407 research outputs found
Rosiglitazone decreases intra- to extramyocellular fat ratio in obese non-diabetic adults with metabolic syndrome
Conselho Nacional de Desenvolvimento CientÃfico e Tecnológico (CNPq)Background Insulin resistance is intrinsically related to intramyocellular (IMCL) rather than extramyocellular (EMCL) triglyceride content. Conflicting results have been reported on the ability of insulin sensitizer agents, such as thiazolidinediones, to modify muscle fat distribution. The aim of this study was to investigate the role of rosiglitazone on muscle fat compartment distribution in an adult population of obese non-diabetic metabolic syndrome patients. Patients and methods Fifteen obese, non-diabetic, metabolic syndrome patients were studied by means of proton nuclear magnetic resonance ((1)H-NMR) spectroscopy before and after treatment with rosiglitazone 8 mg/day for 6 months. Anthropometrical and metabolic variables were assessed. Results After rosiglitazone, body weight and hip circumference increased [100.9 (91.12-138.7) vs. 107.0 (79.6-142.8) kg and 118 (107-126) vs. 122 (110-131) cm]; while waist-hip ratio (WHR) decreased from 0.93 (0.87-1.00) to 0.89 (0.82-0.97) (P < 0.001 for all). Additionally, fasting plasma glucose, insulin and homeostatis model assessment of insulin resistance (HOMA-IR) significantly decreased while adiponectin increased over threefold [9.7 (3.7-17.7) vs. 38.0 (19.3-42.4) mu g/ml] without any changes in resistin. Finally, the IMCL did not change [267.54 (213.94-297.94) vs. 305.75 (230.80-424.75) arbitrary units (AU), P = 0.15] while the EMCL increased [275.53 (210.39-436.66) vs. 411.39 (279.92-556.59) AU; P < 0.01] therefore decreasing the IMCL-to-EMCL (IMCL/EMCL) ratio [1.07 (0.78-1.23) vs. 0.71 (0.53-0.96); P < 0.01]. Conclusion Rosiglitazone treatment increased body weight and hip circumference and decreased WHR. More importantly, it decreased the IMCL/EMCL ratio by increasing the EMCL without any significant change on the IMCL.2712329Conselho Nacional de Desenvolvimento CientÃfico e Tecnológico (CNPq)Research Supporting Agency of Rio de Janeiro State [E-26/150.141/99, E-26/170.522/00]Conselho Nacional de Desenvolvimento CientÃfico e Tecnológico (CNPq)CNPq [CNPq 52 1850/96-7]Research Supporting Agency of Rio de Janeiro State [E-26/150.141/99, E-26/170.522/00
Epidemiological and genomic investigation of chikungunya virus in Rio de Janeiro state, Brazil, between 2015 and 2018
Since 2014, Brazil has experienced an unprecedented epidemic caused by chikungunya virus (CHIKV), with several waves of East-Central-South-African (ECSA) lineage transmission reported across the country. In 2018, Rio de Janeiro state, the third most populous state in Brazil, reported 41% of all chikungunya cases in the country. Here we use evolutionary and epidemiological analysis to estimate the timescale of CHIKV-ECSA-American lineage and its epidemiological patterns in Rio de Janeiro. We show that the CHIKV-ECSA outbreak in Rio de Janeiro derived from two distinct clades introduced from the Northeast region in mid-2015 (clade RJ1, n = 63/67 genomes from Rio de Janeiro) and mid-2017 (clade RJ2, n = 4/67). We detected evidence for positive selection in non-structural proteins linked with viral replication in the RJ1 clade (clade-defining: nsP4-A481D) and the RJ2 clade (nsP1-D531G). Finally, we estimate the CHIKV-ECSA's basic reproduction number (R0) to be between 1.2 to 1.6 and show that its instantaneous reproduction number (Rt) displays a strong seasonal pattern with peaks in transmission coinciding with periods of high Aedes aegypti transmission potential. Our results highlight the need for continued genomic and epidemiological surveillance of CHIKV in Brazil, particularly during periods of high ecological suitability, and show that selective pressures underline the emergence and evolution of the large urban CHIKV-ECSA outbreak in Rio de Janeiro
Population-based prevalence of cervical infection with human papillomavirus genotypes 16 and 18 and other high risk types in Tlaxcala, Mexico
This study was supported by the National Institute of Public Health of
Mexico, the Coordinación de Investigación en Salud del Instituto Mexicano
del Seguro Social, the SecretarÃa de Salud Tlaxcala, the Instituto Nacional de
las Mujeres, and the Consejo Nacional de Ciencia y TecnologÃa [FOSISS 2013
202468]. Additional support has been provided by Roche Diagnostics, BD
Diagnostics, DICIPA and Arbor Vita Corporation. The study sponsors did not
played a role in designing the study, collecting, analyzing or interpreting the
data, writing the report, or submitting this paper for publication. UC Berkeley
Center for Global Public Health, Schoeneman Grant, Joint Medical Program
Thesis Grant, and Cancer Research UK (C569/A10404)
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