Abstract Nonalcoholic fatty liver disease (NAFLD) is a public health problem developed by different etiologies, which induces metabolic dysfunctions and triglycerides accumulation in hepatocytes. This lipid accumulation can generate lipotoxicity, inflammation and the production of reactive oxygen species, collaborating with the progression of liver pathogenesis to more deleterious stage. Among the elements that initiate the establishment of liver diseases, pesticides should be considered. Worldwide, the use of agricultural chemicals to increase food production may accumulate in the environment, affecting non-target organisms. Thus, worldwide legislation must control pesticides use to preserve economies and lives. In this context, to address pesticide toxicity, the alternative animal model, Drosophila melanogaster, emerges as relevant biotechnological tool to investigate molecular connectors of toxic mechanisms in the establishment and development of NAFLD and liver diseases. In this review a comprehensive explanation about pesticides on human health and the use of Drosophila melanogaster as an alternative approach to defeat NAFLD will be presented. (NAFLD etiologies hepatocytes lipotoxicity species stage diseases considered Worldwide environment nontarget non target organisms Thus lives context toxicity model presented

Chagas disease, which is caused by the intracellular protozoanTrypanosoma cruzi, is a serious health problem in Latin America. The heart is one of the major organs affected by this parasitic infection. The pathogenesis of tissue remodelling, particularly regarding cardiomyocyte behaviour after parasite infection, and the molecular mechanisms that occur immediately following parasite entry into host cells are not yet completely understood. Previous studies have reported that the establishment of parasitism is connected to the activation of the phosphatidylinositol-3 kinase (PI3K), which controls important steps in cellular metabolism by regulating the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate. Particularly, the tumour suppressor PTEN is a negative regulator of PI3K signalling. However, mechanistic details of the modulatory activity of PTEN on Chagas disease have not been elucidated. To address this question, H9c2 cells were infected with T. cruzi Berenice 62 strain and the expression of a specific set of microRNAs (miRNAs) were investigated. Our cellular model demonstrated that miRNA-190b is correlated to the decrease of cellular viability rates by negatively modulating PTEN protein expression in T. cruzi-infected cells.

BACKGROUND: A living donor transplant improves the survival and quality of life of a transplant patient. However, the impact of transplantation on postoperative lung function and respiratory muscular strength in kidney donors remains unknown.OBJECTIVE: To evaluate pulmonary function, respiratory muscle strength, quality of life and the incidence of postoperative pulmonary complications (PPCs) in kidney donors undergoing nephrectomy.METHOD: This prospective cohort enrolled 110 consecutive kidney donors undergoing nephrectomy. Subjects underwent pulmonary function (using spirometry) and respiratory muscular strength (using manovacuometry) assessments on the day prior to surgery and 1, 2, 3 and 5 days postoperatively. Quality of life (measured by the SF-36) was evaluated preoperatively and 30 days postoperatively. PPCs were assessed daily by a blinded assessor.RESULTS: Donors exhibited a decrease of 27% in forced vital capacity, 58% in maximum inspiratory capacity and 51% in maximum expiratory pressure on the 1stpostoperative day (p<0.001) but this improved over days 2, 3 and 5 but had not returned to preoperative levels. Patient quality of life was still impaired at 30 days with regards to functional capacity, physical role, pain, vitality and social functioning (p<0.05) but these parameters improved slowly. None of the patients developed PPCs.CONCLUSION: Kidney donors submitted to nephrectomy exhibited a reduction in pulmonary function, respiratory muscular strength and quality of life, most of which were improving toward pre-surgical levels.

Chagas disease, caused by the intracellular protozoan Trypanosoma cruzi, is a serious health problem in Latin America. During this parasitic infection, the heart is one of the major organs affected. The pathogenesis of tissue remodelling, particularly regarding cardiomyocyte behaviour after parasite infection and the molecular mechanisms that occur immediately following parasite entry into host cells are not yet completely understood. When cells are infected with T. cruzi, they develop an inflammatory response, in which cyclooxygenase-2 (COX-2) catalyses rate-limiting steps in the arachidonic acid pathway. However, how the parasite interaction modulates COX-2 activity is poorly understood. In this study, the H9c2 cell line was used as our model and we investigated cellular and biochemical aspects during the initial 48 h of parasitic infection. Oscillatory activity of COX-2 was observed, which correlated with the control of the pro-inflammatory environment in infected cells. Interestingly, subcellular trafficking was also verified, correlated with the control of Cox-2 mRNA or the activated COX-2 protein in cells, which is directly connected with the assemble of stress granules structures. Our collective findings suggest that in the very early stage of the T. cruzi-host cell interaction, the parasite is able to modulate the cellular metabolism in order to survives.

Several molecular methods, such as Southern blotting hybridization, Multilocus Sequence Typing, and DNA microsatellite analysis, have been employed to genotype Candida albicans. The genotype analysis allows to group strains in clades, that is, a group composed of one ancestor and its descendants. These genotype studies demonstrate that clades distribution is influenced by geographic area as well as that antifungal resistance is associated with particular clades. These findings suggested that C. albicans reproduces mainly in a clonal manner, with certain degree of DNA microevolution. Additionally, virulence factors and site of isolation have also been associated with clade specificity. The present article is a brief review about the methods used for Candida genotyping and the correlated clade systems established. Special emphasis is given to Ca3 hybridization, MLST, and Microsatellites. The present work is also focused on the phenotypic and physiological traits associated with Candida clades.

A anemia falciforme é uma doença genética com origem multicêntrica, predominantemente em comunidades africanas, e está presente na população brasileira. A alta frequência de heterozigotos e a gravidade clínica dos homozigotos em nossa população vêm sendo alvo de políticas públicas adotadas pelo Ministério da Saúde e outras instituições governamentais no intuito de dispender cuidado especial ao portador. Foco das investigações científicas desde o esclarecimento de sua base genética, o estudo da anemia falciforme pode ser considerado um tema inesgotável, visto o considerável número de publicações acadêmicas que se reportam à anemia falciforme como temática central e que crescem anualmente. Dentro desse contexto, e no intuito de contribuir com a informação científica sobre a anemia falciforme, o presente estudo tem por objetivo avaliar a comunidade de São José dos Campos, SP, quanto à presença do traço falcêmico, correlacionando os dados obtidos com o histórico do povoamento local. O estudo foi realizado em 93.604 doadores voluntários de sangue, entre os anos de 2004 e 2008 no Serviço de Hematologia e Hemoterapia de São José dos Campos. Dos 93.604 doadores analisados, encontramos 400 portadores heterozigotos do traço falcêmico Hb S (0,43%); nenhum indivíduo homozigoto foi identificado. Esse índice discrepante dos índices nacionais fundamenta-se na história local.

Sickle cell disease is a genetic disease that originated in several different regions, in particular African communities. The disease is present in the Brazilian population. The large number of heterozygotes and the severe clinical symptoms of homozygotes have drawn special attention from the government institutions in Brazil. Since the genetic origin of the disease was elucidated, sickle cell disease has become the focus of an every-growing number of scientific investigations. This investigation was performed to correlate the presence of the sickle cell trait in inhabitants of São José dos Campos, Brazil, with data on immigrants. The study sample consisted of 93,604 blood donors of the Hematology and Hemotherapy Service in São José dos Campos from 2004 to 2008. An analysis of the donors identified 400 heterozygous individuals with the sickle cell trait (Hb S - 0.43%) but no homozygotes. The results are completely different from the national pattern and are strongly supported by local history.

Several mRNAs have been shown to exhibit distinct patterns of poly(A) shortening prior to their decay in vivo. In this study, we show that individual transcripts also demonstrate distinct patterns of deadenylation in in vitro systems derived from HeLa and Jurkat T cell cytoplasmic extracts. The major patterns observed were slow/synchronous and fast/asynchronous poly(A) tail shortening. For all RNA substrates tested, PARN was shown to be the enzyme responsible for the deadenylation patterns that were observed. Sequences in the 3' untranslated regions influenced the deadenylation pattern. Using a fragment of the 3'UTR of the c-fos mRNA as a model, the interaction of CUG-BP, the human homolog of EDEN-BP - a protein previously implicated in regulated deadenylation in Xenopus oocytes - was shown to be associated with changes in PARN-mediated deadenylation patterns. Our results suggest that association of CUG-BP with 3'UTR sequences can modulate the activity of the PARN deadenylase in mammalian cell extracts.