tbuckley/cabot-search huggingface dataset:
Effect of exercise induced hypoxaemia on myocardial repolarisation in severe chronic obstructive pulmonary disease
Authors: R. P Smith, M. K Johnson, J. Ashley, S. T Rudkin, R. J White
Journal: Thorax (1998)

<h3>BACKGROUND</h3> Exercise training is being promoted increasingly for patients with chronic obstructive pulmonary disease (COPD). Many of these patients experience exercise related arterial desaturation but the clinical importance of these hypoxaemic episodes is not known. QTc dispersion is a marker of myocardial repolarisation abnormalities and there has been much interest in its role as a non-invasive predictor of cardiac arrhythmias and sudden death. However, little is known about the dynamic effects that exercise and hypoxaemia have on QTc dispersion in patients with COPD. <h3>METHODS</h3> 20 patients with severe COPD (FEV<sub>1</sub> &lt;40% predicted) undertook two 15 minute treadmill tests at a speed calculated to produce a constant workload of 50% maximum oxygen consumption (Vo<sub>2</sub>max) during which they were blindly given either air or 35% oxygen in random order. Physiological measurements taken throughout exercise included 12 lead electrocardiograms from which QTc dispersion values were calculated according to standard criteria. Nine of the patients who desaturated with exercise were studied further. A similar degree of hypoxaemia was induced at rest by giving them a titrated mixture of air and oxygen and the changes in QTc dispersion were recorded. <h3>RESULTS</h3> 11 of the 20 patients developed significant hypoxaemia (desaturation by ⩾5% to &lt;90%) with exercise breathing air. There were no significant changes in QTc dispersion with either exercise or hypoxaemia. There were no significant changes in QTc dispersion when comparing those who did and did not desaturate, and those with and without a high baseline QTc dispersion values (60 ms). Induced hypoxaemia without exercise also failed to worsen QTc dispersion. <h3>CONCLUSIONS</h3> No evidence was found to suggest that exercise, even when associated with hypoxaemia, causes myocardial repolarisation abnormalities in patients with COPD.
Money and Career Choice
Authors: Robert Steinbrook
Journal: New England Journal of Medicine (1994)

Physicians' incomes are variously decried as contributing to high health care costs in the United States and championed as reasonable compensation for hard work, sobering responsibilities, and long years of training. The public perception is that many doctors earn too much. Yet the promise of a relatively secure financial future helps to attract many top college students to the profession. This infusion of talent contributes to medical progress and a high quality of care.Aggregate statistics on physicians' incomes hide the tremendous variations between specialists and primary care practitioners. In 1992 the median net income for physicians (after expenses but . . .
Different hepatitis C virus dynamics of free-virions and immune-complexes after initiation of interferon-α in patients with chronic hepatitis C
Authors: Naoki Fujita, Masahiko Kaito, Masaki Takeo, Shinichiro Horiike, Hideaki Tanaka, Jiro Ikoma, Shozo Watanabe, Yukihiko Adachi
Journal: Journal of Hepatology (2003)
Pyrimethamine, Sulfadiazine , and Villous Atrophy of the Jejunum
Authors: JAMES B. PUCKETT
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 March 1982Pyrimethamine, Sulfadiazine , and Villous Atrophy of the JejunumJAMES B. PUCKETT, M.D., M. ROBERT COOPER, M.D., JOHN J. STUART, M.D., WALLACE C. WU, M.B.B.S., J. MICHAEL STERCHI, M.D.JAMES B. PUCKETT, M.D.Search for more papers by this author, M. ROBERT COOPER, M.D.Search for more papers by this author, JOHN J. STUART, M.D.Search for more papers by this author, WALLACE C. WU, M.B.B.S.Search for more papers by this author, J. MICHAEL STERCHI, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-96-3-380_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Pyrimethamine and sulfadiazine are useful in treating ocular toxoplasmosis. We recently cared for a patient who was treated for ocular toxoplasmosis with pyrimethamine and sulfadiazine and developed scalp alopecia, bone marrow hypoplasia, and a malabsorption syndrome with total villous atrophy of the jejunum.A 28-year-old woman was treated in 1974 for occular toxoplasmosis with pyrimethamine and sulfadiazine and developed scalp alopecia and diarrhea that persisted for 1 month. In August 1979 she had increased activity of her ocular toxoplasmosis and again was treated with pyrimethamine and sulfadiazine. On the third day of therapy she developed fever, scalp...References1. SCHMIDTHUGHESSCHMIDT LHI. The pharmacological properties of 2,4-diamino-5-p-cholorphenyl-6-ethylpyrimidine (Daraprim). J Pharmacol Exp Ther. 1953;107:92-130. MedlineGoogle Scholar2. RYANHARTCULLIGANGUNKELJACOBSCOOK RWJRLM. Diagnosis and treatment of toxoplasmic uveitis. Trans Am Acad Opthalmol Otolaryngol. 1954;58:867-84. MedlineGoogle Scholar3. FAJARDOFURGIUELELEOPOLD RFI. Treatment of toxoplasmosis uveitis. Arch Opthalmol. 1962;67:712-20. CrossrefMedlineGoogle Scholar4. ROLLO I. Drugs used in the chemotherapy of malaria. In: GOODMAN LS, GILMAN A, eds. The Pharmacological Basis of Therapeutics. 5th ed. New York: MacMillan Publishing Co., Inc.; 1975:1045-58. Google Scholar5. WEINSTEIN L. Antimicrobial agents: sulfonamides and trimethoprim-sulfamethoxazole. In: GOODMAN LS, GILMAN A, eds. The Pharmacological Basis of Therapeutics. 5th ed. New York: MacMillan Publishing Co., Inc.; 1975:1113-29. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Bowman Gray School of Medicine Wake Forest University Winston-Salem, NC 27103 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByAgranulocytosis Associated with Maloprim: Review of Cases 1 March 1982Volume 96, Issue 3Page: 380-380KeywordsAtrophyBone marrowDiarrheaFeversHyperthermiaJejunumPyrimethamineToxoplasmosis Issue Published: 1 March 1982 PDF DownloadLoading ...
Possible mechanisms for a multiple-level model of evolution
Authors: H. C. Plotkin, F. J. Odling
Journal: Behavioral and Brain Sciences (1981)

Many of the commentaries cohere around two major points of criticism. The first is that we have omitted discussion of the mechanisms that are assumed to operate at levels 2, 3, and 4. Campbell, Cloak, Dewsbury, Eckberg, Mundinger, Pulliam, Richerson &amp; Boyd, Slobodkin, Simon, Williams , and Wahlsten all make comments that bear on this point. The second point is that we have omitted discussion of the fact that "organisms change the environment by their activities" ( Lewontin ) and thereby modify the selection pressures that act on them. Apart from Lewontin, this point has been raised in different forms by Barkow, Chase, Hull, Perzigian, Ruyle , and less directly by Slobodkin . Stemming from these two basic omissions there is a third general criticism. Numerous commentators have pointed out that we have failed to discuss sufficiently either the extent or nature of the constraints that may or may not be operating on supraordinate evolutionary processes as a function of their nested relationships to subordinate evolutionary processes within our scheme ( Barkow, Campbell, Cloak, Chase, Lenington, Lewontin, Perzigian, Peterson, Pulliam, Richerson &amp; Boyd, Simon, Slobodkin , and Williams ). We start by acknowledging these three basic omissions. We agree that they exist and that they are serious.
Sexually Transmitted Chlamydial Eye Infections Are Not Trachoma
Authors: Chandler R. Dawson
Journal: JAMA (1978)

The best known human chlamydial diseases include trachoma and lymphogranuloma venereum due to Chlamydia trachomatis strains and psittacosis (or ornithosis) due to avian C psittaci strains. Some C trachomatis strains are among the most common sexually transmitted human pathogens. 1-3 In men, this organism is the major identifiable cause of nongonococcal urethritis and has been associated with epididimytis; in women, it may cause cervicitis and acute salpingitis. 4-7 In newborns, acquired C trachomatis is a common cause of neonatal conjunctivitis and can produce pneumonia. 8,9   The association of chlamydiae with certain eye diseases (trachoma and adult and neonatal inclusion conjunctivitis) was recognized more than 60 years ago. Thus, as early as 1910, most of the epidemiology of C trachomatis infections involving the eye had been elucidated by ophthalmologists who recognized a pattern of eye-to-eye transmission with endemic trachoma and of sexually transmitted infection that occasionally led to the eye diseases
Health risks from increases in methylmercury exposure.
Authors: N K Mottet, C M Shaw, T M Burbacher
Journal: Environmental Health Perspectives (1985)

Our present knowledge of the human health effects of methylmercury exposure is derived from study of major outbreaks of human poisonings in Japan and Iraq and experimental studies on primates. Methylmercury readily passes through such physiological barriers as the blood-brain barrier, blood-testes barrier, and the placenta. Its major pathological effects are on the nervous and reproductive systems and the developing embryo/fetus. The neurotoxicity of methylmercury is well established in both humans and non-human primates. Lesions in the cerebral and cerebellar gray matter consist of necrosis and lysis of neurons, phagocytosis and gliosis. The changes are most prominent in the deep sulci and may have a vascular component. A late effect is cerebral atrophy. At high dose levels the liver, kidneys, and other organs may also have degenerative changes. Although not yet described in humans, a major effect of exposure of female primates is an adverse effect on pregnancy. Maternal female M. fascicularis blood mercury levels above 1 ppm are associated with a decreased pregnancy rate and increased abortion rate. To date our experimental data lack sufficient numbers to detect infrequent pregnancy effects below 1 ppm. Preliminary studies also reveal that methylmercury may also decrease the number and function (swim speed) of sperm. Both human and primate studies demonstrate deleterious effects of methylmercury on the developing embryo/fetus. Autopsies on human and primate infants reveal retarded brain development and the occurrence of a cerebral palsy-like behavior in the newborns, whereas the mother may be free of signs and symptoms of methylmercury toxicity. The fetal blood level of mercury is higher than the maternal level.(ABSTRACT TRUNCATED AT 250 WORDS)
Corporal Punishment in the Schools
Authors: David Orentlicher
Journal: JAMA (1992)

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
Contemporary management and recent advances in paediatric hydrocephalus
Authors: J. Kandasamy, M. D. Jenkinson, C. L. Mallucci
Journal: BMJ (2011)

#### Summary points 

The term hydrocephalus relates to an imbalance between the production and absorption of cerebrospinal fluid that may cause an increase in intracranial pressure. Rather than being a single pathological disease, hydrocephalus may be congenital or may arise secondary to intracranial haemorrhage, infection, or tumours.

Although some reports suggest the incidence of paediatric hydrocephalus has declined in many developed countries, others indicate increased rates because of improved survival of premature infants.1 2 3 4 High rates of neonatal infection and neural tube defects in developing countries are linked to higher rates of hydrocephalus than in the developed world. One prospective observational study of hydrocephalus in east Africa estimated more than 6000 new cases a year, and it continues to be a major source of morbidity and mortality.5

The management of hydrocephalus was revolutionised in the 1950s with the …
378 Efficacy of one year of specific immunotherapy (SIT) with an alginate conjugated parietaria officinalis (PO) extract in parietaria allergic rhinitis
Authors: C Ortolani, EA Pastorello, H Ispano, C Zara, L Farioli, M Fontana, A Sarassi, V Sillano, C Zanussi
Journal: Journal of Allergy and Clinical Immunology (1988)
De-escalation versus continuation of empirical antimicrobial treatment in severe sepsis: a multicenter non-blinded randomized noninferiority trial
Authors: Marc Leone, Carole Bechis, Karine Baumstarck, Jean-Yves Lefrant, Jacques Albanèse, Samir Jaber, Alain Lepape, Jean-Michel Constantin, Laurent Papazian, Nicolas Bruder, Bernard Allaouchiche, Karine Bézulier, François Antonini, Julien Textoris, Claude Martin
Journal: Intensive Care Medicine (2014)
Reactive Hyperemia in Arterioles and Capillaries of Frog Skeletal Muscle following Microocclusion
Authors: ROBERT M. GENTRY, PAUL C. JOHNSON
Journal: Circulation Research (1972)

We studied the localization of blood flow control in skeletal muscle by short-term microocclusions (30-60 seconds) of capillaries and arterioles of the pectoralis muscle in anesthetized frogs ( Rana pipiens ). The muscle was surgically exposed to permit transillumination and measurement of red cell velocity in the microvessels, but innervation and blood supply were kept intact. About one-third of the arterioles showed postocclusion hyperemia. In some muscles every arteriole showed hyperemia following occlusion, but in others none responded, presumably because of preparatory trauma. The average duration of hyperemia after a 1-minute occlusion was 74 ± 45 (SD) seconds. We also compared the effectiveness of arteriolar and capillary occlusions in producing reactive hyperemia in capillaries. Peak capillary blood flow after occlusion of the supply arteriole was 233% above control, and flow debt repayment was 278%. After occlusion of several capillaries, peak capillary blood flow was 67% above control, and flow debt repayment was 74%. In an individual capillary, peak blood flow after occlusion of that capillary was 15% above control, and flow debt repayment was 13%. In a majority of instances there was no discernible reactive hyperemia with single capillary occlusion. The results do not support the concept that flow in individual capillaries is regulated in accordance with each capillary's metabolic environment. Rather, flow in a capillary appears to depend on the metabolic environment of the arteriole supplying that capillary.
CELIPROLOL, BUT NOT ATENOLOL, REDUCES OXIDATIVE STRESS AND ATTENUATES CARDIAC REMODELING INDUCED BY INTERMITTENT HYPOXIA IN MICE
Authors: Atsuo Nomura, Satoshi Nishioka, Waka Uehashi, Ryuji Kato, Yoshikatsu Okada, Nobukazu Ishizaka, Yasuo Matsumura, Tetsuya Hayashi
Journal: Journal of the American College of Cardiology (2013)
Heterogeneity of Ryanodine Receptor Dysfunction in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia
Authors: Randall Loaiza, Nancy A. Benkusky, Patricia P. Powers, Timothy Hacker, Sami Noujaim, Michael J. Ackerman, José Jalife, Héctor H. Valdivia
Journal: Circulation Research (2012)

Rationale: Most cardiac ryanodine receptor (RyR2) mutations associated with catecholaminergic polymorphic ventricular tachycardia (CPVT) are postulated to cause a distinctive form of Ca 2+ release dysfunction. Considering the spread distribution of CPVT mutations, we hypothesized that dysfunctional heterogeneity also was feasible. Objective: To determine the molecular and cellular mechanisms by which a novel RyR2-V2475F mutation associated with CPVT in humans triggers Ca 2+ -dependent arrhythmias in whole hearts and intact mice. Methods and Results: Recombinant channels harboring CPVT-linked RyR2 mutations were functionally characterized using tritiated ryanodine binding and single-channel recordings. Homologous recombination was used to generate a knock-in mouse bearing the RyR2-V2475F mutation. Ventricular myocytes from mice heterozygous for the mutation (RyR2-V2475F +/− ) and their wild-type littermates were Ca 2+ -imaged by confocal microscopy under conditions that mimic stress. The propensity of wild-type and RyR2-V2475F +/− mice to have development of arrhythmias was tested at the whole heart level and in intact animals. Recombinant RyR2-V2475F channels displayed increased cytosolic Ca 2+ activation, abnormal protein kinase A phosphorylation, and increased activation by luminal Ca 2+ . The RyR2-V2475F mutation appears embryonic-lethal in homozygous mice, but heterozygous mice have no alterations at baseline. Spontaneous Ca 2+ release events were more frequent and had shorter latency in isoproterenol-stimulated cardiomyocytes from RyR2-V2475F +/− hearts, but their threshold was unchanged with respect to wild-type. Adrenergically triggered tachyarrhythmias were more frequent in RyR2-V2475F +/− mice. Conclusions: The mutation RyR2-V2475F is phenotypically strong among other CPVT mutations and produces heterogeneous mechanisms of RyR2 dysfunction. In living mice, this mutation appears too severe to be harbored in all RyR2 channels but remains undetected under basal conditions if expressed at relatively low levels. β-adrenergic stimulation breaks the delicate Ca 2+ equilibrium of RyR2-V2475F +/− hearts and triggers life-threatening arrhythmias.
Hemophagocytic lymphohistiocytosis in syntaxin-11–deficient mice: T-cell exhaustion limits fatal disease
Authors: Tamara Kögl, Jürgen Müller, Birthe Jessen, Annette Schmitt-Graeff, Gritta Janka, Stephan Ehl, Udo zur Stadt, Peter Aichele
Journal: Blood (2012)
Hepatofugal portal flow in cirrhosis: Observations on hepatic hemodynamics and the nature of the arterioportal communications
Authors: William G. Rector, John C. Hoefs, Kenneth F. Hossack, Gregory T. Everson
Journal: Hepatology (1988)

Six of 85 patients (7%) with alcoholic liver disease undergoing transhepatic portal pressure measurement had either stagnant (3 patients) or reversed (3 patients) portal blood flow documented by gentle hand injection of 1 to 2 ml of angiographic contrast. Portal blood flow was uniformly hepatopetal in 24 patients with nonalcoholic liver disease. Recurrent spontaneous hepatic encephalopathy and sodium retention occurred in 4 of 6 patients with stagnant or reversed portal flow; gastrointestinal bleeding was not seen. Standard laboratory tests of liver function were widely variable. Net portal pressure was lower in this group than in patients with alcoholic liver disease and forward portal flow (9.2 ± 2.6 vs. 15.6 ± 4.1 mm Hg, p &lt; 0.001). Wedged hepatic vein pressure was 1 to 7 mm Hg higher than portal vein pressure in patients with reversed portal flow. The arterioportal extraction of bile acid was calculated from the difference in concentration between artery and portal vein, and total functional hepatic blood flow was calculated from the hepatic extraction and systemic clearance of indocyanine green. Extraction was 0%, and hepatic blood flow was 0.469 liter per min in a patient with hepatofugal portal flow and recurrent encephalopathy. Extraction was 20%, and hepatic blood flow was 4.014 liters per min in a patient who had never had encephalopathy. These data indicate that arterioportal communications may be sinusoidal or presinusoidal in patients who lose forward portal flow and that the amount of flow in the arterioportal circuit, together with its efficiency, largely determine the clinical outcome.
David Heymann—WHO's public health guru
Authors: Haroon Ashraf
Journal: The Lancet Infectious Diseases (2004)

David Heymann is the Representative of the Director General for polio eradication at the WHO. Before that he was Executive Director of WHO's communicable diseases cluster, which includes WHO's programmes on infectious and tropical diseases, and he led the public-health response to severe acute respiratory syndrome (SARS) in 2003.
571. Increasing BMP Responsiveness in Human Mesenchymal Stem Cells In-Vitro by Delivery of the Osteoinductive LMP-1 Gene
Authors: Manjula Viggeswarapu, Maggie Bargouti, Mesfin Teklemariam, Chantrice Rogers, Liping Zhu, Nancy Baker, Louisa F. Titus, Scott D. Boden
Journal: Molecular Therapy (2006)

BMPs promote the differentiation of osteoprogenitor cells, and also induce osteogenesis in bone marrow stromal cells (MSCs) from rats and mice. However, compared to results with animal models, BMPs are relatively inefficient in inducing human MSCs to undergo osteogenesis, and are much less effective in promoting bone formation in human clinical trials. Previous studies indicated that, while human MSCs respond to Dex with elevated levels of the osteoblast marker alkaline phosphatase, most isolates of human MSCs fail to show alkaline phosphatase induction in response to BMP-2,|[minus]|4 and |[minus]|7. LIM Mineralization Protein-1 (LMP-1) is an intracellular regulatory protein that can induce the expression of multiple BMPs and promote osteoblast differentiation in vitro and in vivo. The purpose of this study was: 1) To determine if delivery of LMP-1 can increase the responsiveness of human MSCs to BMP-2 as evidenced by increasing osteoblastic markers, and 2) To determine if delivery of LMP-1 can potentiate BMP-2 induction of mineralization by human MSC cultures.
Progressive Multifocal Leukoencephalopathy — Progress Made and Lessons Relearned
Authors: John E. Greenlee
Journal: New England Journal of Medicine (1998)

Progressive multifocal leukoencephalopathy is an opportunistic demyelinating infection caused by a ubiquitous, usually nonpathogenic papovavirus known as JC virus. The symptoms and characteristic radiologic findings of progressive multifocal leukoencephalopathy are due to virus-induced lysis of oligodendrocytes, resulting in microscopic foci of myelin breakdown that coalesce to produce increasingly larger lesions.1 The virus also infects astrocytes, in which morphologic features develop that are suggestive of neoplasia, including mitotic figures and multinucleated forms.Progressive multifocal leukoencephalopathy is a disease of immunosuppressed patients. The disease was initially identified by Aström and colleagues as a rare complication of chronic lymphocytic leukemia and Hodgkin's disease. . . .