In the present study, we observed the expression of toll-like receptor 4 (TLR4) and its downstream signal pathway in peripheral blood monocytes (PBMs) from patients with acute cerebral infarct (ACI). The expression of TLR4 and MyD88 by PBMs was determined by flow cytometry and reverse transcriptase-polymerase chain reaction, and nuclear factor-jB (NF-jB) activity was detected by electrophoretic mobility shift assay. Ischemia/reperfusion injury-induced cerebral edema, infarction area, and neurologic impairment scores were determined in MyD88 gene knockout mice. The results indicated a significant increase in circulating TLR4+ monocytes in ACI patients as compared with the control group and the transient ischemia attack (TIA) group. This change paralleled an elevation in TLR4mRNA transcription and serum tumor necrosis factor-a (TNF-a) and interleukin (IL)-6 in the ACI and TIA groups. Correlation analysis showed TLR4 expression to significantly correlate with cytokine levels and stroke severity. MyD88mRNA differed insignificantly among the three groups. Compared with wild-type mice, 6 h of cerebral ischemia followed by 24 h of reperfusion did not significantly change cerebral edema, cerebral infarction area, and neurologic impairment scores in MyD88 gene knockout mice. Compared with the control group, serum heat shock protein (HSP) 60 increased significantly in the ACI and TIA groups, leading to NF-jB activation in TLR4/CD14-transfected HEK293 cells. It is suggested that upregulated TLR4 expression on PMBs may act as one of the peripheral mechanisms of inflammatory injury after ACI. Moreover, circulating HSP60 may be a ligand for TLR4, which is involved in the peripheral mechanism of inflammatory injury after ACI, possibly through an MyD88-independent signal pathway.

1. The present study was conducted to investigate the effects of dietary glutamine (Gln) supplementation on growth performance, carcase characteristics and meat quality in broilers exposed to high ambient temperature. 2. A total of 240 35-d-old male Arbor Acres broilers were randomly assigned to 4 treatment groups (three replicates of 20 birds per cage). The broilers were kept in a temperature-controlled room at either 23 degrees C (no-stress groups, NS) or 28 degrees C (heat stress groups, HS). The broilers were fed either on a basal diet (control, NS) or on the basal diet supplemented with 0, 0.5 or 1.0% Gln (HS). 3. Compared with the NS, the HS (0% Gln) group gained less weight and consumed less feed, had lower final body weight, gain-to-feed ratio, and abdominal fat yield. Breast meat in HS (0% Gln) had lower pH, water-holding capacity (WHC), a* value, ether extract (EE) content and crude protein (CP) content, and had higher shear force (SF) and L* value. 4. Linear increase were found in groups supplemented with Gln (0, 0.5% and 1.0%) for final body weight, weight gain, feed consumption, gain-to-feed ratio and abdominal fat yield. Supplementation with Gln improved breast meat pH, WHC, SF, L* value, a* value, EE content and CP content in broilers exposed to heat stress. No significant difference was observed in all the indices determined between the HS (1% Gln) and the NS. 5. Heat stress caused obvious breast meat discoloration in L*, a* and b* values. However, dietary supplementation with Gln gave a better colour stability. 6. The results indicated that dietary supplementation with Gln may alleviate heat stress-caused deterioration in growth performance, carcase characteristics, meat quality and meat colour stability of broilers.

Previous studies have indicated that there are 3 common haplotypes composed of the -1470, -511, and -31 loci in the interleukin 1beta (IL-1beta) promoter in the Chinese population. The purpose of this study was to investigate the relationship between these haplotypes and lipopolysaccharide (LPS)-stimulated IL-1beta expression by whole blood leukocytes in vitro and to evaluate the effects of these haplotypes on IL-1beta gene transcription. Genomic DNAs were obtained from 105 healthy subjects. The genotypes at the 3 sites of the IL-1beta promoter were determined by restriction fragment length polymorphism analysis. Haplotype frequency was evaluated by using the Arlequin software. Plasma IL-1beta level was measured by enzyme-linked immunosorbent assay. The transcriptional activity of the haplotypes was determined by in vitro reporter gene. The results indicated that after the exposure to LPS, whole blood leukocytes from subjects with the homozygous haplotype -1470G, -511C, and -31T (G-C-T) produced more IL-1beta in vitro than those from subjects with haplotype -1470C, -511T, and -31C (C-T-C) and that the transcriptional activity of the haplotype G-C-T was also higher than that of the haplotype C-T-C. It is suggested that the haplotypes of the IL-1beta promoter influence the expression and transcriptional activity of the IL-1beta gene and that the upregulation of IL-1beta gene expression after LPS exposure in subjects with haplotype G-C-T may be due to an increased transcriptional activity of the haplotype.

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