tbuckley/cabot-search huggingface dataset:
Prospective study on anti-hepatitis C virus–positive patients with persistently normal serum alanine transaminase with or without detectable serum hepatitis C virus RNA
Authors: Michelle Martinot-Peignoux, Nathalie Boyer, Dominique Cazals-Hatem, Bach-Nga Pham, Anne Gervais, Véronique Le Breton, Stéphane Levy, Claude Degott, Dominique-Charles Valla, Patrick Marcellin
Journal: Hepatology (2001)

A significant proportion of patients with detectable antibodies to hepatitis C virus have normal serum alanine transaminase levels. Our aim was to study the outcome of this group. Between 1992 and 1999, 135 consecutive anti-HCV-positive patients with persistently normal ALT were followed for 3.6 +/- 2.3 years (0.5 to 8.5 years), 108 had a liver biopsy at inclusion, and 24 had a second liver biopsy 3.5 +/- 1.0 years later. Serum HCV RNA was detectable with PCR in 94 patients (69%) and not detectable in 41 patients (31%). Patients with and without detectable serum HCV RNA had similar epidemiological characteristics. Serum ALT levels and anti-HCV ratio were lower (P =.001), and histological lesions had lower grade and stage in patients without detectable serum HCV RNA (P =.001). Liver HCV RNA was not detectable with PCR in the 12-serum HCV RNA-negative patients tested. During follow-up, all patients without detectable serum HCV RNA remained HCV RNA-negative and kept normal serum ALT; all patients with detectable serum HCV RNA remained HCV RNA-positive, 20 (21%) had a slight fluctuation of serum ALT above the upper limit of normal. No significant changes were observed in the liver lesions of the 24 patients who underwent a second liver biopsy. In anti-HCV-positive patients with persistently normal serum ALT, histological lesions are significantly lower in HCV RNA-negative than in HCV RNA-positive patients. During follow-up, the HCV RNA status of patients remained unchanged; 21% of the patients with detectable serum HCV RNA had slight increase in serum ALT levels, but histological lesions remained stable.
COMPARISON OF CLINICAL, ELECTROCARDIOGRAPHIC AND PHYSIOLOGICAL SIGNIFICANCE BETWEEN MAIN VERSUS SIDE BRANCHES IN CORONARY BIFURCATION LESIONS
Authors: Bon Kwon Koo, Seung&ndash;Pyo Lee, Ju&ndash;Hee Lee, Kyung Woo Park, Jung&ndash;Won Suh, Woo Young Jung, Joon Hyung Doh, Chang&ndash;Wook Nam, CheolWoong Yu, Bong&ndash;Ki Lee, Dobrin Vassilev, Hong&ndash;Seok Lim, Seung Jea Tahk, Hyo&ndash;Soo Kim
Journal: Journal of the American College of Cardiology (2012)
Toxoplasma gondii alters eicosanoid release by human mononuclear phagocytes: role of leukotrienes in interferon gamma-induced antitoxoplasma activity.
Authors: E C Yong, E Y Chi, W R Henderson
Journal: The Journal of Experimental Medicine (1994)

Toxoplasma gondii tachyzoites markedly alter the profile of eicosanoids released by human mononuclear phagocytes. Freshly isolated, 2-h adherent human monocytes release both cyclooxygenase (e.g., thromboxane [TX] B2, prostaglandin [PG] E2) and 5-lipoxygenase (e.g., leukotriene [LT] B4, LTC4) products of arachidonic acid metabolism after stimulation by the calcium ionophore A23187 or ingestion of opsonized zymosan particles or heat-killed T. gondii. However, after incubation with viable T. gondii, normal and chronic granulomatous disease monocytes release only the cyclooxygenase products TXB2 and PGE2 and fail to form LTB4, LTC4, or other 5-lipoxygenase products. Monocytes maintained in culture for 5 d lose this capacity to release TXB2 and PGE2 after incubation with T. gondii. T. gondii significantly inhibit calcium ionophore A23187-induced LTB4 release by monocyte-derived macrophages; heat-killed organisms do not affect this calcium ionophore A23187-induced release of LTB4. T. gondii-induced inhibition of LTB4 release by calcium ionophore A23187-stimulated monocyte-derived macrophage is reversed by interferon (IFN)-gamma treatment of the monolayers. LTB4 induced extensive damage to the cellular membranes and cytoplasmic contents of the organisms as observed by transmission electron microscopy. Exogenous LTB4 (10(-6) M) induced intracellular killing of ingested T. gondii by non-IFN-gamma-treated monocyte-derived macrophages. IFN-gamma-induced antitoxoplasma activity in monocyte-derived macrophages was inhibited by the selective 5-lipoxygenase inhibitor zileuton but not by the cyclooxygenase inhibitor indomethacin. These findings suggest a novel role for 5-lipoxygenase arachidonic acid products in human macrophage IFN-gamma-induced antitoxoplasma activity.
NOVEL TECHNIQUE FOR AORTIC ROOT MODELING USING REAL-TIME THREE DIMENSIONAL ECHOCARDIOGRAPHY
Authors: Arminder S. Jassar, Benjamin M. Jackson, Liam P. Ryan, Thomas J. Eperjesi, Martin G. St. John Sutton, Victor A. Ferrari, Joseph H. Gorman, Robert C. Gorman
Journal: Journal of the American College of Cardiology (2011)
Carcinoma in situ of the Upper Urinary Tract Treated with Radical Nephroureterectomy – Results from a Multicenter Study
Authors: Jose A. Karam, Vitaly Margulis, Francesco Montorsi, Pierre I. Karakiewicz, Yair Lotan, Eiji Kikuchi, Alon Weizer, Richard Zigeuner, Christian Bolenz, Shahrokh F. Shariat
Journal: European Urology (2008)
Differentiation of constrictive pericarditis from restrictive cardiomyopathy: Assessment of left ventricular diastolic velocities in longitudinal axis by doppler tissue imaging
Authors: Mario J. Garcia, Leonardo Rodriguez, Miguel Ares, Brian P. Griffin, James D. Thomas, Allan L. Klein
Journal: Journal of the American College of Cardiology (1996)

We sought to determine the utility of left ventricular expansion velocities in differentiating constrictive pericarditis from restrictive cardiomyopathy. Several studies have shown that left ventricular diastolic expansion is influenced by the elastic recoil forces of the myocardium. These forces are affected by intrinsic myocardial disease but should be preserved when diastole is impaired as a result of extrinsic causes. Using Doppler tissue imaging, we measured peak early velocity of longitudinal axis expansion (Ea) in 8 patients with constrictive pericarditis, 7 patients with restriction and 15 normal volunteers. Transmitral early (E) and late (A) Doppler flow velocities, left ventricular systolic and diastolic volumes, ejection fraction and mitral annular M-mode displacement were also compared between the groups. The Eavalue was significantly higher in normal subjects (14.5 ± 4.7 cm/s [mean ±SD]) and in patients with constriction (14.8 ± 4.8 cm/s) than in those with restriction (5.1 ± 1.4 cm/s, p < 0.001 constriction vs. restriction). There was weak correlation between Eaand the extent of annular displacement (r = 0.55, p = 0.004) and the E/A ratio (r = 0.44, p = 0.03). There was no correlation between Eaand E (r = 0.33, p = 0.07) or ejection fraction (r = 0.21, p = 0.26). By multivariate analysis, Eawas the best variable for differentiating constriction from restriction. Our study indicates that longitudinal axis expansion velocities are markedly reduced in patients with restrictive cardiomyopathy. The poor correlation found with transvalvular flow velocities suggests that Eamay be relatively preload independent. The measurement of longitudinal axis expansion velocities provides a clinically useful distinction between constrictive pericarditis and restrictive cardiomyopathy and may prove to be valuable in the study of diastolic function.
Misbelief and the neglect of environmental context
Authors: David Dunning
Journal: Behavioral and Brain Sciences (2009)

Abstract Focusing on the individual's internal cognitive architecture, McKay &amp; Dennett (M&amp;D) provide an incomplete analysis because they neglect the crucial role played by the external environment in producing misbeliefs and determining whether those misbeliefs are adaptive. In some environments, positive illusions are not adaptive. Further, misbeliefs often arise because the environment commonly fails to provide crucial information needed to form accurate judgments.
Pharmacological response of quinidine induced early afterdepolarisations in canine cardiac Purkinje fibres: insights into underlying ionic mechanisms
Authors: S. NATTEL, M. A QUANTZ
Journal: Cardiovascular Research (1988)

The purpose of these experiments was to study the pharmacological response of quinidine induced early afterdepolarisations to gain insights into underlying ionic mechanisms. Quinidine (8.5 μM) induced stable early afterdepolarisations at low activation frequencies in 80% of canine cardiac Purkinje fibres superfused with a modified Tyrode's solution. Early afterdepolarisations arose from a secondary plateau in the voltage range of −30 to −60 mV. Calcium channel blockers (verapamil, 1 μM, in 3/6 preparations; verapamil, 10 μM in 6/6 preparations; nifedipine, 0.1 μM in 5/5 preparations) completely eliminated early afterdepolarisations, despite continued quinidine superfusion, without altering the underlying action potential. Isoprenaline (0.2-1 μM) restored them in 75% of these preparations during continued calcium blocker superfusion. Tetrodotoxin (5/5 preparations) eliminated early afterdepolarisations by abbreviating action potentials and reducing or eliminating the quinidine induced secondary plateau. While low concentrations of isoprenaline favoured the occurrence of early afterdepolarisations, larger concentrations eliminated them by enhancing spontaneous automaticity. These experiments suggest that voltage dependent and/or receptor regulated slow inward current plays an important role in quinidine induced early afterdepolarisations. Beta receptor stimulation can enhance or suppress early afterdepolarisations, depending on whether effects on slow inward current (tending to favour them) or on automaticity (suppressing them) predominate.
Sex Differences in Management and Outcome After Acute Myocardial Infarction in the 1990s
Authors: Shmuel Gottlieb, David Harpaz, Avraham Shotan, Valentina Boyko, Jonathan Leor, Miriam Cohen, Lori Mandelzweig, Benjamin Mazouz, Shlomo Stern, Solomon Behar
Journal: Circulation (2000)

Previous studies have suggested that women with acute myocardial infarction (AMI) are less aggressively managed than are men. The aim of this study was to assess sex differences in medical and invasive coronary procedures (angiography, PTCA, and CABG) in AMI patients admitted to cardiac care units (CCUs) in Israel in the mid 1990s and their association with early and 1-year prognosis.We studied 2867 consecutive AMI patients (2125 men, 74%) hospitalized in all 25 CCUs in Israel from 3 prospective nationwide surveys conducted in 1992, 1994, and 1996. Women were, on average, older than men (69 versus 61 years, P:<0.0001) and had a higher prevalence of hypertension, diabetes, Killip class >/=II on admission, and in-hospital complications. Women received aspirin and beta-blockers less often than did men, but these differences were not significant after age adjustment. The unadjusted rates of thrombolysis, angiography, and PTCA/CABG use were lower in women than in men but not after covariate adjustment: 42% versus 48% (adjusted odds ratio [OR] 0.92, 95% CI 0.77 to 1.11), 23% versus 31% (OR 0.88, 95% CI 0.70 to 1.09), and 15% versus 19% (OR 0.93, 95% CI 0.72 to 1.19), respectively. The 30-day mortality was higher in women than in men (17.6% versus 9.6%, respectively; OR 1.39, 95% CI 1.06 to 1.82), but the 30-day to 1-year mortality rate was not (9.1% versus 5.6%, respectively; hazard ratio 1.18, 95% CI 0.84 to 1.66).This prospective nationwide observational community-based study of consecutive AMI patients hospitalized in the CCUs in the mid 1990s indicates that women fare significantly worse than do men at 30 days but not thereafter at 1-year. The difference in 30-day outcome was not influenced by the use of different therapeutic modalities, including thrombolysis and invasive coronary procedures, but was rather due to the older age and greater comorbidity of women; these findings seem also to explain the less frequent use of invasive procedures in women.
Relationship between Fatty-Acid Composition of Platelets and Platelet Aggregation in Rat and Man
Authors: S. RENAUD, K. KUBA, C. GOULET, Y. LEMIRE, C. ALLARD
Journal: Circulation Research (1970)

Male rats fed a diet rich in butter or stearic acid presented a marked predisposition to endotoxin-initiated thrombosis. This was preceded by hypercholesterolemia, hypercoagulability, and an increased susceptibility of platelets to thrombin-induced aggregation. In contrast to this, feeding of corn oil or linoleic or oleic acids did not result in such marked changes in the blood or in severe thrombosis. Gas-liquid chromatographic analysis of total lipids of platelet and plasma indicated that the thrombogenic fat or fatty acid resulted in a highly significant increase, mostly in the platelets, of the ratio of saturated + monounsaturated to polyunsaturated fatty acids (S+M)/P. In patients who had suffered a myocardial infarction as compared with men without risk factors for coronary heart disease, an increase in the (S+M)/P in plasma and platelets was also observed. Among 17 active middle-aged businessmen, the five who presented signs of coronary heart disease also showed the highest susceptibility to thrombin-induced aggregation, but not to ADP or collagen. In these 17 subjects, the results of the thrombin aggregation could be correlated with the platelet (S+M)/P, but not with the plasma or platelet cholesterol. In both the rat and man, a high thrombotic tendency may be associated with a platelet hypersusceptibility to thrombin which, in turn, is related to changes in fatty-acid composition.
The effect of Goeckerman therapy on interferon in serum and suction blister fluid from patients with psoriasis
Authors: J.K. LIVDEN, J.R. BJERKE, M. DEGRE, R. MATRE
Journal: British Journal of Dermatology (1986)

Journal Article The effect of Goeckerman therapy on interferon in serum and suction blister fluid from patients with psoriasis Get access J.K. LIVDEN, J.K. LIVDEN Department of Dermatology, University of Bergen J.K.Livden, Broegelmann Research Laboratory for Microbiology, MFH‐bygget, N‐5016 Haukeland sykehus, Norway. Search for other works by this author on: Oxford Academic Google Scholar J.R. BJERKE, J.R. BJERKE Department of Dermatology, University of Bergen Search for other works by this author on: Oxford Academic Google Scholar M. DEGRE, M. DEGRE National Institute of Public Health, Department of Virology, Oslo, Norway Search for other works by this author on: Oxford Academic Google Scholar R. MATRE R. MATRE Broegelmann Research Laboratory for Microbiology, University of Bergen Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 114, Issue 2, 1 February 1986, Pages 217–225, https://doi.org/10.1111/j.1365-2133.1986.tb02800.x Published: 01 February 1986 Article history Accepted: 31 July 1985 Published: 01 February 1986
Ectopic pregnancy despite intrauterine contraception: a clue to mode of action of I.U.C.D.s.
Authors: G Jonas
Journal: BMJ (1975)

The Detector Circuit Description.-Twotransistors are used in a Darlington connection to provide a high gain.When the resistance between the input terminals Ti and T2 (see fig.) is lowered the transistor collector currents increase and one coil of the remanent relay RL is energized and opens both sets of contacts.The relay remains in this state even if the coil current returns to zero.The contacts RL2 are connected in series with the battery supply to an electric clock and contacts RL1 are connected in series with the internal batteries.The unit, therefore, consumes no current except during the very short time that the relay contacts are actually changing over.When the resistance at the input terminals is raised again the contacts of the remanent relay may be closed by pressing the reset button, which switches the relay back to its resting state.Operating Instructions.-Thesensing pad is connected to push-type terminals on one side of the unit and the clock battery supply is broken through a two-pin plug.If the pad is dry the input terminal resistance is high and the clock will start when the reset button is pressed.The sensitivity control VRI sets the terminal resistance at which the unit operates.
Apolipoprotein E genotype and association between smoking and early onset Alzheimer's disease
Authors: C. M van Duijn, L. M Havekes, C. Van Broeckhoven, P. de Knijff, A. Hofman
Journal: BMJ (1995)

<h3>Abstract</h3> <b>Objective</b>: To investigate the hypothesis that differential survival between smokers and nonsmokers leading to a decrease in the frequency of the e4 allele of the apolipoprotein E gene may explain the inverse relation between smoking history and early onset Alzheimer9s disease. <b>Design</b>: A population based case-control study. <b>Setting</b>: The four northern provinces of the Netherlands and metropolitan Rotterdam. <b>Subjects</b>: 175 patients with early onset Alzheimer9s disease and two independent control groups of 159 and 457 subjects. <b>Main outcome measures</b>: Frequencies of the apolipoprotein e4 allele and relative risk of early onset Alzheimer9s disease. <b>Results</b>: The inverse association between smoking history and early onset Alzheimer9s disease could not be explained by a decrease in the frequency of the apolipoprotein e4 allele. Among carriers of this allele with a family history of dementia subjects with a history of smoking had a strongly reduced risk of early onset Alzheimer9s disease (odds ratio 0.10 (95% confidence interval 0.01 to 0.87)). <b>Conclusions</b>: The results suggest that the inverse relation between smoking history and early onset Alzheimer9s disease cannot be explained by an increased mortality in carriers of the apolipoprotein e4 allele who smoke. The association is strongly modified by the presence of the apolipoprotein e4 allele as well as by a family history of dementia. <h3>Key messages</h3> Key messages This study shows that the inverse association between smoking history and early onset Alzheimer9s disease cannot be explained by a shift in frequency of the apolipoprotein e4 allele The inverse relation was significant only in subjects with a family history of dementia who carry the e4 allele Our study suggests that clinical trials with nicotine or nicotine derivatives have the greatest chance of success in patients with familial Alzheimer9s disease who carry the apolipoprotein e4 allele
PULMONARY REPERFUSION INJURY AFTER THE UNIFOCALIZATION PROCEDURE FOR TETRALOGY OF FALLOT, PULMONARY ATRESIA AND MAJOR AORTOPULMONARY COLLATERAL ARTERIES
Authors: Shiraz Maskatia, Jeffrey A. Feinstein, Beverley Newman, Frank L. Hanley, Stephen J. Roth
Journal: Journal of the American College of Cardiology (2011)
Time‐dependent cleavage of a high‐mannose form of I<sub>i</sub> to p<sup>25</sup> in an intracellular compartment
Authors: Lawrence J. Thomas, Robert E. Humphreys, Walter Knapp, Quoc V. Nguyen
Journal: American Journal of Hematology (1989)

Abstract The cleavage of a high‐mannose form of I i to p 25 was demonstrated in an intracellular compartment of B cells. Subcellular fractions of 72 hr‐activated B cells, separated by Percoll density gradient centrifugation, were immunoprecipitated with anti‐class II or anti‐I serum and characterized for 5′‐nucleotidase, acid phosphatase, and radiolabeled transferrin. The cleavage of p 25 from l i as a C‐terminal fragment occurred from 20 to 60 min after synthesis in an intracellular compartment which was intermediate in density between lysosomal and plasma membrane fractions and coincided with the lighter of two internalized transferrin compartments. Chloroquine or monensin treatments, at maximal nontoxic doses, which block Golgi and lysosomal functions, did not seem to alter the cleavage of 1 i to p 25 . p 25 molecules were reduced to about 10,500 daltons by treatment with endoglycosidases F or H. We conclude that p 25 was generated from a high mannose form of I i in the endoplasmic reticulum or cis‐Golgi. This finding could either implicate that site for class II MHC desetope charging with foreign peptides or reflect a mechanism for degradation of “excess” I i molecules.
Isolated basal keratinocytes express pemphigoid gestationis antigen
Authors: SUSAN E. KELLY, EVA McVITTIE, M. M. BLACK, S. FLEMING
Journal: British Journal of Dermatology (1992)

Journal Article Isolated basal keratinocytes express pemphigoid gestationis antigen Get access SUSAN E. KELLY, SUSAN E. KELLY Department of Dermatology, University of Edinburgh Dr S.E.Kelly, Department of Dermatology, University of Edinburgh, The Royal Infirmary, Edinburgh EH3 9YW. Search for other works by this author on: Oxford Academic Google Scholar EVA McVITTIE, EVA McVITTIE Department of Dermatology, University of Edinburgh Search for other works by this author on: Oxford Academic Google Scholar M. M. BLACK, M. M. BLACK Dowling Skin Unit, St Thomas' Hospital, London Search for other works by this author on: Oxford Academic Google Scholar S. FLEMING S. FLEMING Department of Pathology, University of Edinburgh Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 126, Issue 1, 1 January 1992, Pages 42–46, https://doi.org/10.1111/j.1365-2133.1992.tb08401.x Published: 01 January 1992
Racial Disparities in the Treatment of Depression in Low-Income Persons With Diabetes
Authors: Chandra Y. Osborn, Hollister W. Trott, Maciej S. Buchowski, Kushal A. Patel, Leslie D. Kirby, Margaret K. Hargreaves, William J. Blot, Sarah S. Cohen, David G. Schlundt
Journal: Diabetes Care (2010)

OBJECTIVE Individuals with diabetes are at higher risk for depression than the general population. Although depression can be treated with antidepressant medications, patients with diabetes and comorbid depression often go untreated. The goal of this study was to examine racial disparities in the treatment of depression with antidepressant medication in the southeastern U.S. RESEARCH DESIGN AND METHODS Cross-sectional data were collected at baseline from 69,068 participants (71% African American, 60% female, and 82% with incomes &amp;lt;$25,000) recruited from community health centers and enrolled in the Southern Cohort Community Study (SCCS). The SCCS is a prospective epidemiological cohort study designed to explore causes of health disparities in adults aged 40–79 years. Binary logistic regression was used to identify factors associated with antidepressant use among those with diabetes (n = 14,279). RESULTS Individuals with diagnosed diabetes (14,279) were classified with no depressive symptoms (54.7%), or with mild (24.2%), moderate (12.8%), or severe depressive symptoms (8.3%). After controlling for sex, age, insurance, income, education, BMI, smoking status, alcohol consumption, and level of depression, African Americans with diabetes were much less likely to report taking antidepressant medication than whites (adjusted odds ratio 0.32 [95% CI 0.29–0.35], P &amp;lt; 0.0001). CONCLUSIONS Antidepressant use is much less common among African Americans than among whites with diabetes. Reasons for racial disparities in treatment of depressive symptoms are unclear but may include a combination of differential diagnosis and treatment by health professionals as well as cultural differences in seeking help for emotional distress.