215 resultados para Phospho-inositides


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O objetivo deste estudo foi avaliar o tempo de jejum na granja e a posição dos animais na carroceria do caminhão durante o transporte ao abatedouro sobre o status hormonal e fisiológico de suínos de abate pesados visando obter melhorias no manejo pré-abate e reduzir perdas na qualidade de carne. Foram utilizadas 64 fêmeas com peso médio de 133+11kg, oriundas de duas granjas de terminação. Os tempos de jejum avaliados foram nove, 12, 15 e 18h, enquanto que as posições consideradas na carroceria foram box (frente, meio e atrás), piso (inferior e superior) e lado (lateral direita e esquerda). Ao abate, foram medidos os níveis de glicose, lactato e CPK no sangue. A concentração de cortisol na saliva (CCS) foi medida nas granjas (24 horas antes e após embarque) e no abatedouro (logo após o descarregamento e antes do abate). A freqüência cardíaca foi monitorada durante todo o manejo pré-abate. Foi observado o efeito da interação entre TJG e o local de avaliação sobre a CCS e a freqüência cardíaca. A CCS e a freqüência cardíaca aumentaram significativamente da granja ao desembarque no abatedouro em relação ao descanso pré-abate no abatedouro foi observada uma redução (P<0,05) nos valores. A CCS variou em função do TJG e o local de avaliação da seguinte maneira: suínos com 18 horas de jejum apresentaram menor (P<0,05) variação na CCS durante o transcorrer das diferentes etapas do manejo pré-abate do que suínos com TJG menores e, entre estes, os animais com TJG de nove horas apresentaram a maior (P<0,05) variação. Antes do abate, os suínos com TJG de nove horas apresentaram o maior valor (P<0,05) de CCS quando comparados aos outros TJG. Conclui-se que o TJG promove mudanças (P<0,05) nos valores do cortisol na saliva e na freqüência cardíaca no manejo pré-abate, mas não afetam (P>0,05) os níveis de glicose, lactato e CPK no abate dos suínos.

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O objetivo neste trabalho foi avaliar o efeito do período de descanso (3, 5, 7 e 9 horas) dos suínos no frigorífico (PDF) e da localização dos suínos na carroceria do caminhão (PBO), quando transportados, no inverno ou verão, sobre alguns parâmetros fisiológicos avaliados em 64 fêmeas, com peso médio de 130kg para abate, durante o manejo pré-abate. Para a análise estatística, foram considerados, no modelo de análise da variância, os efeitos de bloco, PDF, PBO e da interação (bloco x PDF), entre outros. O PDF influenciou, significativamente, as concentrações de lactato no sangue e cortisol na saliva. Suínos que descansaram 5 e 7 horas apresentaram maior concentração de lactato em relação aos animais que descansaram 3 e 9 horas. No transporte, a freqüência cardíaca foi muito maior em relação aos demais locais avaliados. Concluiu-se que o incremento do PDF não promove mudanças na freqüência cardíaca, nas concentrações de glicose e CPK no sangue e cortisol na saliva, mas interfere na concentração de lactato no sangue dos suínos.

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The development of strategies for the protection of oral tissues against the adverse effects of resin monomers is primarily based on the elucidation of underlying molecular mechanisms. The generation of reactive oxygen species beyond the capacity of a balanced redox regulation in cells is probably a cause of cell damage. This study was designed to investigate oxidative DNA damage, the activation of ATM, a reporter of DNA damage, and redox-sensitive signal transduction through mitogen-activated protein kinases (MAPKs) by the monomer triethylene glycol dimethacrylate (TEGDMA). TEGDMA concentrations as high as 3-5 mm decreased THP-1 cell viability after a 24 h and 48 h exposure, and levels of 8-oxoguanine (8-oxoG) increased about 3- to 5-fold. The cells were partially protected from toxicity in the presence of N-acetylcysteine (NAC). TEGDMA also induced a delay in the cell cycle. The number of THP-1 cells increased about 2-fold in G1 phase and 5-fold in G2 phase in cultures treated with 3-5 mm TEGDMA. ATM was activated in THP-1 cells by TEGDMA. Likewise, the amounts of phospho-p38 were increased about 3-fold by 3 mm TEGDMA compared to untreated controls after a 24 h and 48 h exposure period, and phospho-ERK1/2 was induced in a very similar way. The activation of both MAPKs was inhibited by NAC. Our findings suggest that the activation of various signal transduction pathways is related to oxidative stress caused by a resin monomer. Signaling through ATM indicates oxidative DNA damage and the activation of MAPK pathways indicates oxidative stress-induced regulation of cell survival and apoptosis. (C) 2008 Elsevier Ltd. All rights reserved.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Pós-graduação em Ciências da Motricidade - IBRC

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Some authors consider minerals from organic sources more bioavailable for pig nutrition in comparison with inorganic sources. To evaluate the relative iron bioavailability from the organic source iron carbo-amino-phospho-chelate (ICAPC) to weanling piglets, it was conducted an experiment with 126 commercial piglets, using iron sulfate monohydrate (S) as standard. The experiment had a randomized block design with seven treatments (diet without adding specific source of iron, diet with 50, 100 and 150 ppm iron from S and diet with 50, 100 and 150 ppm iron from ICAPC), six replications and three animals per experimental unit. Performance parameters (average daily gain - ADG, feed: gain ratio - F:G) and blood variables (hemoglobin - Hb, hematocrit - Ht, transferrin - TR, latent iron-binding capacity - LIBC, total iron-binding capacity - TIBC, serum iron - Fe and transferrin saturation index - TSI) were evaluated. At the end of the experiment a piglet from each experimental unit was slaughtered and its liver and spleen removed for assessment of iron concentration by flame atomic absorption spectrometry (FAAS). The evaluated sources of iron yielded similar results for the variables of interest, but the increase in iron intake was followed by a linear increase in ADG, Hb, Ht, Fe and TSI as well as a linear decrease in the values of F:G, TR, LIBC and TIBC. Iron bioavailabilities from both ICAPC and S sources are similar for weanling piglets.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Two experiments (E) were carried out with the objective of evaluating the effects of fumaric acid and carbo-amino-fosfo-quelato of calcium diets of weaned pigs on performance (E1) and intestinal morphology (E2). A total of 96 and 32 pigs with initial mean weights of 5,66 kg ± 0,44kg and 5,34 ± 0,45kg , in E1 and in E2, were used respectively. Randomized block designs were used in both experiments, with a 2 X 2 factorial arrangement in E1 and a 2 X 2 X 2 factorial arrangement in E2. No interaction between acidifier, source of calcium and phosphorus were found for the variables studied in the two experiments. No treatment effects were found on daily feed intake in evaluating periods. Feed conversion from 0 to 17 days was better (P<0.05) when inorganic sources of Ca and P were fed; however, no difference was observed in other periods. The averages of villus height (AV), crypt depth (PC), AV: PC relationship and mucous membrane of the duodenum and of the jejunum didn’t differ among treatments. Considering the total nursery period, no benefit was found in using an acidifier, however the carbo-amino-fosfo-quelato of calcium studied may replace the inorganic sources in the diets of piglets, with no damage to performance and to intestinal morphology.

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In response to pathogen recognition by Toll-like receptors (TLRs) on their cell surface, macrophages release lipid mediators and cytokines that are widely distributed throughout the body and play essential roles in host responses. Granulocyte macrophage colony-stimulating factor (GM-CSF) is important for the immune response during infections to improve the clearance of microorganisms. In this study, we examined the release of mediators in response to TLR2 ligands by bone marrow-derived macrophages (BMDMs) primed with GM-CSF. We demonstrated that when stimulated with TLR2 ligands, non-primed BMDMs preferentially produced PGE(2) in greater amounts than LTB4. However, GM-CSF priming shifted the release of lipid mediators by BMDMs, resulting in a significant decrease of PGE(2) production in response to the same stimuli. The decrease of PGE(2) production from primed BMDMs was accompanied by a decrease in PGE-synthase mRNA expression and an increase in TNF-alpha and nitric oxide (NO) production. Moreover, some GM-CSF effects were potentiated by the addition of IFN-gamma. Using a variety of TLR2 ligands, we established that PGE(2) release by GM-CSF-primed BMDMs was dependent on TLR2 co-receptors (TLR1, TLR6), CD14, MyD88 and the nuclear translocation of NF kappa B but was not dependent on peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation. Indeed, GM-CSF priming enhanced TLR2, TLR4 and MyD88 mRNA expression and phospho-I kappa B alpha formation. These findings demonstrate that GM-CSF drives BMDMs to present a profile relevant to the host during infections.

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We aimed to investigate the possible role of creatine (CR) supplementation in counteracting dexamethasone-induced muscle wasting and insulin resistance in rats. Also, we examined whether CR intake would modulate molecular pathways involved in muscle remodeling and insulin signaling. Animals were randomly divided into four groups: (1) dexamethasone (DEX); (2) control pair-fed (CON-PF); (3) dexamethasone plus CR (DEX-CR); and (4) CR pair-fed (CR-PF). Dexamethasone (5 mg/kg/day) and CR (5 g/kg/day) were given via drinking water for 7 days. Plantaris and extensor digitorum longus (EDL) muscles were removed for analysis. Plantaris and EDL muscle mass were significantly reduced in the DEX-CR and DEX groups when compared with the CON-PF and CR-PF groups (P < 0.05). Dexamethasone significantly decreased phospho-Ser(473)-Akt protein levels compared to the CON-PF group (P < 0.05) and CR supplementation aggravated this response (P < 0.001). Serum glucose was significantly increased in the DEX group when compared with the CON-PF group (DEX 7.8 +/- A 0.6 vs. CON-PF 5.2 +/- A 0.5 mmol/l; P < 0.05). CR supplementation significantly exacerbated hyperglycemia in the dexamethasone-treated animals (DEX-CR 15.1 +/- A 2.4 mmol/l; P < 0.05 vs. others). Dexamethasone reduced GLUT-4 translocation when compared with the CON-PF and CR-PF (P < 0.05) groups and this response was aggravated by CR supplementation (P < 0.05 vs. others). In conclusion, supplementation with CR resulted in increased insulin resistance and did not attenuate muscle wasting in rats treated with dexamethasone. Given the contrast with the results of human studies that have shown benefits of CR supplementation on muscle atrophy and insulin sensitivity, we suggest caution when extrapolating this animal data to human subjects.

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Objective: We aimed to evaluate the effects of resistance exercise (RE) and leucine (LEU) supplementation on dexamethasone (DEXA)-induced muscle atrophy and insulin resistance. Methods: Male Wistar rats were randomly divided into DEXA(DEX), DEXA + RE (DEX-RE), DEXA + LEU (DEX-LEU), and DEXA + RE + LEU (DEX-RE-LEU) groups. Each group received DEXA 5 mg . kg(-1) . d(-1) for 7 d from drinking water and were pair-fed to the DEX group; LEU-supplemented groups received 0.135 g . kg(-1) . d(-1) through gavage for 7 d; the RE protocol was based on three sessions of squat-type exercise composed by three sets of 10 repetitions at 70% of maximal voluntary strength capacity. Results: The plantaris mass was significantly greater in both trained groups compared with the non-trained groups. Muscle cross-sectional area and fiber areas did not differ between groups. Both trained groups displayed significant increases in the number of intermediated fibers (IIa/IIx), a decreased number of fast-twitch fibers (IIb), an increased ratio of the proteins phospho(Ser2448)/ total mammalian target of rapamycin and phospho(Thr389)/total 70-kDa ribosomal protein S6 kinase. and a decreased ratio of phospho(Ser253)/total Forkhead box protein-3a. Plasma glucose was significantly increased in the DEX-LEU group compared with the DEX group and RE significantly decreased hyperglycemia. The DEX-LEU group displayed decreased glucose transporter-4 translocation compared with the DEX group and RE restored this response. LEU supplementation worsened insulin sensitivity and did not attenuate muscle wasting in rats treated with DEXA. Conversely, RE modulated glucose homeostasis and fiber type transition in the plantaris muscle. Conclusion: Resistance exercise but not LEU supplementation promoted fiber type transition and improved glucose homeostasis in DEXA-treated rats. (C) 2012 Elsevier Inc. All rights reserved.

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Background: Post-rest contraction (PRC) of cardiac muscle provides indirect information about the intracellular calcium handling. Objective: Our aim was to study the behavior of PRC, and its underlying mechanisms, in rats with myocardial infarction. Methods: Six weeks after coronary occlusion, the contractility of papillary muscles (PM) obtained from sham-operated (C, n = 17), moderate infarcted (MMI, n = 10) and large infarcted (LMI, n = 14) rats was evaluated, following rest intervals of 10 to 60 seconds before and after incubation with lithium chloride (Li+) substituting sodium chloride or ryanodine (Ry). Protein expression of SR Ca(2+)-ATPase (SERCA2), Na+/Ca2+ exchanger (NCX), phospholamban (PLB) and phospho-Ser(16)-PLB were analyzed by Western blotting. Results: MMI exhibited reduced PRC potentiation when compared to C. Opposing the normal potentiation for C, post-rest decays of force were observed in LMI muscles. In addition, Ry blocked PRC decay or potentiation observed in LMI and C; Li+ inhibited NCX and converted PRC decay to potentiation in LMI. Although MMI and LMI presented decreased SERCA2 (72 +/- 7% and 47 +/- 9% of Control, respectively) and phospho-Ser(16)-PLB (75 +/- 5% and 46 +/- 11%, respectively) protein expression, overexpression of NCX (175 +/- 20%) was only observed in LMI muscles. Conclusion: Our results showed, for the first time ever, that myocardial remodeling after MI in rats may change the regular potentiation to post-rest decay by affecting myocyte Ca(2+) handling proteins. (Arq Bras Cardiol 2012;98(3):243-251)