Estimativa dos coeficientes específicos de mortalidade infantil segundo peso ao nascer no município de São Paulo (Brasil)

Foi estimada a distribuição do peso ao nascer da coorte dos recém-nascidos que deu origem aos óbitos infantis estudados pela Investigação Interamericana de Mortalidade na Infância no projeto de São Paulo (1968-70) e determinados os riscos de óbito associados a cada intervalo de peso de nascimento. Assim, foram apurados coeficientes de mortalidade infantil de 305,5, 50,2 e 34,4 para recém-nascidos de baixo peso, peso deficiente e peso superior a 3.000 g. A comparação destes coeficientes com os registrados na área americana incluída na investigação citada (Califórnia), revelou excesso de mortalidade, particularmente notável não para os recém-nascidos de baixo peso, mas para os recém-nascidos de peso superior a 3.000 g. O ajuste da mortalidade de São Paulo (Brasil) à distribuição do peso ao nascer observada na Califórnia foi capaz de explicar 15% do excesso da mortalidade infantil e 21% do excesso da mortalidade neonatal de São Paulo.By means of the birth-rate distribution found to exist during the Inter-American Investigation of Mortality in Childhood in S. Paulo (1968-70) the infant death rate association with each birth-weight interval was estimated. The infant mortality rates were 305.5, 50.2 and 34.4 respectively for low birth-weight, deficient weight and weight above 3,000 grams. Compared with the rates found in California, USA, by the same Investigation, the infant mortality rates in S. Paulo are higher, particularly for mortality associated with birth-weight of above 3,000 grams. The adjustment of infant mortality rates in S. Paulo according to the birth-weight distribution found in California led to the conclusion that, at that period, only 15% of the excess of the infant mortality of S. Paulo could be attributed exclusively to birth-weight. In the case of neonatal mortality, 21% of the mortality excess in S. Paulo could be attributed to birth-weight

Decomposition and nutrient release of leguminous plants in coffee agroforestry systems.

Leguminous plants used as green manure are an important nutrient source for coffee plantations, especially for soils with low nutrient levels. Field experiments were conducted in the Zona da Mata of Minas Gerais State, Brazil to evaluate the decomposition and nutrient release rates of four leguminous species used as green manures (Arachis pintoi, Calopogonium mucunoides, Stizolobium aterrimum and Stylosanthes guianensis) in a coffee agroforestry system under two different climate conditions. The initial N contents in plant residues varied from 25.7 to 37.0 g kg-1 and P from 2.4 to 3.0 g kg-1. The lignin/N, lignin/polyphenol and(lignin+polyphenol)/N ratios were low in all residues studied. Mass loss rates were highest in the first 15 days, when 25 % of the residues were decomposed. From 15 to 30 days, the decomposition rate decreased on both farms. On the farm in Pedra Dourada (PD), the decomposition constant k increased in the order C. mucunoides < S. aterrimum < S. guianensis < A. pintoi. On the farm in Araponga (ARA), there was no difference in the decomposition rate among leguminous plants. The N release rates varied from 0.0036 to 0.0096 d-1. Around 32 % of the total N content in the plant material was released in the first 15 days. In ARA, the N concentration in the S. aterrimum residues was always significantly higher than in the other residues. At the end of 360 days, the N released was 78 % in ARA and 89 % in PD of the initial content. Phosphorus was the most rapidly released nutrient (k values from 0.0165 to 0.0394 d-1). Residue decomposition and nutrient release did not correlate with initial residue chemistry and biochemistry, but differences in climatic conditions between the two study sites modified the decomposition rate constants

MAF amplification licenses ERα through epigenetic remodelling to drive breast cancer metastasis

MAF amplification increases the risk of breast cancer (BCa) metastasis through mechanisms that are still poorly understood yet have important clinical implications. Oestrogen-receptor-positive (ER+) BCa requires oestrogen for both growth and metastasis, albeit by ill-known mechanisms. Here we integrate proteomics, transcriptomics, epigenomics, chromatin accessibility and functional assays from human and syngeneic mouse BCa models to show that MAF directly interacts with oestrogen receptor alpha (ERα), thereby promoting a unique chromatin landscape that favours metastatic spread. We identify metastasis-promoting genes that are de novo licensed following oestrogen exposure in a MAF-dependent manner. The histone demethylase KDM1A is key to the epigenomic remodelling that facilitates the expression of the pro-metastatic MAF/oestrogen-driven gene expression program, and loss of KDM1A activity prevents this metastasis. We have thus determined that the molecular basis underlying MAF/oestrogen-mediated metastasis requires genetic, epigenetic and hormone signals from the systemic environment, which influence the ability of BCa cells to metastasize