tbuckley/cabot-search huggingface dataset:
Abstract 20326: Impact of Gender on Clinical Outcomes in Non-Valvular Atrial Fibrillation: Contemporary Perspective From the GARFIELD Registry
Authors: John Camm, Samuel Z Goldhaber, Giuseppe Ambrosio, Petr Jansky, Wael Al Mahmeed, Seil Oh, Martin Van Eickels, Pekka Raatikainen, Jan Steffel, Emily Chu, Gabriele Accetta, Gloria Kayani, Ajay K Kakkar
Journal: Circulation (2014)

Purpose: To evaluate the influence of gender on baseline characteristics and 1-year clinical outcomes in patients with non-valvular atrial fibrillation (AF). Methods: In the ongoing, international registry GARFIELD, a total of 12,458 prospective patients were enrolled at 739 randomly selected sites in 30 countries between March 2010 and January 2013. Results: Compared with men, women with AF were more likely to be older and have a history of hypertension or venous thromboembolism, but less likely to have a history of vascular disease. Use of antithrombotic therapy was similar in the two groups. At 1-year follow-up, the hazard ratio for women versus men, adjusted for age group, use of vitamin K antagonist, Factor Xa inhibitor, direct thrombin inhibitor, and antiplatelet, congestive cardiac failure, hypertension, diabetes, stroke/transient ischaemic attack, and vascular disease, was 0.815 (95% confidence interval, 0.695-0.957) for the incidence of all-cause mortality, 1.414 (1.053-1.899) for the incidence of stroke/systemic embolism (SE), and 1.024 (0.714-1.470) for the incidence of major bleeding. Conclusion: These findings suggest that women with non-valvular AF have a lower mortality rate despite a higher stroke/SE rate compared with men.
Evidence for Improving Palliative Care at the End of Life: A Systematic Review
Authors: Karl A. Lorenz, Joanne Lynn, Sydney M. Dy, Lisa R. Shugarman, Anne Wilkinson, Richard A. Mularski, Sally C. Morton, Ronda G. Hughes, Lara K. Hilton, Margaret Maglione, Shannon L. Rhodes, Cony Rolon, Virginia C. Sun, Paul G. Shekelle
Journal: Annals of Internal Medicine (2008)

Background: Many persons and their families are burdened by serious chronic illness in late life. How to best support quality of life is an important consideration for care. Purpose: To assess evidence about interventions to improve palliative and end-of-life care. Data Sources: English-language citations (January 1990 to November 2005) from MEDLINE, the Database of Abstracts of Reviews of Effects, the National Consensus Project for Quality Palliative Care bibliography, and November 2005 to January 2007 updates from expert reviews and literature surveillance. Study Selection: Systematic reviews that addressed "end of life," including terminal illness (for example, advanced cancer) and chronic, eventually fatal illness with ambiguous prognosis (for example, advanced dementia), and intervention studies (randomized and nonrandomized designs) that addressed pain, dyspnea, depression, advance care planning, continuity, and caregiving. Data Extraction: Single reviewers screened 24 423 titles to find 6381 relevant abstracts and reviewed 1274 articles in detail to identify 33 high-quality systematic reviews and 89 relevant intervention studies. They synthesized the evidence by using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) classification. Data Synthesis: Strong evidence supports treating cancer pain with opioids, nonsteroidals, radionuclides, and radiotherapy; dyspnea from chronic lung disease with short-term opioids; and cancer-associated depression with psychotherapy, tricyclics, and selective serotonin reuptake inhibitors. Strong evidence supports multi component interventions to improve continuity in heart failure. Moderate evidence supports advance care planning led by skilled facilitators who engage key decision makers and interventions to alleviate caregiver burden. Weak evidence addresses cancer-related dyspnea management, and no evidence addresses noncancer pain, symptomatic dyspnea management in advanced heart failure, or short-acting antidepressants in terminal illness. No direct evidence addresses improving continuity for patients with dementia. Evidence was weak for improving caregiver burdens in cancer and was absent for heart failure. Limitations: Variable literature indexing for advanced chronic illness and end of life limited the comprehensiveness of searches, and heterogeneity was too great to do meta-analysis. Conclusion: Strong to moderate evidence supports interventions to improve important aspects of end-of-life care. Future research should quantify these effects and address the generalizability of insights across the conditions and settings of the last part of life. Many critical issues lack high-quality evidence.
Role of Hic-5 in the formation of microvilli-like structures and the monocyte–endothelial interaction that accelerates atherosclerosis
Authors: Shigeko Arita-Okubo, Joo-ri Kim-Kaneyama, Xiao-Feng Lei, Wen-Guang Fu, Koji Ohnishi, Motohiro Takeya, Aya Miyauchi, Hirokazu Honda, Hiroyuki Itabe, Takuro Miyazaki, Akira Miyazaki
Journal: Cardiovascular Research (2015)

The adhesion of circulating monocytes to endothelial cells (ECs) is an early and critical event in the formation of atherosclerotic plaques. Hydrogen peroxide-inducible clone 5 (Hic-5) serves as an adaptor molecule in cell adhesion complexes. However, the role of endothelial Hic-5 in monocyte–EC interaction and atherogenesis remains unclear. We examined the roles of endothelial Hic-5 in monocyte–EC interaction and atherogenesis using mouse models of atherosclerosis and cultured human umbilical vein endothelial cells (HUVECs). Hic-5 was expressed in ECs, but not in monocytes/macrophages. An ex vivo monocyte adhesion assay revealed that adhesion of THP-1 monocytes to aortas isolated from Apoe−/− and LDLR−/− mice stimulated by TNF-α or oxidized LDL was suppressed by Hic-5 deficiency. Scanning electron microscopic observations of aortas harvested from Apoe−/− mice revealed that TNF-α- or oxidized LDL-induced microvilli-like structures were markedly suppressed by Hic-5 deficiency. Relative Hic-5 deficiency suppressed 60% of the atherosclerotic lesions in aortas from Apoe−/− and LDLR−/− mice. In contrast, overexpression of Hic-5 in HUVECs promoted induction of microvilli-like structures and adherence of THP-1 cells in an adhesion receptor such as intercellular adhesion molecule-1- and vascular cell adhesion molecule-1-dependent manner. Hic-5 in ECs plays an important role in the formation of microvilli-like structures and in the interaction between ECs and monocytes, leading to monocyte recruitment and subsequent development of atherosclerosis.
The nitric oxide-induced reduction in cardiac energy supply is not due to inhibition of creatine kinase
Authors: U Decking
Journal: Cardiovascular Research (2001)

Objectives: While nitric oxide (NO) is a potent vasodilator already in the nM range, a cGMP-independent negative inotropic effect is observed at higher concentrations. Since inhibition of creatine kinase (CK) by NO-induced nitrosylation has been proposed as a possible mechanism of action, we measured the flux through CK in the intact heart. Methods: In saline perfused, paced guinea pig hearts 31P NMR spectroscopy was employed to directly assess the cardiac energy status, i.e. free energy of ATP hydrolysis (ΔGATP) and flux through CK using magnetization transfer in absence and presence of NO. Results: NO (50 μM) doubled coronary flow and induced a rapid drop in left ventricular developed pressure (39±10 vs. 81±10 mmHg) and MVO2 (1.3±0.8 vs. 3.7±0.5 μmol/min/g) (n=7). This effect was associated with an immediate decrease in phosphocreatine (PCr) (−69%) and ΔGATP. During the subsequent 35 min of NO infusion cardiac function and MVO2 remained depressed, while PCr partially recovered. NO had no effect on the unidirectional forward flux through CK (98±21 vs. 99±20 μmol/min/g, n=7) which was 5- to 10-fold greater than the rate of ATP turnover. Upon cessation of NO infusion both cardiac function and PCr rapidly returned to baseline values. The NO-induced fall in the myocardial energy status was associated with an increase in mitochondrial NADH (n=7) as assessed by surface fluorescence. The observed change in fluorescence was similar to that observed with short term ischemia. Conclusion: The NO-mediated depression of myocardial function, MVO2 and energy status is not mediated by changes in CK flux. Most likely a partial blockade of mitochondrial oxidative phosphorylation at the level of cytochrome c oxidase is responsible for this effect.
Inhibition of experimental neointimal hyperplasia and thrombosis depends on the type of vascular injury and the site of drug administration.
Authors: C Rogers, M J Karnovsky, E R Edelman
Journal: Circulation (1993)

BACKGROUND Heparin inhibits vascular smooth muscle cell proliferation in tissue culture and limits neointimal hyperplasia after experimental arterial injury but has been ineffective in reducing clinical restenosis. We examined how this discrepancy might reflect suboptimal drug-tissue interactions and/or differences in the vascular response to injury. METHODS AND RESULTS Intravenous infusion was compared with local administration of heparin to injured rabbit iliac arteries either from drug-impregnated polymeric controlled release matrices in the perivascular space or from drug-releasing endovascular stents. Occlusive thrombosis, seen in 42% of control stent-bearing arteries, and partial thrombosis were virtually eliminated by heparin delivery from any route. Intimal area 14 days after balloon withdrawal denudation alone was reduced to an equal extent by continuous systemic heparin or by perivascular heparin for the first 3 days. In contrast, endovascular stents produced more exuberant neointimal hyperplasia, the inhibition of which required continuous rather than only early heparin administration. Neither perivascular delivery limited to the first 3 days nor stent-based delivery reduced neointimal hyperplasia as effectively. CONCLUSIONS The antiproliferative and antithrombotic effects of heparin differ markedly, depending on the type of arterial injury and the mode of drug administration. Different forms of injury may require different therapies, and complications of arterial intervention such as excessive neointimal hyperplasia and thrombosis may demand alternate therapeutic regimens. Duration, dose, and site of delivery rather than frank resistance to therapy may explain why experimentally effective antiproliferative and antithrombotic agents fail clinically.
LOCALIZATION OF ANTIBODIES IN PLASMA CELLS BY ELECTRON MICROSCOPY
Authors: Stefanello de Petris, Gioanna Karlsbad, Benvenuto Pernis
Journal: The Journal of Experimental Medicine (1963)

The localization of antibody in the interior of plasma cells of lymph nodes of rabbits hyperimmunized with ferritin was studied by electron microscopy. The cells were incubated with the antigen (ferritin) which was allowed to penetrate into the cells by suitable methods. Antigen-antibody precipitates were localized in the cisternae of the endoplasmic reticulum and in the perinuclear space. No evident association was found between ferritin and ribosomes or ferritin and outer cell membrane. Cells from control animals immunized with an unrelated antigen, incubated with ferritin, exhibited no labeling. From direct counts of ferritin molecules in plasma cells, a lower limit was evaluated for the antibody concentration in the endoplasmic reticulum (12.2 mg/cm3) and for the total antibody content of a plasma cell (7.0 x 10–3 gm).
Influence of pulmonary vascular disease and fibrosis on prognosis following closed mitral valvotomy
Authors: R. Nicks, V. J. McGovern
Journal: Thorax (1968)

We have examined biopsies of the lingula of the upper lobe of the left lung from 85 patients undergoing mitral valvotomy and have correlated the presence of vascular changes and fibrosis of the lung tissue with pulmonary vascular resistance, the degree and type of mitral stenosis, and the duration of pulmonary symptoms. Factors which significantly affected the prognosis were high pulmonary artery pressures, high vascular resistance, and narrowing of the pulmonary arteries; but, above all, pulmonary fibrosis. The prognosis for patients with mitral incompetence was less favourable than for those without incompetence, especially if there was increased pulmonary vascular resistance and pulmonary hypertension with axis deviation in the electrocardiogram.
Predicting later asthma in toddlers: Do environmental exposure data improve a clinical tool?
Authors: Anina Pescatore, Ben Spycher, Cristian Dogaru, Jennifer Baeuml, Myrofora Goutaki, Erol Gaillard, Claudia Kuehni
Journal: European Respiratory Journal (2013)

Background: We recently developed a simple clinical tool for predicting asthma at school-age in toddlers presenting at the doctor with wheeze or cough (ERJ 2011;38(Supp 55):269-270s). It uses 10 predictors (severity of wheeze, atopic family history, eczema, age and sex), summarized in a score. We now assessed, whether environmental (EV) and socioeconomic (SE) factors improve the predictive performance of this tool.

Methods: From a population-based cohort (UK), we included 1-3 year-olds with current wheeze or recurrent cough and related healthcare visits. Current asthma (wheeze needing inhalers) was assessed 5 yrs later. As potential predictors we included the original prediction score, plus EV (nursery care, siblings, cooking and heating fuel, pets, smoking, breastfeeding) and SE factors (Townsend score, overcrowding, traffic density, urban living, parental education, single parents). We first looked at univariable associations between EV and SE factors and asthma 5 yrs later and then used lasso penalized logistic regression to select predictors in a model including all potential predictors.

Results: 345/1226 (28%) eligible children had asthma 5 yrs after baseline. Cooking with gas and maternal smoking were associated with asthma (p<0.05). However, in the lasso penalized logistic regression only the original score was selected.

Conclusion: Severity of wheeze and family history remain the most important predictors of later asthma in toddlers. Information on EV and SE factors adds little to improve predictive performance of the tool. Further research should investigate the additional value of physiological measurements.

Funding: SNF PDFMP3-123162, SNF 32003B-144068, Asthma UK 07/048.
STUDIES ON THE RECOVERY OF THE IMMUNE RESPONSE IN IRRADIATED MICE THYMECTOMIZED IN ADULT LIFE
Authors: A. Marjorie Cross, Elizabeth Leuchars, J. F. A. P. Miller
Journal: The Journal of Experimental Medicine (1964)

Experiments performed on CBA mice thymectomized in adult life, exposed to lethal doses of irradiation and given tissue therapy are described. Marrow, foetal liver, or spleen cells from syngeneic donors could protect the mice against the lethal effects of irradiation. Between 30 and 70 days' postirradiation, however, marrow-treated, thymectomized irradiated mice showed evidence of trophic disturbances, such as failure to gain weight, in contrast to sham-operated, irradiated, marrow-treated controls. The immune responses of experimental and control mice were tested up to 150 days' postirradiation by challenging with sheep erythrocytes and allogeneic skin grafts. Sham-operated irradiated controls, whether protected with marrow, foetal liver, or spleen cells, produced normal immune responses when challenged at 28, 60, or 150 days after irradiation. Neither foetal liver cells nor marrow cells, in doses of up to 40 million cells per mouse, enabled thymectomized irradiated mice to recover normal immune functions. Spleen cells, from normal donors but not from neonatally thymectomized donors, restored immunological capacity in such mice. It is concluded that immunologically competent cells are present in the spleen of normal adult donors and can function in the absence of the thymus. Bone marrow, on the other hand, does not contain an adequate population of such cells but has lymphoid precursor cells, the descendants of which can become immunologically competent only in the presence of a functioning thymus mechanism.
Effects of amiloride on metabolism and contractility during reoxygenation in perfused rat hearts.
Authors: R G Weiss, E G Lakatta, G Gerstenblith
Journal: Circulation Research (1990)

Myocardial recovery after hypoxia may be determined not only by the extent of metabolic depression during the hypoxic period but also by changes in cation contents as well. Calcium overload during reoxygenation, mediated in part by Na-Ca exchange and supported by the rise in cell sodium during hypoxia, may be one factor. The effects of amiloride (0.1 mM), a diuretic that inhibits Na(+)-H+ and Na-Ca exchanges in cardiac sarcolemma and mitochondria preparations, were studied during hypoxia-reoxygenation in the isovolumic, isolated rat heart. During hypoxia, cell sodium, measured using potassium ethylenediamine tetraacetate cobaltate as an extracellular marker, increased in amiloride and amiloride-free hearts, but there was no increase in cell calcium (3.3 +/- 0.3 vs. 3.6 +/- 0.9 mumol/g dry wt; p = NS). Amiloride did not alter developed pressure (DP), end-diastolic pressure (EDP), pH, or integrated areas of adenosine triphosphate (ATP) and phosphocreatine (PCr) (determined by phosphorus-31-nuclear magnetic resonance spectroscopy) during hypoxia or normal perfusion conditions. Forty minutes after reoxygenation, however, cell calcium was significantly lower in the amiloride (5.1 +/- 1.3 mumol/g dry wt) than in the amiloride-free group (10.4 +/- 1.8 mumol/g dry wt; p less than 0.001), and there was improved recovery of DP (percent of initial) (72 +/- 12% vs. 41 +/- 12%; p less than 0.001), PCr (99 +/- 9% vs. 70 +/- 14%; p less than 0.001), and pH (7.17 +/- 0.17 vs. 6.88 +/- 0.16; p less than 0.001) in the amiloride group. To determine whether this dose of amiloride inhibits the manifestations of sodium-mediated calcium gain in the same model during normoxia, the metabolic and functional sequelae of lithium-substituted low sodium (50 mM) perfusion were studied. Amiloride significantly limited the manifestations of sodium-mediated calcium gain as indexed (all expressed as percent of control) by a lower peak DP (221 +/- 25% vs. 284 +/- 20%) at 3 minutes, improved preservation of PCr (85 +/- 10% vs. 68 +/- 9%) and ATP (104 +/- 12% vs. 84 +/- 9%), lower rise in inorganic phosphate (201 +/- 74% vs. 332 +/- 106%), and a smaller fall in intracellular pH (7.01 +/- 0.04 vs. 6.70 +/- 0.15, p less than 0.05) for all metabolic parameters during a 20-minute period.(ABSTRACT TRUNCATED AT 400 WORDS)
Comparison of two schedules (previous evening versus same morning) of bowel preparation for colonoscopy
Authors: T. Gupta, A. Mandot, D. Desai, P. Abraham, A. Joshi, S. Shah
Journal: Endoscopy (2007)

See also: Commentaire de travail de T. Gupta et al., pp. 706Endoscopy 2007; 39(08): 845-845DOI: 10.1055/s-0032-1308858
Spanish doctors protest against law that excludes immigrants from public healthcare
Authors: A. Garcia Rada
Journal: BMJ (2012)

<h3>BACKGROUND AND PURPOSE:</h3> The accuracy of tumor plasma volume and <i>K</i><sup>trans</sup> estimates obtained with DCE MR imaging may have inaccuracies introduced by a poor estimation of the VIF. In this study, we evaluated the diagnostic accuracy of a novel technique by using a phase-derived VIF and “bookend” T1 measurements in the preoperative grading of patients with suspected gliomas. <h3>MATERIALS AND METHODS:</h3> This prospective study included 46 patients with a new pathologically confirmed diagnosis of glioma. Both magnitude and phase images were acquired during DCE MR imaging for estimates of <i>K</i><sup>trans</sup>_ϕ and V<sub>p_</sub>ϕ (calculated from a phase-derived VIF and bookend T1 measurements) as well as <i>K</i><sup>trans</sup>_SI and V<sub>p_</sub>SI (calculated from a magnitude-derived VIF without T1 measurements). <h3>RESULTS:</h3> Median <i>K</i><sup>trans</sup>_ϕ values were 0.0041 minutes<sup>−1</sup> (95 CI, 0.00062–0.033), 0.031 minutes<sup>−1</sup> (0.011–0.150), and 0.088 minutes<sup>−1</sup> (0.069–0.110) for grade II, III, and IV gliomas, respectively (<i>P</i> ≤ .05 for each). Median V<sub>p_</sub>ϕ values were 0.64 mL/100 g (0.06–1.40), 0.98 mL/100 g (0.34–2.20), and 2.16 mL/100 g (1.8–3.1) with <i>P</i> = .15 between grade II and III gliomas and <i>P</i> = .015 between grade III and IV gliomas. In differentiating low-grade from high-grade gliomas, AUCs for <i>K</i><sup>trans</sup>_ϕ, V<sub>p_</sub>ϕ, <i>K</i><sup>trans</sup>_SI, and V<sub>p_</sub>SI were 0.87 (0.73–1), 0.84 (0.69–0.98), 0.81 (0.59–1), and 0.84 (0.66–0.91). The differences between the AUCs were not statistically significant. <h3>CONCLUSIONS:</h3> <i>K</i><sup>trans</sup>_ϕ and V<sub>p_</sub>ϕ are parameters that can help in differentiating low-grade from high-grade gliomas.
Complement and meningococcal infection.
Authors: B M Greenwood, I I Onyewotu, H C Whittle
Journal: BMJ (1976)

Serum C3 levels were measured in 211 patients with meningococcal disease. Low levels were found in 13 patients with acute meningococcaemia, and complement activation may have contributed to the peripheral circulatory collapse that was responsible for nine deaths. The complement profile of these patients suggested activation of both classical and alternative complement pathways. Patients with meningitis had a higher mean serum C3 level than controls. Serial studies in 13 serum antigen-positive patients with meningitis who subsequently developed arthritis or cutaneous vasculitis showed a transient fall in serum C3 in eight. This fall was probably due to the formation of immune complexes that were responsible for their allergic complications.
Natural selection and schizophrenia
Authors: Roger J. Sullivan, John S. Allen
Journal: Behavioral and Brain Sciences (2004)

Evolutionary theories of schizophrenia must account for the maintenance of putative alleles in past and present populations despite reduced fitness among the affected. Such models must also account for extant intersex and population-level variability in the expression of schizophrenia. We argue that genetic balanced-polymorphism hypotheses remain the most robust in terms of modeling and testing these processes in populations.
Glucosylation of human collagen in aging and diabetes mellitus.
Authors: S L Schnider, R R Kohn
Journal: Journal of Clinical Investigation (1980)

Several of the characteristic complications of diabetes mellitus resemble age-like changes in collagen-rich tissues. It has been reported that increased glucosylation of hemoglobin and serum proteins occurs in diabetes. Glucosylation of insoluble human tendon collagen, a protein with little or no turnover was determined by a thiobarbituric acid method in 23 subjects as a function of age and the presence or absence of diabetes. Amounts of glucose and collagen solubilized by collagenase digestion of the samples were also determined. Glucosylation of collagen was found to increase with age and was markedly increased in juvenile onset diabetes. There appeared to be a limit to the amount of glucosylation that could occur, and older individuals with maturity-onset diabetes demonstrated glucosylation within that limit. The glucose nonenzymatically bound to human collagen may indicate the level of long-term control of the diabetes, and may play a role in the alteration of collagenous tissue properties that occurs in both aging and diabetes.