Dolor osteomuscular y estado de salud mental de trabajadores de dos instituciones de educación superior de Cali, Colombia

Pain is a body's response to fatigue or external factors that can affect the musculoskeletal system and the mental health of the sufferer. Objetive: The aim of this study was to determine the musculoskeletal symptoms and the mental health of workers at two institutions of higher education in Cali, Colombia. Methodology: A descriptive, cross-sectional correlation with participation of 177 workers. Musculoskeletal pain was assessed with the Nordic Questionnaire and mental health status with the General Health Questionnaire of Goldberg (GHQ 12). Results: The workers had a mean age of 38 + / - 9.8 , 42.2 % , a job experience with more than 10 years ( 58.4 %) and seniority between 1 to 5 years , 66.7 % were sedentary , and 43.5 % were overweight with some degree of obesity. Back pain (26.6 %) and knee (11.9 %) were the most prevalent in the last 6 months and 7 days (14.2 % and 6.2 %) and the main causes of medical consultation (14.1 % and 5.6 %). The workers did not show altered behavior or relationships. 43.5 % has been constantly felt under stress, which is statistically associated with the presence of pain in the last 6 months, p value 0.025. Conclusion: statistical relationship between the perception of feeling constantly under pressure in the presence of musculoskeletal pain in the past six months was found. College employees have good mental health.El dolor es una respuesta del organismo a la fatiga o a factores externos, puede afectar el sistema músculo esquelético y la salud mental de quien lo padece. Objetivo: Determinar la sintomatología osteomuscular y el estado de salud mental de trabajadores de dos Instituciones de Educación Superior en Cali Colombia. Metodología: Estudio descriptivo, correlacional de corte transversal con participación de 177 trabajadores. El dolor osteomuscular se evalúo con el Cuestionario Nórdico y el estado de salud mental con el Cuestionario General de Salud de Goldberg (GHQ 12). Resultados: Los trabajadores tuvieron una edad media de 38 +/- 9,8 años (42,2%), experiencia en el oficio mayor a 10 años (58,4%) y antigüedad en la empresa entre 1 y 5 años, 66,7% son sedentarios y 43,5% presentó sobrepeso con algún grado de obesidad. El dolor de espalda (26,6%) y de rodilla (11,9%) fueron los más prevalentes en los últimos 6 meses y 7 días (14,2% y 6,2%) y las principales causas de consulta médica (14,1% y 5,6%). Los trabajadores no presentaron alteración de la conducta ni en las relaciones interpersonales. 43,5% se ha sentido constantemente bajo tensión, lo que se relacionó estadísticamente con la presencia de dolor en los últimos 6 meses, valor p 0,025. Conclusión: Se encontró relación estadística entre la percepción de sentirse constantemente bajo presión con la presencia de dolor osteomuscular en los últimos seis meses. Los trabajadores universitarios gozan de buena salud mental

Morphological alterations and gene and protein expression profiling of bladder tumor cells after treatment with gemcitabine.

Chemical agents used in cancer therapy are associated with cell cycle arrest, activation or deactivation of mechanisms\ud associated to DNA repair and apoptosis. However, due to the complexity of biological systems, the molecular\ud mechanisms responsible for these activities are not fully understood. Thus, studies about gene and protein expression\ud have shown promising results for understanding the mechanisms related to cellular responses and regression of cancer\ud after chemotherapy. This study aimed to evaluate the gene and protein expression profiling in bladder transitional cell\ud carcinoma (TCC) with different TP53 status after gemcitabine (1.56 μM) treatment. The RT4 (grade 1, TP53 wild\ud type), 5637 (grade 2, TP53 mutated) and T24 (grade 3, TP53 mutated) cell lines were used. PCR arrays and mass\ud spectrometry were used to analyze gene and protein expression, respectively. Morphological alterations were observed\ud using scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The results of PCR array\ud showed that gemcitabine activity was mainly related to CDKN1A, GADD45A and SERTDA1 overexpression, and BAX\ud overexpression only in the wild type TP53 cells. Mass spectrometry demonstrated that gemcitabine modulated the protein\ud expression, especially those from genes related to apoptosis, transport of vesicles and stress response. Analyses using SEM\ud and TEM showed changes in cell morphology independently on the cell line studied. The observed decreased number of\ud microvillus suggests low contact among the cells and between cell and extracellular matrix; irregular forms might indicate\ud actin cytoskeleton deregulation; and the reduction in the amount of organelles and core size might indicate reduced\ud cellular metabolism. In conclusion, independently on TP53 status or grade of bladder tumor, gemcitabine modulated\ud genes related to the cell cycle and apoptosis, that reflected in morphological changes indicative of future cell death.FAPESPCNP

Neuroimmune and inflammatory signals in complex disorders of the central nervous system

An extensive microglial-astrocyte-monocyte-neuronal cross talk seems to be crucial for normal brain function, development, and recovery. However, under certain conditions neuroinflammatory interactions between brain cells and neuroimmune cells influence disease outcome and brain pathology. Microglial cells express a range of functional states with dynamically pleomorphic profiles from a surveilling status of synaptic transmission to an active player in major events of development such as synaptic elimination, regeneration, and repair. Also, inflammation mediates a series of neurotoxic roles in neuropsychiatric conditions and neurodegenerative diseases. The present review discusses data on the involvement of neuroinflammatory conditions that alter neuroimmune interactions in four different pathologies. In the first section of this review, we discuss the ability of the early developing brain to respond to a focal lesion with a rapid compensatory plasticity of intact axons and the role of microglial activation and proinflammatory cytokines in brain repair. In the second section, we present data of neuroinflammation and neurodegenerative disorders and discuss the role of reactive astrocytes in motor neuron toxicity and the progression of amyotrophic lateral sclerosis. In the third section, we discuss major depressive disorders as the consequence of dysfunctional interactions between neural and immune signals that result in increased peripheral immune responses and increase proinflammatory cytokines. In the last section, we discuss autism spectrum disorders and altered brain circuitries that emerge from abnormal long-term responses of innate inflammatory cytokines and microglial phenotypic dysfunctions.Fil: Liberman, Ana Clara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigación en Biomedicina de Buenos Aires - Instituto Partner de la Sociedad Max Planck; ArgentinaFil: Trias, Emiliano. Instituto Pasteur de Montevideo; UruguayFil: Da Silva Chagas, Luana. Universidade Federal Fluminense; BrasilFil: Trindade, Pablo. No especifíca;Fil: Dos Santos Pereira, Marissol. Fundación Oswaldo Cruz; Brasil. Universidade Federal do Rio de Janeiro; BrasilFil: Refojo, Damian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigación en Biomedicina de Buenos Aires - Instituto Partner de la Sociedad Max Planck; ArgentinaFil: Hedin Pereira, Cecilia. Universidade Federal do Rio de Janeiro; Brasil. Fundación Oswaldo Cruz; BrasilFil: Serfaty, Claudio A.. Universidade Federal Fluminense; Brasi

cis-Bis[1,1-dibenzyl-3-(furan-2-yl­carbonyl)thio­ureato-κ2 O,S]copper(II)

In the title compound, [Cu(C20H17N2O2S)2], the CuII atom is coordinated by the S and O atoms of two 1,1-dibenzyl-3-(furan-2-ylcarbon­yl)thio­ureate ligands in a distorted square-planar geometry. The two O and two S atoms are mutually cis to each other. The Cu—S and Cu—O bond lengths lie within the ranges of those found in related structures. The dihedral angle between the planes of the two chelating rings is 26.15 (6)°

Abnormal thyroid hormone status differentially affects bone mass accrual and bone strength in C3H/HeJ mice: a mouse model of type I deiodinase deficiency

C3H/HeJ (C3H) mice are deficient of type I deiodinase (D1), an enzyme that activates thyroid hormone (TH), converting thyroxine (T4) to triiodothyronine (T3). Nevertheless, C3H mice present normal serum T3 and a gross euthyroid phenotype. To investigate if a global D1 deficiency interferes in the TH effects on bone, we compared bone growth, bone mass accrual and bone strength of C3H and C57BL/6J (B6) mice under abnormal TH status. Four-week-old female mice of both strains were grouped as Euthyroid, Hypothyroid (pharmacologically-induced), 1xT4 and 10xT4 (hypothyroid animals receiving 1- or 10-fold the physiological dose of T4 /day/16 weeks). Hypothyroidism and TH excess similarly impaired body weight (BW) gain and body growth in both mice strains. In contrast, whereas hypothyroidism only slightly impaired bone mineral density (BMD) accrual in B6 mice, it severely impaired BMD accrual in C3H mice. No differences were observed in serum and bone concentrations of T3 between hypothyroid animals of both strains. Interestingly, treatment with 10xT4 was less deleterious to BMD accrual in C3H than in B6 mice and resulted in less elevated T3 serum levels in B6 than in C3H mice, which is probably explained by the lower D1 activity in C3H mice. In addition, hypothyroidism decreased bone strength only in C3H but not in B6 mice, while TH excess decreased this parameter in both strains. These findings indicate that D1 deficiency contributes to the TH excess-induced differences in bone mass accrual in C3H vs. B6 mice and suggest that deiodinase-unrelated genetic factors might account for the different skeleton responses to hypothyroidism between strains

Infection of Mice by Salmonella enterica Serovar Enteritidis Involves Additional Genes That Are Absent in the Genome of Serovar Typhimurium

Salmonella enterica serovar Enteritidis causes a systemic, typhoid-like infection in newly hatched poultry and mice. In the present study, a library of 54,000 transposon mutants of S. Enteritidis phage type 4 (PT4) strain P125109 was screened for mutants deficient in the in vivo colonization of the BALB/c mouse model using a microarray-based negative-selection screening. Mutants in genes known to contribute to systemic infection (e.g., Salmonella pathogenicity island 2 [SPI-2], aro, rfa, rfb, phoP, and phoQ) and enteric infection (e.g., SPI-1 and SPI-5) in this and other Salmonella serovars displayed colonization defects in our assay. In addition, a strong attenuation was observed for mutants in genes and genomic islands that are not present in S. Typhimurium or in most other Salmonella serovars. These genes include a type I restriction/modification system (SEN4290 to SEN4292), the peg fimbrial operon (SEN2144A to SEN2145B), a putative pathogenicity island (SEN1970 to SEN1999), and a type VI secretion system remnant SEN1001, encoding a hypothetical protein containing a lysin motif (LysM) domain associated with peptidoglycan binding. Proliferation defects for mutants in these individual genes and in exemplar genes for each of these clusters were confirmed in competitive infections with wild-type S. Enteritidis. A ΔSEN1001 mutant was defective for survival within RAW264.7 murine macrophages in vitro. Complementation assays directly linked the SEN1001 gene to phenotypes observed in vivo and in vitro. The genes identified here may perform novel virulence functions not characterized in previous Salmonella models

Thalidomide is Associated With Increased T Cell Activation and Inflammation in Antiretroviral-naive HIV-infected Individuals in a Randomised Clinical Trial of Efficacy and Safety

Trial Design: Open-label, randomised, controlled, pilot proof-of-concept clinical trial. Methods: Participants: Antiretroviral naive adult males with CD4 count >= 350 cells/mm(3). Interventions: Patients were randomised to receive thalidomide 200 mg QD for 3 weeks (Thalidomide group) or not (Control group) and followed for 48 weeks. Objective: We hypothesized that short-term Thalidomide use would reduce HIV related inflammation and HIV replication among antiretroviral naive HIV infected individuals. Outcome: Viral loads, CD4/CD8 counts, ultra-sensitive C-reactive protein (US-CRP), cell activation markers, and plasma lipopolysaccharide (LPS) were analyzed. Randomisation: Unrestricted randomisation. Blinding: No blinding was used. Results: Numbers randomised: Thirty recruited individuals were randomised to Thalidomide (16 patients) or Control (14 patients) groups. Recruitment: Patients were recruited from April 2011 to January 2013. Outcome: Viral loads remained stable in both groups. During thalidomide treatment, a decrease in CD4/CD8 ratio (p = 0.04), a decrease in CD4 count (p = 0.04), an increase in cell activation calculated by the percentage of CD38 (+)/HLA-DR+ CD8 cells (p < 0.05) and an increase in US-CRP (p < 0.01) were observed in the Thalidomide group, with all parameters returning to baseline levels after thalidomide interruption. We confirmed that thalidomide increased HIV replication in vitro of 6 of 7 samples from long-term antiretroviral suppressed individuals. Harms: No class 3/4 adverse events occurred. Conclusions: Short-termuse of thalidomide led to an intense transient increase in T cell activation and inflammation, with a decrease in the CD4(+) cell count without changes to the CD8(+) cell count. We confirmed that thalidomide acts in vitro as a latency reversal agent and speculate that the in vivo results obtained were due to an increase in HIV replication. (C) 2017 The Authors. Published by Elsevier B.V.Fundação de Amparo a Pesquisa do Estado de São Paulo (FAPESP)Univ Fed São Paulo, Lab Retrovirol, São Paulo, BrazilFiocruz MS, Inst Oswaldo Cruz, Lab Interdisciplinar Pesquisas Med, Rio De Janeiro, BrazilSecretaria Municipal Saude Antonio Ribeiro Neto, Rio De Janeiro, BrazilOncohiv, Rio De Janeiro, BrazilUniv Fed Rio de Janeiro, Rio De Janeiro, BrazilInst Fed Educ Ciencia & Tecnol Rio de Janeiro IF, Rio De Janeiro, BrazilUniv Fed São Paulo, Lab Retrovirol, São Paulo, BrazilFAPESP: 04/15856-9Web of Scienc

Endosymbiosis in trypanosomatids: the genomic cooperation between bacterium and host in the synthesis of essential amino acids is heavily influenced by multiple horizontal gene transfers

Background Trypanosomatids of the genera Angomonas and Strigomonas live in a mutualistic association characterized by extensive metabolic cooperation with obligate endosymbiotic Betaproteobacteria. However, the role played by the symbiont has been more guessed by indirect means than evidenced. Symbiont-harboring trypanosomatids, in contrast to their counterparts lacking symbionts, exhibit lower nutritional requirements and are autotrophic for essential amino acids. To evidence the symbiont’s contributions to this autotrophy, entire genomes of symbionts and trypanosomatids with and without symbionts were sequenced here. Results Analyses of the essential amino acid pathways revealed that most biosynthetic routes are in the symbiont genome. By contrast, the host trypanosomatid genome contains fewer genes, about half of which originated from different bacterial groups, perhaps only one of which (ornithine cyclodeaminase, EC:4.3.1.12) derived from the symbiont. Nutritional, enzymatic, and genomic data were jointly analyzed to construct an integrated view of essential amino acid metabolism in symbiont-harboring trypanosomatids. This comprehensive analysis showed perfect concordance among all these data, and revealed that the symbiont contains genes for enzymes that complete essential biosynthetic routes for the host amino acid production, thus explaining the low requirement for these elements in symbiont-harboring trypanosomatids. Phylogenetic analyses show that the cooperation between symbionts and their hosts is complemented by multiple horizontal gene transfers, from bacterial lineages to trypanosomatids, that occurred several times in the course of their evolution. Transfers occur preferentially in parts of the pathways that are missing from other eukaryotes. Conclusion We have herein uncovered the genetic and evolutionary bases of essential amino acid biosynthesis in several trypanosomatids with and without endosymbionts, explaining and complementing decades of experimental results. We uncovered the remarkable plasticity in essential amino acid biosynthesis pathway evolution in these protozoans, demonstrating heavy influence of horizontal gene transfer events, from Bacteria to trypanosomatid nuclei, in the evolution of these pathways

Experimental determination of the surface density for the 6He exotic nucleus

Angular distributions for the elastic scattering of 4,6He on 58Ni have been measured at near-barrier energies. The present data, combined with others for the 4He158Ni system at intermediate energies, allowed the determination of the 4,6He ground-state nuclear densities through an unfolding method. The experimentally extracted nuclear densities are compared with the results of theoretical calculations