tbuckley/cabot-search huggingface dataset:
Bacillary angiomatosis in an HIV seronegative patient on systemic steroid therapy
Authors: R.A. SCHWARTZ, M.A. GALLARDO, R. KAPILA, P. GASCON, J. HERSCU, J. SFEGHL, W.C. LAMBERT
Journal: British Journal of Dermatology (1996)

Journal Article Bacillary angiomatosis in an HIV seronegative patient on systemic steroid therapy Get access R.A. SCHWARTZ, R.A. SCHWARTZ Dermatology, Pathology, Infectious Diseases, Hematology, and preventive Medicine. UMD‐New Jersey Medical School, Newark, New Jersy and Medicine, Bayonne, New Jersey, U.S.A. Prof. R.A. Schwartz. Dermatology. New Jersy Medical School, 185 South Orange Avenue. Newark, New Jersey 07105‐2714, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar M.A. GALLARDO, M.A. GALLARDO Dermatology, Pathology, Infectious Diseases, Hematology, and preventive Medicine. UMD‐New Jersey Medical School, Newark, New Jersy and Medicine, Bayonne, New Jersey, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar R. KAPILA, R. KAPILA Dermatology, Pathology, Infectious Diseases, Hematology, and preventive Medicine. UMD‐New Jersey Medical School, Newark, New Jersy and Medicine, Bayonne, New Jersey, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar P. GASCON, P. GASCON Dermatology, Pathology, Infectious Diseases, Hematology, and preventive Medicine. UMD‐New Jersey Medical School, Newark, New Jersy and Medicine, Bayonne, New Jersey, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar J. HERSCU, J. HERSCU Dermatology, Pathology, Infectious Diseases, Hematology, and preventive Medicine. UMD‐New Jersey Medical School, Newark, New Jersy and Medicine, Bayonne, New Jersey, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar J. SFEGHL, J. SFEGHL Dermatology, Pathology, Infectious Diseases, Hematology, and preventive Medicine. UMD‐New Jersey Medical School, Newark, New Jersy and Medicine, Bayonne, New Jersey, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar W.C. LAMBERT W.C. LAMBERT Dermatology, Pathology, Infectious Diseases, Hematology, and preventive Medicine. UMD‐New Jersey Medical School, Newark, New Jersy and Medicine, Bayonne, New Jersey, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 135, Issue 6, 1 December 1996, Pages 982–987, https://doi.org/10.1046/j.1365-2133.1996.d01-1107.x Published: 01 December 1996 Article history Accepted: 15 April 1996 Published: 01 December 1996
Maximum-Likelihood Inference of Population Size Contractions from Microsatellite Data
Authors: Raphaël Leblois, Pierre Pudlo, Joseph Néron, François Bertaux, Champak Reddy Beeravolu, Renaud Vitalis, François Rousset
Journal: Molecular Biology and Evolution (2014)

Understanding the demographic history of populations and species is a central issue in evolutionary biology and molecular ecology. In this work, we develop a maximum-likelihood method for the inference of past changes in population size from microsatellite allelic data. Our method is based on importance sampling of gene genealogies, extended for new mutation models, notably the generalized stepwise mutation model (GSM). Using simulations, we test its performance to detect and characterize past reductions in population size. First, we test the estimation precision and confidence intervals coverage properties under ideal conditions, then we compare the accuracy of the estimation with another available method (MSVAR) and we finally test its robustness to misspecification of the mutational model and population structure. We show that our method is very competitive compared with alternative ones. Moreover, our implementation of a GSM allows more accurate analysis of microsatellite data, as we show that the violations of a single step mutation assumption induce very high bias toward false contraction detection rates. However, our simulation tests also showed some limits, which most importantly are large computation times for strong disequilibrium scenarios and a strong influence of some form of unaccounted population structure. This inference method is available in the latest implementation of the MIGRAINE software package.
Shortened Ca <sup>2+</sup> Signaling Refractoriness Underlies Cellular Arrhythmogenesis in a Postinfarction Model of Sudden Cardiac Death
Authors: Andriy E. Belevych, Dmitry Terentyev, Radmila Terentyeva, Hsiang-Ting Ho, Inna Gyorke, Ingrid M. Bonilla, Cynthia A. Carnes, George E. Billman, Sandor Györke
Journal: Circulation Research (2012)

Rationale: Diastolic spontaneous Ca 2+ waves (DCWs) are recognized as important contributors to triggered arrhythmias. DCWs are thought to arise when [Ca 2+ ] in sarcoplasmic reticulum ([Ca 2+ ] SR ) reaches a certain threshold level, which might be reduced in cardiac disease as a consequence of sensitization of ryanodine receptors (RyR2s) to luminal Ca 2+ . Objective: We investigated the mechanisms of DCW generation in myocytes from normal and diseased hearts, using a canine model of post–myocardial infarction ventricular fibrillation (VF). Methods and Results: The frequency of DCWs, recorded during periodic pacing in the presence of a β-adrenergic receptor agonist isoproterenol, was significantly higher in VF myocytes than in normal controls. Rather than occurring immediately on reaching a final [Ca 2+ ] SR , DCWs arose with a distinct time delay after attaining steady [Ca 2+ ] SR in both experimental groups. Although the rate of [Ca 2+ ] SR recovery after the SR Ca 2+ release was similar between the groups, in VF myocytes the latency to DCWs was shorter, and the [Ca 2+ ] SR at DCW initiation was lower. The restitution of depolarization-induced Ca 2+ transients, assessed by a 2-pulse protocol, was significantly faster in VF myocytes than in controls. The VF-related alterations in myocyte Ca 2+ cycling were mimicked by the RyR2 agonist, caffeine. The reducing agent, mercaptopropionylglycine, or the CaMKII inhibitor, KN93, decreased DCW frequency and normalized restitution of Ca 2+ release in VF myocytes. Conclusions: The attainment of a certain threshold [Ca 2+ ] SR is not sufficient for the generation of DCWs. Postrelease Ca 2+ signaling refractoriness critically influences the occurrence of DCWs. Shortened Ca 2+ signaling refractoriness due to RyR2 phosphorylation and oxidation is responsible for the increased rate of DCWs observed in VF myocytes and could provide a substrate for synchronization of arrhythmogenic events at the tissue level in hearts prone to VF.
GMP-17-positive T-lymphocytes in renal tubules predict progression in early stages of IgA nephropathy
Authors: L.A. van Es, E. de Heer, L.J. Vleming, A. van der Wal, M. Mallat, I. Bajema, J.A. Bruijn, J.W. de Fijter
Journal: Kidney International (2008)
Remarkable leukemogenic potency and quality of a constitutively active neurotrophin receptor, ΔTrkA
Authors: J Meyer, M Rhein, B Schiedlmeier, O Kustikova, C Rudolph, K Kamino, T Neumann, M Yang, A Wahlers, B Fehse, G W Reuther, B Schlegelberger, A Ganser, C Baum, Z Li
Journal: Leukemia (2007)
Public Health Surveillance for Hereditary Hemochromatosis
Authors: Scott F. Wetterhall
Journal: Annals of Internal Medicine (1998)

The recent realization that hemochromatosis is a common condition has created opportunities to develop unified public health surveillance for this disorder and its complications and to design programs to prevent unnecessary illness and death resulting from this disorder.Public health surveillance for hemochromatosis can be used to measure the magnitude of the problem (for example, to establish the number of persons with evidence of early iron overload); identify research needs; reveal the natural history of the disease; detect changes in health care practices, such as use of screening tests; and evaluate interventions, such as phlebotomy. Existing surveillance has been limited to periodic measurement of morbidity and mortality done by using hospital discharge records, health examination surveys, vital statistics, and data from small research registries. The improvement of surveillance will entail the ongoing collection of information from population-based surveys, such as the Behavioral Risk Factor Surveillance System; the collection of data on provider practices (for example, through the National Ambulatory Medical Care Survey); and the establishment of population-based registries. Creating population-based registries requires consensus on case definitions; strategies to encourage case ascertainment and reporting; policies and procedures for protecting privacy and ensuring confidentiality; and partnerships among providers, researchers, and public health officials. Longitudinal data from population-based registries will provide insight into determinants of disease expression, such as pattern or degree of iron overload. This information is critical for developing evidence-based recommendations for population screening, monitoring changes in medical practices, and assessing the effect of preventive measures.
Human Monoclonal Autoantibodies That React with Multiple Endocrine Organs
Authors: Jo Satoh, Bellur S. Prabhakar, Martin V. Haspel, Fredda Ginsberg-Fellner, Abner L. Notkins
Journal: New England Journal of Medicine (1983)

MANY human diseases have an autoimmune component. In some, such as myasthenia gravis1 and Hashimoto's thyroiditis,2 the autoimmune response is predominantly organ-specific. In other diseases, such as systemic lupus erythematosus3 and polyendocrinopathy,4 5 6 the autoimmune response is very broad, involving several different organs. For example, in patients with polyendocrine diseases, autoantibodies have been found that react with the pancreas, thyroid, pituitary, and gastric mucosa.4 5 6 Because of the low titers of these autoantibodies, as well as the polyclonality of serum, it has been difficult to determine whether there is a variety of autoantibodies, each reacting with a different organ, or whether the . . .
Early Insulin Therapy for Type 2 Diabetic Patients: More Cost Than Benefit
Authors: Mayer B. Davidson
Journal: Diabetes Care (2005)

Let me start by summarizing what we (think we) know and don’t know that pertains to this issue. In the mid-1960s (when I was a fellow), the conventional wisdom was that the complications of diabetes were unrelated to glycemic control; they were genetically determined. Therefore, the clinical goal was simply to keep diabetic patients asymptomatic. Fifteen years later, animal and some retrospective human studies convinced some (1) that near euglycemia would have a beneficial effect on diabetes complications. Controversy surrounding this issue raged until the results of the Diabetes Control and Complications Trial (DCCT) were published (2). Some controversy remained regarding extending the DCCT results to type 2 diabetes (3,4), but with the publication of the U.K. Prospective Diabetes Study (UKPDS) (5,6), the beneficial effects of near euglycemia on microvascular complications were irrefutably established for both type 1 and type 2 diabetic patients. In the past decade, five studies evaluating >2,000 patients with both type 1 (7–9) and type 2 (10,11) diabetes over 6–9 years have demonstrated that development or progression of retinopathy and microalbuminuria were minimal or absent if A1C levels were maintained below 7%, increased only slightly if A1C levels were between 7 and 8%, but increased markedly at values exceeding 8%.

It is important to distinguish between the micro- and macrovascular complications when considering the impact of near euglycemia on diabetes complications because they are often lumped together in arguments for tight control. The relationship between glycemia …
Prophylaxis Against Deep-Vein Thrombosis-Reply
Authors: Graham A. Colditz
Journal: JAMA (1988)

In Reply.  —We are sorry to learn of Lotke and Day's distress about our recent study of the cost-effectiveness of prophylaxis against DVT in orthopedic surgery, in which we reported that such measures can save both lives and health care dollars. They raise a number of issues that we address in turn below.  Was our analysis based only on information concerning the effectiveness of prophylaxis against calf-vein thrombi? As reported, we based our analysis on all reports of randomized, controlled trials of DVT prophylaxis in orthopedic surgery that were published between January 1976 and June 1984. We are unaware of any data that should have been included in our analysis but were not. In these trials, separate rates for proximal- and distal-vein thrombi usually are not reported. Trials that do report both rates, however, indicate comparable reductions in both calf and femoral DVT among patients receiving prophylaxis. 1   Are calf-vein
Seen and not heard
Authors: S. Kumar
Journal: BMJ (2003)

<i>Sanjay Kumar interviews Dr Arun Bal, patients9 rights campaigner in Mumbai, India, who is a founder member and former president of the Association for Consumers9 Action on Safety and Health (ACASH), founder member of the Forum for Medical Ethics, and former editor of <i>Issues in Medical Ethics</i>. After qualifying in surgery, Dr Bal entered private practice in 1977 and for 18 years (1979 to 1996) regularly provided his surgical skills in areas of rural India. Specialising in the diabetic foot for the past 15 years, he is president of the Diabetic Foot Society of India</i>
Phantom breast sensations
Authors: D. J T Webster, E. Jones
Journal: BMJ (1981)

and increasing numbers of students denied university places, no arguments can justify spending £15m of public money in this way, to say nothing of the appalling wastage of more than l1Om of valuable assets at Charterhouse Square.To behave with such reckless abandon at this time of crisis within the universities of this country is surely immoderate.
The Two-Carbon Chain in Metabolism
Authors: Robert E. Olson
Journal: JAMA (1963)

THE IMPACT of the nutritional environment upon an organism cannot be appreciated without reference to cellular physiology and to the biochemical events which underlie cell function. The science of biochemistry, therefore, has become increasingly important in the interpretation of nutritional effects and, for that matter, of all the properties and responses of living matter. Biochemistry can no longer be considered by the medical student or the physician as a dispensable and esoteric subject. It provides the disciplinary base for an increasing number of diagnostic and therapeutic procedures in the practice of medicine. Nutritional therapy can best be understood by visualizing both the pathologic physiology and the effect of nutrition management in biochemical terms. The fate of the 2-carbon chain "active acetate" bears directly on a variety of essential metabolic processes such as energy production, ketone body formation, and fatty acid and cholesterol synthesis. Its functional distribution is dependent upon proper
Foodborne Illness Problems More Than Enteric
Authors: Rebecca Voelker
Journal: JAMA (1994)

IN A MERE 12 months,<i>Escherichia coli</i>0157:H7 has gained renown as a media darling, a target for state legislatures, and a random killer. A year after the potentially deadly bacterial strain struck hundreds of fast-food chain patrons in Washington and three other Western states, federal and state governments are trying to get a better handle on how frequently the pathogen strikes, and how to make it stop. But<i>E coli</i>0157:H7 is just the tip of the iceberg. At last count, foodborne bacterial, viral, and parasitic infections caused 6 million illnesses and 9000 deaths annually. That was in 1983, however. During the intervening years, says the Centers for Disease Control and Prevention (CDC), Atlanta, Ga, no new count has been taken, and public health officials aren't sure if foodborne disease is on the rise or wane. Perhaps the only certainty is that Washington's massive outbreak has ignited new calls
Unique epithelial cell production of hepatocyte growth factor/scatter factor by putative precancerous intestinal metaplasias and associated “intestinal-type” biliary cancer chemically induced in rat liver
Authors: Guan-Hua Lai, Svetlana Radaeva, Toshikazu Nakamura, Alphonse E. Sirica
Journal: Hepatology (2000)

Recently, we observed that Met, the receptor for hepatocyte growth factor/scatter factor (HGF/SF), is overexpressed in epithelial cells of both early-appearing intestinal metaplastic glands in precancerous hepatic cholangiofibrotic tissue and neoplastic glands in later developed intestinal-type of cholangiocarcinoma originated from the furan rat model of cholangiocarcinogenesis when compared with normal and hyperplastic intrahepatic biliary epithelia. We now show that HGF/SF is also aberrantly expressed in a manner closely paralleling that of its receptor in the neoplastic epithelial cells of furan-induced rat cholangiocarcinomas and in a majority of metaplastic epithelial cells within earlier formed precancerous hepatic cholangiofibrotic tissue. Using in situ hybridization and reverse transcription-polymerase chain reaction (RT-PCR), we further showed specific expression of HGF/SF messenger RNA (mRNA) in a novel rat cholangiocarcinoma epithelial cell line overexpressing Met. This cholangiocarcinoma cell line, termed C611B, was established from tumorigenic cells isolated from a furan-induced transplantable tumor. Moreover, we detected by in situ hybridization strong expression of HGF/SF mRNA transcripts in the cancerous epithelial glands of cholangiocarcinoma developed in recipient rats after in vivo cell transplantation of C611B cells. In contrast, mRNA transcripts and protein immunoreactivity for this cytokine were not detected in hepatocytes and biliary epithelial cells in adult normal rat liver nor in rat hyperplastic intrahepatic biliary epithelium. Our results clearly show that HGF/SF becomes aberrantly expressed in cholangiocarcinoma epithelium and in putative precancerous intestinal metaplastic epithelium induced in the liver of furan-treated rats.
Compensatory Mechanisms in Congestive Heart Failure — The Role of the Peripheral Resistance Vessels
Authors: Robert Zelis, Dean T. Mason
Journal: New England Journal of Medicine (1970)

ONE of the principal characteristics of patients with congestive heart failure is the diminished response of cardiac output with physiologic stress.1 There are a number of circulatory mechanisms, both central and peripheral, by which the patient with heart failure compensates for this inability to augment cardiac output adequately. The central compensatory mechanisms include the use of the Frank-Starling principle, development of myocardial hypertrophy and increased sympathetic drive to the heart.2 Thus, the increased blood volume resulting from the renal retention of sodium and secondary aldosteronism leads to an increased ventricular filling pressure and the operation of the ventricle higher on . . .
I Want to Die With Dignity
Authors: Jeff T. Marple
Journal: Annals of Internal Medicine (2014)

Ad Libitum4 February 2014I Want to Die With DignityJeff T. Marple, MDJeff T. Marple, MDFrom Lincoln, Nebraska.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M13-0136 Audio Reading - “I Want to Die With Dignity” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "I Want to Die With Dignity," by J.T. Marple. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail I want to die with dignityand a mechanical heartand a synthetic kidney machine attached to my armand a xenographic liver from a pig that's bred for partsI want to die with dignity when my life span's off the chartsI want to die with dignityand could you add tranquility?I can't get these at home but perhaps at your facilityIt will take a team of dozens to achieve my goal longevitybut if 40 is the new 20 why can't 90 be the new 70?and these politicians to be reelected ... Author, Article, and Disclosure InformationAffiliations: From Lincoln, Nebraska.Current Author Address: Jeff T. Marple, MD; e-mail, [email protected]com. PreviousarticleNextarticle Advertisement Audio Reading - “I Want to Die With Dignity” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "I Want to Die With Dignity," by J.T. Marple. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics 4 February 2014Volume 160, Issue 3Page: 170KeywordsBirthChartsHeartKidneysLiver ePublished: 4 February 2014 Issue Published: 4 February 2014 Copyright & PermissionsCopyright © 2014 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Thrombomodulin Mutations in Atypical Hemolytic–Uremic Syndrome
Authors: Mieke Delvaeye, Marina Noris, Astrid De Vriese, Charles T. Esmon, Naomi L. Esmon, Gary Ferrell, Jurgen Del-Favero, Stephane Plaisance, Bart Claes, Diether Lambrechts, Carla Zoja, Giuseppe Remuzzi, Edward M. Conway
Journal: New England Journal of Medicine (2009)

The hemolytic-uremic syndrome consists of the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. The common form of the syndrome is triggered by infection with Shiga toxin-producing bacteria and has a favorable outcome. The less common form of the syndrome, called atypical hemolytic-uremic syndrome, accounts for about 10% of cases, and patients with this form of the syndrome have a poor prognosis. Approximately half of the patients with atypical hemolytic-uremic syndrome have mutations in genes that regulate the complement system. Genetic factors in the remaining cases are unknown. We studied the role of thrombomodulin, an endothelial glycoprotein with anticoagulant, antiinflammatory, and cytoprotective properties, in atypical hemolytic-uremic syndrome.We sequenced the entire thrombomodulin gene (THBD) in 152 patients with atypical hemolytic-uremic syndrome and in 380 controls. Using purified proteins and cell-expression systems, we investigated whether thrombomodulin regulates the complement system, and we characterized the mechanisms. We evaluated the effects of thrombomodulin missense mutations associated with atypical hemolytic-uremic syndrome on complement activation by expressing thrombomodulin variants in cultured cells.Of 152 patients with atypical hemolytic-uremic syndrome, 7 unrelated patients had six different heterozygous missense THBD mutations. In vitro, thrombomodulin binds to C3b and factor H (CFH) and negatively regulates complement by accelerating factor I-mediated inactivation of C3b in the presence of cofactors, CFH or C4b binding protein. By promoting activation of the plasma procarboxypeptidase B, thrombomodulin also accelerates the inactivation of anaphylatoxins C3a and C5a. Cultured cells expressing thrombomodulin variants associated with atypical hemolytic-uremic syndrome had diminished capacity to inactivate C3b and to activate procarboxypeptidase B and were thus less protected from activated complement.Mutations that impair the function of thrombomodulin occur in about 5% of patients with atypical hemolytic-uremic syndrome.