Energia metabolizável da glicerina bruta e de dietas contendo glicerina bruta para frangos de corte na fase inicial.

Com a variação nos preços dos alimentos a glicerina bruta (GB) pode se tornar uma realidade na substituição parcial ao milho, tornando-se importante a determinação da energia metabolizável aparente (EMAn) deste alimento. Assim sendo, objetivou-se determinar a EMAn da GB e de rações formuladas com níveis crescentes de GB para frangos de corte na fase inicial (7 a 21 dias). Para a avaliação da EMAn das rações foi realizada coleta total de excretas dos 10 aos 18 dias de idade, sendo que os primeiros 4 dias foram de adaptação e os últimos 5 de coleta. Foi utilizado o delineamento experimental inteiramente casualizado com 4 tratamentos (0, 4, 8 e 12% de inclusão de GB nas rações) e 9 repetições de 10 aves por tratamento. Para a avaliação da EMAn da GB foi adicionado um tratamento com a inclusão de 8% de GB na ração referência (0% de GB) e utilizado nove repetições de 10 aves por gaiola. Não houve diferença significativa na EMAn entre os níveis de inclusão de 4 e 8% quando comparados ao controle (0%). Houve efeito linear decrescente para EMAn das dietas avaliadas com a inclusão de GB. A EMAn da GB determinada no ensaio foi de 2651 kcal/kg. Observou-se redução na matéria seca (MS) das excretas e aumento na produção de excretas na MS com o aumento dos níveis de inclusão, fato que pode explicar a reduzida EMAn da GB em inclusões acima de 4%. É necessária a correção do valor de EMAn da GB nas dietas em função do nível de inclusão

Open-coast sandy beaches and coastal dunes

Coastal ecosystems are centres of high biological productivity, but their conservation is often threatened by numerous and complex environmental factors. Citing examples from the major littoral habitats worldwide, such as sandy beaches, salt marshes and mangrove swamps, this text characterises the biodiversity of coastline environments and highlights important aspects of their maintenance and preservation, aided by the analysis of key representative species. Leaders in the field provide reviews of the foremost threats to coastal networks, including the effects of climate change, invasive species and major pollution incidents such as oil spills. Further discussion underscores the intricacies of measuring and managing coastline species in the field, taking into account the difficulties in quantifying biodiversity loss due to indirect cascading effects and trophic skew. Synthesising the current state of species richness with present and projected environmental pressures, the book ultimately establishes a research agenda for implementing and improving conservation practices moving forward. [Book Synopsis

Regulation of neutrophil senescence by microRNAs

Neutrophils are rapidly recruited to sites of tissue injury or infection, where they protect against invading pathogens. Neutrophil functions are limited by a process of neutrophil senescence, which renders the cells unable to respond to chemoattractants, carry out respiratory burst, or degranulate. In parallel, aged neutrophils also undergo spontaneous apoptosis, which can be delayed by factors such as GMCSF. This is then followed by their subsequent removal by phagocytic cells such as macrophages, thereby preventing unwanted inflammation and tissue damage. Neutrophils translate mRNA to make new proteins that are important in maintaining functional longevity. We therefore hypothesised that neutrophil functions and lifespan might be regulated by microRNAs expressed within human neutrophils. Total RNA from highly purified neutrophils was prepared and subjected to microarray analysis using the Agilent human miRNA microarray V3. We found human neutrophils expressed a selected repertoire of 148 microRNAs and that 6 of these were significantly upregulated after a period of 4 hours in culture, at a time when the contribution of apoptosis is negligible. A list of predicted targets for these 6 microRNAs was generated from http://mirecords.biolead.org and compared to mRNA species downregulated over time, revealing 83 genes targeted by at least 2 out of the 6 regulated microRNAs. Pathway analysis of genes containing binding sites for these microRNAs identified the following pathways: chemokine and cytokine signalling, Ras pathway, and regulation of the actin cytoskeleton. Our data suggest that microRNAs may play a role in the regulation of neutrophil senescence and further suggest that manipulation of microRNAs might represent an area of future therapeutic interest for the treatment of inflammatory disease

The proangiogenic capacity of polymorphonuclear neutrophils delineated by microarray technique and by measurement of neovascularization in wounded skin of CD18-deficient mice

Growing evidence supports the concept that polymorphonuclear neutrophils (PMN) are critically involved in inflammation-mediated angiogenesis which is important for wound healing and repair. We employed an oligonucleotide microarray technique to gain further insight into the molecular mechanisms underlying the proangiogenic potential of human PMN. In addition to 18 known angiogenesis-relevant genes, we detected the expression of 10 novel genes, namely midkine, erb-B2, ets-1, transforming growth factor receptor-beta(2) and -beta(3), thrombospondin, tissue inhibitor of metalloproteinase 2, ephrin A2, ephrin B2 and restin in human PMN freshly isolated from the circulation. Gene expression was confi rmed by the RT-PCR technique. In vivo evidence for the role of PMN in neovascularization was provided by studying neovascularization in a skin model of wound healing using CD18-deficient mice which lack PMN infi ltration to sites of lesion. In CD18-deficient animals, neo- vascularization was found to be signifi cantly compromised when compared with wild- type control animals which showed profound neovascularization within the granulation tissue during the wound healing process. Thus, PMN infiltration seems to facilitate inflammation mediated angiogenesis which may be a consequence of the broad spectrum of proangiogenic factors expressed by these cells. Copyright (c) 2006 S. Karger AG, Basel