tbuckley/cabot-search huggingface dataset:
Effect of Low-Dose Aspirin on the Occurrence of Venous Thromboembolism
Authors: Robert J. Glynn, Paul M Ridker, Samuel Z. Goldhaber, Julie E. Buring
Journal: Annals of Internal Medicine (2007)

Background: Short-term aspirin therapy can lower the risk for venous thromboembolism (VTE) in high-risk patients, but whether the long-term use of low-dose aspirin reduces risk in healthy adults is uncertain. Objective: To test the efficacy of long-term aspirin therapy for preventing VTE. Design: Secondary analysis of a 10-year randomized, double-blind, placebo-controlled trial. Setting: U.S. female health care professionals in the Women's Health Study. Participants: 39 876 initially healthy women age 45 years or older (26 779 gave blood samples that were evaluated for factor V Leiden, G20210A prothrombin, and MTHFR 677C>T polymorphisms). Measurements: Documented VTE (deep venous thrombosis or pulmonary embolism) and unprovoked VTE (no recent surgery, trauma, or cancer diagnosis) were prospectively evaluated, secondary end points. Intervention: Aspirin, 100 mg, or placebo on alternate days. Results: Venous thromboembolism occurred in 482 women during follow-up, an incidence higher than that of myocardial infarction and nearly equal to that of stroke. The incidence of VTE (per 1000 person-years) was 1.18 among women randomly assigned to active aspirin, compared with 1.25 among women randomly assigned to placebo (relative hazard, 0.95 [95% CI, 0.79 to 1.13]; rate difference, −0.06 [CI, −0.28 to 0.16]). For unprovoked VTE, the relative hazard was 0.90 (CI, 0.70 to 1.16) and the rate difference was −0.06 (CI, −0.21 to 0.10). Relative hazards associated with aspirin use in higher-risk subgroups were 0.83 (CI, 0.50 to 1.39) among women with either factor V Leiden or the prothrombin mutation and 1.36 (CI, 0.77 to 2.41) among those with a history of VTE. Limitation: Venous thromboembolism was a secondary end point in the Women's Health Study. Conclusion: These data suggest that long-term, low-dose aspirin treatment has little effect on the prevention of VTE in initially healthy women. ClinicalTrials.gov registration number: NCT00000479.
Diagnostic value of blood cytokine concentrations in acute pneumonia.
Authors: P Kragsbjerg, I Jones, T Vikerfors, H Holmberg
Journal: Thorax (1995)

BACKGROUND--The role of cytokines in the pathogenesis of pneumonia is still poorly understood. In a previous study the diagnostic value of measuring blood concentrations of interleukin 6 and interferon gamma was established. In the present study the value of blood concentrations of interleukin 8, granulocyte-colony stimulating factor, and lactoferrin as markers of bacteraemic pneumonia is evaluated. METHODS--The circulating concentrations of interleukin 8 (IL-8), granulocyte-colony stimulating factor (G-CSF), and lactoferrin were measured in 14 patients with bacteraemic pneumococcal pneumonia and 49 patients with atypical pneumonia or influenza A infection using enzyme immunoassays. RESULTS--Serum G-CSF concentrations were higher in the group with bacteraemic pneumococcal pneumonia, and G-CSF values correlated with the white blood cell count and levels of C-reactive protein (CRP). The levels of IL-8 were higher in the group with bacteraemic pneumococcal pneumonia than the groups with Chlamydia pneumonia, Legionella pneumonia, or influenza A infection, but there was no difference when compared with the group with Mycoplasma pneumonia. A white blood cell count of &gt; 15 x 10(9)/l was highly suggestive of bacteraemic pneumonia. The concentrations of lactoferrin were raised in all groups except those with influenza A infection, but no difference was found between the different aetiological groups. A correlation was found between lactoferrin and white blood cell counts. CONCLUSIONS--Serum G-CSF and IL-8 concentrations are potential markers of bacteraemic pneumonia.
Biochemical Aspects of Neurological Disorders
Authors: Donald E. Widmann
Journal: JAMA (1965)

This valuable collection of review articles is based on a series of lectures that was given in 1964 at the Institute of Neurology, the National Hospital, Queen's Square. The subjects covered have a wide range, from myasthenia, muscular dystrophy, and toxic and metabolic neuropathies to depression, retardation, and other mental disorders. For most of the diseases considered excellent reviews of the clinical, genetic, and pathologic aspects precede the biochemical discussions.  The book is well organized and well written. It will appeal to readers who have clinical or research interests in neurology, as well as those concerned with neurologic biochemistry or psychiatry. There is a refreshing absence of jargon, the writing is lucid and easily understood, and the coverage is comprehensive. Anyone interested in neurologic disorders should read this work if only to confirm his faith that good prose still has its place in medical writing. We do not often come
Linking Performance With Payment
Authors: Jordan M. VanLare, Jonathan D. Blum, Patrick H. Conway
Journal: JAMA (2012)

PHYSICIANS ARE LEADERS OF PATIENT CARE TEAMS AND decision makers for system-based investments that facilitate quality improvement. The National Quality Strategy established 3 aims of improving health, improving health care, and reducing cost. The Centers for Medicare & Medicaid Services’ (CMS’s) value-based purchasing (VBP) programs create incentives for physicians to pursue these aims and to reward value more so than volume. Physicians’ leadership role in the health system makes incorporating physicians into the VBP portfolio critical to realizing the potential of these programs. The Physician Value-Based Payment Modifier (value modifier), part of the Affordable Care Act, links physician performance in quality and cost with Medicare Part B payments. Medicare Part B covers services such as laboratory tests, surgeries, and physician visits. CMS recently finalized a rule implementing the value modifier, including initial eligibility, measures of quality and cost, and the effect of physician performance on payment. This Viewpoint provides an overview of the program, its effect on physicians, and aims to engage physicians in a dialogue about how the value modifier should evolve over the course of implementation.
The Right To Be Different: Deviance and Enforced Therapy
Authors: Douglas D. Bond
Journal: JAMA (1972)

The excellence of Professor Kittrie's book lies in the clarity and even temper of its presentation and in the completeness of the documentation. These virtues are particularly welcome in a book which deals with explosive interdisciplinary issues having to do with the personal responsibility in regard to crime and the position of the state as both a punishing parent and a parent whose duty it is to protect, treat, and rehabilitate the wayward child. The history of the law vis-à-vis responsibility is briefly but fascinatingly traced and the brevity helps make clear the constant trend away from demonic possession and vengeance toward concepts of multiple causality, a softening of the concept of individual responsibility, and thus toward "sickness" (which equals "he couldn't help it") and treatment. Many of his points are those put forward by Thomas Szasz, in a somewhat shriller, but no less cogent form. Particular among these are
Does Control of Diabetes Prevent Vascular Complications?
Authors: Robert Matz
Journal: JAMA (1989)

<h3>To the Editor. —</h3> The last part of the conclusion reached by Abbott et al<sup>1</sup>concerning the impact of diabetes on survival following myocardial infarction warrants closer scrutiny. They state, in the abstract: "We conclude... in addition, when cardiac failure appears, control of diabetes assumes added importance, particularly in women, where its effect on survivorship is considerable." The data presented in this communication do not address this issue nor support this statement. While it would be nice to believe that control of diabetes once congestive heart failure supervenes after a myocardial infarction prolongs survival, I am unaware of evidence that supports this theory. Indeed, studies are now ongoing to determine whether control of diabetes can delay or ameliorate the long-term vascular complications of the disease. A second concern is the comment by the authors that diabetes in women also seems to be more severe because a greater percentage of
Targeting transforming growth factor (TGF)-βRI inhibits activation of β1 integrin and blocks vascular invasion in hepatocellular carcinoma
Authors: Emilia Fransvea, Antonio Mazzocca, Salvatore Antonaci, Gianluigi Giannelli
Journal: Hepatology (2008)

Vascular invasion is one of the major negative prognostic factors in patients with hepatocellular carcinoma (HCC), leading to cancer recurrence. To invade, HCC cells must penetrate the vessel wall, consisting of endothelial cells and extracellular matrix components, including fibronectin and fibrinogen. Employing invasive and noninvasive HCC cells, we studied the mechanism underlying vascular invasion. We show that HCC cells invade blood vessels via α5β1, that is equally expressed in invasive and noninvasive cells. However, in the former, the intracytoplasmic tail of β1 integrin is constitutively phosphorylated at threonine 788-789 and the extracellular part is conformationally activated. In noninvasive cells, β1 integrin is not activated. Transforming growth factor (TGF)-β1 specifically phosphorylates β1 integrin (threonine 788-789) via Smad-2 and Smad-3, causing a conformational change of the extracellular component with an inside-out mechanism. This leads noninvasive HCC cells to behave like invasive cells. A selective TGF-βRI inhibitor inhibits phosphorylation of the β1 integrin intracytoplasmic tail, and blocks invasion of HCC cells, both constitutively invasive and with acquired invasive properties. In human HCC tissues with microvascular invasion, phospho-β1 integrin was detected as well as TGF-β1, p-Smad-2, and E-cadherin. Conclusion: TGF-β1 promotes vascular invasion by activating β1 integrin. This suggests a rationale for targeting TGF-βRI in future clinical trials. (HEPATOLOGY 2009.)
Effects of nifedipine on coronary reactive and exercise induced hyperaemia
Authors: R. J BACHE, D. QUANBECK, D. C HOMANS, X.-Z. DAI
Journal: Cardiovascular Research (1987)

Journal Article Effects of nifedipine on coronary reactive and exercise induced hyperaemia Get access ROBERT J BACHE, ROBERT J BACHE From the Division of Cardiology, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar DEBORAH QUANBECK, DEBORAH QUANBECK From the Division of Cardiology, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar DAVID C HOMANS, DAVID C HOMANS From the Division of Cardiology, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar XUE-ZHENG DAI XUE-ZHENG DAI From the Division of Cardiology, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 21, Issue 10, October 1987, Pages 766–771, https://doi.org/10.1093/cvr/21.10.766 Published: 01 October 1987 Article history Received: 27 May 1986 Accepted: 06 May 1987 Published: 01 October 1987
ABIN-2 is required for optimal activation of Erk MAP kinase in innate immune responses
Authors: Stamatia Papoutsopoulou, Antony Symons, Tharsana Tharmalingham, Monica P Belich, Frank Kaiser, Dimitris Kioussis, Anne O'Garra, Victor Tybulewicz, Steven C Ley
Journal: Nature Immunology (2006)
Autophagy regulates endothelial cell processing, maturation and secretion of von Willebrand factor
Authors: Takehiro Torisu, Kumiko Torisu, In Hye Lee, Jie Liu, Daniela Malide, Christian A Combs, Xufeng S Wu, Ilsa I Rovira, Maria M Fergusson, Roberto Weigert, Patricia S Connelly, Mathew P Daniels, Masaaki Komatsu, Liu Cao, Toren Finkel
Journal: Nature Medicine (2013)
Electrophysiologic evaluation of sinus node function in patients with sinus node dysfunction.
Authors: H C Strauss, J T Bigger, A L Saroff, E G Giardina
Journal: Circulation (1976)

Twenty patients of mean age 66.2 years, with suspected sinus node dysfunction, underwent extensive electrophysiologic study. Sinus bradycardia (18), sinus pauses (3), and sinoatrial block (1) were identified in their ECGs prior to study. Also 11 patients had some abnormality of atrioventricular nodal and/or intraventricular conduction prior to study. At the time of electrophysiological study, 10/20 patients (50%) had a mean cycle length exceeding 1000 msec, and mean P-V interval exceeded 210 msec in 7/20 (35%). The estimated "sinoatrial conduction time" exceeded 215 msec in 6/16 (38%) patients. The maximum first escape cycle following pacing at six different rates exceeded a value equal 1.3 X the mean value of the control cycle length + 101 msec (slope of regression line + Y intercept + 1 SD) in 13/9 (68%) patients. Nineteen patients received 1 mg atropine intravenously and mean cycle length decreased by 19%, from 891 +/- 175.8 msec to 718 +/- 182.9 msec. Graded infusion of isoproterenol was employed in 19 patients; four patients required an infusion rate greater than 28.3 ng/kg/min to produce a 20% decrease in spontaneous sinus cycle length. These data would indicate that a variety of interventions are required to characterize the disturbance of sinus node automaticiy and sinoatrial conduction in patients with sinus node dysfunction.
222. Aberrant Striatal Gene Expression in the Striatum of HPRT-Knockout Mouse
Authors: Shaochun Song, C. Ramana Bhasker, Ling Guo, Theodore Friedmann
Journal: Molecular Therapy (2006)

The mechanisms responsible for the dopamine deficit in Lesch Nyhan Disease (LND) and in the HPRT-knockout mouse are poorly understood. We have used microarray transcriptional profiling methods to characterize global patterns of gene expression in the striatum of wild type and HPRT-knockout mice to test our hypothesis that secondary genetic aberrations play a role in the altered CNS function in this disease. We have used the murine full genome GeneChip Mouse Genome 430 2.0 arrays and have identified a small number of genes (>2 fold difference) whose expression in the striatum becomes more than two-fold aberrantly expressed as determined by gene expression studies and as confirmed by quantitative PCR during the 4-8 weeks of post-natal life.
Effect of hypoxia and endothelial loss on vascular smooth muscle cell responsiveness to VEGF-A: role of flt-1/VEGF-receptor-1
Authors: A Parenti
Journal: Cardiovascular Research (2002)

Objective: The influence of hypoxia and endothelial loss on the responsiveness of vascular smooth muscle cells (VSMCs) to vascular endothelial growth factor (VEGF-A) was tested. Methods and results: Exposure to hypoxia induced a potentiation of cultured cell proliferation in response to either the agonist for the VEGF receptor 1 (flt-1) placental growth factor (PlGF-1) or to VEGF-A. This effect was mediated by the mitogen activated protein kinase (MAPK) cascade, since it was inhibited by the MAPK kinase inhibitor PD98059 and by the farnesyl transferase inhibitor II. Accordingly, PlGF-1 activated extracellular signal-regulated kinase1/2. In rat aortic rings deprived of endothelium and cultured in three-dimensional fibrin gels, an increased sprouting of tubular structures in response to VEGF-A was observed only under hypoxia. Studies on rat aorta preparations revealed an endothelium-dependent vasorelaxation in response to either VEGF-A or PlGF1, which was reversed to a contractile response in endothelium-deprived preparations exposed to hypoxia. Western blot and immunohistochemistry of endothelium-deprived preparations exposed to hypoxia showed flt-1 receptor expression in all medial cells. Conversely, flt-1 mRNA, of endothelium-deprived aortic preparations and of tubular structures, was unchanged by hypoxia. Conclusion: These findings demonstrate that experimental conditions mimicking pathological vascular injury can make VSMCs responsive to VEGF-A through the induction of functional flt-1 receptors.
Rapid Resolution of Hypertrophic Pulmonary Osteoarthropathy After Resection of a Lung Mass Caused by Xanthogranulomatous Inflammation
Authors: GANG-UEI HUNG, CHIA-HUNG KAO, WAN-YU LIN, SHYH-JEN WANG
Journal: Clinical Nuclear Medicine (2000)

A 36-year-old woman had hypertrophic pulmonary osteoarthropathy (HPOA) caused by xanthogranulomatous inflammation of the lung. After resection of the lesion, bone pain disappeared dramatically. A bone scan repeated 2 months later revealed resolution of HPOA. This condition is most frequently a result of lung cancer, which occurs in 80% of patients with HPOA. To our knowledge, HPOA in association with xanthogranulomatous inflammation has not been reported before.
Targeting the Heat Shock Factor 1 by RNA Interference: A Potent Tool to Enhance Hyperthermochemotherapy Efficacy in Cervical Cancer
Authors: Antonio Rossi, Stefania Ciafrè, Mirna Balsamo, Pasquale Pierimarchi, M. Gabriella Santoro
Journal: Cancer Research (2006)

Abstract Carcinoma of the uterine cervix is one of the highest causes of mortality in female cancer patients worldwide, and improved treatment options for this type of malignancy are highly needed. Local hyperthermia has been successfully used in combination with systemic administration of cisplatin-based chemotherapy in phase I/II clinical studies. Heat-induced expression of cytoprotective and antiapoptotic heat shock proteins (HSP) is a known complication of hyperthermia, resulting in thermotolerance and chemoresistance and hindering the efficacy of the combination therapy. Heat shock transcription factor 1 (HSF1) is the master regulator of heat-induced HSP expression. In the present report, we used small interfering RNA (siRNA) to silence HSF1 and to examine the effect of HSF1 loss of function on the response to hyperthermia and cisplatin-based chemotherapy in HeLa cervical carcinoma. We have identified the 322-nucleotide to 340-nucleotide HSF1 sequence as an ideal target for siRNA-mediated HSF1 silencing, have created a pSUPER-HSF1 vector able to potently suppress the HSF1 gene, and have generated for the first time human cancer cell lines with stable loss of HSF1 function. We report that, although it surprisingly does not affect cancer cell sensitivity to cisplatin or elevated temperatures up to 43°C when administered separately, loss of HSF1 function causes a dramatic increase in sensitivity to hyperthermochemotherapy, leading to massive (&amp;gt;95%) apoptosis of cancer cells. These findings indicate that disruption of HSF1-induced cytoprotection during hyperthermochemotherapy may represent a powerful strategy to selectively amplify the damage in cancer cells and identify HSF1 as a promising therapeutic target in cervical carcinoma. (Cancer Res 2006; 66(15): 7678-85)
On the Association Between Diabetes and Mental Disorders in a Community Sample
Authors: Johannes Kruse, Norbert Schmitz, Wolfgang Thefeld
Journal: Diabetes Care (2003)

OBJECTIVE—To determine the relationship between mental disorders and diabetes in a representative community sample. RESEARCH DESIGN AND METHODS—This was a cross-sectional study. Data on diabetes and HbA1c values were obtained by structured questionnaires and by laboratory assessments. Current psychiatric disorders were diagnosed by a modified version of the Composite International Diagnostic Interview (CIDI). RESULTS—People with diabetes (PWD) were not more likely to meet Diagnostic and Statistical Manual of Psychiatric Disorders, 4th edition (DSM-IV) criteria for at least one mental disorder than were individuals without diabetes. However, a different diagnostic pattern occurred compared with the general population: odds ratios (ORs) for anxiety disorders in PWD were higher (OR 1.93, 95% CI 1.19–3.14). Although PWD had higher prevalence rates of affective disorders, the relationship between diabetes and affective disorders was not statistically significant after controlling for age, sex, marital status, and socioeconomic status. In contrast, the relationship between diabetes and anxiety disorders remained significant after controlling for these variables. In contrast to individuals without mental disorders, PWD with affective or anxiety disorders more frequently had adequate glycemic control. CONCLUSIONS—Diabetes was associated with an increased likelihood of anxiety disorders. The association between mental disorders, diabetes, and glycemic control should be evaluated carefully in terms of potentially confounding sociodemographic variables, sample characteristics, and definitions of the disorders.
Beyond Cholesterol: The Johns Hopkins Complete Guide for Avoiding Heart Disease
Authors: Donald M. Watkin
Journal: JAMA (1990)

<i>Beyond Cholesterol</i>, written by Peter Kwiterovich, MD, director of the Lipid Research Clinic at The Johns Hopkins School of Medicine, is an exceedingly timely—in fact, almost indispensable— guide for all readers. While addressed to patients, it contains so much justification for its title that it may be considered required reading for physicians who are not themselves at the forefront of lipid research. While Thomas J. Moore ("The Cholesterol Myth,"<i>Atlantic</i>, September 1989 [see previous review]) and others have limited their discussions to total cholesterol, triglycerides, and low-density lipoprotein and high-density lipoprotein cholesterol, Kwiterovich leads readers into, inter alia, hypoHDL and hyperapoB as explanations for why people with low total cholesterol levels may experience the tragedies of myocardial infarction. He uses examples drawn from his own practice to deal with the symptomatology, genetics, laboratory diagnostic findings, treatment, and long-term follow-up of patients; each of the patients he describes presented with a
The Man They Wouldn't Let Die
Authors: James F. Holloran
Journal: JAMA (1965)

Lev Landau, the eminent Russian physicist, lay dying after an automobile accident. His skull was fractured, his pelvis shattered, his viscera ruptured. Four times he seemed to slip away from life, and four times a team of specialists pulled him back.  This dramatic event led the author to prepare a popular biography of Landau the man. And just as dramatic as his return from apparent death is the story of his earlier days, when he assisted at the birth of a new physics. Bohr, Gamow, Pauli, Heisenberg, men who shaped the atomic age, move continually through Landau's life. Landau learned from them, argued with them, and, in turn, taught them.  Interwoven with these intellectual events of the 20's and 30's are the political upheavals of the same era. Russia was in turmoil and the wide-spread persecutions did not spare scientists. Landau himself, thrown into prison, escaped long internment only by