Melhoria da Atenção ao Pré- Natal e Puerpério na UBS/ESF Pedro Bairro Monteiro, Macapá/AP

PINATEL, Enma Rodrigues. Melhoria da Atenção ao Pré- natal e Puerpério na UBS/ESF Pedro Bairro Monteiro, Macapá/AP. 2015. 105 folhas. Trabalho de Conclusão de Curso – Programa de Pós-Graduação em Saúde da Família – Modalidade a Distância, Faculdade de Medicina, Universidade Federal de Pelotas. 2015. Ao realizar um projeto de intervenção através de estudos e levantamento de dados desenvolveu- se uma ação programática prioritária na atenção básica, intervindo na assistência, promoção e prevenção à saúde das gestantes e puérperas da área de abrangência da UBS/ESF Pedro Bairro Monteiro, situado no município de Macapá – Amapá, durante 16 semanas, compreendido entre setembro a dezembro 2014. Nosso objetivo foi melhorar a atenção pré-natal e puerpério, incluindo atenção odontológica, assim como diminuir a morbimortalidade materno – infantil em nossa área. Para realização da intervenção, utilizou- se o banco de dados do SIAB, prontuários e registros específicos, relatos dos ACS, planilha de coletas de dados e ficha-espelho, fornecidos pela Universidade Federal de Pelotas. Alcançou-se o cadastramento adequado no Programa de Pré-natal de 71 gestantes e 74 puérperas, com o 100% de cobertura ao final da intervenção, assim como a solicitação de todos os exames laboratoriais de acordo com o protocolo do Ministério da Saúde, havendo a prescrição de Sulfato Ferroso e Ácido Fólico. Realizou- se a busca ativa às gestantes faltosas as consulta de pré-natal, realizou- se a orientação sobre anticoncepção após o parto, orientação nutricional, aleitamento materno, tabaquismo e higiene bucal. Em relação ao puerpério alcançou- se metas propostas, destacando-se a busca de faltosas, consulta até 30 dias após o parto, orientação sobre cuidados do recém- nascidos, aleitamento materno e planejamento familiar. Em correspondência ao início na intervenção se resultou a melhora qualitativamente e quantitativamente da realização do exame ginecológico, mama e abdominal, a vacinação com dupla adulta (Difteria e Tétano) e Hepatite B, assim como atendimento odontológico em gestantes e puérperas. Palavras-chave: Atenção primária à saúde; saúde da família; saúde da mulher; Pré-natal; puerpério

Lipid-induced hepatocyte-derived extracellular vesicles regulate hepatic stellate cell via microRNAs targeting PPAR-γ.

Background&aimsHepatic stellate cells (HSCs) play a key role in liver fibrosis in various chronic liver disorders including nonalcoholic fatty liver disease (NAFLD). The development of liver fibrosis requires a phenotypic switch from quiescent to activated HSCs. The triggers for HSCs activation in NAFLD remain poorly understood. We investigated the role and molecular mechanism of extracellular vesicles (EVs) released by hepatocytes during lipotoxicity in modulation of HSC phenotype.MethodsEVs were isolated from fat-laden hepatocytes by differential centrifugation and incubated with HSCs. EV internalization and HSCs activation, migration and proliferation were assessed. Loss- and gain-of-functions studies were performed to explore the potential role of PPAR-γ-targeting miRNAs carried by EVs into HSC.ResultsHepatocyte-derived EVs released during lipotoxicity are efficiently internalized by HSCs resulting in their activation, as shown by marked up-regulation of pro-fibrogenic genes (Collagen-I, α-SMA and TIMP-2), proliferation, chemotaxis and wound healing responses. These changes were associated with miRNAs shuttled by EVs and suppression of PPAR-γ expression in HSC. Hepatocyte-derived EVs miRNA content included various miRNAs that are known inhibitors of PPAR-γ expression with miR-128-3p being the most effectively transferred. Furthermore loss- and gain-of-function studies identified miR-128-3p as a central modulator of the effects of EVs on PPAR-γ inhibition and HSC activation.ConclusionOur findings demonstrate a link between fat-laden hepatocyte-derived EVs and liver fibrosis and have potential implications for the development of novel anti-fibrotic targets for NAFLD and other fibrotic diseases

Helicobacter pylori Stress-Response: Definition of the HrcA Regulon

Bacteria respond to different environmental stresses by reprogramming the transcription of specific genes whose proper expression is critical for their survival. In this regard, the heat-shock response, a widespread protective mechanism, triggers a sudden increase in the cellular concentration of different proteins, including molecular chaperones and proteases, to preserve protein folding and maintain cellular homeostasis. In the medically important gastric pathogen Helicobacter pylori the regulation of the principal heat-shock genes is under the transcriptional control of two repressor proteins named HspR and HrcA. To define the HrcA regulon, we carried out whole transcriptome analysis through RNA-sequencing, comparing the transcriptome of the H. pylori G27 wild type strain to that of the isogenic hrcA-knockout strain. Overall, differential gene expression analysis outlined 49 genes to be deregulated upon hrcA gene inactivation. Interestingly, besides controlling the transcription of genes coding for molecular chaperones and stress-related mediators, HrcA is involved in regulating the expression of proteins whose function is linked to several cellular processes crucial for bacterial survival and virulence. These include cell motility, membrane transporters, Lipopolysaccharide modifiers and adhesins. The role of HrcA as a central regulator of H. pylori transcriptome, as well as its interconnections with the HspR regulon are here analyzed and discussed. As the HrcA protein acts as a pleiotropic regulator, influencing the expression of several stress-unrelated genes, it may be considered a promising target for the design of new antimicrobial strategies

Cloned HTLV-1+CD4+, but not CD8+, T-cells display an oncogenic miRNome

HTLV-1 persistence in vivo relies on the persistent clonal expansion of its host cells. These are CD4+ and CD8+ T cells, yet ATL is regularly CD4+. Accordingly, untransformed HTLV-1+CD4+ but not CD8+ T cells cloned from carriers cumulate the features of preleukemic cells, including multinuclearity, chromatin bridges, increased cell cycling and inappropriate telomerase activity. MicroRNAs (miR) modify the maturation of a plethora of T-cells RNA and their deregulation would therefore constitute an appropriate explanation for the Tax-dependent or -independent pleiotropic changes in the phenotype of HTLV-1+CD4+ T cells. As the miRNome of naturally infected untransformed cells has not been investigated to date, we assessed the miR expression profiling of T cells cloned from carriers. Microarray results, confirmed by quantitative RTPCR, showed that, upon infection, CD4+ and CD8+ clones yielded aberrant expression of 15 distinct miRs including miR-34b and miR-494 that were respectively over- and underexpressed in both compartments. The more prominent effect of the infection consisted in the CD4+-restricted overexpression of the cancer-related miRs miR-21, -27b and -23b associated with the CD4+-restricted downregulation of the proapoptotic miR-15 and -16. Data were extended by the analysis of 40 additional CD4+ clones (20 infected). Crossing the miRNome against the whole transcriptome data identified putative miR-targeted genes. In silico, those targeted by miR-23b and -27b defined 2 hitherto unknown pathways involving the cell cycle and genetic disorders. Therefore HTLV-1 triggers a phenotype-specific miR signature consistent with the preleukemic HTLV-1+CD4+ phenoty

Significância prognóstica das micrometástases ocultas em linfonodos no câncer gástrico: estudo histoquímico e imunoistoquímico baseado nas classificações UICC TNM de 1997 e JCGCA de 1998

BACKGROUND: Micrometastasis is a single or a cluster of malignant cells inside the lymph node that are not detected by routine histopathological sections. Micrometastasis is related to poorer prognosis in many gastric cancer studies the real significance of these cells is still controversial. AIM: To evaluate if lymph node micrometastasis is a significant independent prognostic factor and important risk factor for recurrence in gastric cancer. METHODS: A total of 1290 lymph nodes from 28 patients with gastric cancer, since 1998 until 2003, treated by radical resection (D2 and modified D3 lymphadenectomies) were studied. Three sections per lymph node were stained by Hematoxilin-Eosin, histochemical (AB-PAS) and immunohistochemical (AE1-AE3) techniques. Kaplan-Meier's survival curves and Log-rank/Cox tests were used in order to compares lymph node micrometastasis positivity, depth (pT) and location of tumor in gastric wall, histologic type, lymphatic, vascular and perineural invasion, lymph node status (pN) and stage. RESULTS: There were worse prognosis and recurrence in patients with positive lymph node micrometastasis related to vascular and perineural invasions, advanced lymph node status and advanced stages. CONCLUSION: Lymph node micrometastasis seems to be a significant independent prognostic factor and important risk factor for recurrence in gastric cancer, in a context of radical D2 lymphadenectomyRACIONAL: Micrometástases são um conjunto de células malignas dentro de linfonodo que não são detectadas pelos exames histopatológicos de rotina. Elas são relacionadas a prognóstico mais pobre em muitos estudos sobre câncer gástrico, mas a real significância dessas células permanece controversa. OBJETIVO: Avaliar se micrometástase linfonodal é um fator independente de prognóstico e importante para detectar a recurrência do câncer gástrico. MÉTODOS: Um total de 1290 lifonodos de 28 pacientes com câncer gástrico, de 1998 a 2003, tratados com operações radicais (D2 e D3 modificadas) foram revistos. Três secções por linfonodo foram corados por Hematoxilina-Eosina, histoquímica (AB-PAS) e imunoistoquímica (AE1-AE3). Curvas de sobrevida de Kaplan-Meyer e teste de Log-rank/Cox foram usados para comparar positividade das imcrometástases, profundidade (pT) e localização tumoral na parede gástrica, tipo histológico, invasão linfática, vascular e perineural, estado linfonodal (pN) e estádio onde se encontra a doença. RESULTADOS: Houve pior prognóstico e recurrência nos pacientes com linfonodos com micrometástases relacionadas às invasões vascular e perineural , avançado estado de invasão linfática e estadiamento mais elevado. CONCLUSÃO: Micrometástase parece ser importante e independente fator de risco para recurrência no câncer gástrico no contexto das linfadenectomias radicais D2