tbuckley/cabot-search huggingface dataset:
Bronchopulmonary disease in Iranian housewives chronically exposed to indoor smoke
Authors: K Amoli
Journal: European Respiratory Journal (1998)

Tobacco smoking is recognized as the main cause of chronic bronchitis followed by occupational exposure to dust, fumes and gases. Indoor inhalation of smoke is being investigated increasingly but mainly the acute morbidity has been described while the late features and complications which may lead to respiratory disability are less well known. Among the 388 female patients who were referred to the main Bronchoscopy Unit of Tehran University of Medical Sciences between 1986 and 1995, 10 nonsmoking elderly housewives were found with chronic bronchopulmonary lesions characterized by widespread mucosal swelling and anthracotic plaques of the airways. Enquiry into their past history revealed massive exposure to smoke over many years whilst baking household rustic bread inside dwellings. No other source of air pollution was detected. The main clinicopathological features were respiratory disability due to chronic bronchitis with intracellular as well as extracellular black particles. As similar cases may present to medical practitioners even in affluent societies as a result of increasing amounts of immigrants from developing countries, recognition of these patients is important to avoid irrelevant diagnoses and unnecessary interventions.
Treatment of Allergy to Heterologous Monocomponent Insulin With Human Semisynthetic Insulin: Long-Term Study
Authors: Bruno Bruni, Patrizia Barolo, Alberto Blatto, Maurizio Carlini, Silvia Gamba Ansaldi, Giorgio Grassi
Journal: Diabetes Care (1988)

Eight type II (non-insulin-dependent) diabetic subjects (7 women, 1 man, aged 42–61 yr), initially treated with oral hypoglycemic agents and intermittently treated with conventional insulins, were identified as developing allergic reactions to porcine and mixed-species monocomponent insulin. Allergy was systemic (urticaria and nonthrombocytopenic purpura) and local delayed in two subjects and local immediate or biphasic in six subjects. Lipoatrophy was present in two subjects. After treatment with human semisynthetic insulin (Monotard HM and Actrapid HM), systemic allergy disappeared. Local allergy disappeared in five subjects and was reduced in three subjects. No lipoatrophy occurred in new injection areas. The clinical results were accompanied by a significant decrease in serum insulinspecific IgE after 6, 12, 18, 24, 30, and 36 mo. Insulinspecific IgG showed an evident decrease in five of eight patients, but the difference in mean values was not significant after 6, 18, 24, 30, and 36 mo. With one exception, intradermal skin tests were positive to human, bovine, and porcine insulin before and after human insulin treatment.
Consensus meeting agrees distribution of 5-HT3 receptors in mammalian hindbrain
Authors: Gerard D. Pratt, Norman G. Bowery, Gavin J. Kilpatrick, Ronald A. Leslie, Nicholas M. Barnes, Robert J. Naylor, Brian J. Jones, David R. Nelson, JoséM. Palacios, Paul Slater, D.John M. Reynolds
Journal: Trends in Pharmacological Sciences (1990)
Hydrogen Sulfide Inhibits Plasma Renin Activity
Authors: Ming Lu, Yi-Hong Liu, Hong Swen Goh, Josh Jia Xing Wang, Qian-Chen Yong, Rui Wang, Jin-Song Bian
Journal: Journal of the American Society of Nephrology (2010)

The development of renovascular hypertension depends on the release of renin from the juxtaglomerular (JG) cells, a process regulated by intracellular cAMP. Hydrogen sulfide (H2S) downregulates cAMP production in some cell types by inhibiting adenylyl cyclase, suggesting the possibility that it may modulate renin release. Here, we investigated the effect of H2S on plasma renin activity and BP in rat models of renovascular hypertension. In the two-kidney-one-clip (2K1C) model of renovascular hypertension, the H2S donor NaHS prevented and treated hypertension. Compared with vehicle, NaHS significantly attenuated the elevation in plasma renin activity and angiotensin II levels but did not affect plasma angiotensin-converting enzyme activity. Furthermore, NaHS inhibited the upregulation of renin mRNA and protein levels in the clipped kidneys of 2K1C rats. In primary cultures of renin-rich kidney cells, NaHS markedly suppressed forskolin-stimulated renin activity in the medium and the intracellular increase in cAMP. In contrast, NaHS did not affect BP or plasma renin activity in normal or one-kidney-one-clip (1K1C) rats, both of which had normal plasma renin activity. In conclusion, these results demonstrate that H2S may inhibit renin activity by decreasing the synthesis and release of renin, suggesting its potential therapeutic value for renovascular hypertension.
The Perpetual Challenge of Infectious Diseases
Authors: Anthony S. Fauci, David M. Morens
Journal: New England Journal of Medicine (2012)

During the past 200 years, our understanding of infectious diseases has radically evolved from the identification of microbes, to defining their genetic structure, to the development of focused antimicrobial therapies, to the realization of vector biology. This article highlights the tremendous advances that have been made in the field.
How to assess quality in primary care
Authors: Robert Grant, Jim Parle
Journal: BMJ (2015)

Thank you for your interest in spreading the word about The BMJ.NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Username * Your Email * Send To * You are going to email the following How to assess quality in primary care Your Personal Message CAPTCHA This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
O120 REDUCED INCIDENCE OF HEPATOCELLULAR CARCINOMA IN HIV/HBV-COINFECTED PATIENTS RECEIVING TENOFOVIR
Authors: G. Wandeler, D. Kraus, M. Egger, E. Bernasconi, D. Braun, M. Battegay, A. Calmy, M. Cavassini, P. Schmid, H. Furrer, A. Rauch
Journal: Journal of Hepatology (2014)
EUCAST expert rules in antimicrobial susceptibility testing
Authors: R. Leclercq, R. Cantón, D.F.J. Brown, C.G. Giske, P. Heisig, A.P. MacGowan, J.W. Mouton, P. Nordmann, A.C. Rodloff, G.M. Rossolini, C.-J. Soussy, M. Steinbakk, T.G. Winstanley, G. Kahlmeter
Journal: Clinical Microbiology and Infection (2011)
Glucagon-like Peptide-2 Does Not Modify the Growth or Survival of Murine or Human Intestinal Tumor Cells
Authors: Jacqueline A. Koehler, Will Harper, Maja Barnard, Bernardo Yusta, Daniel J. Drucker
Journal: Cancer Research (2008)

Abstract Glucagon-like peptide-2 (GLP-2) secreted from enteroendocrine cells exerts proabsorptive, regenerative, and cytoprotective actions in the normal and injured gut epithelium. Hence, sustained GLP-2 receptor (GLP-2R) activation represents a strategy under investigation for the prevention and treatment of chemotherapy-induced mucositis. Nevertheless, the consequences of increased GLP-2R signaling for the growth and survival of intestinal tumor cells remain poorly understood. We studied the proliferative and cytoprotective actions of GLP-2 in human colon cancer cells stably transfected with the GLP-2R and in nude mice harboring GLP-2R+ human colon cancer cells. The importance of the GLP-2R for tumor growth was also examined in ApcMin/+ mice chronically treated with exogenous GLP-2 and in ApcMin/+:Glp2r−/− mice. GLP-2 increased cyclic AMP accumulation and produced cell-specific activation of growth and survival pathways in DLD-1, SW480, and HT29 cells. However, GLP-2 did not stimulate cell growth or attenuate cycloheximide-, LY294002-, indomethacin-, or chemotherapy-induced cytotoxicity in vitro. Moreover, chronic GLP-2 administration had no effect on the growth of human colon cancer cell xenografts in nude mice in vivo. Daily GLP-2 treatment for 7 weeks increased growth of normal gut mucosa but did not increase the number or size of polyps in ApcMin/+ mice, and genetic disruption of the Glp2r gene in ApcMin/+ mice did not modify polyp size or number. Taken together, although GLP-2R activation engages signaling pathways promoting cell proliferation and cytoprotection in the normal gut epithelium, sustained direct or indirect modulation of GLP-2R signaling does not modify intestinal tumor cell growth or survival. [Cancer Res 2008;68(19):7897–904]
The Metabolic Syndrome Is Frequent in Klinefelter’s Syndrome and Is Associated With Abdominal Obesity and Hypogonadism
Authors: Anders Bojesen, Kurt Kristensen, Niels H. Birkebaek, Jens Fedder, Leif Mosekilde, Paul Bennett, Peter Laurberg, Jan Frystyk, Allan Flyvbjerg, Jens S. Christiansen, Claus H. Gravholt
Journal: Diabetes Care (2006)

OBJECTIVE—Klinefelter’s syndrome is associated with an increased prevalence of diabetes, but the pathogenesis is unknown. Accordingly, the aim of this study was to investigate measures of insulin sensitivity, the metabolic syndrome, and sex hormones in patients with Klinefelter’s syndrome and an age-matched control group. RESEARCH DESIGN AN METHODS—In a cross-sectional study, we examined 71 patients with Klinefelter’s syndrome, of whom 35 received testosterone treatment, and 71 control subjects. Body composition was evaluated using dual-energy X-ray absorptiometry scans. Fasting blood samples were analyzed for sex hormones, plasma glucose, insulin, C-reactive protein (CRP), and adipocytokines. We analyzed differences between patients with untreated Klinefelter’s syndrome and control subjects and subsequently analyzed differences between testosterone-treated and untreated Klinefelter’s syndrome patients. RESULTS—Of the patients with Klinefelter’s syndrome, 44% had metabolic syndrome (according to National Cholesterol Education Program/Adult Treatment Panel III criteria) compared with 10% of control subjects. Insulin sensitivity (assessed by homeostasis model assessment 2 modeling), androgen, and HDL cholesterol levels were significantly decreased, whereas total fat mass and LDL cholesterol, triglyceride, CRP, leptin, and fructosamine levels were significantly increased in untreated Klinefelter’s syndrome patients. In treated Klinefelter’s syndrome patients, LDL cholesterol and adiponectin were significantly decreased, whereas no difference in body composition was found in comparison with untreated Klinefelter’s syndrome patients. Multivariate analyses showed that truncal fat was the major determinant of metabolic syndrome and insulin sensitivity. CONCLUSIONS—The prevalence of metabolic syndrome was greatly increased, whereas insulin sensitivity was decreased in Klinefelter’s syndrome. Both correlated with truncal obesity. Hypogonadism in Klinefelter’s syndrome may cause an unfavorable change in body composition, primarily through increased truncal fat and decreased muscle mass. Testosterone treatment in Klinefelter’s syndrome only partly corrected the unfavorable changes observed in untreated Klinefelter’s syndrome, perhaps due to insufficient testosterone doses.
Retroposon Insertion Patterns of Neoavian Birds: Strong Evidence for an Extensive Incomplete Lineage Sorting Era
Authors: A. Matzke, G. Churakov, P. Berkes, E. M. Arms, D. Kelsey, J. Brosius, J. O. Kriegs, J. Schmitz
Journal: Molecular Biology and Evolution (2012)

More than 150 Ma, the avian lineage separated from that of other dinosaurs and later diversified into the more than 10,000 species extant today. The early neoavian bird radiations most likely occurred in the late Cretaceous (more than 65 Ma) but left behind few if any molecular signals of their archaic evolutionary past. Retroposed elements, once established in an ancestral population, are highly valuable, virtually homoplasy-free markers of species evolution; after applying stringent orthology criteria, their phylogenetically informative presence/absence patterns are free of random noise and independent of evolutionary rate or nucleotide composition effects. We screened for early neoavian orthologous retroposon insertions and identified six markers with conflicting presence/absence patterns, whereas six additional retroposons established before or after the presumed major neoavian radiation show consistent phylogenetic patterns. The exceptionally frequent conflicting retroposon presence/absence patterns of neoavian orders are strong indicators of an extensive incomplete lineage sorting era, potentially induced by an early rapid successive speciation of ancestral Neoaves.
Collagen secretion and growth of mesangial cells require geranylgeranylpyrophosphate
Authors: Motonobu Nishimura, Tomoaki Tanaka, Tatsuji Yasuda, Shinichi Kurakata, Masatoshi Kitagawa, Kenichi Yamada, Yasushi Saito, Aizan Hirai
Journal: Kidney International (1999)
Clinical Pharmacology of Psychotherapeutic Drugs.
Authors: Leo E. Hollister, John G. Csernansky
Journal: Annals of Internal Medicine (1979)

Psychotherapeutic Drugs in the Treatment of Emotional Disorders. Antianxiety Drugs. Hypnotics. Antodepressants. Antipsychotic Drugs. Mood-Stabilizing Drugs. Psychotherapeutic Drugs for Children and Adolescents. Index
Keep your heart in shape: molecular chaperone networks for treating heart disease
Authors: G. Tarone, M. Brancaccio
Journal: Cardiovascular Research (2014)

Despite major advances in the treatment of cardiac diseases, there is still a great need for drugs capable of counteracting the deterioration of cardiac muscle function in congestive heart failure. The role of misfolded protein accumulation as a causal event in the physiopathology of common cardiac diseases is an important emerging concept. Indeed, diverse stress conditions, including mechanical stretching and oxidative stress, can induce misfolded protein accumulation, causing cardiomyocyte death. Cells react to these stress conditions by activating molecular chaperones, a class of proteins that represents an endogenous salvage machinery, essential for rescuing physiological cell functions and sustaining cell survival. Chaperones, also known as heat shock proteins (Hsps), prevent accumulation of damaged proteins by promoting either their refolding or degradation via the proteasome or the autophagosome systems. In addition, molecular chaperones play a key role in intracellular signalling by controlling conformational changes required for activation/deactivation of signalling proteins, and their assembly in specific signalosome complexes. The key role of molecular chaperones in heart function is highlighted by the fact that a number of genetic mutations in chaperone proteins result in different forms of cardiomyopathies. Moreover, a considerable amount of experimental evidence indicates that increasing expression of chaperone proteins leads to an important cardio-protective role in ischaemia/reperfusion injury, heart failure, and arrhythmia, implicating these molecules as potential innovative therapeutic agents.
Linkage to and engagement in HIV care in western Kenya: an observational study using population-based estimates from home-based counselling and testing
Authors: Becky L Genberg, Violet Naanyu, Juddy Wachira, Joseph W Hogan, Edwin Sang, Monicah Nyambura, Michael Odawa, Corey Duefield, Samson Ndege, Paula Braitstein
Journal: The Lancet HIV (2014)
THE PRODUCTION OF STREPTOCOCCUS HEMOLYTICUS BACTEREMIA IN NON-SPECIFICALLY SENSITIZED ANIMALS
Authors: Caspar G. Burn, Caroline A. Chandler, Mildred Hartshorn
Journal: The Journal of Experimental Medicine (1934)

Rabbits sensitized to horse serum developed a bacteremia of 9 to 12 hours' duration when they were inoculated simultaneously with normal horse serum and a strain of Streptococcus hemolyticus, while the bacteria could only be isolated from the blood stream of non-sensitized animals within the first 3 hours after inoculation. On the other hand, when antisera are employed as the antigen for shocking the sensitized rabbits, there is a significant increase in the number of bacteria in the blood stream in contrast to the control animals, but there is no evidence of a prolongation of the bacteremia.
Prostaglandin E2 differentially modulates IL-5 gene expression in activated humanT lymphocytes depending on the costimulatory signal☆☆☆★★★
Authors: Peter Borger, Edo Vellenga, Sonja I. Gringhuis, J.Andre B. Timmerman, Chantal Lummen, Dirkje S. Postma, Henk F. Kauffman
Journal: Journal of Allergy and Clinical Immunology (1998)
Decline in US heart disease slows in younger adults, study finds
Authors: Michael McCarthy
Journal: BMJ (2015)

Despite a marked decline in coronary heart disease (CHD) mortality over the past three decades in the United States a study has found that most of this decline has been due to a reduction in death rates among older men and women but not among younger adults, particularly younger women.

CHD is common in younger adults and women, the researchers noted: patients aged under 50 accounted for as many as 22% of US hospital admissions for acute coronary syndrome, and women under 55 accounted for 25% of all admissions for acute myocardial infarction.

In the study Viola Vaccarino, senior author, from Emory University’s Rollins School of Public Health in Atlanta, Georgia, and colleagues used mortality data on all people aged 25 or older in the US from …
Blockade of Vascular Smooth Muscle Cell Proliferation and Intimal Thickening After Balloon Injury by the Sulfated Oligosaccharide PI-88
Authors: Douglas J. Francis, Christopher R. Parish, Mark McGarry, Fernando S. Santiago, Harry C. Lowe, Kathryn J. Brown, John A. Bingley, Ian P. Hayward, William B. Cowden, Julie H. Campbell, Gordon R. Campbell, Colin N. Chesterman, Levon M. Khachigian
Journal: Circulation Research (2003)

Percutaneous transluminal coronary angioplasty is a frequently used interventional technique to reopen arteries that have narrowed because of atherosclerosis. Restenosis, or renarrowing of the artery shortly after angioplasty, is a major limitation to the success of the procedure and is due mainly to smooth muscle cell accumulation in the artery wall at the site of balloon injury. In the present study, we demonstrate that the antiangiogenic sulfated oligosaccharide, PI-88, inhibits primary vascular smooth muscle cell proliferation and reduces intimal thickening 14 days after balloon angioplasty of rat and rabbit arteries. PI-88 reduced heparan sulfate content in the injured artery wall and prevented change in smooth muscle phenotype. However, the mechanism of PI-88 inhibition was not merely confined to the antiheparanase activity of this compound. PI-88 blocked extracellular signal-regulated kinase-1/2 (ERK1/2) activity within minutes of smooth muscle cell injury. It facilitated FGF-2 release from uninjured smooth muscle cells in vitro, and super-released FGF-2 after injury while inhibiting ERK1/2 activation. PI-88 inhibited the decrease in levels of FGF-2 protein in the rat artery wall within 8 minutes of injury. PI-88 also blocked injury-inducible ERK phosphorylation, without altering the clotting time in these animals. Optical biosensor studies revealed that PI-88 potently inhibited (Ki 10.3 nmol/L) the interaction of FGF-2 with heparan sulfate. These findings show for the first time the capacity of this sulfated oligosaccharide to directly bind FGF-2, block cellular signaling and proliferation in vitro, and inhibit injury-induced smooth muscle cell hyperplasia in two animal models. As such, this study demonstrates a new role for PI-88 as an inhibitor of intimal thickening after balloon angioplasty. The full text of this article is available online at http://www.circresaha.org.
Antibody-enhanced cross-presentation of self antigen breaks T cell tolerance
Authors: Stephanie O. Harbers, Andrea Crocker, Geoffrey Catalano, Vivette D’Agati, Steffen Jung, Dharmesh D. Desai, Raphael Clynes
Journal: Journal of Clinical Investigation (2007)

We have developed a model of autoimmunity to investigate autoantibody-mediated cross-presentation of self antigen. RIP-mOVA mice, expressing OVA in pancreatic β cells, develop severe autoimmune diabetes when given OT-I cells (OVA-specific CD8+ T cells) and anti-OVA IgG but not when given T cells alone. Anti-OVA IgG is not directly injurious to the islets but rather enhances cross-presentation of apoptotic islet antigen to the OT-I cells, leading to their differentiation into potent effector cells. Antibody-driven effector T cell activation is dependent on the presence of activating Fc receptors for IgG (FcγRs) and cross-priming DCs. As a consequence, diabetes incidence and severity was reduced in mice lacking activating FcγRs. An intact complement pathway was also required for disease development, as C3 deficiency was also partially protective. C3-deficient animals exhibited augmented T cell priming overall, indicating a proinflammatory role for complement activation after the T cell priming phase. Thus, we show that autoreactive antibody can potently enhance the activation of effector T cells in response to cross-presented self antigen, thereby contributing to T cell–mediated autoimmunity.
GPR116, an Adhesion G-Protein–Coupled Receptor, Promotes Breast Cancer Metastasis via the Gαq-p63RhoGEF-Rho GTPase Pathway
Authors: Xiaolong Tang, Rongrong Jin, Guojun Qu, Xiu Wang, Zhenxi Li, Zengjin Yuan, Chen Zhao, Stefan Siwko, Tieliu Shi, Ping Wang, Jianru Xiao, Mingyao Liu, Jian Luo
Journal: Cancer Research (2013)

Abstract Adhesion G-protein–coupled receptors (GPCR), which contain adhesion domains in their extracellular region, have been found to play important roles in cell adhesion, motility, embryonic development, and immune response. Because most adhesion molecules with adhesion domains have vital roles in cancer metastasis, we speculated that adhesion GPCRs are potentially involved in cancer metastasis. In this study, we identified GPR116 as a novel regulator of breast cancer metastasis through expression and functional screening of the adhesion GPCR family. We found that knockdown of GPR116 in highly metastatic (MDA-MB-231) breast cancer cells suppressed cell migration and invasion. Conversely, ectopic GPR116 expression in poorly metastatic (MCF-7 and Hs578T) cells promoted cell invasion. We further showed that knockdown of GPR116 inhibited breast cancer cell metastasis in two mammary tumor metastasis mouse models. Moreover, GPR116 modulated the formation of lamellipodia and actin stress fibers in cells in a RhoA- and Rac1-dependent manner. At a molecular level, GPR116 regulated cell motility and morphology through the Gαq-p63RhoGEF-RhoA/Rac1 pathway. The biologic significance of GPR116 in breast cancer is substantiated in human patient samples, where GPR116 expression is significantly correlated with breast tumor progression, recurrence, and poor prognosis. These findings show that GPR116 is crucial for the metastasis of breast cancer and support GPR116 as a potential prognostic marker and drug target against metastatic human breast cancer. Cancer Res; 73(20); 6206–18. ©2013 AACR.
<i>In Utero</i> Exposure to Dioxins and Dioxin-like Compounds and Anogenital Distance in Newborns and Infants
Authors: Marina Vafeiadi, Silvia Agramunt, Eleni Papadopoulou, Harrie Besselink, Kleopatra Mathianaki, Polyxeni Karakosta, Ariana Spanaki, Antonis Koutis, Leda Chatzi, Martine Vrijheid, Manolis Kogevinas
Journal: Environmental Health Perspectives (2012)

Anogenital distance in animals is used as a measure of fetal androgen action. Prenatal exposure to dioxins and dioxin-like compounds in rodents causes reproductive changes in male offspring and decreases anogenital distance.