tbuckley/cabot-search huggingface dataset:
Changes in Quality of Life during Hemodialysis and Peritoneal Dialysis Treatment
Authors: Albert W. Wu, Nancy E. Fink, Jane V.R. Marsh-Manzi, Klemens B. Meyer, Frederic O. Finkelstein, Michelle M. Chapman, Neil R. Powe
Journal: Journal of the American Society of Nephrology (2004)

Despite more than 20 yr of use, relative differences in health-related quality of life (HRQOL) between hemodialysis (HD) and peritoneal dialysis (PD) are not clearly known. The objective of this study was to compare self-reported HRQOL and overall health status for HD and PD patients at the initiation of dialysis therapy and 1 yr later. A prospective cohort of incident ESRD patients was enrolled between October 1995 and June 1998 at 81 outpatient dialysis units in 19 states and included 698 HD and 230 PD patients who completed a baseline CHOICE Health Experience Questionnaire. The main outcome measured was change in qualify-of-life scores from start of dialysis to 1 yr on dialysis and overall health status. Of 928 patients who completed the baseline questionnaire, 585 also completed the 12-mo questionnaire; 101 had died, 55 had received a kidney transplant, and 88 had moved to a new dialysis clinic. PD patients were slightly younger, were more likely to be white, were well-educated, were employed, were married, had less comorbidity, and had higher hematocrit. Unadjusted baseline scores showed better HRQOL for PD patients in both generic and ESRD domains (bodily pain, travel, diet restrictions, and dialysis access [P < 0.05]). At 1 yr, SF-36 scores improved, whereas some ESRD domains improved and others deteriorated. HD patients had greater improvements in two SF-36 domains (physical functioning and general health perception) than PD patients, but results were mixed for ESRD domains (PD is better for finances, HD is better for sleep and overall quality of life). HD and PD patients did not differ in change in overall health status. HD and PD are associated with similar HRQOL outcomes at 1 yr. Generic HRQOL in two domains improved more for HD patients. However, for ESRD-specific HRQOL, results were not consistent; some domains were better for PD patients whereas others were better for HD patients. In advising patients about modality choices, trade-offs should be discussed and individual preferences for specific aspects of HRQOL should be elicited.
Polycystin-2 Immunolocalization and Function in Zebrafish
Authors: Tomoko Obara, Steven Mangos, Yan Liu, Jinhua Zhao, Stephanie Wiessner, Albrecht G Kramer-Zucker, Felix Olale, Alexander F Schier, Iain A Drummond
Journal: Journal of the American Society of Nephrology (2006)

Polycystin-2 functions as a cation-permeable transient receptor potential ion channel in kidney epithelial cells and when mutated results in human autosomal dominant polycystic kidney disease. For further exploration of the <i>in vivo</i> functions of Polycystin-2, this study examined its expression and function during zebrafish embryogenesis. <i>pkd2</i> mRNA is ubiquitously expressed, and its presence in the larval kidney could be confirmed by reverse transcription–PCR on isolated pronephroi. Immunostaining with anti-zebrafish Polycystin-2 antibody revealed protein expression in motile kidney epithelial cell cilia and intracellular cell membranes. Intracellular localization was segment specific; in the proximal nephron segment, Polycystin-2 was localized to basolateral cell membranes, whereas in the caudal pronephric segment, Polycystin-2 was concentrated in subapical cytoplasmic vesicles. Polycystin-2 also was expressed in muscle cells and in a variety of sensory cells that are associated with mechanotransduction, including cells of the ear, the lateral line organ, and the olfactory placodes. Disruption of Polycystin-2 mRNA expression resulted in pronephric kidney cysts, body axis curvature, organ laterality defects, and hydrocephalus—defects that could be rescued by expression of a human PKD2 mRNA. In-frame deletions in the first extracellular loop and C-terminal phosphofurin acidic cluster sorting protein–1 (PACS-1) binding sites in the cytoplasmic tail caused Polycystin-2 mislocalization to the apical cell surface. Unlike zebrafish intraflagellar transport protein (IFT) mutants, cyst formation was not associated with cilia defects and instead correlated with reduced kidney fluid output, expansion of caudal duct apical cell membranes, and occlusion of the caudal pronephric nephron segment.
Hemodynamic effects of nitric oxide synthase inhibition at steady state and following tumor necrosis factor-α-induced myodepression
Authors: D Murray
Journal: Cardiovascular Research (1999)

Objective: Nitric oxide (NO) has been proposed as a common mediator of tumor necrosis factor-α (TNFα)-induced vasodilation and myocardial dysfunction. Accordingly, we performed an extensive assessment of the influence of NO synthase inhibition on left ventricle (LV) and circulatory performance in conscious dogs at steady state and after establishment of TNFα mediated myodepression. Methods: Autonomically blocked, chronically instrumented dogs were studied at steady state and 6 h after initiation of a 1-h rhTNFα infusion (40 μg/kg). Ventricular performance was evaluated using the pressure–volume framework. Dogs were then treated with either NG-nitro-l-arginine methylester (l-NAME, 40 mg/kg bolus) or angiotensin II (250–500 ng/kg). Results:l-NAME, under control conditions or following recombinant human (rh)TNFα-induced ventricular dysfunction, produced marked increases in afterload with attendant increases in LV pressure, volume, and prolonged isovolumic relaxation without adversely influencing coronary blood flow. Regardless of whether the dogs received rhTNFα, l-NAME did not affect the slopes of the end-systolic pressure–volume and stroke-work (SW)-end-diastolic volume (EDV) relations (force-based measure of contractility), whereas the slope of the dP/dtmax–EDV relation, a velocity dependent parameter of LV systolic function, declined. Overall ventricular performance, as seen by the circulation, was reduced by l-NAME in control as well as rhTNFα-treated dogs, evidenced by rightward shifts of the SW–EDV and dP/dtmax–EDV relations. Similar findings were observed in the separate cohorts of dogs, at steady state and 6 h after rhTNFα, following angiotensin II at matched systolic pressure. Conclusions: Systemic NO synthase inhibition with l-NAME does not acutely reverse rhTNFα-induced myocardial dysfunction. The detrimental influence of l-NAME on LV size, relaxation, and velocity-based measures of contractility is likely attributable to its effects on increasing afterload.
Effect of physical training on calcium transport by rat cardiac sarcoplasmic reticulum.
Authors: S Penpargkul, D I Repke, A M Katz, J Scheuer
Journal: Circulation Research (1977)

Cardiac microsomes enriched in fragmented sarcoplasmic reticulum (SR) were isolated from hearts of physically trained rats and were compared to those from sedentary rats. Preparations from conditioned rats were found to transport calcium to a greater extent than those from sedentary rats both in the absence and in the presence of 1 mM oxalate. Higher oxalate concentrations abolished the differences in calcium accumulation by cardiac microsomes from conditioned and sedentary rats and indicated a qualitative change in SR from conditioned hearts. We conclude that the increased transport by SR from hearts of conditioned rats may provide one mechanism for enhanced contractile reserve in these hearts.
New α2 globin chain variant with low oxygen affinity affecting the N‐terminal residue and leading to N‐acetylation [Hb Lyon‐Bron α 1(NA1)Val→Ac‐Ala]
Authors: P. Lacan, G. Souillet, M. Aubry, D. Promé, S. Richelme‐David, J. Kister, H. Wajcman, A. Francina
Journal: American Journal of Hematology (2002)

Hemoglobin Lyon-Bron was found in two members of a family of German ascent presenting with a moderate normocytic anemia. In this alpha 2 globin variant, the N-terminal valine of the chain was replaced by an alanine. Electrospray mass spectrometry of the alpha chain showed that, as normally, the initiator methionine was cleaved during globin processing but that the N alpha-terminal group was totally acetylated. This resulted in structural modifications of a region crucial for oxygen binding. As a consequence, hemoglobin Lyon-Bron displayed both a reduced chloride effect and a decreased oxygen affinity, this last point explaining the apparent anemia.
In vivo and in vitro inactivation of bovine surfactant by an anti-surfactant monoclonal antibody
Authors: E P Eijking, D S Strayer, G J van Daal, R Tenbrinck, T A Merritt, E Hannappel, B Lachmann
Journal: European Respiratory Journal (1991)

In this study the importance of a low-weight surfactant protein (11 kDa) is demonstrated by selectively blocking this protein with a monoclonal antibody. In adult rats respiratory failure was induced by repeated bronchoalveolar lavage to remove all pulmonary surfactant. It was shown that surfactant mixed with the antibody was not capable of restoring lung function when compared with surfactant alone or surfactant mixed with control serum. Using the pulsating bubble surfactometer, it could be demonstrated that surfactant mixed with this antibody had a significant higher minimum surface tension when compared with surfactant alone, or surfactant mixed with an unrelated mouse immunoglobulin G (IgG). The inhibition of surfactant function by the monoclonal antibody suggests the importance of the 11 kDa protein for normal surfactant function.
Effect of non-invasive ventilation on pH, carbon dioxide and bicarbonate, in acute, hypercapnic, respiratory failure
Authors: Premenath Balakrishnan, Graeme Wilson
Journal: European Respiratory Journal (2012)

Acute type II respiratory failure is defined by the presence of PaCO2 > 6.6 kPa and pH   We undertook an audit of patients admitted to a high dependency unit in a large teaching hospital setting. The patients were in acute type II respiratory failure as defined by above. They had an arterial blood gas (ABG) recorded before initiation of NIV, after 1-2 hours, after a further 4 hours and at discharge from NIV. We have shown the data for pre NIV and at the end of NIV treatment. The data is therefore for patients who successfully completed NIV therapy. The study was carried out over a twelve month period. The data was entered into the database by the ward junior doctor at the time of the patient9s admission and subsequent discharge.  We had complete data for 44 patients. The p value was derived from the t-test for paired data  This study confirms the findings of previous studies that the successful use of NIV in acute, hypercapnic, respiratory failure leads to significant improvements in both the pH and PaCO 2 . This improvement appears to be directly due to improved alveolar ventilation leading to a reduction in PaCO 2 ; from this data there does not appear to be a significant contribution from renal buffering.
Virus-Induced Cellular Immunity to Simian Virus 40 Tumor-Specific Surface Antigen(s) in Adult LVG:LAK Hamsters&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: W. A. Weppner, J. H. Coggin
Journal: JNCI Journal of the National Cancer Institute (1980)

Cell-mediated Immunity directed against simian virus 40 (SV40) tumor-specific surface antigen(s) (TSSA) was detected in SV40-immunized noninbred LVG:LAK hamsters with the use of a lymphocyte transformation assay. Sensitized spleen cells underwent a proliferative response in the presence of cells of an SV40-induced hamster sarcoma cell line (WF5-1) or the plasma membranes from these cells. In addition, 3-M KCI extracts of the plasma membranes of WF5-1 cells elicited such a lymphocyte proliferative response. Neither the cells of a chemically induced sarcoma cell line (OBT), their plasma membranes, nor 3-M KCI extracts of these membranes caused a similar proliferative response. These results established that immunization of adult hamsters with SV40 resulted in a specific autochthonous cell-mediated immune response against SV40 TSSA. The in vitro demonstration of this virus-induced immunity provided a unique method for the investigation of the SV40 TSSA Involved in the establishment or rejection of tumors. The described lymphocyte transformation assay was also used to follow the solubilization and purification of the SV40 TSSA.
Linear IgA disease: the IgA and IgG response to dermal antigens demonstrates a chiefly IgA response to LAD285 and a dermal 180-kDa protein
Authors: J. Allen, F. Wojnarowska
Journal: British Journal of Dermatology (2003)

Background Linear IgA disease (LAD) of adults and children is mediated by IgA antibodies that target proteins of the epithelial adhesion complex. Most studies have concentrated on the epidermal-associated antigens; the dermal antigens remain unresolved. Objectives To determine the dermal antigen repertoire of IgA and IgG antibodies in LAD. Methods Immunoblotting was carried out on salt-split and urea-extracted dermal skin extracts with IgA antibodies (63 adult and 34 childhood sera) and with IgG antibodies (49 adult and 18 childhood sera). Results Antigens were identified by IgA (61%), IgG (27%) and by both antibody isotypes (19%). LAD285 and an antigen of 180 kDa were the major dermal antigens identified, and antigens of 230 kDa, collagen VII and a protein under 100 kDa were identified less commonly. IgA autoantibodies from adults bound single antigens more frequently than multiple antigens; from children they bound single and multiple antigens equally. The binding of multiple antigens was, however, more common in children than adults. The IgG response was weaker. The 180-kDa antigen was the main IgG dermal target, and with a single exception, IgG autoantibodies targeted single antigens. Conclusions There was an IgA and IgG response to dermal antigens in LAD; however, the dual antibody response was limited. The antibody response to LAD285 and a 180-kDa antigen (probably BP180) suggests that intermolecular epitope spreading of the antigens associated with the extracellular matrix/dermal components of the basement membrane contributes to the immunopathology of the disease. The restricted IgG response suggests that dermal-binding IgG autoantibodies are not pathologically significant.
Comparison of Changes in Mesenteric Resistance Following Splanchnic Nerve Stimulation with Responses to Epinephrine and Norepinephrine
Authors: C. P. DEAL, HAROLD D. GREEN
Journal: Circulation Research (1956)

This is a study of the characteristics of the splanchnic nerve supply to the mesenteric vascular circuit. The flow and pressure responses in the dog's superior mesenteric artery to splanchnic nerve stimulation and to intraarterial injections of epinephrine and norepinephrine, before and during various levels of adrenergic blockade, are analyzed. The results suggest that the splanchnic nerve contains only vasoconstrictor fibers, the mediator of which is probably norepinephrine, but that it also contains fibers which induce the release of epinephrine from the adrenal gland. No evidence for the presence of cholinergic dilator fibers was found.
A30: Assessment of Construct and Discriminative Validity of the 3-Variable JADAS in Relation of Parent-Reported Outcomes
Authors: Alessandro Consolaro, Giorgia Negro, Maria C. Gallo, Sara Verazza, Serena Calandra, Cristina Robbiano, Nicolino Ruperto, Alberto Martini, Angelo Ravelli
Journal: Arthritis & Rheumatology (2014)

Background/Purpose:

An established approach to the measurement of disease activity in juvenile idiopathic arthritis (JIA) is based on the Juvenile Arthritis Disease Activity Score (JADAS). The feasibility of the JADAS for use in standard clinical practice might be enhanced by implementing of a 3-variable version, which does not include the acute phase reactant. Recently, the 3-variable JADAS was found to correlate closely with the original tool. However, the validity of this simplified version of the JADAS in the clinical setting is still insufficiently documented. Aim of the study was to further validate the 3-variable version of the JADAS, hence named clinical JADAS (cJADAS), by assessing its relationship with parent-reported outcomes (excluding the parent's rating of overall well-being, which is included in the JADAS).



Methods:

The study was conducted in a cohort of 175 newly-diagnosed consecutive JIA patients, first seen between 2007–2011 and then followed for 2 years. Clinical assessments were made at baseline and then at 6, 12, 18 and 24 months. At each visit, all parent reported outcomes included in the Juvenile Arthritis Multidimensional Assessment Report (JAMAR) were assessed by a parent of each patient. Construct validity of the cJADAS was computed by calculating its Spearman's correlation with pain visual analog scale (VAS) and disease activity VAS. Discriminative validity was evaluated, by means of the non-parametric analysis of variance (Kruskal-Wallis test) or Mann-Whitney U test, by examining the ability of cJADAS to discriminate between: 1) different categories of disease state (remission, persistent activity or flare), rated subjectively by the parents; 2) different categories of disease course (improved, stable or worsened), rated subjectively by the parents; 3) visit in which parents declared themselves as satisfied or not satisfied with the outcome of the illness; 4) different duration of morning stiffness.



Results:

The cJADAS was strongly correlated with pain VAS (r=0.71) and disease activity VAS (r=0.77). The cJADAS was significantly lower in patients rated as being in remission than in patients rated as being in persistent activity or flare (p < 0.0001), in patients rated as improved or stable than in patients rated as worsened (p < 0001), and in patients whose parents were satisfied with illness outcome than in those who were not (p < 0.0001). The cJADAS was proportionally greater in parallel with the progressive increase in morning stiffness (p < 0001).



Conclusion:

The cJADAS was strongly associated with all parent-reported outcomes, which indicates that it reflects well the parent perception of the child's disease status and course.
Systems Training for Emotional Predictability and Problem Solving (STEPPS) for Outpatients With Borderline Personality Disorder: A Randomized Controlled Trial and 1-Year Follow-Up
Authors: Nancee Blum, Don St. John, Bruce Pfohl, Scott Stuart, Brett McCormick, Jeff Allen, Stephan Arndt, Donald W. Black
Journal: American Journal of Psychiatry (2008)

Objective: Systems Training for Emotional Predictability and Problem Solving (STEPPS) is a 20-week manual-based group treatment program for outpatients with borderline personality disorder that combines cognitive behavioral elements and skills training with a systems component. The authors compared STEPPS plus treatment as usual with treatment as usual alone in a randomized controlled trial. Method: Subjects with borderline personality disorder were randomly assigned to STEPPS plus treatment as usual or treatment as usual alone. Total score on the Zanarini Rating Scale for Borderline Personality Disorder was the primary outcome measure. Secondary outcomes included measures of global functioning, depression, impulsivity, and social functioning; suicide attempts and self-harm acts; and crisis utilization. Subjects were followed 1 year posttreatment. A linear mixed-effects model was used in the analysis. Results: Data pertaining to 124 subjects (STEPPS plus treatment as usual [N=65]; treatment as usual alone [N=59]) were analyzed. Subjects assigned to STEPPS plus treatment as usual experienced greater improvement in the Zanarini Rating Scale for Borderline Personality Disorder total score and subscales assessing affective, cognitive, interpersonal, and impulsive domains. STEPPS plus treatment as usual also led to greater improvements in impulsivity, negative affectivity, mood, and global functioning. These differences yielded moderate to large effect sizes. There were no differences between groups for suicide attempts, self-harm acts, or hospitalizations. Most gains attributed to STEPPS were maintained during follow-up. Fewer STEPPS plus treatment as usual subjects had emergency department visits during treatment and follow-up. The discontinuation rate was high in both groups. Conclusions: STEPPS, an adjunctive group treatment, can deliver clinically meaningful improvements in borderline personality disorder-related symptoms and behaviors, enhance global functioning, and relieve depression.
THE EFFECT OF ANTIBACTERIAL DRUGS ON THE WEIGHT OF MICE
Authors: Rene Dubos, Russell W. Schaedler, Richard L. Costello
Journal: The Journal of Experimental Medicine (1963)

NCS mice gained weight rapidly when fed a gluten diet deficient in several amino acids, but their weight gain on the same regimen was very much retarded if they were given antibacterial drugs, even for a short period of time. This retardation of growth could not be entirely corrected by supplementing the gluten diet with lysine and threonine. The decrease in growth rate brought about by antibacterial drugs could probably be traced to the alteration in intestinal flora resulting from drug treatment. The intensity and duration of both types of changes were related to the dose of drug administered, and to the length of the treatment period. Whatever the nutritional regimen, treatment with penicillin caused a retardation of weight gain in NCS mice. The retardation was more pronounced, and longer lasting, when the animals were fed semisynthetic regimens (containing casein or gluten) than when they were fed crude diets (pellets) containing natural materials of ill defined composition. These differences probably had their origin in the fact that the changes in fecal flora induced by the drugs were profoundly influenced by the composition of the diet. Antibacterial drugs which retarded weight gain of Swiss NCS mice, in contrast increased weight gain in ordinary Swiss mice raised under usual conditions. It is probable that this difference in response to the antibacterial drugs resulted from the fact that ordinary Swiss mice have a much more complex intestinal flora than NCS animals.
Cardiac Hypertrophy After Transplantation Is Associated With Persistent Expression of Tumor Necrosis Factor-α
Authors: Sonny J. Stetson, Ale Perez-Verdia, Wojceich Mazur, John A. Farmer, Michael M. Koerner, Donald G. Weilbaecher, Mark L. Entman, Miguel A. Quiñones, George P. Noon, Guillermo Torre-Amione
Journal: Circulation (2001)

Background — The mechanisms that contribute to cardiac allograft hypertrophy are not known; however, the rapid progression and severity of hypertrophy suggest that nonhemodynamic factors may play a contributory role. Tumor necrosis factor-α (TNF-α) is a cytokine produced in cardiac allografts and capable of producing hypertrophy and fibrosis; therefore, we suggest that TNF-α may play a contributory role. Accordingly, the aims of our study were to define the role of systemic hypertension in the development of hypertrophy, characterize the histological determinants of hypertrophy, and characterize the expression of myocardial TNF-α after heart transplantation. Methods and Results — To separate the effect of hypertension from immune injury in the development of cardiac allograft hypertrophy, we measured the gain in left ventricular mass by 2D echocardiography in heart transplant recipients and lung transplant recipients who developed similar rates of systemic hypertension. The gain in left ventricular mass was 73% in heart transplant recipients and 7% in lung transplant recipients ( P &lt;0.0001). By comparing myocardial samples obtained during the first week after transplant and at 1 year, we found that there was a significant increase in total collagen content ( P &lt;0.0001), collagen I ( P &lt;0.0001), collagen III ( P &lt;0.0001), and myocyte size ( P &lt;0.0001). These changes were associated with persistent myocardial TNF-α expression. Conclusions — We suggest that the contribution of hypertension to cardiac allograft hypertrophy is minimal and that persistent intracardiac expression of TNF-α may contribute to the development of cardiac allograft hypertrophy.