tbuckley/cabot-search huggingface dataset:
Lester's Getting a Bottle
Authors: Keith Luther
Journal: Annals of Internal Medicine (1999)

On Being a Patient5 January 1999Lester's Getting a BottleKeith Luther, MDKeith Luther, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-1-199901050-00016 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Henry stepped off the bus onto the curb at the corner of Broadway and Sheridan. It was March and cold in Chicago, but the sun was bright and Henry narrowed his eyes to the light. He stood holding a plastic grocery bag under his arm as the bus pulled away from its exhaust. He crossed Broadway into the shadow of the Hotel Chateau.“Where you been, Henry?” said the manager from behind his glass.“Hospital.”The manager moved his face close to the hole for talking. “Tomorrow's the first, don't forget.”A few men reclined on broken-down couches in the ... Author, Article, and Disclosure InformationAffiliations: Corresponding Author: Keith Luther, MD, Tulane University Medical Center, 1430 Tulane Avenue, New Orleans, LA 70112.Note: This paper was adapted from an earlier version that appeared in the Spring 1994 issue of Body Electric. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByLife on the Receiving End: A Qualitative Analysis of Health Providers??? Illness Narratives 5 January 1999Volume 130, Issue 1Page: 73-74KeywordsBlood countsEmotionsHospitalizationsKidneysNervesOral medicinePancreasPancreatitisPharynxStomach Issue Published: 5 January 1999 CopyrightCopyright © 1999 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
The capture of phosphoproteins by 14-3-3 proteins mediates actions of insulin
Authors: Shuai Chen, Silvia Synowsky, Michele Tinti, Carol MacKintosh
Journal: Trends in Endocrinology and Metabolism (2011)

How does signalling via PI3K-PKB (AKT)-mTORC1-p70S6K and ERK-p90RSK mediate wide-ranging physiological responses to insulin? Quantitative proteomics and biochemical experiments are revealing that these signalling pathways induce the phosphorylation of large and overlapping sets of proteins, which are then captured by phosphoprotein-binding proteins named 14-3-3s. The 14-3-3s are dimers that dock onto dual-phosphorylated sites in a configuration with special signalling and mechanical properties. They interact with the Rab GTPase-activating proteins AS160 and TBC1D1 to regulate glucose uptake into target tissues in response to insulin and energy stress. Dynamic patterns in the 14-3-3-binding phosphoproteome are providing new insights into how insulin triggers coherent shifts in metabolism that are integrated with other cellular response systems.
GW25-e3097 Two birds with one stone: α-blocker therapy on LUTS/BPH in men concomitant with mild hypertension
Authors: Xiao Hengjun, Pang Jun, Hu Cheng, Wu Jieying, Chen Jun, Pu Xiaoyong, Li Dong, Gao Xin
Journal: Journal of the American College of Cardiology (2014)
Milton Keynes is first acute trust to install Microsoft's integrated patient records system
Authors: M. Cross
Journal: BMJ (2010)

The prospect of NHS patients managing their own healthcare records on a private online system moved closer last week with the announcement of a deal between the software giant Microsoft and an NHS acute trust. Milton Keynes Hospital NHS Foundation Trust is to become the first UK user of a Microsoft product for combining health data produced by disparate IT systems.

Milton …
Is thrombin a key player in the 'coagulation-atherogenesis' maze?
Authors: J. I. Borissoff, H. M.H. Spronk, S. Heeneman, H. ten Cate
Journal: Cardiovascular Research (2009)

In addition to its established roles in the haemostatic system, thrombin is an intriguing coagulation protease demonstrating an array of effects on endothelial cells, vascular smooth muscle cells (VSMC), monocytes, and platelets, all of which are involved in the pathophysiology of atherosclerosis. There is mounting evidence that thrombin acts as a powerful modulator of many processes like regulation of vascular tone, permeability, migration and proliferation of VSMC, recruitment of monocytes into the atherosclerotic lesions, induction of diverse pro-inflammatory markers, and all of these are related to the progression of cardiovascular disease. Recent studies in transgenic mice models indicate that the deletion of the natural thrombin inhibitor heparin cofactor II promotes an accelerated atherogenic state. Moreover, the reduction of thrombin activity levels in apolipoprotein E-deficient mice, because of the administration of the direct thrombin inhibitor melagatran, attenuates plaque progression and promotes stability in advanced atherosclerotic lesions. The combined evidence points to thrombin as a pivotal contributor to vascular pathophysiology. Considering the clinical development of selective anticoagulants including direct thrombin inhibitors, it is a relevant moment to review the different thrombin-induced mechanisms that contribute to the initiation, formation, progression, and destabilization of atherosclerotic plaques.
NUCLEAR MEDICINE CROSS-MATCH OF HETEROLOGOUS BLOOD UNITS IN HEMOLYTIC ANEMIA
Authors: J. Morrison, A. Ramos-Gabatin, J. Brown, Major T. Dougherty, M. Dominik, J. Collet, J. Powell
Journal: Clinical Nuclear Medicine (1993)

Morrison, J.; Ramos-Gabatin, A.; Brown, J.; Dougherty, Major T.; Dominik, M.; Collet, J.; Powell, J. Author Information
Study progression in application of process analytical technologies on film coating
Authors: Tingting Peng, Ying Huang, Liling Mei, Linna Wu, Longkai Chen, Xin Pan, Chuanbin Wu
Journal: Asian Journal of Pharmaceutical Sciences (2014)

Abstract   Film coating is an important unit operation to produce solid dosage forms, thereby, the monitoring of this process is helpful to find problems in time and improve the quality of coated products. Traditional methods adopted to monitor this process include measurement of coating weight gain, performance of disintegration and dissolution test, etc. However, not only do these methods cause destruction to the samples, but also consume time and energy. There have recently emerged the applications of process analytical technologies (PAT) on film coating, especially some novel spectroscopic and imaging technologies, which have the potential to real-time track the progress in film coating and optimize production efficiency. This article gives an overview on the application of such technologies for film coating, with the goal to provide a reference for the further researches.
Cardiovascular Effects of Weight Reduction
Authors: JAMES K. ALEXANDER, KIRK L. PETERSON
Journal: Circulation (1972)

Weight reduction programs usually improve the exercise capacity of patients with chronic exogenous obesity. However, the reversibility of left ventricular hypertrophy and dysfunction associated with obesity is unknown. Accordingly, an analysis was made of hemodynamic data obtained by cardiac catheterization and standard chest roentgenograms in nine markedly obese patients before and after weight loss of 39 to 84 kg (24 to 55% of control weight) over periods of 4 to 34 months. In each case body oxygen uptake (360 to 297 ml/min), blood volume (7.8 to 6.1 liters), cardiac output (7.9 to 6.2 liters/min), and arteriovenous oxygen difference (4.6 to 4.0 vol. %) were significantly reduced after weight loss. Systemic arterial pressure declined (102 to 87 mm Hg) while systemic vascular resistance changed insignificantly (1,067 to 1,141 dynes-sec-cm -5 ). In seven subjects comparable chest roentgenograms before and after weight reduction revealed decrease in the cardiothoracic ratio, suggesting a reduction in left ventricular dimensions. These results have been interpreted as indicating that the circulatory effects of gross obesity are largely reversible with weight loss. Despite reductions in left ventricular stroke work, stroke volume, and cavity size at rest, the average left ventricular filling pressure rose with exercise to a comparable and abnormal level (20 mm Hg) both before and after weight loss. Thus, evidence of left ventricular dysfunction persisted, suggesting that myocardial hypertrophy and reduced ventricular compliance did not regress significantly with weight loss over periods as long as 3 years.
Cardiac Sarcoidosis
Authors: David L. Chamovitz
Journal: JAMA (1962)

CARDIAC SARCOIDOSIS has been encountered frequently enough to warrant its consideration in the differential diagnosis of heart disease of unknown origin. It is the purpose of this report to describe an autopsied case and to emphasize sarcoidosis as a cause of paroxysmal ventricular tachycardia. Report of a Case A 40-year-old Italian male was first admitted to the Aliquippa Hospital on June 4, 1957, because of severe anterior chest pain radiating down the inner aspect of the left arm. Mild pain had been present for 2 weeks. In 1937, in Italy, the patient was told that he had "suffocating heart disease." Nevertheless, he served in the Italian Army without restriction. During a preemployment examination in 1953, shortly after arriving in this country, again he was told he had heart trouble, but again was permitted to do manual labor. The patient was first examined 6 months prior to admission because of right
An Outline of Scientific Writing
Authors: J. Kirkman
Journal: BMJ (1996)

Jen Tsi Yang World Scientific Publishing, Singapore and London, £12.00, pp 160 ISBN 981 02 2466 4

“There are already many excellent texts on scientific writing in English. Why, then …,” asks Professor Yang in his preface, “… would an author whose first language is Chinese write another book on the subject?”

His answer made me look forward to reading his book: “As an author in English for over 40 years, I understand the unique writing challenge that we Asians face.” He subtitles his book For Researchers with …
Kidney Disease: Acute Renal Failure
Authors: J P Merrill
Journal: Annual Review of Medicine (1960)

The subject of  renal  is an important one. It is important because this condition may be one of the most critical with which the physi­ cian must deal and yet it is also compatible with complete and lasting recov­ ery. It i s unfortunate, therefore; that the term acute renal  has led to so much semantic confusion. Acute renal failure, in the functional sense, has been confused with  urinary suppression and  renal insuffi­ ciency. From an anatomical standpoint it has been variously classified as shock kidney, crush syndrome,  tubular necrosis and first, but least ac­ curately, as lower nephron nephrosis ( 1) . The word failure is defined by Webster's Collegiate Dictionary, fourth edition, as omission to perform, and  as wanting in strength, power, capacity; incompetent. These definitions certainly imply functional parameters. The functional as­ pect seems important. For instance, one recent excellent review (2) states that  glomerular nephritis cannot be included in the category of acute renal insufficiency. However, in functional terms which is the ultimate concern of the patient, if not the semanticist,  glomerular nephritis may certainly produce any and all degrees of incompetence of the kidney. Acute urinary suppression, on the other hand, would seem to imply the sup­ pression of urinary function by influences from without the kidney. Whether or not this is semantically justified, it is convenient from a diagnostic stand­ point to divide the general subject of  renal  into (a) pre renal, (b) renal, and (c) postrenal. This division, in turn, implies that only in cate­ gory (b) is there renal parenchymal damage and, by the same token, prerenal or postrenal defects may mask a kidney whose functioning parenchyma is intact. This has important connotations for immediate diagnosis and treat­ ment. A further division that has seemed useful in the past (3) has been a division of  renal insufficiency and  renal failure. Acute renal in­ sufficiency is defined as inability to perform standard tests of function, whereas  renal failur.e implies inability to excrete at normal plasma levels the load of metabolite presented. As will be pointed out,  in­ sufficiency may appear to be  when the metabolic load becomes so great that even the normal functioning kidney cannot eliminate it at normal plasma levels. This fact was pointed out by Addis (4) in citing the fact that the blood urea nitrogen may rise dramatically in normal young men whose
1025 MARKERS OF ENDOTHELIAL DYSFUNCTION AS PREDICTORS OF ASCITIC DECOMPENSATION IN PATIENTS WITH LIVER CIRRHOSIS
Authors: M. Fiorini, M. Marcacci, C. Boni, F. Zappia, G. Roveri, G. Venturelli, A. Pietrangelo, P. Ventura
Journal: Journal of Hepatology (2013)
Daily Peak Flow Measurements in the Assessment of Steroid Therapy for Airway Obstruction
Authors: S. W. Epstein, C. M. Fletcher, E. A. Oppenheimer
Journal: BMJ (1969)

Measurements of peak expiratory flow can be made by outpatients on themselves. This technique, which may be carried out at home, has proved to be valuable in assessing the effect of steroids and other bronchodilator drugs in relieving airway obstruction.
Organic Mental Disease
Authors: Lawrence C. McHenry
Journal: JAMA (1982)

"The potentially curable causes of progressive intellectual deterioration represent the most overlooked treatable medical conditions in America" (Geschwind). Freemon's monograph on these conditions is a well-written and comprehensive modern introduction to the phenomena of organic mental disease. Pointing out the brain-mind relationship, he reminds us all of the dilemma as to whether these are neurological or psychiatric conditions. Specialists in both fields, as well as the general physician, still have the tendency to slough these problems off. After reading Freemon's book, one is able to grasp a better understanding of the problem and the potential for better management of these patients. Failure to recognize and accept these conditions is probably the single greatest impediment to understanding organic mental dysfunction and to proper and human treatment of the many patients who suffer from these disorders. Freemon's 11 chapters begin with a general discussion of neuroanatomy and physiology in chapters on the
FOXO1 is a tumor suppressor in classical Hodgkin lymphoma
Authors: Linka Xie, Alexey Ushmorov, Frank Leithäuser, Hanfeng Guan, Christian Steidl, Johanna Färbinger, Christin Pelzer, Marion J. Vogel, Harald J. Maier, Randy D. Gascoyne, Peter Möller, Thomas Wirth
Journal: Blood (2012)
Endostatin, the Proteolytic Fragment of Collagen XVIII, Induces Vasorelaxation
Authors: D. Wenzel, A. Schmidt, K. Reimann, J. Hescheler, G. Pfitzer, W. Bloch, B.K. Fleischmann
Journal: Circulation Research (2006)

Collagen XVIII is an important component of the extracellular matrix and is expressed in basement membranes. Its degradation results in the generation of endostatin claimed to possess antiangiogenic activity. To date, only limited knowledge exists with regard to the cellular signaling of this molecule. We show in single-cell measurements using the Ca 2+ indicator fura-2 acetoxy methylester (fura-2 AM) and the nitric oxide (NO) indicator 4,5-diaminofluorescein diacetate that application of endostatin (ES) (5 pmol/L, 100 ng/mL) induced Ca 2+ spikes and an increase of NO production in human and murine endothelial cells. The NO response was independent of an increase in cytosolic Ca 2+ and blocked by the endothelial NO synthase (eNOS) inhibitor N G -nitro- l -arginine methyl ester and by incubation with pertussis toxin known to inhibit G i/o proteins. The physiological relevance of this novel signaling pathway of ES was assessed with isometric force measurements in large and small arteries of mouse. Physiological concentrations of ES were found to decrease vascular tone in an endothelium-dependent manner. This occurred via an Arg-Gly-Asp (RGD) peptide–independent pathway through activation of G i/o proteins, phosphatidylinositol 3-kinase, Akt, and eNOS. We conclude that the proteolytic matrix fragment ES is a prominent vasorelaxing agent. Because ES is constantly released into the blood, it is a novel regulator of blood pressure and, therefore, represents an interesting pharmacological target.
Can the Intensive Care Unit Be Harmful?-Reply
Authors: William A. Knaus
Journal: JAMA (1983)

<h3>In Reply.—</h3> Using clinical trials to evaluate ICU use would be one good way to improve our use of these units. In my opinion, the best way to reach Dr Spodick's objective of identifying patients for whom ICU care is harmful would be to select patients from diagnostic groups that we already know contain a substantial number of patients who may not benefit from intensive care.<sup>1,2</sup>This would make it possible to use random allocation rather than an expert panel to select which patients to admit to the unit. Another way to investigate the value both of ICU care and of the many invasive aspects of its use is to scrutinize the natural differences in use that occur among hospitals. For example, within our current research effort in 15 tertiary-care ICUs, we find substantial variation in admitting practices and the use of pulmonary artery catheters. Whether we use classical
Personalizing Oncology: Perspectives and Prospects
Authors: John Mendelsohn
Journal: Journal of Clinical Oncology (2013)

This article provides an overview of the research, beginning a century ago, that has led to the current use of genomically informed methods for selection of targeted therapies to treat individual patients with cancer—so-called precision cancer medicine. Until 1980, most research on cancer therapy was not targeted in the sense we use the word today. Since then, there has been an acceleration in research identifying genetic and molecular targets and in clinical trials using biomarkers that identify the presence of genetic or molecular markers in a patient's cancer to select appropriate targeted therapy. This approach has been made possible by increased knowledge of the genetic pathogenesis of cancer and by increased capacity to sequence genes and genomes in clinically useful timeframes and at a reasonable cost. However, many challenges and pitfalls remain in selecting optimal targets, interpreting data on genetic aberrations, designing effective targeted drugs and antibodies, dealing with resistance to treatments, identifying appropriate combinations of therapies, and performing the complex clinical trials that are required. Future clinical research with experimental targeted agents is likely to be more informative because of appropriate preselection of patients enrolled onto trials and performance of genetic and molecular studies on specimens of a patient's cancer before and after treatment.
Increased Fluidity of Human Platelet Membranes during Complement-Mediated Immune Platelet Injury
Authors: Sanford J. Shattil, Douglas B. Cines, Alan D. Schreiber
Journal: Journal of Clinical Investigation (1978)

Complement appears to be involved in the destruction of platelets in certain clinical disorders, such as quinidine purpura and post-transfusion purpura. In both disorders, the classical complement sequence is activated by antigen-antibody complexes. It has been suggested that the terminal components of the complement sequence insert into the hydrophobic core of cell surface membranes and that this process leads to cell lysis. Fluidity is a fundamental property of lipids within the membrane's hydrophobic core. To examine the interaction of complement with membranes, we investigated the effect of complement activation on the fluidity of human platelet membranes. Complement was fixed to platelets using a post-transfusion purpura antibody, and membrane lipid fluidity was assessed in terms of fluorescence anisotropy using two fluorescent probes, 1,6-diphenyl-1,3,5-hexatriene and 9-(12-anthroyl) stearic acid. Microviscosity, expressed in poise, was derived from the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene.Post-transfusion purpura antibody plus complement made platelet membranes more fluid as evidenced by a 21% decrease in anisotropy and a 35% decrease in microviscosity of platelets at 37 degrees C, and this was associated with platelet lysis ((51)Cr release). Complement damage to platelets was accompanied by a 10-15% increase in DeltaE, the fusion activation energy for microviscosity, indicating that complement not only decreased membrane microviscosity but also made membrane lipids less ordered. These changes were consistent and rapid, with platelet lysis and the reduction in microviscosity being half-maximal by 6 min. They were prevented by inactivation of complement with heat or with EDTA, and they were not observed when C5-deficient plasma was used as the complement source. Qualitatively similar changes in platelet membrane fluidity were observed when complement was fixed to platelets by a quinidine-dependent anti-platelet antibody rather than by post-transfusion purpura antibody. Post-transfusion purpura antibody plus complement also decreased the microviscosity of isolated platelet membranes. Moreover, the lipids extracted from platelets lysed by complement had a 22% decrease in microviscosity (P < 0.01), with no associated changes in the amount of cholesterol relative to phospholipid or in the amounts of the various phospholipids. These studies demonstrate that lipids within the hydrophobic core of platelet membranes damaged by complement become more fluid, and this is associated with platelet lysis. These findings are consistent with the concept that the insertion of the terminal complement components into the platelet membrane bilayer perturbs lipid-lipid interactions within the membrane's hydrophobic core.
Morbidity and mortality study of shale oil workers in the United States.
Authors: J Costello
Journal: Environmental Health Perspectives (1979)

The study of the carcinogenic potential of domestic U. S. shale oil has increased significantly in importance because of the present energy problem and resulting research into alternative sources of fuel. With the increased scope of planned oil shale activity on the Colorado Plateau, it is important that an attempt be made to determine the health effects, if any, of occupational exposure to shale oil. This paper briefly reviews some past work of Soviet and British investigators concerning potential health hazards of shale oil. It reviews the results and conclusions of the 1952-1955 dermatological study of oil shale workers by the U. S. Public Health Service, and it discusses in detail the plans of a NIOSH morbidity and mortality study currently under way.