tbuckley/cabot-search huggingface dataset:
Triggers of onset of acute cardiovascular disease.
Authors: L A Soloff
Journal: Circulation (1990)

Vesterqvist's normal subjects regular joggers?Is strenuous exer- cise associated with increased activation of endothelial cells and faster recovery from aspirin?Certainly, under the conditions existing immediately after a myocardial infarction, sufficient stim- ulation of endothelial cells may occur to accelerate their recovery from aspirin.Both our study and that of Vesterqvist suggest that significant long-term aspirin therapy (300 mg daily or 500 mg every third day) can occur with much less inhibition of PGI2 than thromboxane.As we found and as has also been shown by Kyrle et al,8 long-term lower doses of aspirin appear to have a greater suppressive effect on vascular prostacyclin.It will be important to better understand the basis for these results and whether they reflect changes from quiescent to stimulated endothelial cells, an induction of endothe- lial cyclooxygenase, an effect of residual salicylate to block aspirin acetylation of the vessel wall cyclooxygenase, or relate in some way to the capacity of the liver or other tissues to degrade aspirin.
The allergenic relevance of profilin (Ole e 2) from <i>Olea europaea</i> pollen
Authors: A. Martínez, J. A. Asturias, J. Monteseirín, V. Moreno, A. García‐Cubillana, M. Hernández, A. De La Calle, C. Sánchez‐Hernández, J. L. Pérez‐Formoso, J. Conde
Journal: Allergy (2002)

Many works have dealt with the study of the allergenic relevance of profilin from allergenic extracts, mainly derived from pollens and vegetable foods. Olive pollen extracts also contain a profilin allergen (Ole e 2). This protein has been characterized in detail, so the aminoacid sequence of three isoforms and the structural model of one of them are already known. The prevalence of Ole e 2 for olive allergenic patients has been evaluated by different in vivo and in vitro methods, and the results compared with those obtained for another pollen profilins.
Lipoprotein (a) accumulates intracellularly in coronary atherectomy specimens obtained from primary and restenotic lesions after PTCA
Authors: Daniel I. Simon, Frederick J. Sehoen, Gunther M. Fless, Angelo M. Scanu, Dwayne A. Schmidt, Robert D. Safian, William F. Penny, Donald S. Baim, Joseph Loscalzo
Journal: Journal of the American College of Cardiology (1991)
Is everyone Bayes? On the testable implications of Bayesian Fundamentalism
Authors: Maarten Speekenbrink, David R. Shanks
Journal: Behavioral and Brain Sciences (2011)

Abstract A central claim of Jones &amp; Love's (J&amp;L's) article is that Bayesian Fundamentalism is empirically unconstrained. Unless constraints are placed on prior beliefs, likelihood, and utility functions, all behaviour – it is proposed – is consistent with Bayesian rationality. Although such claims are commonplace, their basis is rarely justified. We fill this gap by sketching a proof, and we discuss possible solutions that would make Bayesian approaches empirically interesting.
Differential subunit composition of the G protein–activated inward-rectifier potassium channel during cardiac development
Authors: Bernd K. Fleischmann, Yaqi Duan, Yun Fan, Torsten Schoneberg, Andreas Ehlich, Nibedita Lenka, Serge Viatchenko-Karpinski, Lutz Pott, Juergen Hescheler, Bernd Fakler
Journal: Journal of Clinical Investigation (2004)

Parasympathetic slowing of the heart rate is predominantly mediated by acetylcholine-dependent activation of the G protein–gated potassium (K+) channel (IK,ACh). This channel is composed of 2 inward-rectifier K+ (Kir) channel subunits, Kir3.1 and Kir3.4, that display distinct functional properties. Here we show that subunit composition of IK,ACh changes during embryonic development. At early stages, IK,ACh is primarily formed by Kir3.1, while in late embryonic and adult cells, Kir3.4 is the predominant subunit. This change in subunit composition results in reduced rectification of IK,ACh, allowing for marked K+ currents over the whole physiological voltage range. As a consequence, IK,ACh is able to generate the membrane hyperpolarization that underlies the strong negative chronotropy occurring in late- but not early-stage atrial cardiomyocytes upon application of muscarinic agonists. Both strong negative chronotropy and membrane hyperpolarization can be induced in early-stage cardiomyocytes by viral overexpression of the mildly rectifying Kir3.4 subunit. Thus, a switch in subunit composition is used to adopt IK,ACh to its functional role in adult cardiomyocytes.
Outlier Status of U.S. Health Care Costs
Authors: Steven D. Hanks
Journal: Annals of Internal Medicine (2005)

Letters15 November 2005Outlier Status of U.S. Health Care CostsSteven D. Hanks, MDSteven D. Hanks, MDFrom Central Connecticut Health Alliance, New Britain, CT 06050.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-143-10-200511150-00024 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:In the first of his 4-part series on health care costs, Bodenheimer (1) lists 7 varying perspectives on why health care costs are high and what should be done to solve the problem. There is an eighth perspective that he does not mention, however—one that economists have discussed for almost 40 years. Health care costs have risen relative to the price of other goods as a result of differing levels of productivity growth in health care as opposed to other industries. This phenomenon of unbalanced productivity growth was first described by New York University economist William Baumol ...References1. Bodenheimer T. High and rising health care costs. Part 1: seeking an explanation. Ann Intern Med. 2005;142:847-54. [PMID: 15897535] LinkGoogle Scholar2. Baumol WJ. Macroeconomics of unbalanced growth. Am Econ Rev. 1967;62:415-26. Google Scholar3. Baumol WJ. Anatomy of an illusion: do health care costs matter? The New Republic. 22 November 1993:16-8. Google Scholar4. Triplett JE, Bosworth BP. Productivity Measurement Issues in Service Industries: Baumol's Disease Has Been Cured. Federal Reserve Bank of New York Economic Policy Review. New York: Federal Reserve Bank of New York; 2003:23-30. Google Scholar Author, Article, and Disclosure InformationAuthors: Steven D. Hanks, MDAffiliations: From Central Connecticut Health Alliance, New Britain, CT 06050.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoHigh and Rising Health Care Costs. Part 1: Seeking an Explanation Thomas Bodenheimer Outlier Status of U.S. Health Care Costs Thomas Bodenheimer Outlier Status of U.S. Health Care Costs Michael J. Keberlein Metrics 15 November 2005Volume 143, Issue 10Page: 759KeywordsConflicts of interestFallsForecastingHealth careHealth care sectorHealth information technologyInformation technologyInpatients ePublished: 15 November 2005 Issue Published: 15 November 2005 Copyright & PermissionsCopyright © 2005 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Effect of simvastatin and/or pioglitazone on insulin resistance, insulin secretion, adiponectin, and proinsulin levels in nondiabetic patients at cardiovascular risk—the PIOSTAT Study
Authors: Thomas Forst, Andreas Pfützner, Georg Lübben, Matthias Weber, Nikolaus Marx, Efstrathios Karagiannis, Carsta Koehler, Werner Baurecht, Cloth Hohberg, Markolf Hanefeld
Journal: Metabolism (2007)
Identical-Twin Bone Marrow Transplants for Leukemia
Authors: Robert Peter Gale
Journal: Annals of Internal Medicine (1994)

Objective: To compare outcomes of identical-twin with HLA-identical sibling bone marrow transplants for leukemia. Design: Matched-pair analysis comparing relapse, treatment-related mortality, and leukemia-free survival in cohorts matched for disease and variables correlated with transplant outcome, with and without adjustment for graft-versus-host disease. Setting: 163 institutions worldwide between 1978 and 1990, reporting to the International Bone Marrow Transplant Registry. Participants: 103 identical-twin transplants: 24 for acute lymphoblastic leukemia (ALL) in first remission, 45 for acute myelogenous leukemia (AML) in first remission, and 34 for chronic myelogenous leukemia (CML) in first chronic phase. Results were compared with those in 1030 concurrent HLA-identical sibling transplants matched for prognostic factors. Results: Three-year probabilities of relapse after identical-twin compared with HLA-identical sibling transplants were as follows: ALL, 36% (95% CI, 17% to 55%) compared with 26% (CI, 20% to 32%); AML, 52% (CI, 37% to 67%) compared with 16% (CI, 12% to 20%); and CML, 40% (CI, 23% to 57%) compared with 7% (CI, 4% to 10%). Increased relapse risks in AML and CML persisted after adjusting for graft-versus-host disease (relative risk, 3.1 [CI, 1.9 to 5.1] and 5.5 [CI, 2.8 to 11.0], respectively). Although twins had less treatment-related mortality than HLA-identical siblings, leukemia-free survival was similar. Three-year leukemia-free survival probabilities after twin compared with HLA-identical sibling transplants were as follows: ALL, 57% (CI, 37% to 77%) compared with 58% (CI, 52% to 64%); AML, 42% (CI, 27% to 57%) compared with 55% (CI, 50% to 60%); and CML, 59% (CI, 42% to 76%) compared with 61% (CI, 56% to 66%). Conclusions: Identical-twin transplants in AML and CML are associated with increased relapse risk compared with HLA-identical sibling transplants. A similar trend was observed in ALL but was not statistically significant. Increased relapse in twin transplants is not explained by lack of graft-versus-host disease. Leukemia-free survival after twin and HLA-identical sibling transplants is similar because increased relapse in twins is offset by decreased treatment-related mortality.
Diesel Exhaust Particles Activate the Matrix-Metalloproteinase-1 Gene in Human Bronchial Epithelia in a β-Arrestin–Dependent Manner via Activation of RAS
Authors: Jinju Li, Andrew J. Ghio, Seung-Hyun Cho, Constance E. Brinckerhoff, Sidney A. Simon, Wolfgang Liedtke
Journal: Environmental Health Perspectives (2008)

BackgroundDiesel exhaust particles (DEPs) are globally relevant air pollutants that exert a detrimental human health impact. However, mechanisms of damage by DEP exposure to human respiratory health and human susceptibility factors are only partially known. Matrix metalloproteinase-1 (MMP-1) has been implied as an (etio)pathogenic factor in human lung and airway diseases such as emphysema, chronic obstructive pulmonary disease, chronic asthma, tuberculosis, and bronchial carcinoma and has been reported to be regulated by DEPs.ObjectiveWe elucidated the molecular mechanisms of DEPs' up-regulation of MMP-1.Methods/ResultsUsing permanent and primary human bronchial epithelial (HBE) cells at air–liquid interface, we show that DEPs activate the human MMP-1 gene via RAS and subsequent activation of RAF-MEK-ERK1/2 mitogen-activated protein kinase signaling, which can be scaffolded by β-arrestins. Short interfering RNA mediated β-arrestin1/2 knockout eliminated formation, subsequent nuclear trafficking of phosphorylated ERK1/2, and resulting MMP-1 transcriptional activation. Transcriptional regulation of the human MMP-1 promoter was strongly influenced by the presence of the –1607GG polymorphism, present in 60–80% of humans, which led to striking up-regulation of MMP-1 transcriptional activation.ConclusionOur results confirm up-regulation of MMP-1 in response to DEPs in HBE and provide new mechanistic insight into how these epithelia, the first line of protection against environmental insults, up-regulate MMP-1 in response to DEP inhalation. These mechanisms include a role for the human –1607GG polymorphism as a susceptibility factor for an accentuated response, which critically depends on the ability of β-arrestin1/2 to generate scaffolding and nuclear trafficking of phosphorylated ERK1/2.
Malaria Prophylaxis-Reply
Authors: Donald Catino
Journal: JAMA (1983)

<h3>In Reply.—</h3> I completely agree with most of what Dr Schwartz and colleagues say in their letter. They echo many of the points made in our original article, which was shortened considerably to be published as a letter to the editor. They took exception to our statement concerning "the responsibility for the dissemination of such health information." We refer them to Dr Myron Schultz, director of their own Parasitic Disease Division, who wrote to us in 1979, stating: The sources of information (for travelers) on malaria prophylaxis and the quality of that information is unknown to us in any meaningful statistical manner. This is an important subject since any remedial action to correct the problem should be targeted to the most appropriate recipients. My suspicion is that there are deficiencies all along the chain of (mis)information. We have been trying to determine the identities of "the most appropriate recipients." The
Practolol in angina.
Authors: D N Phear
Journal: BMJ (1971)

This hepatotoxic effect of busulphan ther- apy appears to be rare and in this case was associated with prolonged therapy.However, we suggest that jaundice in patients under treatment for chronic granulocytic leukaemia may be attributable to busulphan therapy rather than severe leukaemic infiltration of the liver.-Weare, etc.,
Lack of Evidence for Contact Sensitization by <i>Pfiesteria</i> Extract
Authors: Rachel M. Patterson, Edward Noga, Dori Germolec
Journal: Environmental Health Perspectives (2007)

Members of the estuarine dinoflagellate genus Pfiesteria are reported to have been responsible for massive fish kills in the southeastern United States. Some reports suggest that exposure to waters having Pfiesteria blooms or occupation-related exposure might result in Pfiesteria-induced dermal irritation and inflammation. Although the toxin has not been isolated and purified, the original data suggested both hydrophilic and hydrophobic toxic components. Some investigators propose that dermonecrotic properties are associated with a hydrophobic fraction.
A missense mutation in the glucagon receptor gene is associated with non–insulin–dependent diabetes mellitus
Authors: J. Hager, L. Hansen, C. Vaisse, N. Vionnet, A. Philippi, W. Poller, G. Velho, C. Carcassi, L. Contu, C. Julier, F. Cambien, P. Passa, M. Lathrop, W. Kindsvogel, F. Demenais, E. Nishimura, P. Froguel
Journal: Nature Genetics (1995)
Primary hypothyroidism presenting as pituitary failure.
Authors: W M Tunbridge, J C Marshall, C W Burke
Journal: BMJ (1973)

Plasma cortisol and growth hormone levels did not rise when hypoglycaemia was induced, but plasma cortisol rose after an intramuscular injection of 5U of vasopressin.Further, the plasma thyroid-stimulating hormone level measured by radioimmunoassay, responded to thyrotrophin-releasing hormone 200 ,g given intra- venously (see table ).No evidence of tumour recurrence was found at operation, and replacement therapy with cortisone, testosterone, and thyroxine produced increased energy, hair growth, and decreased cold sensitivity.
Health Insurance: Definitions and Distinctions
Authors: Bert A. Loftman
Journal: JAMA (1995)

<h3>To the Editor.</h3> —The article by Dr Safran and colleagues<sup>1</sup>proposed to compare fee-for-service with prepaid health care systems. The comparison is misleading because the former is an employer-provided, fee-for-service medical care system with utilization review. This is really nothing more than another form of managed care, and definitely not true fee-for-service. A true fee-for-service system would not incorporate any utilization review because the user would be able to purchase medical care from any physician or hospital. The patient would not be limited by his or her insurance carrier. A more accurate comparison would have used a fee-for-service example whereby the patient has a high-deductible, patient-paid medical insurance plan without the current tax penalty under which patient-paid medical care must function. Any medical care or insurance that a patient buys is purchased with after-tax dollars, while employer-paid medical care benefits are purchased with the employees' pretax dollars. This occurs
Cardiac Myocyte Z-Line Calmodulin Is Mainly RyR2-Bound, and Reduction Is Arrhythmogenic and Occurs in Heart Failure
Authors: Yi Yang, Tao Guo, Tetsuro Oda, Asima Chakraborty, Le Chen, Hitoshi Uchinoumi, Anne A. Knowlton, Bradley R. Fruen, Razvan L. Cornea, Gerhard Meissner, Donald M. Bers
Journal: Circulation Research (2013)

Calmodulin (CaM) associates with cardiac ryanodine receptor type-2 (RyR2) as an important regulator. Defective CaM-RyR2 interaction may occur in heart failure, cardiac hypertrophy, and catecholaminergic polymorphic ventricular tachycardia. However, the in situ binding properties for CaM-RyR2 are unknown.We sought to measure the in situ binding affinity and kinetics for CaM-RyR2 in normal and heart failure ventricular myocytes, estimate the percentage of Z-line-localized CaM that is RyR2-bound, and test cellular function of defective CaM-RyR2 interaction.Using fluorescence resonance energy transfer in permeabilized myocytes, we specifically resolved RyR2-bound CaM from other potential binding targets and measured CaM-RyR2 binding affinity in situ (Kd=10-20 nmol/L). Using RyR2(ADA/+) knock-in mice, in which half of the CaM-RyR2 binding is suppressed, we estimated that >90% of Z-line CaM is RyR2-bound. Functional tests indicated a higher propensity for Ca2+ wave production and stress-induced ventricular arrhythmia in RyR2(ADA/+) mice. In a post-myocardial infarction rat heart failure model, we detected a decrease in the CaM-RyR2 binding affinity (Kd≈51 nmol/L; ≈3-fold increase) and unaltered RyR2 affinity for the FK506-binding protein FKBP12.6 (Kd~0.8 nmol/L).CaM binds to RyR2 with high affinity in cardiac myocytes. Physiologically, CaM is bound to >70% of RyR2 monomers and inhibits sarcoplasmic reticulum Ca2+ release. RyR2 is the major binding site for CaM along the Z-line in cardiomyocytes, and dissociating CaM from RyR2 can cause severe ventricular arrhythmia. In heart failure, RyR2 shows decreased CaM affinity, but unaltered FKBP 12.6 affinity.
ASSESSMENT OF PLAQUE BURDEN USING CORONARY CT CALCIUM SCORES IN POLICE OFFICERS AND FIREFIGHTERS IN NEW YORK STATE
Authors: M. Zubair Jafar, Navdeep Bhatti, Danyaal Moin, Lisa Pedevillano, Lakshmi Munnangi, Asma Siddiqui, Daniel O’Dea, Larry Schek, Mike Yen, Julie Ling, Larry Solomon
Journal: Journal of the American College of Cardiology (2010)
T6 TRAIL is a potential novel therapeutic target in pulmonary arterial hypertension
Authors: A. G. Hameed, N. D. Arnold, J. Pickworth, J. C. Chamberlain, C. M. H. Newman, D. C. Crossman, S. E. Francis, A. Lawrie
Journal: Thorax (2011)

<h3>Introduction and Objectives</h3> Pulmonary Arterial Hypertension (PAH) is a life threatening disease characterised by the progressive narrowing and occlusion of small pulmonary arteries, driven by the dysregulated growth of vascular cells. Current therapies are unable to reverse PAH and so identifying key pathways in disease pathogenesis should permit the development of more targeted therapeutics. The cytokine, Tumour Necrosis Factor (TNF)-Related Apoptosis-Inducing Ligand (TRAIL) induces EC apoptosis and SMC proliferation in the systemic circulation, but hitherto has not been studied in PAH. We recently determined that TRAIL is a mitogen for human PA-SMCs in-vitro and was associated with pulmonary vascular lesions in humans and rodent models. We thus hypothesised that TRAIL is an important mediator in the pathogenesis of PAH and now describe the potential therapeutic benefits of targeting TRAIL in-vivo using two animal models. <h3>Methods</h3> To test whether blocking TRAIL could prevent the development of PAH, an anti-TRAIL antibody was delivered via osmotic mini-pump coincident with the induction of PAH in the MCT rat model. We also tested whether genetic deletion of TRAIL (ApoE−/−/TRAIL−/− mice) would confer protection to diet-induced PAH. To test whether inhibiting TRAIL could reverse established disease we again treated both models with an anti-TRAIL antibody starting from day 21 in the rat and 8 weeks in the ApoE−/− mouse. Phenotyping included echocardiography, closed chest cardiac catheterisation followed by immuno-histological and biochemical analyses of the lung. <h3>Results</h3> Antibody blockade (MCT) and genetic deletion (ApoE−/−) of TRAIL prevented the development of PAH in both models. Interestingly a PAH disease phenotype was restored in ApoE−/−/TRAIL−/− mice by the administration of recombinant TRAIL. In rodents with established PAH, an anti-TRAIL antibody, significantly increased survival and reduced pulmonary vascular remodelling in the fatal rat MCT model (p&lt;0.05 cf control). In the murine model, an anti-TRAIL antibody treatment reversed both haemodynamics (RVSP 27 mm Hg vs 88 mm Hg, p&lt;0.001) and pulmonary vascular remodelling. <h3>Conclusions</h3> Our preclinical investigations are the first to determine the importance of TRAIL to disease pathogenesis and highlight its potential as a novel and rational target to direct future translational therapies for PAH.
Hemodynamic Effects of Intravenous Digoxin in Acute Myocardial Infarction.
Authors: Harry Lipp
Journal: Annals of Internal Medicine (1972)

Meeting Abstracts1 May 1972Hemodynamic Effects of Intravenous Digoxin in Acute Myocardial Infarction.Harry Lipp, M.B.B.S., Pablo Denes, M.D., Miguel Gambetta, M.D., Leon Resnekov, M.D.Harry Lipp, M.B.B.S.Search for more papers by this author, Pablo Denes, M.D.Search for more papers by this author, Miguel Gambetta, M.D.Search for more papers by this author, Leon Resnekov, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-76-5-865_4 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptEight patients with acute myocardial infarction, three not in failure and five in moderate or severe clinical or hemodynamic failure, were investigated after the intravenous administration of 0.5 to 0.75 mg digoxin. Mean aortic pressure (Ao), mean pulmonary arterial pressure (PA), left ventricular filling pressure (LVFP), cardiac index (CI), stroke index (SI), arterial PO2, pulmonary arterial oxygen saturation (pulmonary arterial So2), systemic vascular resistance (SVR), left ventricular stroke work index (LVSWI), left ventricular minute work index (LVMWI), and tension time index (TTI) were obtained before and 1 hour after intravenous digoxin. Patients in moderate or severe failure had significant changes... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Harry Lipp, M.B.B.S.; Pablo Denes, M.D.; Miguel Gambetta, M.D.; Leon Resnekov, M.D.Affiliations: Chicago, Ill. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1972Volume 76, Issue 5Page: 865-866KeywordsAcute myocardial infarctionBlood pressureHemodynamicsOxygenPartial pressure of oxygenPulmonary arteryStrokeSystemic vascular resistance ePublished: 1 December 2008 Issue Published: 1 May 1972 PDF downloadLoading ...