tbuckley/cabot-search huggingface dataset:
New York outbreak of E coli poisoning affects 1000 and kills two
Authors: F. Charatan
Journal: BMJ (1999)

The shortage of organs for transplantation by its nature prompts ethical dilemmas. For example, although there is an imperative to save human life and reduce suffering by maximising the supply of vital organs, there is an equally important obligation to ensure that the process by which we increase the supply respects the rights of all stakeholders. In a relatively unexamined practice in the USA, organs are procured from unrepresented decedents without their express consent. Unrepresented decedents have no known healthcare wishes or advance care planning document; they also lack a surrogate. The Revised Uniform Anatomical Gift Act (RUAGA) of 2006 sends a mixed message about the procurement of organs from this patient population and there are hospitals that authorise donation. In addition, in adopting the RUAGA, some states included provisions that clearly allow organ procurement from unrepresented decedents. An important unanswered question is whether this practice meets the canons of ethical permissibility. The current Brief Report presents two principled approaches to the topic as a way of highlighting some of the complexities involved. Concluding remarks offer suggestions for future research and discussion.
424 PLATELET COUNT/SPLEEN DIAMETER RATIO IS MORE ACCURATE FOR PREDICTION OF SIGNIFICANT AND EXTENSIVE FIBROSIS THAN AST-TO-PLATELET RATIO INDEX (APRI) IN PATIENTS WITH CHRONIC HEPATITIS C
Authors: J.H. Sohn, T.Y. Kim, D.W. Jun, C.S. Eun, Y.C. Jeon, D.S. Han
Journal: Journal of Hepatology (2010)
Residual inflammation after rituximab treatment is associated with sustained synovial plasma cell infiltration and enhanced B cell repopulation
Authors: Y K O Teng, E W N Levarht, R. E M Toes, T. W J Huizinga, J. M van Laar
Journal: Annals of the Rheumatic Diseases (2008)

<h3>Objective:</h3> To investigate the clinical effects of rituximab treatment in relation to immunological effects of rituximab on tissue-derived B lineage cells and repopulation of circulating B cells. <h3>Methods:</h3> A total of 24 patients with rheumatoid arthritis (RA) were treated with 2×1000 mg rituximab and assessed clinically at 4, 12, 18 and 24 weeks using a 44-joint Disease Activity Score (DAS<sub>44</sub>). Synovial biopsies were analysed with immunohistochemistry at baseline and 12 weeks after treatment. Peripheral blood mononuclear cells were analysed by high sensitivity flow cytometry at all timepoints. <h3>Results:</h3> In this study, a cohort of patients was dichotomised according to those who achieved a low disease activity score (DAS<sub>44</sub>&lt;2.4: LoA group) and those with persistent disease activity (DAS<sub>44</sub>&gt;2.4: HiA group) at any time after rituximab treatment. At baseline, the low activity (LoA) group had significantly lower DAS<sub>44</sub> scores (median 3.33, range 2.84 to 4.23) than the high activity (HiA) group (median 3.73, range 3.03 to 5.23; p = 0.022) and significantly less histological inflammation in synovium (median 6.7, range 1 to 15 vs 16.6, range 4 to 22; p = 0.036). DAS<sub>44</sub> scores before and after rituximab treatment were associated with synovial infiltration of CD79a+ CD20− B cells, morphologically resembling plasma cells. Following treatment with rituximab, the LoA group had significantly reduced repopulation of circulating pre-switched IgD+ B cells (median 0.044%, range 0.002 to 0.66 vs 0.45%, range 0.07 to 9.47; p = 0.006) and post-switched CD27+ B cells (median 0.17%, range 0.04 to 0.39 vs 0.67, range 0.08 to 2.05; p = 0.005) compared to the HiA group. <h3>Conclusion:</h3> The present study demonstrated that a low disease activity state following rituximab was associated with reduced infiltration of CD79a+ CD20− plasma cells in synovium and reduced B cell repopulation.
Streptomycin in the Treatment of Salmonella Enteritis in Infants
Authors: Sidney Ross, Frederic G. Burke, E. Clarence Rice, Harold Bischoff, John A. Washington
Journal: New England Journal of Medicine (1949)

THE susceptibility of various strains of salmonella in vitro to streptomycin has been adequately demonstrated by West et al.1 However, the clinical efficacy of this antibiotic in salmonella enteritis has not been too extensively investigated, and relatively few cases have been reported thus far among children. Seligmann et al.2 used streptomycin in 5 cases of enteritis due to Salmonella typhimurium in the newborn period and observed only a transitory sterilization of the bowel, and in all 5 cases the pathogenic organism reappeared in the stool, usually within forty-eight hours after the drug had been discontinued. A relatively small oral dose . . .
Sickness and Health in America: Readings in the History of Medicine and Public Health
Authors: Thomas Novotny
Journal: JAMA (1987)

Modern American physicians and public health professionals perceive illness and the condition that we call "health" in ways different from those of our forebears. Medical education short-changes medical history, and, as a consequence, we risk forgetting the lessons of the past. This excellent collection of historical vignettes provides useful and captivating reading for health professionals at all levels. It is not a collection of accolades to a few prominent physicians but rather a series of descriptions of important ideas, movements, and concepts in the evolution of modern medicine and public health. In the overview, the editors emphasize that food and filth are as important as physicians and hospitals in the decline of illness and the prolongation of life. The essays, therefore, describe lay and professional successes and failures ranging from "physicians to patent medicines, from masturbation to smallpox, from birthing to bacteriology." The book further affirms that "to understand sickness
CD4 T Cell Tolerance to Human C-reactive Protein, an Inducible Serum Protein, Is Mediated by Medullary Thymic Epithelium
Authors: Ludger Klein, Thomas Klein, Ulrich Rüther, Bruno Kyewski
Journal: The Journal of Experimental Medicine (1998)

Inducible serum proteins whose concentrations oscillate between nontolerogenic and tolerogenic levels pose a particular challenge to the maintenance of self-tolerance. Temporal restrictions of intrathymic antigen supply should prevent continuous central tolerization of T cells, in analogy to the spatial limitation imposed by tissue-restricted antigen expression. Major acute-phase proteins such as human C-reactive protein (hCRP) are typical examples for such inducible self-antigens. The circulating concentration of hCRP, which is secreted by hepatocytes, is induced up to 1,000-fold during an acute-phase reaction. We have analyzed tolerance to hCRP expressed in transgenic mice under its autologous regulatory regions. Physiological regulation of basal levels (<10(-9) M) and inducibility (>500-fold) are preserved in female transgenics, whereas male transgenics constitutively display induced levels. Surprisingly, crossing of hCRP transgenic mice to two lines of T cell receptor transgenic mice (specific for either a dominant or a subdominant epitope) showed that tolerance is mediated by intrathymic deletion of immature thymocytes, irrespective of widely differing serum levels. In the absence of induction, hCRP expressed by thymic medullary epithelial cells rather than liver-derived hCRP is necessary and sufficient to induce tolerance. Importantly, medullary epithelial cells also express two homologous mouse acute-phase proteins. These results support a physiological role of "ectopic" thymic expression in tolerance induction to acute-phase proteins and possibly other inducible self-antigens and have implications for delineating the relative contributions of central versus peripheral tolerance.
Clinical guidelines: Potential benefits, limitations, and harms of clinical guidelines
Authors: S. H Woolf, R. Grol, A. Hutchinson, M. Eccles, J. Grimshaw
Journal: BMJ (1999)

This is the first in a series of four articles on issues in the development and use of clinical guidelines

Over the past decade, clinical guidelines have increasingly become a familiar part of clinical practice. Every day, clinical decisions at the bedside, rules of operation at hospitals and clinics, and health spending by governments and insurers are being influenced by guidelines. As defined by the Institute of Medicine, clinical guidelines are “systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances.”1 They may offer concise instructions on which diagnostic or screening tests to order, how to provide medical or surgical services, how long patients should stay in hospital, or other details of clinical practice

The broad interest in clinical guidelines that is stretching across Europe, North America, Australia, New Zealand, and Africa (box) has its origin in issues that most healthcare systems face: rising healthcare costs, fueled by increased demand for care, more expensive technologies, and an ageing population; variations in service delivery among providers, hospitals, and geographical regions and the presumption that at least some of this variation stems from inappropriate care, either overuse or underuse of services; and the intrinsic desire of healthcare professionals to offer, and of patients to receive, the best care possible. Clinicians, policy makers, and payers see guidelines as a tool for making care more consistent and efficient and for closing the gap between what clinicians do and what scientific evidence supports.

As guidelines diffuse into medicine, there are important lessons to learn from the firsthand experience of those who develop, evaluate, and use them.3 This article, the first of a four part series to reflect on these lessons, examines the potential benefits, limitations, and harms of clinical guidelines. Future articles will review lessons learned …
Physicians' Utilization and Charges for Outpatient Diagnostic Imaging in a Medicare Population
Authors: Bruce J. Hillman
Journal: JAMA (1992)

For 10 common clinical presentations, we assessed differences in physicians' utilization of and charges for diagnostic imaging, depending on whether they performed imaging examinations in their offices (self-referral) or referred their patients to radiologists (radiologist-referral).Using previously developed methodologies, we generated episodes of medical care from an insurance claims database. Within each episode, we determined whether diagnostic imaging had been performed, and if so, whether by a self-referring physician or a radiologist. For each of the 10 clinical presentations, we compared the mean imaging frequency, mean imaging charges per episode of care, and mean imaging charges for diagnostic imaging attributable to self- and radiologist-referral.Depending on the clinical presentation, self-referral resulted in 1.7 to 7.7 times more frequent performance of imaging examinations than radiologist-referral (P < .01, all presentations). Within all physician specialties, self-referral uniformly led to significantly greater utilization of diagnostic imaging than radiologist-referral. Mean imaging charges per episode of medical care (calculated as the product of the frequency of utilization and mean imaging charges) were 1.6 to 6.2 times greater for self-referral than for radiologist-referral (P < .01, all presentations). When imaging examinations were performed--including those performed in both physicians' offices and hospital outpatient departments--mean imaging charges were significantly greater for radiologists than for self-referring physicians in seven of the clinical presentations (P < .01). This result is related to the high technical charges of hospital outpatient departments; in office practice, radiologists' mean charges for imaging examinations were significantly less than those of self-referring physicians for seven clinical presentations (P < .01).Nonradiologist physicians who operate diagnostic imaging equipment in their offices perform imaging examinations more frequently, resulting in higher imaging charges per episode of medical care. These results extend our previous research on this subject by their focus on a broader range of clinical presentations; a mostly elderly, retired population; and the inclusion of higher-technology imaging examinations.
Jaundice and Oxyphenisatin
Authors: Gordon McHardy
Journal: JAMA (1970)

Two middle-aged women were hospitalized with a similar, moderately severe illness consisting of fatigue, vague abdominal symptoms, and jaundice. Laboratory abnormalities consisted of elevated levels of serum glutamic oxaloacetic transaminase (SGOT), serum bilirubin, and serum alkaline phosphatase. Physical findings included mild hepatic enlargement and tenderness. Results of cholecystographic studies were normal. Each patient had been taking a laxative mixture containing oxyphenisatin acetate, dioctyl sodium sulfosuccinate, and carboxymethylcellulose sodium (Dialose Plus) prior to the illness. Improvement followed fortuitous discontinuance of the Dialose Plus in both patients upon hospitalization. Clinical and laboratory relapse occurred, in both patients, shortly after resumption of Dialose Plus. Recovery seems to have followed final discontinuance of the medication.
The T−786C Endothelial Nitric Oxide Synthase Genotype Predicts Cardiovascular Mortality in High-Risk Patients
Authors: Gian Paolo Rossi, Giuseppe Maiolino, Mario Zanchetta, Daniele Sticchi, Luigi Pedon, Maurizio Cesari, Domenico Montemurro, Renzo De Toni, Silvia Zavattiero, Achille C. Pessina
Journal: Journal of the American College of Cardiology (2006)
HIF-1α deletion partially rescues defects of hematopoietic stem cell quiescence caused by Cited2 deficiency
Authors: Jinwei Du, Yu Chen, Qiang Li, Xiangzi Han, Cindy Cheng, Zhengqi Wang, David Danielpour, Sally L. Dunwoodie, Kevin D. Bunting, Yu-Chung Yang
Journal: Blood (2012)
K————x-Rated Therapy
Authors: MARVIN J. BITTNER
Journal: Annals of Internal Medicine (1980)

Ad Libitum1 October 1980K————x-Rated TherapyMARVIN J. BITTNER, M.D.MARVIN J. BITTNER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-93-4-636 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIt started with as promising a pain as any that can wake you up at two in the morning. I woke up with a painful, red, swollen great toe. Podagra? With a uric acid maven like Kelley as chief, what better illness could a Michigan medical resident contract? Gout is rich in heritage, treatable, better understood biochemically than many diseases, and free of the worrisome prognosis of hepatitis and the stigma of gonorrhea. Many of my peers had shown interest in it, but who else had gone far enough to contract it? True, it could be the first sign of... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: MARVIN J. BITTNER, M.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCarbohydratesK- - - -X-Rated Therapy:—Another ViewRODNEY K. KUSUMI, M.D. 1 October 1980Volume 93, Issue 4Page: 636-636KeywordsGonorrheaGoutHepatitisUric acid ePublished: 1 December 2008 Issue Published: 1 October 1980 PDF downloadLoading ...
Opening of the mitochondrial permeability transition pore causes matrix expansion and outer membrane rupture in fas-mediated hepatic apoptosis in mice
Authors: Gérard Feldmann, Delphine Haouzi, Alain Moreau, Anne-Marie Durand-Schneider, Annie Bringuier, Alain Berson, Abdellah Mansouri, Daniel Fau, Dominique Pessayre
Journal: Hepatology (2000)

Although Fas stimulation has been reported to cause outer mitochondrial membrane rupture in Jurkat cells, the mechanism of this effect is debated, and it is not known if outer membrane rupture also occurs in hepatocyte mitochondria. We studied the in vivo effects of Fas stimulation on ultrastructural lesions and mitochondrial function in mice. Four hours after administration of an agonistic anti-Fas antibody (8 μg/animal), caspase activity increased 5.4-fold. Nuclear DNA showed internucleosomal fragmentation, whereas supercoiled mitochondrial DNA was replaced by circular and linear forms. Mitochondrial cytochrome c was partly released into the cytosol. Ultrastructurally, mitochondrial lesions were observed in both apoptotic hepatocytes (with nuclear chromatin condensation/fragmentation) and nonapoptotic hepatocytes (without nuclear changes). In nonapoptotic cells, outer mitochondrial membrane rupture allowed herniation of the inner membrane and matrix through the outer membrane gap. In apoptotic hepatocytes, the matrix became electron-lucent and no longer protruded through the outer membrane gap. Mitochondria clustered around the nucleus, whereas rough endoplasmic reticulum cisternae became peripheral. In liver mitochondria isolated after Fas stimulation, the membrane potential decreased, whereas basal respiration increased. Pretreatment with either z-VAD-fmk (an inhibitor of caspases) or cyclosporin A (a permeability transition inhibitor) totally or mostly prevented mitochondrial outer membrane rupture, membrane potential decrease, cytochrome c release, and apoptosis. In conclusion, in vivo Fas stimulation causes caspase activation, mitochondrial permeability transition (decreasing the membrane potential and increasing basal respiration), mitochondrial matrix expansion (as shown by matrix herniation), outer mitochondrial membrane rupture, and cytochrome c release.
Renin — From Beginning to End
Authors: David C. Kem, Ronald D. Brown
Journal: New England Journal of Medicine (1990)

IN 1898 Tigerstedt and Bergman1 observed a sustained pressor response after the infusion of a saline extract of renal tissue into a rabbit. This ultimately led to elucidation of the renin–angiotensin–aldosterone system, the components of which are essential for homeostatic control of blood pressure and fluid and electrolyte balance. The aspartyl proteinase renin is released from juxtaglomerular cells encircling the afferent arterioles in the kidney. It acts on the α2-globulin angiotensinogen, produced in the liver, to form the nonpressor decapeptide angiotensin I. This in turn is cleaved by the peptidyl dipeptidase angiotensin-converting enzyme to angiotensin II, which has . . .
Left behind: the legacy of hurricane Katrina
Authors: David Atkins, Ernest M Moy
Journal: BMJ (2005)

Hurricane Katrina puts the health effects of poverty and race in plain view 

T he sinking of the Titanic , during which women in first class cabins were more likely to survive than those booked into cheaper decks, has been used to illustrate the effects of income and social class on health (T LaVeist, personal communication, 2005). In the aftermath of hurricane Katrina, Americans have been shocked and shamed to realise that they still don't have enough lifeboats for all of our citizens. Live images of uncollected corpses and families clinging to rooftops made vivid what decades of statistics could not: that being poor in America, and especially being poor and black in a poor southern state, is still hazardous to your health.

This may truly be a “teachable moment” about the impact of poverty and race on health. The gap in health between white and black Americans has been estimated to cause 84 000 excess deaths a year in the United States, a virtual Katrina every week.1 Because the victims gradually succumb to various diseases such as diabetes, cardiovascular disease, alcohol and drug abuse, cancer, and HIV infection, they rarely capture the public's attention in the way the victims of Katrina have. As a result, health inequality has persisted despite decades of important health gains, economic growth, and progress on racial issues in the United States.

It would be a mistake, however, to assume …
Myocardial KRASG12D expression does not cause cardiomyopathy in mice
Authors: Martin G. Dalin, Zhiyuan Zou, Margareta Scharin-Täng, Roghaiyeh Safari, Christin Karlsson, Martin O. Bergo
Journal: Cardiovascular Research (2013)

AimsGerm-line mutations in genes encoding components of the RAS/mitogen-activated protein kinase (MAPK) pathway cause developmental disorders called RASopathies. Hypertrophic cardiomyopathy (HCM) is the most common myocardial pathology and a leading cause of death in RASopathy patients. KRAS mutations are found in Noonan and cardio-facio-cutaneous syndromes. KRAS mutations, unlike mutations of RAF1 and HRAS, are rarely associated with HCM. This has been attributed to the fact that germ-line KRAS mutations cause only a moderate up-regulation of the MAPK pathway. Highly bioactive KRAS mutations have been hypothesized to cause severe cardiomyopathy incompatible with life. The aim of this study was to define the impact of KRASG12D expression in the heart.
Is measurable cyclic variation of integrated backscatter present in all standard echo-views in dilated cardiomyopathies?
Authors: Konstantina Bouki, Aleksandra Lange, Przemyslaw Palka, auCarmel M. Moran, Lynn Fenn, M.Pautiina Ramo, Thomas R.D. Shaw, W.Norman McDicken, George R. Sutherland
Journal: Journal of the American College of Cardiology (1996)
Long-term Anticoagulant Therapy after Myocardial Infarction in Women
Authors: Chr. F. Borchgrevink, Chr. Bjerkelund, A. M. Abrahamsen, G. Bay, P. Borgen, B. Grande, I. Helle, H. Kjorstad, A. M. Petersen, T. Rorvik, R. Thorsen, A. Odegaard
Journal: BMJ (1968)

A multicentre trial from five medical departments in Oslo has been carried out to determine the value in women patients of one year9s long-term anticoagulant therapy. Follow-up long-term laboratory control and anticoagulant dosage were performed at one centre (the Rikshospitalet). One hundred and fifty-nine patients were assigned randomly into two similar well-matched groups (control and treatment). Dosage was controlled by Thrombotest, aiming at 10–20% levels, and 50% of the tests were less than 14%. Compared with the control group, the treatment group showed a significant reduction in mortality and in reinfarction rate. No serious bleeding complications occurred. It is concluded that women benefit as much as men from long-term anticoagulant therapy.
Local Anesthesia for Neonatal Circumcision
Authors: Gerald N. Weiss
Journal: JAMA (1988)

To the Editor.—  The ORIGINAL CONTRIBUTION by Stang et al 1 is a commendable scientific study, but it may be based on questionable assumptions. It has never been proved that a neonate undergoing surgery experiences pain. In 1987, Fitzgerald 2 reported the following:  Understanding and treatment of infant pain depends on the wider study of developmental processes. As yet, this is just beginning. It is apparent in rats that peripheral nociceptors develop prenatally, but levels of peptides and other neurochemicals within their terminals build up slowly over the postnatal period. Furthermore, substance P receptors in the spinal cord initially are distributed diffusely and become localized postnatally. Cells in the dorsal horn that process nociceptive information have poorly organized responses at birth and develop segmental and descending controls postnatally. Enkephalin levels within the spinal cord also increase postnatally, and there is a differential development of opiate receptors, with K-receptors appearing first
Evolutionary toggling of the MAPT 17q21.31 inversion region
Authors: Michael C Zody, Zhaoshi Jiang, Hon-Chung Fung, Francesca Antonacci, LaDeana W Hillier, Maria Francesca Cardone, Tina A Graves, Jeffrey M Kidd, Ze Cheng, Amr Abouelleil, Lin Chen, John Wallis, Jarret Glasscock, Richard K Wilson, Amy Denise Reily, Jaime Duckworth, Mario Ventura, John Hardy, Wesley C Warren, Evan E Eichler
Journal: Nature Genetics (2008)