tbuckley/cabot-search huggingface dataset:
Current Status of Bicarbonate in CKD
Authors: Mirela Dobre, Mahboob Rahman, Thomas H. Hostetter
Journal: Journal of the American Society of Nephrology (2014)

Metabolic acidosis was one of the earliest complications to be recognized and explained pathologically in patients with CKD. Despite the accumulated evidence of deleterious effects of acidosis, treatment of acidosis has been tested very little, especially with respect to standard clinical outcomes. On the basis of fundamental research and small alkali supplementation trials, correcting metabolic acidosis has a strikingly broad array of potential benefits. This review summarizes the published evidence on the association between serum bicarbonate and clinical outcomes. We discuss the role of alkali supplementation in CKD as it relates to retarding kidney disease progression, improving metabolic and musculoskeletal complications.
Naturally Occurring Tolerance Acquisition to Foods in Children Previously Allergic to Egg and Peanut Is Characterized By Antigen Specificity and Associated with Increased Subsets of Regulatory T Cells
Authors: Nashmia Qamar, Anna B. Fishbein, Kristin A. Erickson, Miao Cai, Christine Szychlinski, Paul Bryce, Robert P. Schleimer, Ramsay L. Fuleihan, Anne Marie Singh
Journal: Journal of Allergy and Clinical Immunology (2015)
Effectiveness of National Implementation of Prolonged Exposure Therapy in Veterans Affairs Care
Authors: Afsoon Eftekhari, Josef I Ruzek, Jill J Crowley, Craig S Rosen, Mark A Greenbaum, Bradley E Karlin
Journal: JAMA Psychiatry (2013)

Posttraumatic stress disorder (PTSD) is a pervasive and often debilitating condition that affects many individuals in the general population and military service members. Effective treatments for PTSD are greatly needed for both veterans returning from Iraq and Afghanistan and veterans of other eras. Prolonged exposure (PE) therapy has been shown to be highly efficacious in clinical trials involving women with noncombat trauma, but there are limited data on its effectiveness in real-world clinical practice settings and with veterans.To evaluate the effectiveness of PE as implemented with veterans with PTSD in a large health care system.This evaluation included 1931 veterans treated by 804 clinicians participating in the Department of Veterans Affairs (VA) PE Training Program. After completing a 4-day experiential PE training workshop, clinicians implemented PE (while receiving consultation) with a minimum of 2 veteran patients who had a primary diagnosis of PTSD.Changes in PTSD and depression symptoms were assessed with the PTSD Checklist and the Beck Depression Inventory II, measured at baseline and at the final treatment session. Multiple and single imputation were used to estimate the posttest scores of patients who left treatment before completing 8 sessions. Demographic predictors of treatment dropout were also examined.Intent-to-treat analyses indicate that PE is effective in reducing symptoms of both PTSD (pre-post d = 0.87) and depression (pre-post d = 0.66), with effect sizes comparable to those reported in previous efficacy trials. The proportion of patients screening positive for PTSD on the PTSD Checklist decreased from 87.6% to 46.2%.Clinically significant reductions in PTSD symptoms were achieved among male and female veterans of all war eras and veterans with combat-related and non-combat-related PTSD. Results also indicate that PE is effective in reducing depression symptoms, even though depression is not a direct target of the treatment.
EPIDEMIOLOGICAL STUDY OF INJURY AND ILLNESS IN GREAT BRITAIN SHORT-TRACK SPEED SKATING
Authors: D Palmer-Green, M Brownlow, J Hopkins, J Eley, R Jaques, G Hunter
Journal: British Journal of Sports Medicine (2014)

Background Prevention of injury and illness in elite sport can have not only athlete health benefits but also potential positive performance gains. As the first step towards prevention, valid injury/illness surveillance data is needed. Objective Provide injury/illness epidemiology information on the Great Britain (GB) short-track speed skating squad. Design Longitudinal prospective surveillance study, recording injury/illness, and training/competition exposure data. Definitions for injury/illness, time-loss and performance-restriction were used to identify the rate and severity of athlete injuries/illnesses. Setting GB short-track speed skating National training centre, including domestic and international training/competition venues during the 2009/2010 season. Participants 11 (7 male; 4 female) National team athletes. Interventions Standardised report forms for injuries/illnesses were completed by medical, and competition/training exposure by coaching, support staff. Main outcome measure Injury/illness rate, severity and causes. Results There were 14 training (2.7/1000 athlete training hrs) and 2 competition (13/100 competition starts) injuries, and 12 illnesses. Equating 64% and 73% of the squad suffering at least one injury/illness, with 29 days and 5 days lost per injury/illness, respectively. Injuries to the thigh (38%), lumbar spine and knee (19% each) were most common, with 8, 19, and 43 days lost per injury, respectively. Overuse (gradual/sudden-onset: 38%), non-contact trauma (31%) and contact – static object (25%) were the most common causes of injury, with contact – static object (59d) and overuse (33d) most severe. Upper respiratory tract infection was the most common illness (75%), occurring more frequently around periods of competition and long haul travel. Conclusions Injury and illness seasonal prevalence was similar, but severity greater for injuries. Prevention initiatives targeting common and severe injuries/illnesses may be beneficial in reducing the number of athlete days lost to training/competition.
Maternal Hypercholesterolemia and Treatment During Pregnancy Influence the Long-Term Progression of Atherosclerosis in Offspring of Rabbits
Authors: Wulf Palinski, Francesco P. D’Armiento, Joseph L. Witztum, Filomena de Nigris, Florencia Casanada, Mario Condorelli, Mercedes Silvestre, Claudio Napoli
Journal: Circulation Research (2001)

Maternal hypercholesterolemia during pregnancy is associated with enhanced fatty streak formation in human fetuses and faster progression of atherosclerosis during childhood even under normocholesterolemic conditions. A causal role of maternal hypercholesterolemia in lesion formation during fetal development has previously been established in rabbits. The same experimental model is now used to establish that maternal hypercholesterolemia or ensuing pathogenic events in fetal arteries enhance atherogenesis later in life. Five groups of rabbit mothers were fed chow, cholesterol-enriched chow, or cholesterol-enriched chow plus 1000 IU vitamin E, 3% cholestyramine, or both during pregnancy. Offspring of all groups (n=136) were fed a mildly hypercholesterolemic diet for up to a year and had similar cholesterol levels. Aortic lesion sizes and lipid peroxidation products in plasma and lesions in offspring were determined at birth, 6 months, or 12 months. Lesion progression in offspring of hypercholesterolemic mothers was greater than in all other groups. At each time point, offspring of hypercholesterolemic mothers had 1.5- to 3-fold larger lesions than offspring of normocholesterolemic mothers ( P &lt;0.01), with the greatest absolute differences at 12 months. Maternal treatment reduced lesions by 19% to 53%, compared with offspring of untreated hypercholesterolemic mothers ( P &lt;0.01), with the greatest effect in the vitamin E groups. At 12 months, lesions in offspring of all vitamin E and cholestyramine-treated mothers were similar to those of normocholesterolemic mothers. Lipid peroxidation end-products in lesions and plasma showed analogous differences between groups as lesions ( P &lt;0.01). Thus, pathogenic programming in utero increases the susceptibility to atherogenic risk factors later in life and maternal intervention with cholesterol-lowering drugs or antioxidants reduce postnatal lipid peroxidation and atherosclerosis in their offspring.
Cephalosporin-induced hemolysis: A case report and review of the literature
Authors: W. Christopher Ehmann
Journal: American Journal of Hematology (1992)

Abstract Cephalosporins are commonly used drugs that interact with red blood cell membranes. They frequently cause a positive direct antiglobulin test but rarely cause hemolysis. A case of cefotetan‐induced hemolytic anemia is described in which two types of antibodies were detected. One reacted with red blood cells by a hapten mechanism, the other reacted with drug to form immune complexes. This case is compared with the 13 cases of cephalosporin‐induced hemolytic anemia reported to date. Understanding the interactions of red blood cells and cephalosporins is critical to the safe use of these commonly prescribed drugs. © 1992 Wiley‐Liss, Inc.
Cosegregation Analysis in Genetic Crosses Suggests a Protective Role for Atrial Natriuretic Factor Against Ventricular Hypertrophy
Authors: S. Masciotra, S. Picard, C. F. Deschepper
Journal: Circulation Research (1999)

Abstract —In most rat models studied to date, increased ventricular mass is associated with high ventricular expression of the atrial natriuretic factor (ANF) gene. However, it is unknown whether ANF plays a beneficial or detrimental role in the course of left ventricular hypertrophy or whether ANF gene expression could be genetically linked to cardiac mass. To address such questions, we performed a cosegregation analysis in genetic crosses of inbred strains of rats. To select strains with the appropriate phenotypic characteristics, we first compared the ventricular abundance of ANF mRNA to ventricular mass (corrected for body weight) in 2 recombinant inbred strains derived from Wistar-Kyoto (WKY)/spontaneously hypertensive rat (SHR) hybrid crosses, ie, WKY-derived hyperactive (WKHA) and WKY-derived hypertensive (WKHT) rats, as well as in their parental inbred strains. In the 2 such strains that were normotensive, we observed that ventricular mass was higher in WKHA than in WKY rats, yet ventricular ANF mRNA was less abundant in WKHA than in WKY rats. Within a segregating population of F2 animals generated from a cross between WKY and WKHA genitors, the abundance of ventricular ANF mRNA and peptide correlated inversely with left ventricular mass, in contrast to the positive correlation observed with β-myosin heavy chain mRNA. Finally, in the equally hypertensive SHR and WKHT strains, we found that ventricular mass was higher in SHR than in WKHT, yet ventricular ANF mRNA was less abundant in SHR than in WKHT. These results demonstrate for the first time that low ventricular ANF gene expression can be linked genetically to high cardiac mass independently of blood pressure and are consistent with a protective role for ANF against left ventricular hypertrophy.
Occurrence of symptomatic knee osteoarthrosis in rural Finland: a prospective follow up study.
Authors: P Kannus, M Jarvinen, H Kontiala, L Bergius, E Hyssy, E Salminen, A Tuomi, T Unkila, I Valtanen
Journal: Annals of the Rheumatic Diseases (1987)

All visits to physicians in the Orivesi Region Federation of Municipalities for Public Health Work in Finland paid due to symptomatic osteoarthrosis of the knee joint were prospectively recorded over a period of one year. Two hundred and thirty four visits were made, accounting for 0.63% of all visits. The prevalence of knee osteoarthrosis was 1.11% (men 0.45%, women 1.72%), and the incidence was 0.60%. The disease occurred almost twice as often in the right knee than in the left. The study provides basic information about patients needing medical help because of symptomatic knee osteoarthrosis. The results can be used as an aid to the planning of examination and treatment resources and in assessment of the need for such services.
SCP Phosphatases Suppress Renal Cell Carcinoma by Stabilizing PML and Inhibiting mTOR/HIF Signaling
Authors: Yu-Ching Lin, Li-Ting Lu, Hsin-Yi Chen, Xueyan Duan, Xia Lin, Xin-Hua Feng, Ming-Jer Tang, Ruey-Hwa Chen
Journal: Cancer Research (2014)

Abstract The tumor-suppressor protein promyelocytic leukemia (PML) is aberrantly degraded in multiple types of human cancers through mechanisms that are incompletely understood. Here, we show that the phosphatase SCP1 and its isoforms SCP2/3 dephosphorylate PML at S518, thereby blocking PML ubiquitination and degradation mediated by the prolyl isomerase Pin1 and the ubiquitin ligase KLHL20. Clinically, SCP1 and SCP3 are downregulated in clear cell renal cell carcinoma (ccRCC) and these events correlated with PMLS518 phosphorylation, PML turnover, and high-grade tumors. Restoring SCP1-mediated PML stabilization not only inhibited malignant features of ccRCC, including proliferation, migration, invasion, tumor growth, and tumor angiogenesis, but also suppressed the mTOR–HIF pathway. Furthermore, blocking PML degradation in ccRCC by SCP1 overexpression or Pin1 inhibition enhanced the tumor-suppressive effects of the mTOR inhibitor temsirolimus. Taken together, our results define a novel pathway of PML degradation in ccRCC that involves SCP downregulation, revealing contributions of this pathway to ccRCC progression and offering a mechanistic rationale for combination therapies that jointly target PML degradation and mTOR inhibition for ccRCC treatment. Cancer Res; 74(23); 6935–46. ©2014 AACR.
Molecular cloning, expression, and chromosomal localization of the human earliest lymphocyte activation antigen AIM/CD69, a new member of the C-type animal lectin superfamily of signal-transmitting receptors.
Authors: M López-Cabrera, A G Santis, E Fernández-Ruiz, R Blacher, F Esch, P Sánchez-Mateos, F Sánchez-Madrid
Journal: The Journal of Experimental Medicine (1993)

The activation of T lymphocytes, both in vivo and in vitro, induces the expression of CD69. This molecule, which appears to be the earliest inducible cell surface glycoprotein acquired during lymphoid activation, is involved in lymphocyte proliferation and functions as a signal transmitting receptor in lymphocytes, natural killer (NK) cells, and platelets. To determine the structural basis for CD69 function, the cDNA coding for CD69 was isolated by a polymerase chain reaction-based strategy using oligonucleotides deduced from peptide sequences of the purified protein. The isolated cDNA exhibited a single open reading frame of 597 bp coding for CD69, and predicted a 199-amino acid protein of type II membrane topology, with extracellular (COOH-terminal), transmembrane, and intracellular domains. The CD69 clone hybridized to a 1.7-kb mRNA species, which was rapidly induced and degraded after lymphocyte stimulation, consistent with the presence of rapid degradation signals at the 3' untranslated region. Transient expression of the polypeptide encoded by CD69 cDNA in COS-7 cells demonstrated that it presented properties comparable to native CD69 protein. The CD69 gene was regionally mapped to chromosome 12 p13-p12 by both somatic cell hybrid DNA analysis and fluorescence in situ hybridization coupled with GTG banding (G bands by trypsin using Giemsa). Protein sequence homology search revealed that CD69 is a new member of the Ca(2+)-dependent (C-type) lectin superfamily of type II transmembrane receptors, which includes the human NKG2, the rat NKR-P1, and the mouse NKR-P1 families of NK cell-specific genes. CD69 also has a structural homology with other type II lectin cell surface receptors, such as the T cell antigen Ly49, the low avidity immunoglobulin E receptor (CD23), and the hepatic asialoglycoprotein receptors. The CD69 protein also shares functional characteristics with most members of this superfamily, which act as transmembrane signaling receptors in early phases of cellular activation.
Trends in End-of-Life Decision Making in Patients With and Without Cancer
Authors: Koen Pardon, Kenneth Chambaere, H. Roeline W. Pasman, Reginald Deschepper, Judith Rietjens, Luc Deliens
Journal: Journal of Clinical Oncology (2013)

Purpose Because of cancer's high symptom burden and specific disease course, patients with cancer are more likely than other patients to face end-of-life decisions that have possible or certain life-shortening effects (ELDs). This study examines the incidence of ELDs in patients with cancer compared with patients without cancer and the trends in ELD incidence from 1998-2007. Patients and Methods A nationwide death certificate study in Flanders, Belgium, was conducted in 2007, analogous to one completed in 1998. Physicians who had signed selected death certificates (n = 6,927) were sent a questionnaire. Results The response rate was 58.4%. Nonsudden deaths were studied. Intensified symptom alleviation occurred more in patients with cancer than in those without (53.8% v 31.7%; P &lt; .001) as did euthanasia (6.8% v 0.9%; P &lt; .001). There was no difference between groups in nontreatment decisions and life-ending acts without patient's explicit request. Patients with cancer were less involved in the end-of-life decision-making process than patients without cancer (69.7% v 83.5%; P = .001). From 1998 to 2007, ELD incidence has increased in patients with cancer (+6.7%) and even more in patients without cancer (+14.9%) because of an increase in intensified symptom alleviation. In patients with cancer, euthanasia rates increased strongly and life-ending acts without the patient's explicit request decreased. Conclusion The higher ELD incidence in patients with cancer compared with those without is probably related to differences in disease trajectories and access to end-of-life care. During the period from 1998 to 2007, when euthanasia was legalized and palliative care intensified, overall ELDs increased, including those as a result of symptom alleviation and euthanasia, with a decrease in life-ending acts without explicit request.
In Search of a Common European Approach to a Healthy Indoor Environment
Authors: Olaf C.G. Adan, Julie Ng-A-Tham, Wojtek Hanke, Torben Sigsgaard, Peter van den Hazel, Felicia Wu
Journal: Environmental Health Perspectives (2007)

Increasingly, policymakers in Europe and around the world are realizing the importance of healthy indoor environments for public health. Certain member states of the European Union (EU) have already achieved successes in improving indoor environmental quality, such as controlling certain contaminants (e.g., environmental tobacco smoke) or developing nationwide policies that address indoor air generally. However, a common European approach to achieving healthy indoor environments is desirable for several reasons including providing a broader recognition of the problem of unhealthy indoor air, setting a policy example for all 27 EU member states, and achieving greater public health equity across the different European nations. In this article we address the question "Why is it so difficult in the EU to develop a coherent approach on indoor environment?" We identify and describe four main barriers: a) the subsidiarity principle in EU policymaking, introducing decentralization of decision making to the member states; b) fragmentation of the topic of the indoor environment; c) the differences in climate and governance among different member states that make a common policy difficult; and d) economic issues. We discuss potential lessons and recommendations from EU and U.S. successes in achieving healthier indoor environments through various policy mechanisms.
Exposure to Diesel Exhaust Aggravates Nasal Allergic Reaction in Guinea Pigs
Authors: TAKAHIRO KOBAYASHI
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

Diesel exhaust particulates (DEP) (1) and exposure to diesel exhaust (DE) induce nasal mucosal hyperresponsiveness to histamine. Therefore, in the present study, we investigated whether or not exposing guinea pigs to DE aggravates the nasal allergic reaction induced by repeated nasal administration of ovalbumin (OVA). Guinea pigs were exposed to filtered air or to DE (DE containing 0.3 or 1.0 mg/m3 of DEP) for 5 wk. During exposure to filtered air or to DE, guinea pigs were administered 1% of OVA in saline into the nasal cavities once a week. Sneezes were counted and nasal secretions were measured as indices of sneezing responses and rhinorrhea for 20 min after OVA administration. Titers of specific anti-OVA-IgG and anti-OVA-IgE and the number of eosinophils infiltrated into both nasal epithelium and subepithelium were measured at the end of the exposure to DE. Exposure to DE enhanced the number of sneezes and the amount of nasal secretions induced by OVA. Titers of specific anti-OVA-IgG and anti-OVA-IgE also significantly increased in DE-exposed animals. Exposure to DE also augmented the number of eosinophils that infiltrated both the nasal epithelium and the subepithelium induced by OVA. These results suggest that exposure to DE enhances the nasal allergic reaction induced by repeated antigen administration in guinea pigs.
Mechanisms of the Puromycin-Induced Defects in the Transglomerular Passage of Water and Macromolecules
Authors: Michael P. Bohrer, Christine Baylis, Channing R. Robertson, Barry M. Brenner, Julia L. Troy, Wayne T. Willis
Journal: Journal of Clinical Investigation (1977)

To investigate the mechanism(s) of increased filtration of serum proteins after glomerular injury, polydisperse samples of uncharged [3H]dextran (D) or anionic [3H]dextran sulfate (DS) were infused into 14 control and 16 puromycin aminonucleoside- (PAN) treated Munich-Wistar rats. Fractional clearances of D or DS ranging in radius from 18 to 42Å were determined in these rats, together with direct measurements of the forces governing the glomerular filtration rate of water. Whole kidney and single nephron glomerular filtration rates were ∼40% lower in PAN-treated rats, relative to controls, due mainly to a marked reduction in the glomerular capillary ultrafiltration coefficient and, to a lesser extent, to a small reduction in glomerular plasma flow rate as well. In PAN-treated rats, as in normal controls, inulin was found to permeate the glomerular capillary wall without measurable restriction, and both D and DS were shown to be neither secreted nor reabsorbed. Fractional clearances of uncharged D were reduced after PAN administration, falling significantly for effective D radii from 22 to 38Å. Utilizing a theory based on macromolecular transport through pores, these results indicate that in PAN-treated rats, effective pore radius is the same as in controls, ∼44Å. In PAN nephrosis, however, the ratio of total pore surface area/pore length, a measure of pore density, is reduced to approximately one-third that of control, due very likely to a reduction in filtration surface area. In contrast to the results with uncharged D, fractional clearances of DS were found to increase after PAN administration for all DS radii studied. These results with D and DS suggest that proteinuria in PAN nephrosis is due, not to an increase in effective pore radius or number of pores, but rather to a diminution of the electrostatic barrier function of the glomerular capillary wall, thereby allowing increased passage of polyanions such as DS and albumin.