tbuckley/cabot-search huggingface dataset:
Cerebral Protection During Surgery for Acute Aortic Dissection Type A
Authors: Tobias Krüger, Ernst Weigang, Isabell Hoffmann, Maria Blettner, Hermann Aebert
Journal: Circulation (2011)

Background— Cerebral protection during surgery for acute aortic dissection type A relies on hypothermic circulatory arrest, either alone or in conjunction with cerebral perfusion. Methods and Results— The perioperative and intraoperative conditions of 1558 patients submitted from 44 cardiac surgery centers in German-speaking countries were analyzed. Among patients with acute aortic dissection type A, 355 (22.8%) underwent surgery with hypothermic circulatory arrest alone. In 1115 patients (71.6%), cerebral perfusion was used: Unilateral antegrade cerebral perfusion (ACP) in 628 (40.3%), bilateral ACP in 453 (29.1%), and retrograde perfusion in 34 patients (2.2%). For 88 patients with acute aortic dissection type A (5.6%), no circulatory arrest and arch intervention were reported (cardiopulmonary bypass–only group). End points of the study were 30-day mortality (15.9% overall) and mortality-corrected permanent neurological dysfunction (10.5% overall). The respective values for the cardiopulmonary bypass–only group were 11.4% and 9.1%. Hypothermic circulatory arrest alone resulted in a 30-day mortality rate of 19.4% and a mortality-corrected permanent neurological dysfunction rate of 11.5%, whereas the rates were 13.9% and 10.0%, respectively, for unilateral ACP and 15.9% and 11.0%, respectively, for bilateral ACP. In contrast with the ACP groups, there was a profound increase in mortality when systemic circulatory arrest times exceeded 30 minutes in the hypothermic circulatory arrest group ( P &lt;0.001). Mortality-corrected permanent neurological dysfunction correlated significantly with perfusion pressure in the ACP groups. Conclusions— This study reflects current surgical practice for acute aortic dissection type A in Central Europe. For arrest times less than 30 minutes, hypothermic circulatory arrest and ACP lead to similar results. For longer arrest periods, ACP with sufficient pressure is advisable. Outcomes with unilateral and bilateral ACP were equivalent.
Abnormal Cardiac Conduction and Morphogenesis in Connexin40 and Connexin43 Double-Deficient Mice
Authors: Susanne Kirchhoff, Jung-Sun Kim, Andreas Hagendorff, Eva Thönnissen, Olaf Krüger, Wouter H. Lamers, Klaus Willecke
Journal: Circulation Research (2000)

Connexin40-deficient (Cx40(-/-)/Cx43(+/+)) and connexin43-heterozygous knockout mice (Cx40(+/+)/Cx43(+/-)) are viable but show cardiac conduction abnormalities. The ECGs of adult double heterozygous animals (Cx40(+/-)/Cx43(+/-)) suggest additive effects of Cx40 and Cx43 haploinsufficiency on ventricular, but not on atrial, conduction. We also observed additive effects of both connexins on cardiac morphogenesis. Approximately half of the Cx40(-/-)/Cx43(+/+) embryos died during the septation period, and an additional 16% died after birth. The majority of the latter mice had cardiac hypertrophy in conjunction with common atrioventricular junction or a ventricular septal defect. All Cx40(-/-)/Cx43(+/-) progeny exhibited cardiac malformations and died neonatally. The most frequent defect was common atrioventricular junction with abnormal atrioventricular connection, which was more severe than that seen in Cx40(-/-)/Cx43(+/+) mice. Furthermore, muscular ventricular septal defects, premature closure of the ductus arteriosus, and subcutaneous edema were noticed in these embryos. Cx40(+/-)/Cx43(-/-) embryos showed the same phenotype (ie, obstructed right ventricular outflow tract) as reported for Cx40(+/+)/Cx43(-/-) mice. These findings demonstrate that Cx43 haploinsufficiency aggravates the abnormalities observed in the Cx40(-/-) phenotype, whereas Cx40 haploinsufficiency does not worsen the Cx43(-/-) phenotype. We conclude that the gap-junctional proteins Cx40 and Cx43 contribute to morphogenesis of the heart in an isotype-specific manner.
Does removal of aids/devices and help make a difference in the Childhood Health Assessment Questionnaire disability index?
Authors: C Saad-Magalhães, A Pistorio, A Ravelli, G Filocamo, S Viola, R Brik, D Mihaylova, R ten Cate, B Andersson-Gare, V Ferriani, K Minden, P Hashkes, M Rygg, M-J Sauvain, H Venning, A Martini, N Ruperto
Journal: Annals of the Rheumatic Diseases (2009)

Objective: To assess whether the removal of aids/devices and/or help from another person in the Childhood Health Assessment Questionnaire (C-HAQ) leads to a significant change in the disability index (DI) score and responsiveness in juvenile idiopathic arthritis (JIA). Methods: Changes in the C-HAQ DI score in a cross-sectional sample of 2663 children with JIA and in 530 active patients with JIA in a trial of methotrexate (MTX) were compared. Results: Patients in the MTX trial had higher disease activity and disability than the cross-sectional sample. The frequency of aids/devices (range 1.2–10.2%) was similar between the two samples, while help (range 5.3–38.1%) was more frequently used in the MTX group. Correlation between disease severity variables and the two different C-HAQ DI scoring methods did not change substantially. There was a decrease in the C-HAQ DI score for both the cross-sectional (mean score from 0.64 with the original method to 0.54 without aids/devices and help, p&lt;0.0001) and the MTX sample (mean score from 1.23 to 1.07, p&lt;0.0001). A linear regression analysis of the original C-HAQ DI score versus the score without aids/devices and help demonstrated the substantial overlap of the different scoring methods. Responsiveness in the responders to MTX treatment did not change with the different C-HAQ DI scoring methods (range 0.86–0.82). Conclusion: The removal of aids/devices and help from the C-HAQ does not alter the interpretation of disability at a group level. The simplified C-HAQ is a more feasible and valid alternative for the evaluation of disability in patients with JIA.
The Ambulatory Pediatric Association Fellowship in Pediatric Environmental Health: A 5-Year Assessment
Authors: Philip J. Landrigan, Alan D. Woolf, Ben Gitterman, Bruce Lanphear, Joel Forman, Catherine Karr, Erin L. Moshier, James Godbold, Ellen Crain
Journal: Environmental Health Perspectives (2007)

Evidence is mounting that environmental exposures contribute to causation of disease in children. Yet few pediatricians are trained to diagnose, treat, or prevent disease of environmental origin.To develop a cadre of future leaders in pediatric environmental health (PEH), the Ambulatory Pediatric Association (APA) launched a new 3-year fellowship in 2001-the world's first formal training program in PEH. Sites were established at Boston Children's Hospital, Mount Sinai School of Medicine, George Washington University, University of Cincinnati, and University of Washington. Fellows are trained in epidemiology, biostatistics, toxicology, risk assessment, and preventive medicine. They gain clinical experience in environmental pediatrics and mentored training in clinical research, policy development, and evidence-based advocacy. Thirteen fellows have graduated. Two sites have secured follow-on federal funding to enable them to continue PEH training.To assess objectively the program's success in preparing fellows for leadership careers in PEH, we conducted a mailed survey in 2006 with follow-up in 2007.Fifteen (88%) of 17 fellows and graduates participated; program directors provided information on the remaining two. Nine graduates are pursuing full-time academic careers, and two have leadership positions in governmental and environmental organizations. Ten have published one or more first-authored papers. Seven graduates are principal investigators on federal or foundation grants. The strongest predictors of academic success are remaining affiliated with the fellowship training site and devoting < 20% of fellowship time to clinical practice.The APA fellowship program is proving successful in preparing pediatricians for leadership careers in PEH.
461 INCOMPLETE REVERSAL OF COGNITIVE DYSFUNCTION AFTER LIVER TRANSPLANTATION IN INDIVIDUALS WHO HAD HAD OVERT HEPATIC ENCEPHALOPATHY BEFORE LIVER TRANSPLANTATION
Authors: F. Campagna, A. Biancardi, S. Montagnese, P. Angeli, D. Mapelli, C. Poci, S. Schiff, U. Cillo, A. Gatta, P. Amodio
Journal: Journal of Hepatology (2010)
Transgenic Mice and Analysis of B-Cell Tolerance
Authors: C C Goodnow
Journal: Annual Review of Immunology (1992)

Understanding the mechanism of immunological tolerance to self-antigens remains a fundamental problem in immunology. Transgenic mice carrying rearranged antigen-receptor genes have provided a window into the events involved in this process, by allowing the development and fate of antigen-specific lymphocytes to be followed in vivo. In the B-cell lineage, as in T cells, self-reactive cells have been found to undergo several distinct fates in vivo: they can be physically eliminated, functionally inactivated, or they can persist unchanged or become activated. As discussed in this review, direct visualization of the fate of self-reactive cells resolves one of the key issues in tolerance. Achieving a precise understanding of the cellular and molecular events leading to lymphocyte deletion, anergy, or activation nevertheless remains a challenge for the future.
Insulin Sensitivity and Insulin Binding to Monocytes in Maturity-Onset Diabetes
Authors: Ralph Defronzo, David Deibert, Rosa Hendler, Philip Felig, Vijay Soman
Journal: Journal of Clinical Investigation (1979)

Tissue sensitive to insulin and insulin binding to monocytes were evaluated in 15 nonobese maturity-onset diabetics and in 16 healthy controls. Insulin sensitivity was determined by the insulin clamp technique in which the plasma insulin is acutely raised and maintained 100 μU/ml above the fasting level and plasma glucose is held constant at fasting levels by a variable glucose infusion. The amount of glucose infused is a measure of overall tissue sensitivity to insulin.
Spontaneous and pokeweed mitogen induced production of rheumatoid factor and immunoglobulins in type II essential mixed cryoglobulinaemia.
Authors: R.A Sinico, G Fiorini, A Fornasieri, P Bernasconi, S Benuzzi, M.L Paracchini, G D'Amico
Journal: Annals of the Rheumatic Diseases (1986)

In order to evaluate functional lymphocyte defects in type II essential mixed cryoglobulinaemia (EMC) in vitro production of immunoglobulins (Ig) and rheumatoid factor (RF) has been studied in basal conditions and under pokeweed mitogen (PWM) stimulation in 15 patients and in 17 control subjects. The major finding was a significantly high basal and inducible production of RF by EMC lymphocytes as compared with the RF production in controls, while synthesis of polyclonal Ig was unaffected. A good correlation existed between in vitro production and serum levels of RF. Peripheral blood SmIg+ and Ia+ cells were also significantly increased. The possibility that EMC shares some pathogenetic mechanism with rheumatoid arthritis on the one hand and with lymphoproliferative diseases on the other is considered.
Extra hepatic portal venous obstruction.
Authors: D R Triger
Journal: Gut (1987)

Editorial. Causes possibles: infection, traumatisme, neoplasme, troubles de la coagulation, cirrhose; l'obstruction peut etre idiopathique et peut-etre congenitale. En cas d'obstruction de la beine porte extrahepatique des examens approfondis sont necessaire pour exclure la cirrhose qui peut amener les complications les plus serieurses
Angiopoietin/Tie2 Pathway Influences Smooth Muscle Hyperplasia in Idiopathic Pulmonary Hypertension
Authors: Laurence Dewachter, Serge Adnot, Elie Fadel, Marc Humbert, Bernard Maitre, Anne-Marie Barlier-Mur, Gerald Simonneau, Michel Hamon, Robert Naeije, Saadia Eddahibi
Journal: American Journal of Respiratory and Critical Care Medicine (2006)

Angiopoietins are involved in blood vessel maturation and remodeling.One consequence of endothelium-specific tyrosine kinase-2 (Tie2) receptor activation by angiopoietin-1 (Ang1) is the release of endothelium-derived growth factors that recruit vascular wall cells. We investigated this process in idiopathic pulmonary arterial hypertension (iPAH).Ang1, Ang2, and total and phosphorylated Tie2 expression (mRNA and protein) was evaluated in human lung specimens and in cultured pulmonary artery smooth muscle cells (PA-SMCs) and pulmonary endothelial cells (P-ECs) isolated from patients with iPAH and control subjects. Media collected from Ang1-treated P-ECs were assessed for their PA-SMC growth-promoting effect.Tie2 receptor was fourfold higher in lungs and P-ECs from patients with iPAH than in those from control subjects, with a parallel increase in phosphorylated lung Tie2 receptor. In contrast, Ang1 and Ang2 expression in lungs, P-ECs, and PA-SMCs did not differ. Incubation of PA-SMCs with medium collected from P-EC cultures induced marked proliferation, and this effect was stronger when using P-ECs from patients with iPAH than from control subjects. Ang1 pretreatment of P-ECs from either patients or control subjects induced a further increase in PA-SMC proliferation. Fluoxetine, an inhibitor of the mitogenic action of serotonin, reduced the growth-promoting effect of P-EC media. Ang1 added to P-ECs from patients with iPAH increased the production of endothelin-1 (ET-1) and serotonin, but not of platelet-derived growth factor-BB or epidermal growth factor, and increased the amount of mRNA encoding tryptophan hydroxylase-1 (the rate-limiting enzyme of serotonin synthesis), preproET-1, and ET-1-converting enzyme.The Ang1/Tie2 pathway is potentiated in iPAH, contributing to PA-SMC hyperplasia via increased stimulation of endothelium-derived growth factors synthesis by P-ECs.
Effects of immunotherapy on symptoms, PEFR, spirometry, and airway responsiveness in patients with allergic asthma to house‐dust mites (<i>D. pteronyssinus</i>) on inhaled steroid therapy
Authors: J. C. Torres Costa, J. I. Plácido, J. P. Moreira Silva, L. Delgado, M. Vaz
Journal: Allergy (1996)

The present study was designed to investigate the effects of immunotherapy (IT) with an extract of Dermatophagoides pteronyssinus (Alergo‐Merck Depot®) during a 27‐month period in patients with allergic asthma to house‐dust mites. We included 11 patients (mean age 18 years) treated with a combination of IT and inhaled beclomethasone dipropionate (BDP) in comparison to another II (mean age 22 years) treated with BDP alone. We evaluated symptom scores, salbutamol use, peak expiratory flow rates (PEFR), spirometry, and bronchial hyperresponsiveness (BHR) during 18 months of therapy with BDP and in the 9 months after BDP interruption. The two kinds of treatment were efficient and comparable in relation to symptom score, salbutamol use, morning PEFR, FVC, and FEV 1 , but patients treated with IT and BDP had a faster improvement of BHR and PEFR variability. The interruption of BDP after 18 months of therapy was linked to an impairment of all end points, which were more pronounced in patients previously treated only with BDP. These findings suggest that in selected asthmatic patients allergic to house‐dust mites, the association of IT and BDP is more effective than therapy with this inhaled steroid alone due to a faster and more striking improvement during the first months of treatment and to a lower rate of relapse after the interruption of therapy with BDP.
Relative contributions of arginine vasopressin and angiotensin II to maintenance of systemic arterial pressure in the anesthetized water-deprived rat.
Authors: C E Andrews, B M Brenner
Journal: Circulation Research (1981)

We used a structural analogue of arginine vasopressin (AVP) and investigated the role of AVP in the maintenance of mean arterial pressure (AP) in anesthetized, water-deprived rats. The administration of [1(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 4-valine-8-D-arginine] vasopressin, d(CH2)5VDAVP, completely inhibited to 30-40 mma Hg rise in AP which normally accompanied the administration of 50 mU exogenous AVP (group 1). Thus, d(CH2)5VDAVP is a specific antagonist of the vascular effects of AVP. d(CH2)5VDAVP failed to significantly alter AP in water diuretic rats (group 3) and was without effect on urine osmolality during water diuresis or antidiuresis. However, bolus injection of d(CH2)5VDAVP into water deprived rats (group 2) prompted an abrupt fall in AP from 112 +/- 4 to 94 +/- 4 mm Hg (P less than 0.001). This fall in AP was transient, with return of AP to 110 +/- 4 mm Hg within 15 minutes. Administration of saralasin, an angiotensin II antagonist, not only prevented the compensation in AP, but also significantly magnified the maximal hypotensive response seen following d(CH2)5VDAVP (group 4). Discontinuing the saralasin allowed AP to return to baseline. Bilateral nephrectomy (group 5) also prevented the return of AP, further implicating endogenous angiotensin II as the specific mediator of the compensation in AP following d(CH2)5VDAVP administration. These studies clearly demonstrate that circulating AVP contributes to the maintenance of AP during water deprivation in the anesthetized rat. When this vascular action of AVP is blocked, angiotensin II assumes major responsibility for blood pressure regulation in the antidiuretic state.
P58 An audit of treatment outcomes for patients with tuberculosis diagnosed at an inner London teaching hospital between 2000 and 2010: Abstract P58 Table 1
Authors: E Togun, S Stephens, O Sewo, FM Perrin, RD Barker
Journal: Thorax (2012)

<h3>Background</h3> The WHO has the ambition that 85% of patients starting treatment for TB achieve treatment success (cure or treatment complete).<sup>1</sup> There has been considerable anxiety that poor treatment completion rates would lead to increased transmission of tuberculosis and perhaps drive increased drug resistance. We have been monitoring treatment outcomes for patients registering at our hospital since the year 2000. Here we report outcomes and analyse risk factors for treatment interruption for patients with tuberculosis registering up until 2010. <h3>Methods</h3> All patients diagnosed with tuberculosis at an inner London teaching hospital between 2000 and 2010 were included in the study. Outcomes were recorded, as defined by the requirements of the London TB Register. Follow-up of patients is predominantly nurse-led with little day-to-day involvement from doctors. Samples are sent to the National Mycobacterial Reference Laboratory – Whitechapel, for culture and sensitivity testing with first line anti-tuberculous drugs. Sex, Age (Decade), HIV status, disease site (pulmonary or extra pulmonary) and resistance to any first line drug were evaluated to see whether they were associated with “ost to follow up”, as opposed to all other outcomes, using chi-square test for proportions. <h3>Results</h3> One thousand two hundred and forty two patients were identified. Ten patients (1%) had MDRTB, 714 58% were male, 981 (79%) were born abroad, 160 (13%) aged 0–20 years, 679 (55%) 21–40 years, 279 22% (41–60), 124 10% &gt; 60, 164 (13%) were known to be HIV, 596 (48%) had pulmonary disease 147 (18%) of 803 with positive cultures had any drug resistance. None of the variables assessed were significantly associated with being lost to follow up. <h3>Discussion</h3> Our nurse led TB programme has resulted in outcomes that meet international standards. Less than 5% of patients interrupt treatment. The results would probably improve if we obtained treatment outcomes for those who transferred out. None of the variables examined should be used as indicators for enhanced supervision. World Health Organization - Stop TB Partnership. The Stop TB Strategy, 2006.
Family Psychiatry: From Research to Practice
Authors: Alison M. Heru
Journal: American Journal of Psychiatry (2006)

Objective: The purpose of this article is to review current research evidence for clinicians involving families in the assessment and treatment of their patients. Method: Research on effects of family support on illness outcome and outcomes of family-centered treatment in medicine, pediatrics, and psychiatry are reviewed. Results: Research in many medical fields shows that families have powerful influences on health that are equal to or surpass other risk factors and that brief family interventions increase health and decrease the risk of relapse in chronic illnesses. Research in psychiatry affirms that family interventions reduce the rate of relapse, improve recovery, and increase family well-being. Conclusions: Current evidence supports increased emphasis on family-oriented psychiatric practice.
Neutrophil function in patients with primary Sjogren's syndrome: relation to infection propensity.
Authors: B Gudbjornsson, N Feltelius, R Hallgren, P Venge
Journal: Annals of the Rheumatic Diseases (1991)

The function of neutrophils was studied in 23 consecutive patients with primary Sjögren9s syndrome and in 35 healthy controls. Nineteen patients (83%) had extraglandular symptoms and nine patients (39%) had recurrent bacterial infections. The patients had a marked reduction of neutrophil adherence, especially those with recurrent bacterial infections, and reduced opsonic activity of plasma. Increased random migration of isolated neutrophils was found in the patients with a propensity for bacterial infections. Chemotaxis and chemokinesis, phagocytosis, chemiluminescence production, and the intracellular neutrophil contents of lactoferrin and lysozyme were normal. The various aspects of neutrophil function tested in this study were not related to disease duration or to inflammatory disease activity. The impaired neutrophil adherence may play a part in the increased propensity for bacterial infections seen in patients with primary Sjögren9s syndrome.
Efficacy of a chemotherapy combination for the treatment of metastatic neuroendocrine tumours
Authors: E. Bajetta, L. Ferrari, G. Procopio, L. Catena, E. Ferrario, A. Martinetti, M. Di Bartolomeo, R. Buzzoni, L. Celio, M. Vitali, E. Beretta, E. Seregni, E. Bombardieri
Journal: Annals of Oncology (2002)
THE HEME OXYGENASE SYSTEM:A Regulator of Second Messenger Gases
Authors: Mahin D. Maines
Journal: The Annual Review of Pharmacology and Toxicology (1997)

▪ Abstract The heme oxygenase (HO) system consists of two forms identified to date: the oxidative stress–inducible protein HO-1 (HSP32) and the constitutive isozyme HO-2. These proteins, which are different gene products, have little in common in primary structure, regulation, or tissue distribution. Both, however, catalyze oxidation of heme to biologically active molecules: iron, a gene regulator; biliverdin, an antioxidant; and carbon monoxide, a heme ligand. Finding the impressive heme-degrading activity of brain led to the suggestion that “HO in brain has functions aside from heme degradation” and to subsequent exploration of carbon monoxide as a promising and potentially significant messenger molecule. There is much parallelism between the biological actions and functions of the CO- and NO-generating systems; and their regulation is intimately linked. This review highlights the current information on molecular and biochemical properties of HO-1 and HO-2 and addresses the possible mechanisms for mutual regulatory interactions between the CO- and NO-generating systems.
Crack Cocaine Abuse: An Epidemic with Many Public Health Consequences
Authors: James W. Cornish, Charles P. O'Brien
Journal: Annual Review of Public Health (1996)

In the mid-1980s a new, smokable form of cocaine, called crack, was introduced in the United States. Soon thereafter, it became apparent that crack cocaine abuse was a serious and important public health concern. Over the past several years, crack cocaine use has increasingly been associated with a myriad of immediate and long-term adverse effects. Duing this same period, crack cocaine use has progressively moved away from experimentation and recreational use to chronic and compulsive drug use.