Remoção de fósforo de efluentes da suinocultura.

Projeto/Plano de Ação: 03.11.09.01

Tecnologias para tratamento de dejeto de suínos.

Projeto/Plano de Ação: 03.11.09.012

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

Comparação das exigências nutricionais para suínos machos castrados recomendadas pelas Tabelas Brasileiras (2011) e pelo NRC (2012).

bitstream/item/78981/1/Comunicado-508.pdfProjeto/Plano de Ação: 03.12.01.025

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

Interference with glycosaminoglycan-chemokine interactions with a probe to alter leukocyte recruitment and inflammation in vivo

In vivo leukocyte recruitment is not fully understood and may result from interactions of chemokines with glycosaminoglycans/GAGs. We previously showed that chlorite-oxidized oxyamylose/COAM binds the neutrophil chemokine GCP-2/CXCL6. Here, mouse chemokine binding by COAM was studied systematically and binding affinities of chemokines to COAM versus GAGs were compared. COAM and heparan sulphate bound the mouse CXC chemokines KC/CXCL1, MIP-2/CXCL2, IP-10/CXCL10 and I-TAC/CXCL11 and the CC chemokine RANTES/CCL5 with affinities in the nanomolar range, whereas no binding interactions were observed for mouse MCP-1/CCL2, MIP-1α/CCL3 and MIP-1β/CCL4. The affinities of COAM-interacting chemokines were similar to or higher than those observed for heparan sulphate. Although COAM did not display chemotactic activity by itself, its co-administration with mouse GCP-2/CXCL6 and MIP-2/CXCL2 or its binding of endogenous chemokines resulted in fast and cooperative peritoneal neutrophil recruitment and in extravasation into the cremaster muscle in vivo. These local GAG mimetic features by COAM within tissues superseded systemic effects and were sufficient and applicable to reduce LPS-induced liver-specific neutrophil recruitment and activation. COAM mimics glycosaminoglycans and is a nontoxic probe for the study of leukocyte recruitment and inflammation in vivo

Neutralization of (NK-cell-derived) B-cell activating factor by Belimumab restores sensitivity of chronic lymphoid leukemia cells to direct and Rituximab-induced NK lysis.

Natural killer (NK) cells are cytotoxic lymphocytes that substantially contribute to the therapeutic benefit of antitumor antibodies like Rituximab, a crucial component in the treatment of B-cell malignancies. In chronic lymphocytic leukemia (CLL), the ability of NK cells to lyse the malignant cells and to mediate antibody-dependent cellular cytotoxicity upon Fc receptor stimulation is compromised, but the underlying mechanisms are largely unclear. We report here that NK-cells activation-dependently produce the tumor necrosis factor family member 'B-cell activating factor' (BAFF) in soluble form with no detectable surface expression, also in response to Fc receptor triggering by therapeutic CD20-antibodies. BAFF in turn enhanced the metabolic activity of primary CLL cells and impaired direct and Rituximab-induced lysis of CLL cells without affecting NK reactivity per se. The neutralizing BAFF antibody Belimumab, which is approved for treatment of systemic lupus erythematosus, prevented the effects of BAFF on the metabolism of CLL cells and restored their susceptibility to direct and Rituximab-induced NK-cell killing in allogeneic and autologous experimental systems. Our findings unravel the involvement of BAFF in the resistance of CLL cells to NK-cell antitumor immunity and Rituximab treatment and point to a benefit of combinatory approaches employing BAFF-neutralizing drugs in B-cell malignancies