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Departamento de Computação
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Departamento de Física
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Departamento de Biologia
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Publication History View all

  • Source
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    ABSTRACT: Introdução Dentre as poucas informações existentes sobre as operações pré-abate, sabe-se que muitos são os fatores que contribuem com o estresse das aves durante estas etapas e que a intensidade destes efeitos determina o nível elevado de perdas por mortalidade na chegada ("Death on arrival" – DOA). No entanto, a busca pela localização destes pontos críticos tornou-se um dos principais desafios da cadeia produtiva de frangos de corte, com o objetivo de reduzir as perdas nesta fase, e consequentemente aumentar a lucratividade para todos os atores envolvidos no cenário avícola. Destaca-se nesta abordagem a operação de espera nos abatedouros, que consiste no momento em que as aves aguardam na carga o momento de abate. Esta etapa é uma das mais importantes e decisivas quanto ao sucesso obtido entre a retirada das aves das granjas e sua chegada à linha de abate, dentro de condições que facilitem a comercialização de um produto final de qualidade superior. Todavia, mesmo com todos os cuidados tomados nas etapas de pega, carregamento e transporte, estes podem ser perdidos em poucas horas durante a espera, caso esta seja mal planejada para o objetivo de oferecer um ambiente térmico adequado para os animais. Pouco se sabe das condições ideais que possam contribuir para a redução da carga de estresse do animal, proveniente das etapas anteriores.
    AVESUI'09; 09/2014
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    ABSTRACT: Our previous findings enable us to hypothesize that the sesquiterpene (-)-α-bisabolol acts as inhibitor of voltage-dependent Ca(2+) channels in smooth muscle cells. The current study was aimed at consolidating such hypothesis through the recording of isometric tension in isolated aortic preparations, measurement of intracellular Ca(2+) by imaging technique as well as discovery of channel target using in silico analysis method. In rat aortic rings, (-)-α-bisabolol (1-1000μM) fully relaxed KCl- and phenylephrine-elicited contractions, but the IC50 values to produce such effects differed significantly (22.8 [17.6-27.7] and 200.7 [120.4-334.6] μM, respectively). Its ability to relax phenylephrine-induced contractions remained unaffected by L-NAME, indomethacin, 1H-[1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one, tetraethylammonium, glibenclamide or KT-5720. Under Ca(2+)-free conditions, (-)-α-bisabolol (100μM) did not alter the contractions evoked by phenylephrine or caffeine whereas it reduced those evoked by CaCl2 in KCl-, but not in PHE (in the presence of nifedipine)-stimulated preparations. (-)-α-Bisabolol did not significantly alter the contractions induced by the extracellular Ca(2+) restoration in cyclopiazonic acid-treated aortic rings or those evoked by phorbol 12,13-dibutyrate. In mesenteric artery rings loaded with Fluo-4AM, simultaneous measurement of force and cytosolic Ca(2+) revealed that (-)-α-bisabolol blunted the cytosolic levels of Ca(2+) in response to K(+) but not to norepinephrine. Silico docking analysis of the Cavβ2a subunit of voltage-dependent Ca(2+) channel indicated the existence of putative docking sites for (-)-α-bisabolol. The findings from confocal imaging and in silico analysis reinforce the ability of (-)-α-bisabolol to inhibit preferentially contractile responses evoked by Ca(2+) influx through voltage-dependent Ca(2+) channels.
    Vascular pharmacology. 08/2014;
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    ABSTRACT: The nitroderivative 1-nitro-2-phenylethane (NPE) was recently described as a compound possessing heme-dependent soluble guanylyl cyclase (sGC) stimulating properties in vascular smooth muscle cells. In this study, we tested such pharmacological property of NPE in mice pancreatic acinar cells subjected to the bile salt taurocholate, a type of pathological stimulus that simulates pancreatitis. Here, isolated acinar cells were treated with NPE in order to assess the role of sGC on the detrimental effects induced by taurocholate. NPE reduced taurocholate-elicited Ca(2+) overload, production of reactive oxygen species (ROS), apoptosis, necrosis, and exerted a protective effect against mitochondrial membrane potential (ΔΨm) dissipation. These NPE-induced effects were abolished by pretreatment with ODQ and KT 5823, and after the blockade of nitric oxide (NO) synthase with L-NAME, inhibitors of key components of the sGC pathway. Contrarily to cGMP that alone increased ΔΨm collapse and cell damage, the cytoprotective effect of NPE on ΔΨm and cell necrosis was almost reproduced by 8-nitro-cGMP, a second messenger generated by sGC under oxidative stress conditions. In conclusion, putative sGC stimulation with NPE reveals its cytoprotective profile on pancreatic cells subjected to taurocholate. Moreover, ROS and NO conjunctly appear to drive sGC activity in pancreatic acinar cells to implement an adaptive mechanism in response to oxidative and Ca(2+) stress through 8-nitro-cGMPsynthesis.
    Biochemical pharmacology. 08/2014;

Information

  • Address
    Av. da Universidade, 2853 Benfica, 60020-181, Fortaleza, Ceará, Brazil
  • Head of Institution
    Prof. Jesualdo Pereira Farias
  • Website
    http://www.ufc.br
  • Phone
    +55 (85) 3366 7300
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Oecologia Australis 07/2012; 16(2):156-164.
63 Downloads
 
Revista Latino-Americana de Enfermagem. 01/2002;
49 Downloads

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