tbuckley/cabot-search huggingface dataset:
Epidemic of Pulmonary Tuberculosis in a Closed Community
Authors: C. Protheroe
Journal: BMJ (1957)

The first scientific study of the epidemiology of tuber- culosis was made by Villemin in 1868.He stressed the high incidence of the disease among those living in closed communities, such as prisoners, inmates of mental institutions, soldiers, and religious bodies.Tuberculosis among troops living in barracks was very common com- pared with those in the field or those living at home.He -quoted, as an example, the Allied armies before Sebasto- pol during the winter of 1854-5.Although these troops were living under most unhygienic conditions, with poor food, and subjected to severe cold and excessive fatigue,
German union threatens strike over doctors' long hours
Authors: Jane Burgermeister
Journal: BMJ (2004)

A dispute over doctors' working hours in hospitals in Germany is escalating, after the county's largest union of doctors warned that it would take strike action unless hospitals implemented an EU court ruling to cut doctors' working hours.

The Marburger Union—which represents 80 000 of the 122 000 clinical doctors in Germany—said that doctors are still working up to 80 hours a week in hospitals despite a ruling by the European Court, which was incorporated into German law and which required doctors' working hours to be …
Israel's health minister stuns experts by ending mandatory fluoridation
Authors: J. Siegel-Itzkovich
Journal: BMJ (2014)

<h3>Objective</h3> Hepatitis D virus (HDV) is a circular RNA virus coinfecting hepatocytes with hepatitis B virus. Chronic hepatitis D results in severe liver disease and an increased risk of liver cancer. Efficient therapeutic approaches against HDV are absent. <h3>Design</h3> Here, we combined an RNAi loss-of-function and small molecule screen to uncover host-dependency factors for HDV infection. <h3>Results</h3> Functional screening unravelled the hypoxia-inducible factor (HIF)-signalling and insulin-resistance pathways, RNA polymerase II, glycosaminoglycan biosynthesis and the pyrimidine metabolism as virus-hepatocyte dependency networks. Validation studies in primary human hepatocytes identified the carbamoyl-phosphatesynthetase 2, aspartate transcarbamylase and dihydroorotase (CAD) enzyme and estrogen receptor alpha (encoded by <i>ESR1</i>) as key host factors for HDV life cycle. Mechanistic studies revealed that the two host factors are required for viral replication. Inhibition studies using N-(phosphonoacetyl)-L-aspartic acid and fulvestrant, specific CAD and ESR1 inhibitors, respectively, uncovered their impact as antiviral targets. <h3>Conclusion</h3> The discovery of HDV host-dependency factors elucidates the pathogenesis of viral disease biology and opens therapeutic strategies for HDV cure.
Adding age and genetic risk to PSA test could improve screening for prostate cancer
Authors: Z. Kmietowicz
Journal: BMJ (2012)

Targeting tests for prostate cancer at the men most likely to develop the disease could halve the number needed to be screened, reduce overdiagnosis, and potentially save the NHS millions of pounds, suggests research.

With funding from Cancer Research UK, researchers from London and Cambridge developed a model to estimate the cost and quality adjusted life years (QALYs) of a personalised screening programme compared with an age based screening strategy using data from English cancer registries and the ProtecT study (http://www.hta.ac.uk/1230) into the treatments for clinically localised prostate cancer.

Both strategies used the prostate specific antigen test …
Abstract 208: Metformin represses stem cell properties and induces apoptosis in human breast cancer cells and mouse mammary epithelial cells
Authors: Eun Joo Kang, Jae Hong Seo, Jun Suk Kim, Ji Young Kim
Journal: Cancer Research (2014)

Abstract Cancer stem cells (CSCs) are small portions of cancer cells that have important self-renewal and proliferation characteristics, and therefore, they play a significant role in cancer development and metastasis. Recently, several studies have revealed CSCs of several solid tumors. The identification and targeting of CSCs are expected to advance treatment outcomes, but until now, only a few drugs that specifically target CSCs have been developed. Metformin, an antidiabetic drug used for the treatment of type 2 diabetes mellitus, suppresses gluconeogenesis in the liver and increases insulin sensitivity and glucose uptake in peripheral tissues such as muscles. Moreover, the drug has shown an anti-cancer effect by inhibiting cellular proliferation and protein synthesis in several cancer cell lines. Additionally, many clinical and epidemiological studies have suggested that metformin might be associated with a decreased risk of cancer development and an increased response to chemotherapy. In addition to its anticarcinogenic effect, studies about the anti-cancer stem cell effect of metformin have been recently reported. Several reports revealed that metformin could preferentially kill cancer stem cells, including breast cancer stem cells. However, the mechanism of anti-cancer stem cell activity is not well known. Therefore, this study was planned to confirm the cytotoxicity of metformin, especially for breast cancer stem cells as well as breast cancer cells. To this end, several human breast cancer cell lines and normal mouse mammary epithelial cell lines were used. In this study, metformin showed cell growth inhibition in human breast cancer cells and mouse mammary epithelial cells by inducing cell cycle arrest and apoptosis. Moreover, metformin specifically killed breast cancer stem cells. Metformin showed reduced mammosphere formation in all cell lines. In addition, decreasing breast cancer stem cell population by metformin treatment was identified through FACS analysis. For the mechanism of anti-cancer stem cell activity, western blot assay was performed. We identified decreased levels of cyclin D and cycline E and increased levels of Bax in secondary mammaospheres according to metformin treatment. In conclusion, this present study show that metformin kills breast cancer stem cells as well as breast cancer cells, and these phenomena occur by the induction of cell cycle arrest and apoptosis. Citation Format: Eun Joo Kang, Jae Hong Seo, Jun Suk Kim, Ji Young Kim. Metformin represses stem cell properties and induces apoptosis in human breast cancer cells and mouse mammary epithelial cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 208. doi:10.1158/1538-7445.AM2014-208
Altered protein expression profile associated with phenotypic changes in lung fibroblasts co-cultured with gold nanoparticle-treated small airway epithelial cells
Authors: Cheng-Teng Ng, Lin-Yue Lanry Yung, Hannah Lee-Foon Swa, Rebecca Wan-Yan Poh, Jayantha Gunaratne, Boon-Huat Bay
Journal: Biomaterials (2014)
Obstetric care must change if Netherlands is to regain reputation for safe childbirth
Authors: Tony Sheldon
Journal: BMJ (2008)

<h3>Background</h3> Allostatic load, a measure of early ageing or ‘wear and tear’ from adapting to environmental challenges, has been suggested as a framework with which to understand the stress-related disruption of multiple biological systems which may be linked to asthma. Considering the socioeconomic context is also critical given asthma and allostatic overload are more common in lower socioeconomic groups. <h3>Aims</h3> Estimate the relationship between allostatic load and its constituent biomarkers, asthma and corticosteroid prescribing while controlling for socioeconomic status. <h3>Methods</h3> Data from <i>Understanding Society</i> (a nationally representative survey of UK community-dwelling adults) waves 1–3 (2009–2012) allowed the identification of a sex-specific risk profile across 12 biomarkers used to construct an Allostatic Load Index for a sample of 9816 adults. Regression analyses were used to examine the association of asthma status and corticosteroid prescriptions with allostatic load and its constituent biomarkers while controlling for socioeconomic status (n=9805). <h3>Results</h3> Subjects with currently treated asthma and no corticosteroid prescription have an allostatic load 1.21 times higher than those without asthma (p&lt;0.001). Asthmatic subjects in receipt of inhaled corticosteroids had an allostatic load, approximately 1.12 times higher than those without asthma (p&lt;0.001). This association persisted in sensitivity analyses and appeared to be driven by an association with specific biomarkers (dehydroepiandrosterone-sulfate, waist-to-height ratio and C-reactive protein). <h3>Conclusion</h3> Early ageing, in the form of a higher allostatic load, was present even in the mildest asthma group not receiving inhaled corticosteroids. Allostatic load is helpful in understanding the increased all-cause mortality and multimorbidity observed in asthma.
344 PROTECTIVE EFFECT OF BILIVERDIN AND BILIVERDIN REDUCTASE AGAINST BILE ACID-INDUCED TOXICITY IN LIVER CELLS
Authors: E. Gonzalez-Sanchez, M.J. Perez, N.S. Nytofte, O. Briz, M.A. Serrano, M.J. Monte, F. Jimenez, F. Gonzalez-San Martin, J.J.G. Marin
Journal: Journal of Hepatology (2012)
Handbook of Human Immunology
Authors: Roshini S. Abraham
Journal: JAMA (2008)

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
Expression and localization of inducible and endothelial nitric oxide synthase in the rat ovary. Effects of gonadotropin stimulation in vivo.
Authors: B J Van Voorhis, K Moore, P J Strijbos, S Nelson, S A Baylis, D Grzybicki, C P Weiner
Journal: Journal of Clinical Investigation (1995)

Nitric oxide is reportedly involved in the regulation of several ovarian processes, yet the isoforms of nitric oxide synthase (NOS) expressed in the ovary are unknown. Our purpose was to identify and localize NOS isoenzymes in the rat ovary and to examine++ if mRNA expression of NOS isoenzymes change after gonadotropin stimulation. Using reverse transcriptase-PCR, we demonstrated that inducible (iNOS) and endothelial (eNOS), but not neuronal, NOS mRNAs are expressed in the ovary. In a gonadotropin-stimulated rat model, unstimulated ovaries had the highest levels of iNOS mRNA as quantified by ribonuclease protection assay. After gonadotropin injection, iNOS mRNA declined to undetectable levels in ovaries containing ovulatory follicles before increasing slighty in ovaries containing copora lutea. In situ hybridization studies localized iNOS to granulosa cells of secondary follicles and small antral follicles. Western blots of unstimulated ovaries demonstrated iNOS protein. In contrast to iNOS, eNOS mRNA levels, determined by quantitative PCR, increased after gonadotropin stimulation and peaked in ovaries containing ovulatory follicles before declining in the luteal phase. eNOS protein was localized to blood vessels in the ovary by immunohistochemistry. We conclude that two isoforms of NOS are expressed in the ovary and the mRNA levels for these isozymes are differentially regulated.
An evolution of professionalism
Authors: Andrew Vallance-Owen
Journal: Journal of the Royal Society of Medicine (2011)

I would agree with the components of the current preferred model of new professionalism1 outlined by Dr Stanton et al., but I believe there is something missing when they talk about accountability. They cover the dynamic between patients and professionals and the benefit of assuming a stronger sense of responsibility for the ways in which the wider health system works, but they seem to miss a fundamental plank of professionalism which is accountability to and for your peers.

For my part, I feel it is vital that the profession is seen to tackle issues apparent in its own back yard. Revalidation, rightly in my view, is going to depend absolutely on annual appraisal, hopefully whole practice appraisal to cover all aspects of a doctor's practice (NHS and/or private). If appraisal is really going to work to protect patients and encourage continuous quality improvement, then it must be a rigorous and fair peer review. As soon as a doctor with doubtful data or unanswered issues is ‘let off the hook’, the appraiser has failed in that accountability, both to peers and public. It is a big responsibility, but surely crucial to be carried out consistently and effectively if we are to maintain our independence as a profession.

An area which might be tackled via appraisal, but which professionals need to be aware of between appraisals, is significant unwarranted variation (particularly outliers, say outside three standard deviations from the mean). I was talking to an orthopaedic audience recently and used the example of knee arthroscopy for osteoarthritis, for which there is almost no evidence of effectiveness in the absence of mechanical locking. To be fair, they were astounded when I told them about the thousands of knee arthroscopies that health insurers pay for per annum; that the rate in private practice was substantially more than the rate in the NHS and that we knew of one orthopaedic surgeon who was probably doing around 2000 a year overall in his private practice. The point I was making was that in this, and multiple other situations in both public and private sectors, professional colleagues often sense where there are elements of poor practice and, as clinical data feedback improves, outliers in local clinical practice will now be increasingly exposed; so, it must surely be up to the profession to tackle these issues because, if they don't, others (e.g. health insurers) will which, while it may protect patients, will undermine professionalism, old or new … but, sadly, the professionals will only have themselves to blame.
LOW AMPLITUDE VAGUS NERVE STIMULATION AFFECTS HEART RATE AND NEUROHORMONES IN HUMANS
Authors: Katherine Fan, Raymond Yee, Lorna Gula, Cathy Bentley, Avram Scheiner, Sum Lam, Macrina Wong, Maria Parke, Ruth Nicholson Klepfer, Allan Skanes
Journal: Journal of the American College of Cardiology (2010)
MORBILLIFORM ERUPTION FOLLOWING USE OF SULFAGUANIDINE
Authors: Robert Turell
Journal: JAMA (1942)

The occurrence of dermatitis following sulfaguanidine therapy has apparently not yet been recorded. This report deals with a patient who had a generalized morbilliform eruption which appeared about sixteen days after the institution of sulfaguanidine therapy but who had previously been treated with sulfanilamide, sulfathiazole and sulfadiazine without cutaneous complications. <h3>REPORT OF CASE</h3> A white woman aged 40 was first seen on Jan. 21, 1941 at which time a diagnosis of nonspecific ulcerative colitis was made. One week later she was sent to the Mount Sinai Hospital where 1 Gm. of sulfathiazole in suspension was given every four hours by rectum. After a total of 42 Gm. had been administered there was only a trace of sulfathiazole in each 100 cc. of blood. The patient, however, made a good temporary recovery, as evidenced by the clinical course and sigmoidoscopic studies. Because of a recurrence of the colitis, the patient reentered
Cardiac Hypertrophy and Reduced Contractility in Hearts Deficient in the Titin Kinase Region
Authors: Jun Peng, Katy Raddatz, Jeffery D. Molkentin, Yiming Wu, Siegfried Labeit, Henk Granzier, Michael Gotthardt
Journal: Circulation (2007)

Background— Titin is a giant protein crucial for the assembly and elasticity of the sarcomere. Recently, titin has been linked to signal transduction through its kinase domain, which has been proposed to sense mechanical load. We developed a knockout in which expression of M-line–deficient titin can be induced in adult mice and investigated the role of the titin kinase region in cardiac function. Methods and Results— Isolated heart experiments revealed that in titin M-line–deficient mice, the contractile response to β-adrenergic agonists and extracellular calcium is reduced. However, the Ca 2+ sensitivity and cooperativity of activation of skinned cardiac muscle were unchanged. In knockout mice, calcium transients showed a reduced rate of calcium uptake, and expression analysis showed reduced levels of calmodulin, phospholamban, and SERCA2. Ultimately, knockout mice developed cardiac hypertrophy and heart failure, which involves protein kinase C signal transduction but not the mitogen-activated protein kinase pathway. Conclusions— The titin kinase region emerges as a regulator of contractile function through effects on calcium handling and hypertrophy through protein kinase signal transduction. These novel functions of titin might provide a rationale for future therapeutic approaches to attenuate or reverse symptoms of heart failure.
Postoperative deep vein thrombosis in Nigerians on high-fibre diets.
Authors: C Latto
Journal: BMJ (1979)

capsid antigen.The IgM titre was screened routinely at 1/8 but no further dilutions were assayed.The discrepancy in the titres re- ported from Manchester and Colindale on roughly contemporaneous samples can only be attributed to methodological differences.Antibodies to cytomegalovirus were de- tected in the laboratory of Professor Harold Stern, St George's Hospital Medical School, using complement fixation as stated in our article.Numerous attempts were made to isolate this virus from the patient's urine but without success.Because of limitations of space, we could only summarise the serological data in our article and we could not fully discuss the diagnostic possibilities.We agree that one cannot be dogmatic about the nature of this patient's illness.It is our belief that the most likely explanation is that she had a primary infection with EB virus to which she was unable to make an adequate immunological response.Indeed, the antibody titres to cyto- megalovirus may be attributable to cross- reaction of antibody between this virus and EB virus.'However, we agree that we cannot exclude the possibility that this patient had a double infection with both viruses and that the impaired response to EB virus reflects the immunosuppression induced by cytomegalovirus.
The Literature of Medicine: Reviews and Notes: Ethics in Clinical Practice: Author's Name
Authors: Howard B. Burchell
Journal: Annals of Internal Medicine (1995)

Corrections1 August 1995The Literature of Medicine: Reviews and Notes: Ethics in Clinical Practice: Author's NameFREEHoward B. BurchellHoward B. BurchellSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-3-199508010-00023 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In a recent book review, the name of the first author of Ethics in Clinical Practice was incorrectly given as J. C. Aronheim. The correct name is J. C. Ahronheim.REFERENCE1. Burchell HB. Review of Ethics in Clinical Practice. Ann Intern Med. 1995; 122:320. Google Scholar Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 August 1995Volume 123, Issue 3Page: 238 ePublished: 15 August 2000 Issue Published: 1 August 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Serum Creatine Phosphokinase in Leptospirosis
Authors: Warren D. Johnson
Journal: JAMA (1975)

Serum creatine phosphokinase (CPK) and serum glutamic oxaloacetic and pyruvic transaminase (SGOT, SGPT) levels were determined in 61 patients with leptospirosis and 16 with viral hepatitis during the acute phase of illness. The CPK value was elevated in 29 leptospirosis patients and normal in all 16 hepatitis patients. Conversely, mean SGOT and SGPT levels were lower in leptospirosis patients. The CPK determination is a simple test that may provide diagnostic information in a jaundiced patient, particularly when characteristic manifestations of leptospirosis are absent. The pattern of greatly elevated CPK levels with only modest elevations in transaminase values in an acutely jaundiced patient should strongly suggest a diagnosis of leptospirosis.
Tacrolimus (FK506) ointment for atopic dermatitis: A phase I study in adults and children
Authors: Samer Alaiti, Sewon Kang, Virginia C. Fiedler, Charles N. Ellis, David V. Spurlin, Darrell Fader, Grigoriy Ulyanov, Shrikant D. Gadgil, Atsushi Tanase, Ira Lawrence, Patricia Scotellaro, Kathleen Raye, Ihor Bekersky
Journal: Journal of the American Academy of Dermatology (1998)
Binding to Cysteinyl-Leukotriene Receptors
Authors: SIMONETTA NICOSIA, VALÉRIE CAPRA, SAULA RAVASI, G. ENRICO ROVATI
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

It is widely accepted that leukotrienes (LTs) exert their actions through high-affinity specific receptors, although only the LTB 4  receptor has been cloned so far (1). Given the differences between the two classes of LTs (LTB 4  versus LTC 4 , LTD 4 , and LTE 4 , i.e., cysteine-containing leukotrienes or cysteinyl-LTs) in terms of both structure and profile of biological activity, it is not unexpected that the receptors for LTB 4  are totally different from those for cysteinyl-LTs and no cross-reactivity has been shown among the two classes. The first hint of the existence of leukotriene receptors had been given even before their structure had been elucidated. FPL-55712 had been proposed as an antagonist of slow-reacting substance of anaphylaxis (SRS-A) when it was not yet known that the latter was composed mainly of LTs (2). Subsequently, the recognition of strict structural requirements for LT action (3, 4), their high potency (in the nanomolar range), and the development of a number of specific antagonists (5) made it clear that these lipid mediators elicit their biological actions through specific receptors. The existence of different classes of Cys-LT receptors in human tissues is the subject of this article. Cysteinyl-LTs have been recognized to play a key role in asthma (6), and, as a consequence, the large majority of studies aimed at the characterization of their receptors have been performed in the respiratory system. Asthma is a multifactorial disease, characterized by the presence of reversible airway obstruction, inflammation, and hyperresponsiveness (7). The most significant discovery in the more recent research on asthma pathophysiology has been the revelation that airway inflammation is the key component of this condition. Of the different mediators that are known to be involved in asthma, leukotrienes are considered to be among the most important because they participate both in bronchoconstriction and in the inflammatory component of this disease.