tbuckley/cabot-search huggingface dataset:
More education is needed before we burden women with their HPV status
Authors: E. D. Butterfield
Journal: BMJ (2014)

Elfstrom and colleagues do not discuss the ethics of human papillomavirus (HPV) testing, which will become a more contentious problem as more women are screened for HPV.1

We encourage patients diagnosed with sexually transmitted infections to tell their sexual partners. It is mandatory for patients to inform their partners of potentially life threatening infections like HIV: if the patient …
Commentary: Economics of diabetes care must move forwards
Authors: P D Home
Journal: BMJ (1995)

A problem of clinical science, albeit ultimately a happy one, is that it does not stop moving forwards. Even this autumn, the observations by the Gentofte group that percentage survival after onset of diabetic nephropathy over 16 years has quintupled and that median survival time has trebled, in association with lower blood pressure, will lead many to intensify their efforts to control even minor degrees of hypertension (>140/90 mm Hg) in these patients.1 So much is consistent with the current paper, but meanwhile the Gentofte group has also defined a 75% reduction (40% to 10%) over eight years in progression to proteinuria (albumin excretion >300 mg/day) in those patients with type 1 diabetes treated …
Forecasting Physician Workforce Requirements
Authors: Jonathan Zucker
Journal: JAMA (1995)

To the Editor.  —In a recent article by Dr Weiner, 1 the evidence from HMO staffing patterns, as reported in his Table 2, is faulty and inconsistent.  For example, in the column pertaining to Group Health Cooperative of Puget Sound in Table 2, the author has reported the number of neurosurgeon and anesthesiologist physician specialists per 100 000 population as 0.4 and 9.0, respectively. However, Group Health Cooperative (475 000 population) employs four neurosurgeons and 21 anesthesiologists. Is there any explanation for not reporting correctly the numbers for these physician specialists as 0.8 and 4.4, respectively?  As a result of the reported staffing patterns in that article, we anesthesiologists in the employ of Group Health Cooperative of Puget Sound easily forecast the daunting prospect of having to defend ourselves against a charge that we have twice as many physicians as comparable groups. Our unique early warning may forecast a broader
Heparin inhibits the expression of tissue-type plasminogen activator by smooth muscle cells in injured rat carotid artery.
Authors: A W Clowes, M M Clowes, T R Kirkman, C L Jackson, Y P Au, R Kenagy
Journal: Circulation Research (1992)

Smooth muscle cells (SMCs) in balloon-injured rat carotid artery express tissue-type plasminogen activator (t-PA) at a time when they are migrating from the media to the intima. Since heparin inhibits SMC migration and intimal thickening, we have examined the possibility that heparin might also inhibit t-PA expression. Heparin (nonanticoagulant fraction; molecular weight, approximately 6,000) was administered by continuous intravenous infusion (1.0 mg/kg per hour) to Sprague-Dawley rats subjected to balloon injury of the left common carotid artery. At various times up to 14 days after injury, plasminogen activator expression was analyzed by zymography, plasmin generation, enzyme-linked immunosorbent assay, Northern blotting, and in situ hybridization. This dose of heparin inhibited SMC accumulation at 14 days by 60%. Both urokinase plasminogen activator (u-PA) and t-PA activity increased in injured arteries and reached a maximum at 7 days. Heparin treatment decreased t-PA, but not u-PA, activity. Total t-PA protein was decreased by treatment with heparin but not chondroitin sulfate, and the decrease in t-PA protein was associated with decreased t-PA mRNA in the media. These results in the injured rat carotid artery agree with our earlier observations that heparin inhibits t-PA gene expression in cultured baboon aortic SMCs. They also provide support for the hypothesis that heparin interferes with the expression of certain proteases required for SMC migration and proliferation.
A CASE OF SEPTICAEMIC MENINGITIS, WITH RECOVERY
Authors: J. Dunbar
Journal: BMJ (1918)

SEPTICAEMIC MENINGITIS.EM DIT OU1wA I87After the patient has had a good rest and been radiographed.Besley's or other callipers with weight and pulley extension in the line of the thigh are, as a routine procedure, applied to the femur just above the knee, and the points are inserted down to the bone, but not penetrating into it;
Deficiency of tumour necrosis factor- and interferon- in bone marrow cells synergistically inhibits neointimal formation following vascular injury
Authors: H. Murayama, M. Takahashi, M. Takamoto, Y. Shiba, H. Ise, J. Koyama, Y.-i. Tagawa, Y. Iwakura, U. Ikeda
Journal: Cardiovascular Research (2008)

Neointimal formation after percutaneous coronary intervention (PCI), termed restenosis, limits therapeutic revascularization. Since it is now known that vascular injury involves an inflammatory response, we examined the role of tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in the neointimal formation after injury. Control (BALB/c), TNF-α-deficient (Tnf−/−), IFN-γ-deficient (Ifng−/−), or double-deficient (Tnf−/−Ifng−/−) mice were subjected to wire-mediated vascular injury of the right femoral artery. Neointimal formation after injury was significantly reduced after the injury in the Tnf−/−Ifng−/− mice, compared to that in the control, Tnf−/−, and Ifng−/− mice. Immunohistochemical analysis showed that TNF-α and IFN-γ were expressed in neointimal lesions in the control mice, but not in mice with deficiency of the corresponding cytokine. No significant difference in re-endothelialization was observed among these groups. The number of proliferating cell nuclear antigen in the neointimal lesions was significantly decreased in the Tnf−/−Ifng−/− mice. Bone marrow transplantation experiments revealed that deficiency of TNF-α and IFN-γ specifically in bone marrow cells significantly inhibited neointimal formation after vascular injury. The absence of TNF-α and IFN-γ in bone marrow cells synergistically inhibits neointimal formation following vascular injury, and thus, may provide new insights into the mechanisms underlying restenosis after PCI.
A Gpr120-selective agonist improves insulin resistance and chronic inflammation in obese mice
Authors: Da Young Oh, Evelyn Walenta, Taro E Akiyama, William S Lagakos, Denise Lackey, Ariane R Pessentheiner, Roman Sasik, Nasun Hah, Tyler J Chi, Jason M Cox, Mary Ann Powels, Jerry Di Salvo, Christopher Sinz, Steven M Watkins, Aaron M Armando, Heekyung Chung, Ronald M Evans, Oswald Quehenberger, Joanne McNelis, Juliane G Bogner-Strauss, Jerrold M Olefsky
Journal: Nature Medicine (2014)
S30 An evaluation of the systemic inflammatory response to endurance walking in patients with COPD: comparison with healthy individuals
Authors: J. L. Canavan, M. Moreton-Clack, A. Lewko, B. Linton-Willoughby, A. Jewell, R. Garrod
Journal: Thorax (2011)

<h3>Introduction</h3> Chronic low grade systemic inflammation is well described in stable COPD and may affect exercise tolerance in this population (Broekhuizen <i>et al</i>, 2006). Some studies investigating the systemic inflammatory (SI) response to exercise in COPD have reported increased cytokine responses to exercise in COPD patients (Rabinovich <i>et al</i>, 2003) and all have used protocols where the individual patient and healthy comparator perform exercise at a percentage of their own maximal oxygen consumption or muscle strength. This inevitably leads to discrepancies in exercise duration and absolute intensity between COPD and healthy groups, meaning we are unable to determine the effect of COPD on the exercise-induced cytokine response. We hypothesised that COPD patients would have an enhanced systemic inflammatory response compared with healthy comparators completing an identical walking protocol. <h3>Method</h3> 16 clinically stable COPD patients (5M: 11F) completed one treadmill endurance walking test at 85% VO<sub>2</sub>max until volitional exhaustion. Following this 16 age, sex-matched healthy participants completed identical walking protocols (speed, distance, duration) to that achieved by the 16 COPD patients. The concentration of systemic inflammatory markers (CRP, IL-6, TNF-α, IL-17) were analysed from venous blood taken at rest and post-walk. The exercise induced CRP and cytokine response was evaluated within groups using paired t tests or Wilcoxon sign tests. Comparison of the cytokine response data between groups was analysed using Wilcoxon sign tests. <h3>Results</h3> Results are presented as median (25th, 75th percentile) or mean change (95% CI). Baseline concentrations of the systemic inflammatory markers were not significantly different between the COPD (FEV<sub>1</sub> 50 (38 to 87) %) and healthy participants (Abstract S30 table 1). IL-6 increased significantly post-walk in the COPD group (0.25 (95% CI 0.49 to 0.008) but not in the healthy participants. TNF-α, IL-17 and CRP were not significantly increased with exercise in either group. No significant differences were found between groups for the change (pre- to post-walk) in any inflammatory markers (CRP: p=0.07; IL-6: p=0.51; TNF-α: p=0.22; IL-17: p=0.44). <h3>Conclusion</h3> Despite a significant increase in IL-6, the magnitude of the systemic inflammatory response to matched absolute workloads in COPD patients is not greater than in healthy comparators.
Controlling Abuse of Drugs From the Anesthesia Department-Reply
Authors: Gerald R. Adler
Journal: JAMA (1985)

<h3>In Reply.—</h3> Dr Patt's comments regarding our article are pertinent. No control and accounting system is foolproof. In a military environment, however, control measures can be more rigorous. Now, after 20 months, we still have not identified a drug abuser. We like to assume that this fact indicates no such individual is present in our department, but we also believe three other factors are operative: (1) the residents know that we constantly monitor their drug use and will detect any abrupt or gradual increase in drug use; (2) the quantities of abused drugs available to each resident are insufficient to support a drug habit (ie, no residents are consistently using greater than 10 mL a day of fentanyl when in contrast, past confirmed drug abusers were using 20 to 60 mL of this drug per day); and (3) the attending staff are denied access to the supplies of controlled substances.
Inhibition of Primary ADP-Induced Platelet Aggregation in Normal Subjects after Administration of Nitrofurantoin (Furadantin)
Authors: Ennio C. Rossi, Nathan W. Levin
Journal: Journal of Clinical Investigation (1973)

The evidence indicating that platelets may play a role in the occurrence of certain thromboembolic phenomena has stimulated a search for inhibitors of platelet function. This report presents data to indicate that nitrofurantoin is a potent inhibitor of primary ADP-induced platelet aggregation. The addition of 10 μM nitrofurantoin to citrated platelet-rich plasma obtained from 12 normal subjects produced a 29±6% (2 SD) inhibition of the velocity of platelet aggregation induced by 2 μM ADP. The inhibitory effect of nitrofurantoin demonstrated competitive kinetics in respect to ADP. The intravenous (180 mg) or oral (200 mg) administration of nitrofurantoin produced a serum nitrofurantoin concentration ranging from 2.7 to 23 μM in 28 normal subjects. Platelet-rich plasma obtained from these subjects demonstrated inhibition of the velocity of ADP-induced platelet aggregation that correlated with the log of the serum nitrofurantoin concentration (P < 0.001). Collagen-induced platelet aggregation was also inhibited in a dose-related manner, and the bleeding time was significantly prolonged in the two subjects with the highest serum nitrofurantoin concentration. These studies indicate that nitrofurantoin in vivo inhibits platelet function to a degree that is proportional to the serum nitrofurantoin concentration.
The Future Use of in Vitro Data in Risk Assessment to Set Human Exposure Standards: Challenging Problems and Familiar Solutions
Authors: Kenny S. Crump, Chao Chen, Thomas A. Louis
Journal: Environmental Health Perspectives (2010)

The vision of a National Research Council (NRC) committee (the Committee on Toxicity Testing and Assessment of Environmental Agents) for future toxicity testing involves the testing of human cells in in vitro assays for "toxicity pathways"--normal signaling pathways that when perturbed can lead to adverse effects. Risk assessments would eventually be conducted using mathematical models of toxicity pathways (TP models) to estimate exposures that will not cause biologically significant perturbations in these pathways.In this commentary we present our vision of how risk assessment to support exposure standards will be developed once a suitable suite of in vitro assays becomes available.Issues to be faced basing risk assessments on in vitro data are more complex than, but conceptually similar to, those faced currently when applying in vivo data. Absent some unforeseen technical breakthrough, in vitro data will be used in ways similar to current practices that involve applying uncertainty or safety factors to no observed adverse effect levels or benchmark doses. TP models are unlikely to contribute quantitatively to risk assessments for several reasons, including that the statistical variability inherent in such complex models severely limits their usefulness in estimating small changes in response, and that such models will likely continue to involve empirical modeling of dose responses.The vision of the committee predicts that chemicals will be tested more quickly and cheaply and that animal testing will be reduced or eliminated. Progress toward achieving these goals will be expedited if the issues raised herein are given careful consideration.
Adverse Events and Quadrivalent Human Papillomavirus Recombinant Vaccine
Authors: Vicky Debold
Journal: JAMA (2009)

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
An open-label phase 2 trial of entospletinib (GS-9973), a selective spleen tyrosine kinase inhibitor, in chronic lymphocytic leukemia
Authors: Jeff Sharman, Michael Hawkins, Kathryn Kolibaba, Michael Boxer, Leonard Klein, Meihua Wu, Jing Hu, Steve Abella, Chris Yasenchak
Journal: Blood (2015)
Presence of a non-HLA B cell antigen in rheumatic fever patients and their families as defined by a monoclonal antibody.
Authors: A K Khanna, D R Buskirk, R C Williams, A Gibofsky, M K Crow, A Menon, M Fotino, H M Reid, T Poon-King, P Rubinstein
Journal: Journal of Clinical Investigation (1989)

Numerous investigators have suspected that there is a genetic predisposition to rheumatic fever (RF). In this context we have recently produced a series of monoclonal antibodies directed against B cells obtained from RF patients one of which, labeled D8/17, identifies a B cell antigen present in 100% of all RF patients studied. While the highest percentage of positive cells were exhibited by RF probands (33.5% +/- SE), the percentage of cells in unaffected siblings and parents was 14.6 and 13%, respectively. The percentage of positive cells in APSGN probands, unaffected siblings, and parents was 2.96, 3.86, and 2.8%, respectively. A low level of B cells (5-7%) bearing the D8/17 marker was seen in control patients. The segregation pattern of the phenotypes defined by the percentage of D8/17 positive cells within HLA-typed RF families are consistent with an autosomal recessive mode of inheritance not associated with the human MHC system. We postulate that these phenotypes indicate the presence of at least one necessary genetic factor for susceptibility to RF.
THE POSSIBLE ROLE OF GENETIC VARIANTS IN PREDICTING ANTRACICLYNE-INDUCED CARDIOTOXICITY
Authors: Savina Nodari, Marco Triggiani, Martina Fragni, Graziella Bonetti, Vito Amoroso, Edda Lucia Simoncini, Annalisa Pizzuto, Ilaria Papa, Sara Capellini, Luca Ambrosiani, Sandra Sigala
Journal: Journal of the American College of Cardiology (2014)
Effects of ximelagatran, an oral direct thrombin inhibitor, r-hirudin and enoxaparin on thrombin generation and platelet activation in healthy male subjects
Authors: Troy C Sarich, Michael Wolzt, Ulf G Eriksson, Christer Mattsson, Alice Schmidt, Susanne Elg, Magnus Andersson, Maria Wollbratt, Gunnar Fager, David Gustafsson
Journal: Journal of the American College of Cardiology (2003)
Tacrolimus 0.1% ointment for seborrhoeic dermatitis: an open-label pilot study
Authors: T.J. Braza, J.B. DiCarlo, S.L. Soon, C.O. McCall
Journal: British Journal of Dermatology (2003)

Journal Article Tacrolimus 0·1% ointment for seborrhoeic dermatitis: an open‐label pilot study T.J. Braza, T.J. Braza Department of Dermatology, Emory University School of Medicine, Atlanta, GA, U.S.A Search for other works by this author on: Oxford Academic Google Scholar J.B. DiCarlo, J.B. DiCarlo Department of Dermatology, Emory University School of Medicine, Atlanta, GA, U.S.A Search for other works by this author on: Oxford Academic Google Scholar S.L. Soon, S.L. Soon Department of Dermatology, Emory University School of Medicine, Atlanta, GA, U.S.A Dr Seaver Soon. E‐mail: seaversoon@hotmail.com Search for other works by this author on: Oxford Academic Google Scholar C.O. McCall C.O. McCall Department of Dermatology, Emory University School of Medicine, Atlanta, GA, U.S.A Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 148, Issue 6, 1 June 2003, Pages 1242–1244, https://doi.org/10.1046/j.1365-2133.2003.05383.x Published: 01 June 2003 Article history Accepted: 01 January 2003 Published: 01 June 2003
Smoking reduction may lead to decreased lung cancer risk
Authors: D Rogers
Journal: Thorax (2005)

▴ Godtfredsen NS, Prescott E, Osler M. Effect of smoking reduction on lung cancer risk. JAMA2005;294:1505–10 [OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4] Since many smokers are unable or unwilling to totally quit smoking, the concept of harm reduction is raised. This study, with up to 31 years of follow up, studied the smoking habits of 11 151 men and 8563 women aged between 20 and 93 years. 864 cases of primary lung cancer occurred … [1]: {openurl}?query=rft.jtitle%253DJAMA%26rft.stitle%253DJAMA%26rft.issn%253D0002-9955%26rft.aulast%253DGodtfredsen%26rft.auinit1%253DN.%2BS.%26rft.volume%253D294%26rft.issue%253D12%26rft.spage%253D1505%26rft.epage%253D1510%26rft.atitle%253DEffect%2Bof%2BSmoking%2BReduction%2Bon%2BLung%2BCancer%2BRisk%26rft_id%253Dinfo%253Adoi%252F10.1001%252Fjama.294.12.1505%26rft_id%253Dinfo%253Apmid%252F16189363%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/external-ref?access_num=10.1001/jama.294.12.1505&link_type=DOI [3]: /lookup/external-ref?access_num=16189363&link_type=MED&atom=%2Fthoraxjnl%2F60%2F12%2F1058.atom [4]: /lookup/external-ref?access_num=000232113400020&link_type=ISI
Diagnosis and management of the antiphospholipid syndrome
Authors: D. Cohen, S. P. Berger, G. M. Steup-Beekman, K. W. M. Bloemenkamp, I. M. Bajema
Journal: BMJ (2010)

#### Summary points

Antiphospholipid syndrome was first described 27 years ago in patients with systemic lupus erythematosus (SLE) and positive anticardiolipin antibodies, who presented with a clotting syndrome that affected arteries and veins.1 Female patients had a high risk of recurrent miscarriage and late fetal loss. The international classification criteria for this syndrome used today are based on those initial clinical observations.2

The syndrome is under-recognised and underdiagnosed and can have devastating consequences if untreated, mainly because of uncontrolled thrombosis. Difficulties in diagnosis are compounded by a lack of standardisation of diagnostic tests. Early recognition is crucial, because treatment can reduce mortality and morbidity in relatively young people who often present with diseases such as stroke, myocardial infarction, and deep vein thrombosis.

Because of its variable clinical presentation, patients with antiphospholipid syndrome present to a variety of medical practitioners. Here, we introduce this complicated and intriguing syndrome, and provide basic guiding principles for the recognition, diagnosis, and management of affected patients.

#### Sources and selection criteria

We searched the following databases for evidence from systematic reviews, clinical trials, and prospective cohort studies: PubMed (1949 to January 2010), Embase (1980 to January 2010), Web of Science (1945 to January 2010), Cochrane Library (1990 to January 2010), CINAHL (1982 to January 2010), and Academic Search Premier (1865 to January 2010). All relevant keyword variations were used. In general, the …
Psychiatric Education in the Americas
Authors: EUGENE B. BRODY
Journal: American Journal of Psychiatry (1971)

Changing values regarding the delivery of reparative and preventive health services require increased social sensitivity as well as public health competence on the part of psychiatrists. These goals and more adequate behavioral science education for clinicians may be achieved by a program leading to an M.D. degree with a major in human behavior. Our lack of basic knowledge, however, makes it essential that additional qualified students be trained as psychiatric investigators via post-M.D. research oriented programs. This raises questions about diverse patterns of training and the development of different categories of psychiatric practitioners or specialists. The formulation of internationally recognized accrediting standards would facilitate the development of rational training sequences, reduce the brain drain from less to more industrialized nations, and produce competent psychiatrists whose credentials would be acceptable throughout the hemisphere.
The Relman Years at the Journal
Authors: Jerome P. Kassirer
Journal: New England Journal of Medicine (1991)

Arnold S. Relman, M.D., retired this week after 14 years as Editor-in-Chief of the New England Journal of Medicine. As he departs, the Journal is recognized as the leading general-interest medical journal and is widely acknowledged to be at the forefront of clinical medicine, health economics, medical ethics, and the legal aspects of medical practice. Because he won the respect, sometimes grudging, of economists, legislators, and policy makers with his incisive analyses of problems in their ostensibly exclusive domains, his personal influence extends far beyond the covers of the Journal.Numbers alone tell a story. The Journal now . . .