Mortalidade pós-neonatal no território brasileiro: uma revisão da literatura

O presente trabalho trata-se de revisão sistemática, referente ao período de 2004 a 2009, sobre o tema mortalidade pós-neonatal. Teve o objetivo de identificar como se colocam na literatura, as causas da morte e a relação com as condições socioeconômicas. Foram selecionados 27 artigos, 74,4% publicados em periódicos da área da Saúde Pública e 66,7%, de desenho do tipo ecológico. Quase a totalidade versava sobre grupos de causas e seus componentes (66,7%), seguidos pelo terço restante, sobre a identificação dos fatores determinantes dos óbitos. A região Sudeste produziu mais de 37% dos estudos. Na maioria dos municípios e estados brasileiros, a redução superou 50% no final da década de 1990. Dentre os grupos de causas de óbitos, predominou o grupamento diarreia-pneumonia, seguido pelas malformações congênitas. As condições de vida segundo indicadores socioeconômicos - moradia, saneamento básico, educação e acesso à saúde - foram determinantes para os maiores índices de mortalidade pós-neonatal por causas passíveis de redução.

Cause-specific mortality and income inequality in Sao Paulo, Brazil

OBJECTIVE: To analyze cause-specifi c mortality rates according to the relative income hypothesis. METHODS: All 96 administrative areas of the city of Sao Paulo, southeastern Brazil, were divided into two groups based on the Gini coefficient of income inequality: high (>= 0.25) and low (<0.25). The propensity score matching method was applied to control for confounders associated with socioeconomic differences among areas. RESULTS: The difference between high and low income inequality areas was statistically significant for homicide (8.57 per 10,000; 95% CI: 2.60; 14.53); ischemic heart disease (5.47 per 10,000 [95% CI 0.76; 10.17]); HIV/AIDS (3.58 per 10,000 [95% CI 0.58; 6.57]); and respiratory diseases (3.56 per 10,000 [95% CI 0.18; 6.94]). The ten most common causes of death accounted for 72.30% of the mortality difference. Infant mortality also had signifi cantly higher age-adjusted rates in high inequality areas (2.80 per 10,000 [95% CI 0.86; 4.74]), as well as among males (27.37 per 10,000 [95% CI 6.19; 48.55]) and females (15.07 per 10,000 [95% CI 3.65; 26.48]). CONCLUSIONS: The study results support the relative income hypothesis. After propensity score matching cause-specifi c mortality rates was higher in more unequal areas. Studies on income inequality in smaller areas should take proper accounting of heterogeneity of social and demographic characteristics.

MyD88 signaling is directly involved in the development of murine placental Malaria

Malaria is a widespread infectious disease caused by the parasite Plasmodium. During pregnancy, malaria infection leads to a range of complications that can affect both the mother and fetus, including stillbirth, infant mortality, and low birth weight. In this study, we utilized a mouse model of placental malaria (PM) infection to determine the importance of the protein MyD88 in the host immune response to Plasmodium during pregnancy. Initially, we demonstrated that Plasmodium berghei NK65GFP adhered to placental tissue via chondroitin sulfate A and induced PM in mice with a C57BL/6 genetic background. To evaluate the involvement of MyD88 in the pathology of PM, we performed a histopathological analysis of placentas obtained from MyD88(-/-) and wild-type (WT) mice following infection on the 19th gestational day. Our data demonstrated that the detrimental placental alterations observed in the infected mice were correlated with the expression of MyD88. Moreover, in the absence of this protein, production of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) was significantly reduced in the infected mice. More importantly, in contrast to fetuses from infected WT mice, which exhibited a reduction in body weight, the fetuses from infected MyD88(-/-) mice did not display significant weight loss compared to their noninfected littermates. In addition, we observed a decrement of maternal care associated with malaria infection, which was attenuated in the MyD88-deficient mice. Collectively, the results of this study illustrate the pivotal importance of the MyD88 signaling pathway in the pathogenesis of placental malaria, thus presenting new possibilities for targeting MyD88 in therapeutic interventions.