The objective of this study was to evaluate the effects of low ambient temperature (LAT) and dietary vitamin C (VC) supplementation on pulmonary vascular remodeling (PVR) and the relative expression of hypoxia inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF) and its receptor 2 (VEGFR-2) mRNA of lungs in 21-d-old broilers. 400 1-d-old male Cobb broilers were assigned randomly to 4 treatments as follows for 21 d: 1) LAT and a basal diet; 2) LAT and a basal diet supplemented with 1 000 mg kg–1 VC (LAT+VC); 3) normal ambient temperature (NAT) and a basal diet; 4) NAT and a basal diet supplemented with 1 000 mg kg–1 VC (NAT+VC). Each treatment was composed of 10 replicates of 10 birds per replicate. Samples of lung were collected after the broilers were killed at d 21. LAT increased the ratio of vessel wall area to vessel total area (WA/TA, %) and mean media thickness in pulmonary arterioles (mMTPA, %) (P<0.05). Dietary VC supplementation decreased mMTPA (P<0.05), but had no effect on the WA/TA. LAT increased (P<0.05) the relative mRNA expression of HIF-1α, VEGF and VEGFR-2, while adding VC to the diet could decrease (P<0.05) their relative mRNA expression. A significant positive correlation existed between the level of VEGF mRNA expression and the value of WA/WT (P<0.05) or mMTPA (P<0.05). These results suggested LAT resulted in pulmonary vascular remodeling, and the increase of HIF-1α, VEGF and VEGFR-2 mRNA expression, and dietary VC supplementation can alleviate pulmonary vascular remodeling in broiler by affecting these gene expression.

The β-1,3-glucan from yeast has been extensively examined for its immuno-enhancing effects in animals. However, investigation on the relationship among β-glucan, gut microbiota and immune-modulating effects remains limited particularly in pigs. Considering the critical roles of gut methanogens in the microbial fermentation, energy metabolism and disease resistance, we investigated the phylogenetic diversity of methanogens from fermented cultures of porcine colonic digesta with (G) or without (N) yeast β-glucan based on sequences of the archaeal 16S rRNA gene. A total of 145 sequences in the G library were assigned into 8 operational taxonomic units (OTUs) with the majority of sequences (114/145) related to strains Methanobrevibacter millerae or Methanobrevibacter gottschalkii with high identities ranging from 97.9 to 98.6%, followed by 23 sequences to Methanobrevibacter ruminantium, 2 sequences to Methanobrevibacter smithii and one sequence to Methanobrevibacter wolinii. The 142 sequences in the N library were assigned to 2 OTUs with most sequences (127/142) related to strains M. millerae or M. gottschalkii with sequence identities ranging from 97.9 to 98.5%, and 15 sequences related to M. gottschalkii with 97.9% identity. Shannon diversity index showed that the G library exhibited significantly higher archaeal diversity (P<0.05) and Libshuff analysis indicated the differences in the community structure between the two libraries were significant (P<0.0001). In conclusion, the current study provides evidence that addition of yeast β-glucan significantly increased the diversity of methanogens in in vitro fermented porcine colonic digesta.

To investigate the tissue deposition and elimination of melamine (MEL) in broilers, a total of 1 920 commercial 1-d-old male Cobb broilers were randomly allotted to 6 treatments with diets contaminated by MEL at 0, 2, 10, 30, 50, 100 mg kg-1 of diet for 42 d, and followed MEL withdrawal from diet at 50 or 100 mg kg-1 of diet for 96 h. The MEL was found in residue of plasma, liver, kidney, breast, and leg muscle with the highest level in kidney and in dose response manner (except in kidney), but no time response (except in plasma). The MEL residue in organ tissue was below the safe level of 50 μg mL-1 in blood or 50 μg kg-1 in tissues proposed by the US FSIS when MEL in diet was lower (2 mg kg-1). The MEL in tissues was eliminated by withdrawal MEL from diets. The elimination half-life of MEL was from 3.2 to 6.6 h, and the clearance time, when MEL residue concentration under limit detection, was from 18.0 to 31.4 h.