tbuckley/cabot-search huggingface dataset:
The Insulin Resistance Syndrome in Native Hawaiians
Authors: Marjorie K Mau, Andrew Grandinetti, Richard F Arakaki, Healani K Chang, Everett K Kinney, J David Curb
Journal: Diabetes Care (1997)

OBJECTIVE To investigate whether fasting hyperinsulinemia is associated with a clustering of cardiovascular disease (CVD) risk factors, manifesting as the insulin resistance syndrome (IRS), in a population of native Hawaiians. RESEARCH DESIGN AND METHODS A total of 574 native Hawaiians ≥ 30 years of age were examined for blood pressure, waist-to-hip ratio (WHR), BMI, oral glucose tolerance, and fasting lipid, insulin, and C-peptide concentrations. All statistical analyses (n = 384) excluded 190 individuals who had NIDDM or who were taking hypertension medication. Using logistic regression analysis, fasting insulin and C-peptide levels were compared with CVD risk factors (glucose intolerance, hypertension, central adiposity, elevated triglyceride levels, and low HDL cholesterol levels) after adjusting for age and obesity. RESULTS Sixty-six percent of native Hawaiians were overweight or obese, and 70% were found to have central adiposity. Fasting insulin concentrations were correlated with BMI, WHR, blood pressure, and triglyceride, HDL cholesterol, and glucose concentrations. Fasting insulin was also significantly associated with an increasing number of CVD risk factors in each participant (P &amp;lt; 0.001). Fasting insulin and C-peptide concentrations were independently associated with glucose intolerance, high triglyceride levels, and low HDL cholesterol levels. However, only fasting C-peptide concentrations were independently associated with hypertension and central adiposity. Apparent differences in the correlates of fasting insulin and C-peptide may be related to multiple factors and warrant further evaluation. CONCLUSIONS This study provides cross-sectional data confirming the existence of the IRS in native Hawaiians. However, further longitudinal studies are needed to examine the relationship of insulin resistance and/or surrogate markers to increased rates of NIDDM and CVD mortality in native Hawaiians.
CAPAP in acute pancreatitis: just another marker or real progress?
Authors: M W BÜCHLER, W UHL, Å ANDRÉN-SANDBERG
Journal: Gut (1998)

See article on page97 

There are no pathognomonic symptoms in acute pancreatitis. In reaching a diagnosis the patient’s history, physical findings, and serum amylase or lipase concentrations have to be considered. Serum amylase is one of the oldest clinically useful laboratory tests, having been around for almost 70 years.1 However, too great a reliance on amylase or lipase will lead to underdiagnosis owing to the lack of sensitivity and specificity.2 

Up to 20% of patients with acute pancreatitis run a severe clinical course and these patients must be identified as quickly as possible. The “gold standard” for staging patients with acute pancreatitis is dynamic contrast enhanced computed tomography.3 Disease severity, however, may only become apparent at laparotomy (or necropsy). Operative intervention is not needed in uncomplicated cases and should be avoided if at all posssible in severe acute pancreatitis. Researchers have also attempted to differentiate between mild and severe forms of acute pancreatitis using so-called indicators of necrosis in blood or urine. Examples of these parameters are C-reactive protein (CRP), PMN elastase, phospholipase A2, antiproteases, and cytokines.4-8 CRP …
THE WORK OF THE MEDICAL ADVISORY BOARDS
Authors: Henry E. Hale
Journal: JAMA (1918)

<h3>To the Editor:</h3> —I have seen the comment inThe Journal(Feb. 23, 1918, p. 541) concerning the work of the medical advisory boards. As chairman of Board No. 3, Columbia University Group, I wish to express my appreciation of your suggestion, and hope that such recognition will be secured. My particular board would prefer some insignia to wear and a certificate to put away in a strong box.
Delayed publication of vaccine trials
Authors: C. W. Jones, T. F. Platts-Mills
Journal: BMJ (2014)

Why are we waiting? Sponsors, authors, and editors all contribute to delays

Among medical interventions to improve human health, vaccination has been and remains one of the most important.1 Given the huge number of deaths from influenza pandemics in recent history, the ability to rapidly develop effective vaccines for new strains of influenza is particularly critical. Making and testing a new influenza vaccine that can be administered to the public takes six months or less.2 For example, the pandemic A/H1N1 2009 influenza strain was first identified in April of 2009; four vaccines were approved by the US Food and Drug Administration in September. After the approval of a vaccine, however, important questions remain regarding dosage, effectiveness, and safety. These questions are best answered by randomized clinical trials, and getting complete results from these trials to policy makers, clinicians, and the general public in a timely manner is essential.

The problems of delayed publication and non-publication of clinical trials have been described in a variety of settings.3 4 5 In this issue of The BMJ , Manzoli and colleagues (doi:10.1136/bmj.g3058) examine delays to publication and non-publication for the vitally important area of vaccine trials.6 The authors searched …
IL-15 but not IL-2 rapidly induces lethal xenogeneic graft-versus-host disease
Authors: Sameek Roychowdhury, Bradley W. Blaser, Aharon G. Freud, Kerry Katz, Darshna Bhatt, Amy K. Ferketich, Valerie Bergdall, Donna Kusewitt, Robert A. Baiocchi, Michael A. Caligiuri
Journal: Blood (2005)
Interferon regulatory factor 3 and type I interferons are protective in alcoholic liver injury in mice by way of crosstalk of parenchymal and myeloid cells
Authors: Jan Petrasek, Angela Dolganiuc, Timea Csak, Bharath Nath, Istvan Hritz, Karen Kodys, Donna Catalano, Evelyn Kurt-Jones, Pranoti Mandrekar, Gyongyi Szabo
Journal: Hepatology (2010)

Alcoholic liver disease (ALD) features increased hepatic exposure to bacterial lipopolysaccharide (LPS). Toll-like receptor-4 (TLR4) recognizes LPS and activates signaling pathways depending on MyD88 or TRIF adaptors. We previously showed that MyD88 is dispensable in ALD. TLR4 induces Type I interferons (IFNs) in an MyD88-independent manner that involves interferon regulatory factor-3 (IRF3). We fed alcohol or control diets to wild-type (WT) and IRF3 knock-out (KO) mice, and to mice with selective IRF3 deficiency in liver parenchymal and bone marrow-derived cells. Whole-body IRF3-KO mice were protected from alcohol-induced liver injury, steatosis, and inflammation. In contrast to WT or bone marrow-specific IRF3-KO mice, deficiency of IRF3 only in parenchymal cells aggravated alcohol-induced liver injury, associated with increased proinflammatory cytokines, lower antiinflammatory cytokine interleukin 10 (IL-10), and lower Type I IFNs compared to WT mice. Coculture of WT primary murine hepatocytes with liver mononuclear cells (LMNC) resulted in higher LPS-induced IL-10 and IFN-β, and lower tumor necrosis factor alpha (TNF-α) levels compared to LMNC alone. Type I IFN was important because cocultures of hepatocytes with LMNC from Type I IFN receptor KO mice showed attenuated IL-10 levels compared to control cocultures from WT mice. We further identified that Type I IFNs potentiated LPS-induced IL-10 and inhibited inflammatory cytokine production in both murine macrophages and human leukocytes, indicating preserved cross-species effects. These findings suggest that liver parenchymal cells are the dominant source of Type I IFN in a TLR4/IRF3-dependent manner. Further, parenchymal cell-derived Type I IFNs increase antiinflammatory and suppress proinflammatory cytokines production by LMNC in paracrine manner.Our results indicate that IRF3 activation in parenchymal cells and resulting type I IFNs have protective effects in ALD by way of modulation of inflammatory functions in macrophages. These results suggest potential therapeutic targets in ALD.
Complications of Selective Percutaneous Transfemoral Coronary Arteriography and their Prevention
Authors: GERALD S. GREEN, C. MALCOLM MCKINNON, JOSEF RÖSCH, MELVIN P. JUDKINS
Journal: Circulation (1972)

Complications encountered during a typical 12-month period of routine work with the Judkins percutaneous transfemoral method of selective coronary arteriography are reviewed. In 445 examinations, 20 complications (16 local and four cardiac) occurred. Local complications included nine delayed hemorrhages, five thromboses of femoral arteries, and two peripheral emboli. Cardiac complications included one ventricular fibrillation, one significant bradyarrhythmia, and two myocardial infarctions. Causes of individual complications are analyzed and means for their prevention discussed. Guidelines of the procedure are proposed to minimize the complications of selective coronary arteriography. Emphasis is placed on patient evaluation, preparation for the procedure, and meticulous examination technique.
Gum disease may increase the risk of stroke
Authors: Roger Dobson
Journal: BMJ (2006)

People with antibodies to Porphyromonas gingivalis , the organism most strongly associated with periodontal disease, were more likely to have a stroke, a new study has found.

Women who were exposed to the pathogen were up to 2.3 times more likely than other women to have a stroke, shows the research, which was published online ahead of print publication on 26 July in Atherosclerosis (http://www.sciencedirect.com/, doi: 10.1016/j.atherosclerosis.2006.06.027).

“We found that systemic exposure to a main periodontal pathogen, P. gingivalis , was an independent risk factor for …
Immunoperoxidase study of the secretory immunoglobulin system and lysozyme in normal and diseased gastric mucosa.
Authors: P Isaacson
Journal: Gut (1982)

Using an immunoperoxidase technique the distribution of secretory component, IgA, and lysozyme has been investigated in normal, inflamed, dysplastic, and carcinomatous gastric mucosa. Apart from pyloric glands which contain lysozyme, normal gastric mucosa stains negatively for all three antigens. In gastric mucosa neck cells appear to adapt by synthesising secretory component and lysozyme and transporting IgA. Intense staining for the three antigens is seen in dysplastic gastric epithelium and in well-differentiated intestinal type carcinomas. With progressive de-differentiation the tumours lose the ability to synthesise secretory component and lysozyme. Carcinomas of the diffuse type stain positively for secretory component and lysozyme and individual cells appear to take up IgA even in the absence of surrounding IgA containing plasma cells. These functional properties are retained in lymph node metastases. It is suggested that secretory component synthesising malignant cells might take up circulating dimeric IgA and that this could be a reflection of an important physiological mechanism.
Lymphokine stimulation of collagen accumulation.
Authors: R L Johnson, M Ziff
Journal: Journal of Clinical Investigation (1976)

Lymphokine-rich supernates from normal human peripheral blood mononuclear cells, stimulated by the mitogen phytohemagglutinin, have been shown to cause enhanced collagen accumulation by human embryonic lung fibroblasts (WI-38), as measured by hydroxyproline content of fibroblast monolayers, [14C] proline incorporation into soluble collagen and collagenase release of radioactivity in supernates and monolayers of cultures incubated with [14C] proline. This fibroblast-stimulating activity, demonstrable by suitable dilutions of the supernates, coexisted with a number of other lymphokine activities such as lymphotoxin, proliferation inhibitory factor, and cloning inhibitory factor, which tend to reduce the numbers of function of fibroblasts. The increased content of collagen appeared to be the product of selected surviving and responding fibroblasts. The factor causing this increased collagen accumulation was nondialyzable and stable at -70 degrees C. It represents the first described lymphoid cell-derived activity capable of enhancing collagen accumulation. Fibroblast-stimulating activity may be implicated in the abnormal fibrosis seen in association with chronic inflammation in a variety of disease states. It may have special relevance to progressive systemic sclerosis.
Rationing Intensive Care — Physician Responses to a Resource Shortage
Authors: Daniel E. Singer, Phyllis L. Carr, Albert G. Mulley, George E. Thibault
Journal: New England Journal of Medicine (1983)

Abstract To determine how physicians ration limited critical resources, we studied the allocation of intensive-care-unit (ICU) beds during a shortage caused by a lack of nurses. As the bed capacity of the medical ICU decreased from 18 to 8, the percentage of days on which one or more beds were available decreased from 95 to 55 per cent, and monthly admissions decreased from 122 to 95. Physicians responded by restricting ICU admissions to acutely ill patients and reducing the proportion of patients admitted primarily for monitoring. Among patients admitted because of chest pain, the proportion actually sustaining a myocardial infarction increased linearly with the restriction in bed capacity. Although more patients with myocardial infarction were admitted to non–intensive-care areas, there was no increase in mortality. In addition, physicians transferred patients out of the ICU sooner. There was no apparent withdrawal of care from dying patients. Our results suggest that physicians can respond to moderate resource limitations by more efficient use of intensive-care resources. (N Engl J Med 1983; 309:1155–60.)
Laboratory-Acquired Infections: History, Incidence, Causes and Prevention
Authors: Josephine A. Morello
Journal: JAMA (1988)

This book from Britain is a detailed treatise on the History, Incidence, Causes and Prevention of laboratory-acquired infections. The author, an adviser to the World Health Organization in the Special Programme on Safety Measures in Microbiology, has considerable experience in this area and presents the subject in a highly readable manner.  He begins by reviewing and expanding on previous surveys that document the extent of laboratory-acquired infections. Of interest is the changing incidence of some diseases. Although brucellosis remains number one among the top ten, only one laboratory-acquired case has been reported since 1978. In the United States, typhoid fever has been moving up the list as a result of infections acquired from proficiency testing samples. Nevertheless, clinical microbiologists will not be surprised to learn that more than half of reported laboratory infections have been acquired in research rather than diagnostic laboratories.  A chapter on minimizing equipment- and technique-related hazards
The Differential Effects of Mutant <i>p53</i> Alleles on Advanced Murine Lung Cancer
Authors: Erica L. Jackson, Kenneth P. Olive, David A. Tuveson, Roderick Bronson, Denise Crowley, Michael Brown, Tyler Jacks
Journal: Cancer Research (2005)

Abstract We report a direct comparison of the differential effects of individual p53 mutations on lung tumor growth and progression, and the creation of a murine model of spontaneous advanced lung adenocarcinoma that closely recapitulates several aspects of advanced human pulmonary adenocarcinoma. We generated compound conditional knock-in mice with mutations in K-ras combined with one of three p53 alleles: a contact mutant, a structural mutant, or a null allele. p53 loss strongly promoted the progression of K-ras–induced lung adenocarcinomas, yielding a mouse model that is strikingly reminiscent of advanced human lung adenocarcinoma. The influence of p53 loss on malignant progression was observed as early as 6 weeks after tumor initiation. Furthermore, we found that the contact mutant p53R270H, but not the structural mutant p53R172H, acted in a partially dominant-negative fashion to promote K-ras–initiated lung adenocarcinomas. However, for both mutants, loss-of-heterozygosity occurred uniformly in advanced tumors, highlighting a residual tumor-suppressive function conferred by the remaining wild-type allele of p53. Finally, a subset of mice also developed sinonasal adenocarcinomas. In contrast to the lung tumors, expression of the point-mutant p53 alleles strongly promoted the development of sinonasal adenocarcinomas compared with simple loss-of-function, suggesting a tissue-specific gain-of-function.
Lipid Research Clinics Program
Authors: Michael S. Conjalka
Journal: JAMA (1984)

<h3>To the Editor.—</h3> The report from the LRC-CPPT<sup>1</sup>documents that hypercholesteremic men randomly allocated to receive cholestyramine and dietary treatment for their type II hyperlipoproteinemia had fewer CHD events than did hypercholesteremic men who were treated with placebo and diet. However, while the incidence of CHD events was significantly reduced in the group receiving cholestyramine, there was no significant survival advantage for this cholestyramine-treated group. Analysis by the Lipid Research Clinics Program revealed that this lack of survival advantage for the cholestyramine-treated group was due, in large part, to an increased number of deaths secondary to trauma among those patients receiving cholestyramine. In this exhaustive study, the program also documented that patients receiving cholestyramine had significantly lower serum carotene levels than did patients receiving placebo, thus suggesting that cholestyramine was in fact causing malabsorption of other fat-soluble materials besides cholesterol. Indeed, for years it has been known that cholestyramine
LONG-TERM BLEEDING IN PATIENTS ON PROLONGED DUAL ORAL ANTIPLATELET THERAPY AFTER DES IMPLANTATION: PREVALENCE, PREDICTORS, AND PROGNOSTIC IMPLICATIONS
Authors: Roberta Rossini, Giuseppe Musumeci, Corrado Lettieri, Giuseppe Biondi Zoccai, Tamar Nijaradze, Nicola Cicorella, Nikoloz Lortkipanidze, Michele Romano, Giuseppe Tarantini, Antonello Gavazzi, Dominick J. Angiolillo
Journal: Journal of the American College of Cardiology (2010)
Nitric Oxide Inhibits Numerous Features of Mast Cell–Induced Inflammation
Authors: Jeffrey P. Gaboury, Xiao-Fei Niu, Paul Kubes
Journal: Circulation (1996)

Background We previously reported that mast cell degranulation causes histamine and P-selectin–dependent leukocyte rolling and platelet-activating factor (PAF)- and CD18-associated leukocyte adhesion, whereas others have reported serotonin-induced edema formation. The purpose of the present study was to determine whether nitric oxide (NO) could inhibit the mast cell–induced multistep recruitment of leukocytes and the associated microvascular dysfunction in single inflamed venules. Methods and Results Intravital fluorescence microscopy was used to demonstrate increased leukocyte rolling and adhesion and increased albumin extravasation in single 25- to 40-μm venules that were treated with the mast cell–degranulating agent compound 48/80 (CMP 48/80). The mast cell–induced histamine-dependent rolling and PAF-dependent adhesion were completely inhibited by the addition of the NO donor spermine NO. However, spermine NO did not directly inhibit histamine-induced leukocyte rolling and only partly affected PAF-induced leukocyte adhesion. Compound 48/80–activated mast cells evoked a significant increase in PAF-dependent neutrophil adhesion in vitro. Spermine-NO prevented the mast cell–dependent neutrophil adhesion but failed to affect direct adhesion with PAF. The mast cell–induced albumin leakage was also inhibited by the NO donor. Conclusions Taken together, these results suggest that exogenous NO can modulate leukocyte recruitment and microvascular permeability alterations elicited by mast cell activation and raises the possibility that the use of NO donors may be a reasonable therapeutic approach to reducing mast cell–dependent inflammation.
Genetic Deficit of SK3 and IK1 Channels Disrupts the Endothelium-Derived Hyperpolarizing Factor Vasodilator Pathway and Causes Hypertension
Authors: Sebastian Brähler, Anuradha Kaistha, Volker J. Schmidt, Stephanie E. Wölfle, Christoph Busch, Brajesh P. Kaistha, Michael Kacik, Anna-Lena Hasenau, Ivica Grgic, Han Si, Chris T. Bond, John P. Adelman, Heike Wulff, Cor de Wit, Joachim Hoyer, Ralf Köhler
Journal: Circulation (2009)

It has been proposed that activation of endothelial SK3 (K(Ca)2.3) and IK1 (K(Ca)3.1) K+ channels plays a role in the arteriolar dilation attributed to an endothelium-derived hyperpolarizing factor (EDHF). However, our understanding of the precise function of SK3 and IK1 in the EDHF dilator response and in blood pressure control remains incomplete. To clarify the roles of SK3 and IK1 channels in the EDHF dilator response and their contribution to blood pressure control in vivo, we generated mice deficient for both channels.Expression and function of endothelial SK3 and IK1 in IK1(-/-)/SK3(T/T) mice was characterized by patch-clamp, membrane potential measurements, pressure myography, and intravital microscopy. Blood pressure was measured in conscious mice by telemetry. Combined IK1/SK3 deficiency in IK1(-/-)/SK3(T/T) (+doxycycline) mice abolished endothelial K(Ca) currents and impaired acetylcholine-induced smooth muscle hyperpolarization and EDHF-mediated dilation in conduit arteries and in resistance arterioles in vivo. IK1 deficiency had a severe impact on acetylcholine-induced EDHF-mediated vasodilation, whereas SK3 deficiency impaired NO-mediated dilation to acetylcholine and to shear stress stimulation. As a consequence, SK3/IK1-deficient mice exhibited an elevated arterial blood pressure, which was most prominent during physical activity. Overexpression of SK3 in IK1(-/-)/SK3(T/T) mice partially restored EDHF- and nitric oxide-mediated vasodilation and lowered elevated blood pressure. The IK1-opener SKA-31 enhanced EDHF-mediated vasodilation and lowered blood pressure in SK3-deficient IK1(+/+)/SK3(T/T) (+doxycycline) mice to normotensive levels.Our study demonstrates that endothelial SK3 and IK1 channels have distinct stimulus-dependent functions, are major players in the EDHF pathway, and significantly contribute to arterial blood pressure regulation. Endothelial K(Ca) channels may represent novel therapeutic targets for the treatment of hypertension.
5 IODO-2'-DEOXYURIDINE IN THE TREATMENT OF HERPES ZOSTER.
Authors: D. I. McCALLUM, E. N. M. JOHNSTON, B. H. RAJU
Journal: British Journal of Dermatology (1964)

Journal Article 5 IODO‐2′‐DEOXYURIDINE IN THE TREATMENT OF HERPES ZOSTER. Get access D. I. McCALLUM, D. I. McCALLUM Skin Department, General Hospital, Nottingham Search for other works by this author on: Oxford Academic Google Scholar E. N. M. JOHNSTON, E. N. M. JOHNSTON Skin Department, General Hospital, Nottingham Search for other works by this author on: Oxford Academic Google Scholar B. H. RAJU B. H. RAJU Skin Department, General Hospital, Nottingham Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 76, Issue 11, 1 November 1964, Pages 459–462, https://doi.org/10.1111/j.1365-2133.1964.tb15484.x Published: 01 November 1964
Nine-ball Neck
Authors: Richard Dean Smith
Journal: JAMA (1989)

To the Editor.—  Billiards may not look like a sport that could induce injury, but one case illustrates its danger.  Report of a Case.—  A 56-year-old man complained of tightness of the right cervical muscles and soreness of the right shoulder that occasionally interfered with sleep, was associated with brief morning stiffness, and was noted to be worse a day or two after playing pocket billiards, especially nine-ball. Muscular tenderness of the nuchal and trapezius muscles on the right side with trigger points at the base of the skull, the midtrapezius muscle, and anteromedial to the shoulder was present, as well as skinfold tenderness. Forced abduction produced a sensation of pulling in the shoulder.  Treatment was successful with conditioning exercises, proper instruction in technique, massage of tender muscles, application of local heat, and more frequent participation in billiards. Therapy with muscle relaxants, anti-inflammatory drugs, and analgesics was not required.  Comment.—