tbuckley/cabot-search huggingface dataset:
Body weight and comorbidity predict mortality in COPD patients treated with oxygen therapy
Authors: S. Marti, X. Muñoz, J. Rios, F. Morell, J. Ferrer
Journal: European Respiratory Journal (2006)

The aim of this study was to investigate the association between clinical variables and all-cause and respiratory mortality in patients with chronic obstructive pulmonary disease (COPD) undergoing long-term oxygen therapy (LTOT). The authors retrospectively studied a historic cohort of 128 patients with COPD (126 males, mean age± sd 68.9±9.7 yrs, body mass index (BMI) 25.1±4.5 kg·m −2 , and forced expiratory volume in one second 25.4±8.8% predicted), who were being treated with long-term oxygen therapy in a tertiary teaching hospital between 1992 and 1999. Comorbidity, assessed with the Charlson Index, was present in 38% of the patients. Vital status and cause of death were assessed through the population death registry. A total of 78 patients (61%) had died by the end of follow-up. Three-year survival was 55%. Death was due to respiratory causes in 77% of cases. On Cox analysis, BMI &lt;25 kg·m −2 , comorbid conditions, age ≥70 yrs and cor pulmonale were associated with all-cause mortality. The BMI and comorbidity were the only significant predictive factors when the analysis was restricted to respiratory mortality. In conclusion, body mass index &lt;25 kg·m −2 and comorbidity were predictors of all-cause and respiratory mortality in a cohort of chronic obstructive pulmonary disease patients treated with long-term oxygen therapy. These factors should be taken into account when considering the management and prognosis of these patients.
Effects of Citalopram and Interpersonal Psychotherapy on Depression in Patients With Coronary Artery Disease
Authors: François Lespérance, Nancy Frasure-Smith, Diana Koszycki, Marc-André Laliberté, Louis T. van Zyl, Brian Baker, John Robert Swenson, Kayhan Ghatavi, Beth L. Abramson, Paul Dorian, Marie-Claude Guertin, for the CREATE Investigators
Journal: JAMA (2007)

INCE THE EARLY 1990S, STUDIES have reported prevalences of major depression between 17% and 27% in hospitalized patients with coronary artery disease (CAD). 1 Most have also demonstrated that depression has a negative cardiac prognostic impact. 2,3 Only 1 large randomized trial, the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study, 4 has tried to determine whether treating depression could improve cardiac prognosis in CAD patients.Although ENRICHD demonstrated that a combination of short-term individual cognitive behavior therapy (CBT) and a selective serotonin reuptake inhibitor (SSRI), when needed, was significantly better than usual care at reducing depressive symptoms over 6 months in depressed or socially iso-For editorial comment see p 411.
Social Entrepreneurship for Sexual Health (SESH): A New Approach for Enabling Delivery of Sexual Health Services among Most-at-Risk Populations
Authors: Joseph D. Tucker, Kevin A. Fenton, Robert Peckham, Rosanna W. Peeling
Journal: PLoS Medicine (2012)

Each year there are over one billion estimated new curable sexually transmitted infections [1]. This is a daunting number, especially in the face of dwindling public health resources and difficulty reaching and retaining individuals in most-at-risk populations, who are the main drivers of these infections. Yet a growing number of community-based organizations focused on reaching most-at-risk populations have the capacity to move beyond condom distribution and conventional outreach to deliver novel point-of-care HIV/sexually transmitted disease (STD) testing [2], enhance partner notification [3], and link patients into treatment and care programs. The growing organizational and technical capacity of community-based organizations has been recognized by the Global Fund to Fight AIDS, Tuberculosis and Malaria, the GAVI Alliance, and the Joint United Nations Programme on HIV/AIDS, all of which have community-based organization representation at their highest levels [4]. But community-based organizations' growing capacity has yet to reach its full potential for service delivery since a substantial portion of most-at-risk populations in regions with substantial sexual disease burden remain out of care, untested, and unengaged [5].

Social entrepreneurship provides a new approach to more completely realize this full potential through identifying new prevention, treatment, and retention strategies. Optimizing health systems and program implementation are increasingly understood to be key drivers for improving health [6]. Social entrepreneurship uses entrepreneurial principles to promote the sustainable and innovative use of human, fiscal, and technological resources for social good. In the context of sexual health, social entrepreneurship focuses on developing novel, sustainable, community-responsive sexual health services. A number of social entrepreneurial tools, such as social marketing, conditional cash transfers, and microenterprise, have been effective in sexual health promotion in small pilot studies, but they have not been widely applied or systematically evaluated. Here we discuss the shortcomings of the dominant sexual health approach, explain the benefit of using social entrepreneurship for sexual health (SESH), and articulate key principles for moving forward.
Diagnosis of Pheochromocytoma
Authors: Tomas Lenz, Jan Gossmann, Karl-Ludwig Schulte, Lothar Salewski, Helmut Geiger
Journal: New England Journal of Medicine (1988)

The purpose of this article is to give an overview on recent advances in the diagnosis, localization by imaging and treatment of pheochromocytoma. Pheochromocytoma is a mostly benign tumor (malignancy rate 10-15%) which arises from chromaffin cells with excessive catecholamine production and secretion. Most tumors are localized in the adrenals but 15-18% of the lesions are found extraadrenally (paragangliomas). Pheochromocytoma is a rare form of secondary hypertension; it can also be found as a feature of familial disease (e.g. von Hippel-Lindau disease, MEN type II) due to genetic mutations of several genes that have been identified recently. In familial pheochromocytoma molecular genetic analysis has improved the diagnostic modalities. In such patients the tumor can occur bilaterally and patients often remain normotensive until the tumor produces sufficient catecholamines to have hemodynamic effects. The extreme importance of recognizing this tumor is evident from the fact that it can be successfully removed in about 90% of the cases, whereas if unrecognized the tumor poses great risk of death or devastating complications. Diagnostic screening includes measurement of catecholamines and their metabolites (metanephrines) in plasma and/or urine. Furthermore, pharmacological testing (e.g. clonidine suppression test) may be indicated in patients with moderately elevated catecholamines or when the diagnosis is still uncertain. Several imaging techniques are applied to localize the tumor. Abdominal CT scan is still considered the "gold standard" since about 98% of the tumors lie infradiaphragmatically. Magnetic resonance imaging (MRI) and MIBG-scanning are other useful methods. Recently, positron emission tomography (PET) based techniques have also been developed. After the diagnosis is made tumor removal following pharmacological pretreatment is the decisive therapeutic measure.
GM2 Expression in Renal Cell Carcinoma: Potential Role in Tumor-Induced T-Cell Dysfunction
Authors: Kaushik Biswas, Amy Richmond, Patricia Rayman, Soumika Biswas, Mark Thornton, Gaurisankar Sa, Tanya Das, Renliang Zhang, Ali Chahlavi, Charles S. Tannenbaum, Andrew Novick, Ronald Bukowski, James H. Finke
Journal: Cancer Research (2006)

Abstract Multiple mechanisms have been proposed to account for immune escape by tumors. Although gangliosides have long been known to suppress T-cell immunity, few studies have examined the effect of human tumor-derived gangliosides on immune responses. Here, we show that gangliosides isolated from renal cell carcinoma (RCC) cell lines and clear cell tumor tissue can induce apoptosis in peripheral blood T cells. The RCC tissue-derived gangliosides also suppressed IFN-γ and, in many cases, interleukin-4 production by CD4+ T cells at concentrations (1 ng/mL-100 pg/mL) well below those that induce any detectable T-cell death (4-20 μg/mL). Additional findings show that GM2 expressed by RCC plays a significant role in promoting T-cell dysfunction. This is supported by the demonstration that all RCC cell lines examined (n = 5) expressed GM2 as did the majority of tumors (15 of 18) derived from patients with clear cell RCC. Furthermore, an antibody specific for GM2 (DMF10.167.4) partially blocked (50-60%) T-cell apoptosis induced by coculturing lymphocytes with RCC cell lines or with RCC tissue-derived gangliosides. DMF10.167.4 also partially blocked the suppression of IFN-γ production induced by RCC tissue-derived gangliosides, suggesting that GM2 plays a role in down-regulating cytokine production by CD4+ T cells. (Cancer Res 2006; 66(13): 6816-25)
ALPHA-INTERFERON THERAPY FOR ESSENTIAL THROMBOCYTHAEMIA
Authors: F.J Giles, A.G Gray, M Brozovic, I.R Grant, S.J Machin, J.D.M Richards, S Venutas, C.R.J Singer, K.L Yong, S.C Davies, A.V Hoffbrand, A.B Mehta, M.J.G Thomas, A.H Goldstone
Journal: The Lancet (1988)
Urinary levels of seven phthalate metabolites in the U.S. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000.
Authors: Manori J Silva, Dana B Barr, John A Reidy, Nicole A Malek, Carolyn C Hodge, Samuel P Caudill, John W Brock, Larry L Needham, Antonia M Calafat
Journal: Environmental Health Perspectives (2003)

We measured the urinary monoester metabolites of seven commonly used phthalates in approximately 2,540 samples collected from participants of the National Health and Nutrition Examination Survey (NHANES), 1999-2000, who were greater than or equal to 6 years of age. We found detectable levels of metabolites monoethyl phthalate (MEP), monobutyl phthalate (MBP), monobenzyl phthalate (MBzP), and mono-(2-ethylhexyl) phthalate (MEHP) in > 75% of the samples, suggesting widespread exposure in the United States to diethyl phthalate, dibutyl phthalate or diisobutylphthalate, benzylbutyl phthalate, and di-(2-ethylhexyl) phthalate, respectively. We infrequently detected monoisononyl phthalate, mono-cyclohexyl phthalate, and mono-n-octyl phthalate, suggesting that human exposures to di-isononyl phthalate, dioctylphthalate, and dicyclohexyl phthalate, respectively, are lower than those listed above, or the pathways, routes of exposure, or pharmacokinetic factors such as absorption, distribution, metabolism, and elimination are different. Non-Hispanic blacks had significantly higher concentrations of MEP than did Mexican Americans and non-Hispanic whites. Compared with adolescents and adults, children had significantly higher levels of MBP, MBzP, and MEHP but had significantly lower concentrations of MEP. Females had significantly higher concentrations of MEP and MBzP than did males, but similar MEHP levels. Of particular interest, females of all ages had significantly higher concentrations of the reproductive toxicant MBP than did males of all ages; however, women of reproductive age (i.e., 20-39 years of age) had concentrations similar to adolescent girls and women 40 years of age. These population data on exposure to phthalates will serve an important role in public health by helping to set research priorities and by establishing a nationally representative baseline of exposure with which population levels can be compared.
Identification of the First Gene Locus (SSNS1) for Steroid-Sensitive Nephrotic Syndrome on Chromosome 2p
Authors: Rainer G. Ruf, Arno Fuchshuber, Stephanie M. Karle, Arnaud Lemainque, Kirsten Huck, Thomas Wienker, Edgar Otto, Friedhelm Hildebrandt
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. Disease mechanisms of steroid-sensitive nephrotic syndrome (SSNS) remain unknown. Whereas gene identification has furthered the understanding of pathomechanisms in steroid-resistant nephrotic syndrome (SRNS), not even a gene locus is known for SSNS. Total genome linkage analysis was performed in a consanguineous SSNS kindred to identify a gene locus for SSNS. Homozygosity mapping identified a locus for SSNS on chromosome 2p12-p13.2 between markers D2S292 and D2S289 (multipoint LOD score Z<sub>max</sub> = 3.01 at D2S145). The first gene locus for SSNS, as a first step to detect the responsible gene, was thus identified. There was clear evidence for genetic locus heterogeneity upon examination of ten additional families with SSNS. E-Mail: fhilde@umich.edu
Tumor Necrosis Factor Receptor 1 Signaling Resistance in the Female Myocardium During Ischemia
Authors: Meijing Wang, Ben M. Tsai, Paul R. Crisostomo, Daniel R. Meldrum
Journal: Circulation (2006)

Background— Tumor necrosis factor-α (TNF) is increased in myocardial tissue after ischemia and reperfusion (I/R). TNF contributes to postischemic myocardial dysfunction and induces proinflammatory signaling, which may be mediated by the 55-kDa TNF receptor (TNFR1). In humans, there is a direct correlation between functional capacity, survival, and circulating TNF levels. Although decreasing the TNF level in animals was beneficial after myocardial ischemia, simply decreasing the bioavailability of TNF in humans with heart failure was not beneficial. This led to the important appreciation that TNF may have beneficial or deleterious effects in the heart, depending on which of its receptors is activated. Females have a lower incidence of heart failure and a higher heart failure survival than males. We hypothesized that TNFR1 signaling resistance occurs in the female myocardium during ischemia. Methods and Results— Hearts from male and female TNFR1-knockout and wild-type (WT) mice were subjected to I/R. Female WT mice had better postischemic recovery than did male WT mice, an effect that appeared to be due to TNFR1 signaling resistance in females. Female WT mice had less myocardial depression after TNF infusion despite equivalent TNFR1 expression. Interestingly, TNFR1 ablation improved postischemic myocardial function, decreased activation of p38 mitogen-activated protein kinase, and reduced expression of interleukins-1β and -6 in males but not in females. Furthermore, WT females expressed more of the suppressor of cytokine signaling protein 3 after I/R, which may in part explain TNFR1 signaling resistance in the female myocardium. Conclusions— This study demonstrates that sex differences exist in myocardial TNF signaling by TNFR1 after I/R.
Carotid Sinus Reflex Control of Coronary Blood Flow
Authors: ERIC O. FEIGL
Journal: Circulation Research (1968)

The role of the carotid sinus reflex in control of the blood flow in the left circumflex coronary artery was studied in nine open-chest dogs anesthetized with chloralose. Flow was measured with an electromagnetic flowmeter. The effects of bilateral common carotid occlusion were examined in a three-part experiment in each dog. (1) Under vagotomy (control) conditions, occlusion of both common carotid arteries resulted in tachycardia, increased blood pressure, and a decrease in coronary artery resistance. (2) After beta-receptor blockade with propranolol, 1.0 mg/kg, carotid sinus hypotension still resulted in increased blood pressure but the tachycardia was blocked, and coronary artery resistance increased. (3) Following rapid cardiac sympathectomy, carotid sinus hypotension still resulted in a reflex rise in systemic blood pressure but coronary resistance remained steady. This demonstrated the reflex nature of the increased coronary resistance observed after beta-receptor blockade. It is concluded that the coronary circulation is under reflex control and that sympathetic coronary artery vasomotion is a part of a carotid sinus reflex.
Comparative Effectiveness of Clozapine and Standard Antipsychotic Treatment in Adults With Schizophrenia
Authors: T. Scott Stroup, Tobias Gerhard, Stephen Crystal, Cecilia Huang, Mark Olfson
Journal: American Journal of Psychiatry (2015)

The authors compared the effectiveness of initiating treatment with either clozapine or a standard antipsychotic among adults with evidence of treatment-resistant schizophrenia in routine clinical practice.U.S. national Medicaid data from 2001 to 2009 were used to examine treatment outcomes in a cohort of patients with schizophrenia and evidence of treatment resistance that initiated clozapine (N=3,123) and in a propensity score-matched cohort that initiated a standard antipsychotic (N=3,123). Interventions were new initiation of clozapine or a standard antipsychotic medication, defined as no exposure to the new medication in the prior 365 days. The primary outcome was hospital admission for a mental disorder. Secondary outcomes included discontinuation of the index antipsychotic, use of an additional antipsychotic, incidence of serious medical conditions, and mortality.Initiation of clozapine was associated with a significantly decreased rate of psychiatric hospital admission (hazard ratio=0.78, 95% CI=0.69-0.88), index antipsychotic discontinuation (hazard ratio=0.60, 95% CI=0.55-0.65), and use of an additional antipsychotic (hazard ratio=0.76, 95% CI=0.70-0.82). Clozapine was associated with significantly increased incidence of diabetes mellitus (2.8% for clozapine vs. 1.4% for standard antipsychotic; hazard ratio=1.63, 95% CI=0.98-2.70), hyperlipidemia (12.9% for clozapine vs. 8.5% for standard antipsychotic; hazard ratio=1.40, 95%CI=1.09-1.78), and intestinal obstruction (0.9% for clozapine vs. 0.3% for standard antipsychotic; hazard ratio=2.50, 95% CI=0.97-6.44).In adults with schizophrenia and evidence of treatment resistance, initiating clozapine compared with initiating a standard antipsychotic was associated with greater effectiveness on several important outcomes. Increasing the judicious use of clozapine is warranted together with vigilance to prevent and detect serious medical adverse effects.
What have worm models told us about the mechanisms of neuronal dysfunction in human neurodegenerative diseases?
Authors: Dawn Teschendorf, Christopher D Link
Journal: Molecular Neurodegeneration (2009)

The nematode worm Caenorhabditis elegans has become an intensely studied model organism, and worm studies have made significant contributions to developmental biology and other fields. The experimental advantages of C. elegans, particularly its simple anatomy, optical transparency, short lifespan, and facile genetics, have also led researchers to use this model to investigate neuronal cell degeneration and death. Worm studies of neurodegeneration can be divided into two general classes: studies in which mutations of C. elegans genes lead to neuronal dysfunction and death, and studies in which external manipulations (e.g., chemical treatments or introduction of engineered transgenes) are used to induce neurodegeneration. For both types of studies the primary approach has been to use forward genetic, reverse genetic, or candidate gene approaches to identify genes that modify neurodegeneration. The ease and relatively low cost of C. elegans propagation also suggests a role for these C. elegans models for compound screening. An excellent review has been previously published that summarizes much of the work done on mutationally-induced neuronal death in C. elegans 1. This review focuses on studies that have attempted to model specific human neurodegenerative diseases using transgenic approaches. These studies have given us a variety of insights into the specific disruptions of cellular processes that may underlie human neurodegenerative diseases.
Comparative Clinical Effectiveness and Value of Novel Interferon-Free Combination Therapy for Hepatitis C Genotype 1
Authors: Jeffrey A. Tice, Harinder S. Chahal, Daniel A. Ollendorf
Journal: JAMA Internal Medicine (2015)

This evidence report on interferon-free therapy for chronic hepatitis C virus infection includes a systematic review of the literature, a cost-effectiveness model, and a budget impact assessment to support a December 2014 public meeting of the California Technology Assessment Forum.
Effectiveness of dynamic muscle training, relaxation training, or ordinary activity for chronic neck pain: randomised controlled trial
Authors: M. Viljanen
Journal: BMJ (2003)

<h3>Abstract</h3> <b>Objective</b> To determine the effectiveness of dynamic muscle training and relaxation training for chronic neck pain. <b>Design</b> Randomised controlled trial. <b>Setting</b> Five occupational healthcare centres, Tampere, Finland. <b>Participants</b> 393 female office workers (mean age 45 years) with chronic non-specific neck pain randomly assigned to 12 weeks of dynamic muscle training (n = 135) or relaxation training (n = 128), plus one week of reinforcement training six months after baseline; or ordinary activity (control group; n = 130). <b>Main outcome measure</b> Change in intensity of neck pain at three, six, and 12 months. <b>Results</b> No significant difference was found in neck pain between the groups at follow up. However, the range of motion for cervical rotation and lateral flexion increased more in the training groups than in the control group. <b>Conclusions</b> Dynamic muscle training and relaxation training do not lead to better improvements in neck pain compared with ordinary activity.
Chemoprevention of ultraviolet radiation-induced skin cancer.
Authors: R D Ley, V E Reeve
Journal: Environmental Health Perspectives (1997)

The use of chemical and physical sunscreening agents has increased dramatically during the last two to three decades as an effective means of preventing sunbum. The use of high sunprotection factor sunscreens has also been widely promoted for the prevention of skin cancer, including melanoma. Whereas sunscreens are undoubtedly effective in preventing sunbum, their efficacy in preventing skin cancer, especially melanoma, is currently under considerable debate. Sunscreens have been shown to prevent the induction of DNA damage that presumably results from the direct effects of ultraviolet radiation (UVR) on DNA. DNA damage has been identified as an initiator of skin cancer formation. However, both laboratory and epidemiological studies indicate that sunscreens may not block the initiation or promotion of melanoma formation. These studies suggest that the action spectrum for erythema induction is different than the action spectrum for the induction of melanoma. Indeed, recent reports on the wavelength dependency for the induction of melanoma in a fish model indicate that the efficacy of ultraviolet A wavelengths (320-400 nm) to induce melanoma is orders of magnitude higher than would be predicted from the induction of erythema in man or nonmelanoma skin tumors in mice. Other strategies for the chemoprevention of skin cancer have also been reported. Low levels and degree of unsaturation of dietary fats protect against UVR-induced skin cancer in mice humens. Compounds with antioxidant activity, including green tea extracts (polyphenols), have been reported to inhibit UVR-induced skin carcinogenesis.
Mechanisms and implications of phosphoinositide 3-kinase δ in promoting neutrophil trafficking into inflamed tissue
Authors: Kamal D. Puri, Teresa A. Doggett, Jason Douangpanya, Yonghao Hou, William T. Tino, Tim Wilson, Thomas Graf, Elizabeth Clayton, Martin Turner, Joel S. Hayflick, Thomas G. Diacovo
Journal: Blood (2004)