To investigate the effects of a synthetic soybean isoflavone (ISF) on growth performance, meat quality, and antioxidation in male broilers, 1,500 birds that were 42 d old were allotted to 5 treatments with 6 replicates per treatment (50 birds per replicate). Birds were fed diets supplemented with 0, 10, 20, 40, or 80 mg of ISF/kg, respectively, for a period of 3 wk ad libitum. The results showed that dietary supplementations with 10 or 20 mg of ISF/kg increased weight gain by 13.6 and 16.2% (P < 0.01) and elevated feed intake by 7.37% (P < 0.05) and 11.2% (P < 0.01), respectively. Addition of 10 mg of ISF/kg decreased feed:gain by 5.5% (P < 0.05). Supplementation with 40 mg of ISF/kg in the diet slightly increased water-holding capacity by 17.24% (P < 0.1), and the addition of 20 or 40 mg/kg of ISF significantly increased the pH value of meat (P < 0.01), although adding 40 or 80 mg of ISF/kg increased the lightness of meat color (P < 0.05). Malondialdehyde production was slightly reduced in plasma of 20 mg of ISF/kg supplemented chickens (P < 0.1) and significantly decreased in breast muscles of 20, 40, or 80 mg of ISF/kg supplemented chickens (P < 0.01). The addition of 40 or 80 mg of ISF/kg significantly increased total antioxidant capability (P < 0.01) and slightly elevated total superoxide dismutase activity (P < 0.1) in plasma of chickens. The dose of 80 mg of ISF/kg slightly improved catalase activity in plasma (P < 0.06). In breast muscle, treatment of birds with 40 or 80 mg of ISF/kg caused an increase of total superoxide dismutase activity by 25.36% (P < 0.05) or 63.93% (P < 0.01). Catalase activity significantly increased by 70.61% by the supplemental ISF at the 40-mg level (P < 0.05). Also, 10, 20, or 40 mg doses of ISF/kg decreased lactic acid production (P < 0.05). The results of this study indicate that dietary ISF could improve growth performance and meat quality by decreasing lipid peroxidation and improving antioxidative status in male broilers.

An efficient near-infrared (NIR) quantum cutting (QC) in GdAl3(BO3)4:RE3+,Yb3+ (RE=Pr, Tb, and Tm) phosphors has been demonstrated, which involves the conversion of the visible photon into the NIR emission with an optimal quantum efficiency approaching 200%, by exploring the cooperative downconversion mechanism from RE3+ (RE=Pr, Tb, and Tm) excitons to the two activator ions, Yb3+. The development of NIR QC phosphors could open up a new approach in achieving high efficiency silicon-based solar cells by means of downconversion in the visible part of the solar spectrum to ∼1000nm photons with a twofold increase in the photon number.

The present study was performed to investigate the preventative effect of Lactobacillus plantarum on diarrhea in relation to intestinal barrier function in young piglets challenged with enterotoxigenic Escherichia coli (ETEC) K88. Seventy-two male piglets (4 d old) were assigned to 2 diets (antibiotic-free basal diet with or without L. plantarum, 5 × 10(10) cfu/kg diet) and subsequently challenged or not with ETEC K88 (1 × 10(8) cfu per pig) on d 15 in a 2 × 2 factorial arrangement of treatments. Feed intake and BW were measured on d 15 and 18 (3 d after challenge) for determination of growth performance. On d 18, 1 piglet from each pen was slaughtered to evaluate small intestinal morphology and expression of tight junction proteins at the mRNA and protein levels while another piglet was used for the intestinal permeability test. Before and after ETEC K88 challenge, piglets fed L. plantarum had greater BW, ADG, and ADFI (P< 0.05) and marginally greater G:F (P < 0.10) compared to piglets fed the unsupplemented diet. After ETEC K88 challenge, the challenged piglets did not show an impaired growth performance but had greater incidence of diarrhea compared to the nonchallenged piglets. There was an interaction between dietary L. plantarum and ETEC K88 challenge (P < 0.05) as L. plantarum prevented the ETEC K88-induced diarrhea. Piglets challenged with ETEC K88 also had greater urinary lactulose:mannitol and plasma concentration of endotoxin, shorter villi, deeper crypt depth, and reduced villous height:crypt depth in the duodenum and jejunum and decreased zonula occludens-1 mRNA and occludin mRNA and protein expression in the jejunum (P < 0.05). These deleterious effects caused by ETEC K88 were inhibited by feeding L. plantarum (P < 0.05). There were no effects of either treatment on the morphology and expression of tight junction proteins in ileum. In conclusion, L. plantarum, given to piglets in early life, improved performance and effectively prevented the diarrhea in young piglets induced by ETEC K88 challenge by improving function of the intestinal barrier by protecting intestinal morphology and intestinal permeability and the expression of genes for tight junction proteins (zonula occludens-1 and occludin).

The present study was conducted to test the hypothesis that dietary arginine supplementation may improve meat quality of finishing pigs. Beginning at approximately 60 kg body weight, pigs were fed a corn- and soybean meal-based diet supplemented with 0, 0.5 or 1% L-arginine until they reached a body weight of approximately 110 kg. On the last day of the experiment, pigs were food-deprived for 16 h before blood samples were obtained for analysis of amino acids, insulin, and other metabolites. Immediately thereafter, pigs were slaughtered for determination of carcass composition, muscle biochemical parameters, and meat quality. The result showed that arginine did not affect pig growth performance or carcass traits. However, 1% arginine decreased drip loss of pork muscle at 48 h postmortem, while increasing intramuscular fat content (P < 0.05). Supplementing 0.5 or 1% arginine to the diet increased arginine concentration and decreased cortisol level in serum, while enhancing antioxidative capacity and glutathione peroxidase activity in serum (P < 0.05). Additionally, 1% arginine increased antioxidative capacity in skeletal muscle (P < 0.05). Furthermore, 0.5 or 1% arginine decreased the cortisol receptor mRNA level in muscle (P < 0.05). Collectively, these results indicate that supplemental arginine improved meat quality and attenuated oxidative stress of finishing pigs.

No abstract

Stomach and intestines are involved in the secretion of gastrointestinal fluids and the absorption of nutrients and fluids, which ensure normal gut functions. Aquaporin water channels (AQPs) represent a major transcellular route for water transport in the gastrointestinal tract. Until now, at least 11 AQPs (AQP1–11) have been found to be present in the stomach, small and large intestines. These AQPs are distributed in different cell types in the stomach and intestines, including gastric epithelial cells, gastric glands cells, absorptive epithelial cells (enterocytes), goblet cells and Paneth cells. AQP1 is abundantly distributed in the endothelial cells of the gastrointestinal tract. AQP3 and AQP4 are mainly distributed in the basolateral membrane of epithelial cells in the stomach and intestines. AQP7, AQP8, AQP10 and AQP11 are distributed in the apical of enterocytes in the small and large intestines. Although AQP-null mice displayed almost no phenotypes in gastrointestinal tracts, the alterations of the expression and localization of these AQPs have been shown to be associated with the pathology of gastrointestinal disorders, which suggests that AQPs play important roles serving as potential therapeutic targets. Therefore, this review provides an overview of the expression, localization and distribution of AQPs in the stomach, small and large intestine of human and animals. Furthermore, this review emphasizes the potential roles of AQPs in the physiology and pathophysiology of stomach and intestines.

Suboptimal embryonic/fetal survival and growth remains a significant problem in mammals. Using a swine model, we tested the hypothesis that dietary L-arginine supplementation during gestation may improve pregnancy outcomes through enhancing placental growth and modulating hormonal secretions. Gestating pigs (Yorkshire×Landrace, n=108) were assigned randomly into two groups based on parity and body weight, representing dietary supplementation with 1.0% L-arginine-HCl or 1.7% L-alanine (isonitrogenous control) between days 22 and 114 of gestation. Blood samples were obtained from the ear vein on days 22, 40, 70 and 90 of gestation. On days 40, 70 and 90 of gestation, concentrations of estradiol in plasma were higher (P<0.05) in arginine-supplemented than in control sows. Moreover, arginine supplementation increased (P<0.05) the concentrations of arginine, proline and ornithine in plasma, but concentrations of urea or progesterone in plasma did not differ between the two groups of sows. Compared with the control, arginine supplementation increased (P<0.05) the total number of piglets by 1.31 per litter, the number of live-born piglets by 1.10 per litter, the litter birth weight for all piglets by 1.36 kg, and the litter birth weight for live-born piglets by 1.70 kg. Furthermore, arginine supplementation enhanced (P<0.05) placental weight by 16.2%. The weaning-to-estrus interval of sows was not affected by arginine supplementation during gestation. These results indicate that dietary arginine supplementation beneficially enhances placental growth and the reproductive performance of sows.

Deoxynivalenol (DON), a common mycotoxin, usually induces oxidative stress and affects the intestinal health of humans and animals. This study investigated the protective effect of resveratrol (RES), a natural antioxidant, on alleviating the cytotoxicity induced by DON in the porcine intestinal-epithelial cell line (IPEC-J2). Cells were incubated with RES for 24 h and then exposed to DON for another 24 h. Cell viability, proliferation, apoptosis, and oxidative-stress indicators were determined. In comparison with DON-only-treated cells, pretreatment with RES (15 μM) increased the cell viability (79.74 ± 2.02 vs 90.98 ± 2.66%, P < 0.01), improved proliferation (EdU-positive cells, 26.42 ± 1.12 vs 32.05 ± 0.78%, P < 0.01), decreased accumulation of intracellular reactive oxygen species (ROS, 1.68 ± 0.05 vs 1.29 ± 0.06, P < 0.01), stabilized mitochondrial-membrane potential (MMP, 8.98 ± 1.40 vs 2.29 ± 0.76, P < 0.001), and prevented apoptosis induced by DON (13.91 ± 1.20 vs 6.83 ± 0.52%, P < 0.01). RES activated the Nrf2 signaling pathway, and transfection with Nrf2 siRNA abrogated the protection of RES against DON-induced cytotoxicity, accumulation of intracellular ROS, and mitochondria-dependent apoptosis. Collectively, RES protects IPEC-J2 cells against DON-induced damage at least partly via the Nrf2 signaling pathway.