, Crystal Miller, Giovanni Barosi, Lewis R. Silverman, Giuseppe Prosperini, Roberto Marchioli, Ronald Hoffman
Journal: Blood (2014)
Propranolol and Digoxin for Angina Pectoris
Authors: JACK J. STEIN
Journal: Annals of Internal Medicine (1976)

Comments and Correction1 January 1976Propranolol and Digoxin for Angina PectorisJACK J. STEIN, M.D.JACK J. STEIN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-84-1-99_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In their recent paper "Combined Propranolol and Digoxin Therapy in Angina Pectoris" (Ann Intern Med 83:449-455, 1975), Crawford and associates, having proved combination therapy effective, leave an important question unanswered, namely, what are the indications for its use.The patients in their study had apparently never been given a trial of nitrates, although some physicians believe that nitrates are the drugs of choice in stable angina (1), particularly when only one coronary artery is involved (2), and that propranolol is useful as a second-line drug when nitrates fail.The point to be made is that, in the...References1. ARONOW W: Drug therapy: management of stable angina. N Engl J Med 289:516-520, 1973 CrossrefMedlineGoogle Scholar2. MUNDTH E and AUSTEN W: Surgical measures for coronary heart disease. N Engl J Med 293:13-18, 75-80, 123-130, 1975 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: JACK J. STEIN, M.D. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1976Volume 84, Issue 1Page: 99-99KeywordsAnginaCoronary arteriesDrugsNitrates ePublished: 1 December 2008 Issue Published: 1 January 1976 PDF downloadLoading ...
Walking and Type 2 Diabetes
Authors: James O. Hill
Journal: Diabetes Care (2005)

If you need another reason to prioritize physical activity for your patients with type 2 diabetes, it is provided in the study by Di Loreto et al. (1) published in this issue of Diabetes Care . Results from the study show that you can get impressive improvements in health and reductions in health care costs just by getting your patients with type 2 diabetes to make modest increases in physical activity. A second message is that you can produce these increases in physical activity in a large proportion of your patients with a simple counseling program that requires only a modest commitment of time and effort.

A unique aspect of the study is that the results were analyzed in a way to provide some guidance on how much physical activity is required for health and financial benefits in this population. Keep in mind that these analyses were obtained from a post hoc analysis of the data and must be treated with caution until confirmed by other prospective studies. Nonetheless, the results strongly suggest that small, achievable increases in physical activity can have a big impact on health in this population. In this study, all patients were given a counseling program designed to increase physical activity by at least 10 MET h/week. After 2 years, the results were analyzed based on how much physical activity was actually performed. The authors found significant health benefits with increases in physical activity of >10 MET h/week, and they suggest that this is the minimum increase in physical activity required to achieve health and financial benefits in sedentary patients with type 2 diabetes. Further, they found that the health benefits of …
NOVEL ORAL ANTICOAGULANTS AND CONCOMITANT ANTIPLATELET THERAPY FOR STROKE PREVENTION IN PATIENTS WITH ATRIAL FIBRILLATION: A META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS
Authors: Shashi Kumar, Stephan B. Danik, Robert K. Altman, Conor D. Barrett, Gary S. Roubin, Andrea Natale, Jacqueline S. Danik
Journal: Journal of the American College of Cardiology (2014)
Approval of TMJ Prosthesis
Authors: Jane E. Henney
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
Role of Depression As a Predictor of Mortality Among Cancer Patients After Stem-Cell Transplantation
Authors: Jesús M. Prieto, Jorge Atala, Jordi Blanch, Enric Carreras, Montserrat Rovira, Esteve Cirera, Anna Espinal, Cristóbal Gasto
Journal: Journal of Clinical Oncology (2005)

Purpose To determine the association between depression and survival among cancer patients at 1, 3, and 5 years after stem-cell transplantation (SCT). Patients and Methods This was a prospective cohort study of 199 hematologic cancer patients who survived longer than 90 days after SCT and who were recruited in a University-based hospital between July 1994 and August 1997. Patients received a psychiatric assessment at four consecutive time points during hospitalization for SCT, yielding a total of 781 interviews. Depression diagnoses were determined on the basis of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Results Eighteen (9.0%) and 17 patients (8.5%) met criteria for major and minor depression, respectively. Multivariate Cox regression models found major depression to be predictive of higher 1-year (hazard ratio [HR], 2.59; 95% CI, 1.21 to 5.53; P = .014) and 3-year mortality (HR, 2.04; 95% CI, 1.03 to 4.02; P = .041) but not 5-year mortality (HR, 1.48; 95% CI, 0.76 to 2.87; P = .249). Minor depression had no effect on any mortality outcome. Other multivariate significant predictors of higher mortality were higher regimen toxicity in the 1-, 3-, and 5-year models; older age and acute lymphoblastic leukemia in the 3- and 5-year models; chronic myelogenous leukemia in the 3-year model; and lower functional status and intermediate/higher risk status in the 5-year model. Use of peripheral-blood stem cells predicted lower mortality in the 5-year model. Conclusion After adjusting for multiple factors, major depression predicted higher 1- and 3-year mortality among cancer patients after SCT, underscoring the importance of adequate diagnosis and treatment of major depression.
Reconsidering the Politics of Public Health
Authors: Dave A. Chokshi, Nicholas W. Stine
Journal: JAMA (2013)

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
Targeted Sarcoplasmic Reticulum Ca <sup>2+</sup> ATPase 2a Gene Delivery to Restore Electrical Stability in the Failing Heart
Authors: Michael J. Cutler, Xiaoping Wan, Bradley N. Plummer, Haiyan Liu, Isabelle Deschenes, Kenneth R. Laurita, Roger J. Hajjar, David S. Rosenbaum
Journal: Circulation (2012)

Recently, we reported that sarcoplasmic reticulum Ca(2+) ATPase 2a (SERCA2a), the pump responsible for reuptake of cytosolic calcium during diastole, plays a central role in the molecular mechanism of cardiac alternans. Heart failure (HF) is associated with impaired myocardial calcium handling, deficient SERCA2a, and increased susceptibility to cardiac alternans. Therefore, we hypothesized that restoring deficient SERCA2a by gene transfer will significantly reduce arrhythmogenic cardiac alternans in the failing heart.Adult guinea pigs were divided into 3 groups: control, HF, and HF+AAV9.SERCA2a gene transfer. HF resulted in a decrease in left ventricular fractional shortening compared with controls (P<0.001). As expected, isolated HF myocytes demonstrated slower sarcoplasmic reticulum calcium uptake, decreased Ca(2+) release, and increased diastolic Ca(2+) (P<0.05) compared with controls. Moreover, SERCA2a, cardiac ryanodine receptor 2, and sodium-calcium exchanger protein expression was decreased in HF compared with control (P<0.05). As predicted, HF increased susceptibility to cardiac alternans, as evidenced by decreased heart rate thresholds for both V(m) alternans and Ca alternans compared with controls (P<0.01). Interestingly, in vivo gene transfer of AAV9.SERCA2a in the failing heart improved left ventricular contractile function (P<0.01), suppressed cardiac alternans (P<0.01), and reduced ryanodine receptor 2 P(o) secondary to reduction of ryanodine receptor 2-P(S2814) (P<0.01). This ultimately resulted in a decreased incidence of inducible ventricular arrhythmias (P=0.05).These data show that SERCA2a gene transfer in the failing heart not only improves contractile function but also directly restores electric stability through the amelioration of key arrhythmogenic substrate (ie, cardiac alternans) and triggers (ie, sarcoplasmic reticulum Ca(2+) leak).
Variants Weakly Correlated with <i>CHRNA5</i> D398N Polymorphism Should be Considered in Transcriptional Deregulation at the 15q25 Locus Associated with Lung Cancer Risk
Authors: Jen C. Wang, Laura J. Bierut, Alison M. Goate
Journal: Clinical Cancer Research (2009)

To the Editors: A recent article by Falvella et al. (1) reports a significant up-regulation of CHRNA5 transcript levels in lung adenocarcinomas, a confirmation of an association between the CHRNA5 D398N variant and lung cancer risk, and an association of the D398N variant (rs16969968) with CHRNA5 mRNA levels in lung tissue. This study highlights the candidacy of CHRNA5 as the 15q25 locus associated with lung cancer risk. The authors reported that CHRNA5 mRNA levels are up-regulated 30-fold in lung adenocarcinoma compared with normal lung tissue and that CHRNA5 mRNA levels were about 2.5-fold lower in individuals homozygous for the risk allele (N398) compared with individuals homozygous for the nonrisk allele. However, there is insufficient evidence to conclude that the risk allele of the D398N variant is biologically associated with higher CHRNA5 mRNA expression in lung adenocarcinoma. Our work provides evidence for two distinct biological mechanisms altering the risk related to developing nicotine dependence and lung cancer. One mechanism involves the variant rs16969968 (D398N), which likely alters protein structure and receptor function in vitro (2). A second potential mechanism is altered mRNA expression of CHRNA5. In our study using human brain tissue, we showed that several variants located upstream of the coding region of CHRNA5 (i.e., rs588765) are much more strongly associated with the variability in CHRNA5 mRNA expression observed in human frontal cortex than rs16969968 (3, 4). Subjects homozygous for the minor allele of rs588765 showed a 2.9-fold increase in CHRNA5 mRNA expression compared with subjects homozygous for the major allele (3, 4). The polymorphism rs588765 and highly correlated variants are only weakly correlated with the D398N variant. Using diplotype analysis, we observed that the variant N398, which greatly increases risk for nicotine dependence and lung cancer, primarily occurs on the background of low mRNA expression of CHRNA5. The nonrisk variant D398 occurs on both high and low expression alleles. When D398 occurs on the background of low CHRNA5 mRNA expression, the risk for nicotine dependence and lung cancer is significantly lower compared with those with the high CHRNA5 mRNA expression (4). Thus, for an optimal translational application of their findings, variants tagged by rs588765 are recommended in further testing of the association observed between the D398N variant and CHRNA5 mRNA levels in lung tissue.Drs. L.J. Bierut, A.M. Goate, and J.C. Wang are listed as inventors on a patent (US 20070258898) held by Perlegen Sciences, Inc., covering the use of certain single nucleotide polymorphisms in determining the diagnosis, prognosis, and treatment of addiction. Dr. Bierut has acted as a consultant for Pfizer, Inc., in 2008.
ROENTGEN-RAY SILHOUETTES: A METHOD OF CASE RECORDING
Authors: John J. Moorhead
Journal: JAMA (1923)

A number of methods have been designed for recording roentgen-ray findings, particularly in cases of fracture. These methods vary from a simple tracing to an elaborate colored photograph. During the war, the French had a very good idea in which colored chalk was used; but while this method is excellent and graphic, it requires considerable time and experience. At the Post-Graduate and Beekman Street hospitals I have recently been using a modification of this French plan; our roentgen-ray records are now in black and white, and for want of a better name, I call them silhouettes. An ordinary tracing is first made (<i>A</i>) on architect's tracing paper (sometimes called vellum), and then the interosseous and extra-osseous parts are painted solid black (<i>B</i>) with a small brush, a dull black paint, such as black japan, being used. The parchment-like tracing paper is quite absorptive, and the paint will not run. An
A role for adenosine deaminase in human monocyte maturation.
Authors: D Fischer, M B Van der Weyden, R Snyderman, W N Kelley
Journal: Journal of Clinical Investigation (1976)

The occurrence of a deficiency of adenosine deaminase (ADA) activity in some patients with severe combined immunodeficiency suggests a possible relationship between the activity of ADA and the aberration of the immune system. To help delineate the function of ADA in the immune response we have examined its role in monocyte maturation. When incubated in vitro, peripheral blood monocytes transformed, within 3 days, to macrophagea as assessed by phase-contrast microscopy and an increase in the specific activity of the lysosomal enzyme acid phosphatase. The specific activity of ADA increased as much as ninefold, reaching a peak after the 1st day in culture, while the activities of other enzymes involved in the purine salvage pathway were not altered. Sucrose density ultracentrifugation of extracts prepared immediately after the isolation of monocytes revealed the presence of two forms of ADA with molecular weights of approximately 30,000 and 110,000. The increase in ADA specific activity during monocyte cultivation correlated with an increase in the activity of the smaller molecular species. A specific inhibitor ADA, erythro-9-(2-hydroxy-3-nonyl) adenine, prevented the increase in acid phosphatase activity, as well as the morphological changes associated with the monocyte maturation. These data suggest a role for ADA in monocyte to macrophage maturation. In view of the central role of macrophages in immune function, this observation may relate to the association of combined immunodeficiency and a deficiency of this enzyme.