Water-treated maize stems were subjected to delignification with peroxymonosulfuric acid at 20 degrees C for 144 h, with peroxyformic acid at 80 degrees C for 6 h, with peracetic acid at 50 degrees C for 6 h, and with 2% hydrogen peroxide at 45 degrees C for 12 h at pH 1.5, 4.4, 9.5, 11.5, 12.0, and 12.6, respectively, which solubilized 47.1, 91.3, 33.3, 16.6, 15.9, 17.4, 86.2, 87.7, and 91. 3% of the original lignin, respectively. Substantial lignins were released during the treatment with peroxyformic acid and hydrogen peroxide at pH > or =11.5, whereas an insignificant effect on delignification was observed by using peroxymonosulfuric acid, peracetic acid, and hydrogen peroxide under acidic, natural, and weakly alkaline media conditions. The structures of the isolated lignin preparations were investigated by chemical analysis, gel permeation chromatography, and UV, FT-IR, and (13)C NMR spectroscopy.

ABSTRACT. Two hundred and forty one-day-old male broiler chickens (Ross-308) were fed corn-soybean basal diets with 0, 40, 80, or 160 mg/ kg of an acid protease preparation from 1 to 42 days of age, in order to investigate the effects of an exogenous enzyme on growth performance, pancreatic trypsin activity and mRNA expression. Average daily gain (ADG) was greatest in the 160-mg/kg treatment group at 1-21 days, which was significantly higher than that in the control. After 42 days, average daily feed intake (ADFI) and ADG had significantly increased in the 80-and 160-mg/kg treatments (P < 0.05), with the 80-mg/kg treatment group having the highest ADFI and ADG values. The feed conversion ratio was not affected. Dietary acid protease at 80 and 160 mg/kg significantly decreased trypsin activity in the pancreas (relative to the control group) by 35.71 and 47.29%, respectively (P < 0.05). After 42 days, trypsin mRNA expression in the pancreas had significantly decreased by 19.5% in the 80-mg/kg treatment group relative to the control (P < 0.05). After 21 and 42 days, the diet supplemented with 160 mg/kg acid protease significantly decreased pancreatic trypsin mRNA by 19.6 and 37.7%, respectively, compared to the control. There were no significant differences between the 40-mg/kg treatment group and the control. Our results suggest that the amount of acid protease in the diet significantly affects trypsin activity and mRNA expression in broilers.

Neo-intimal hyperplasia is one of the major causes of restenosis in which stromal cell-derived factor-1 (SDF-1α) and its receptor CXCR4 play an important role. In a rat common carotid artery balloon injury model, the number of CD34+CXCR4+ cells was significantly increased immediately after injury (p < 0.01), followed by a gradual decrease to baseline seven days after the injury. Furthermore, the plasma (SDF-1α) level was markedly elevated, and peaked 24 hours after injury (p < 0.01), followed by a rapid decrease to baseline level seven days after the injury. In the injured common carotid artery, the mRNA expression of (SDF-1α) was elevated immediately after injury, followed by a gradual decline, but that of CXCR4 was increased four days after injury.Immuno-histochemistry displayed CXCR4-positive staining one day after injury, which then gradually increased and continued for at least one month. In addition, administration of AMD3100 (200 ng/kg, i.p.), a CXCR4 antagonist, did not affect the number of CD34+CXCR4+ cells, the elevated level of plasma (SDF-1α) and expression of (SDF-1α) mRNA. The expression of CXCR4 mRNA and protein however was markedly decreased, and detectable CXCR4-positive cells occurred four days after injury, followed by a decreased intensity of staining. We also found that, three months after balloon injury, stenosis of the carotid artery intima in the group that received AMD3100 was significantly less than in the untreated group (p < 0.05). Therefore, (SDF-1α)/CXCR4 played a crucial role in the intimal hyperplasia, and restenosis may have be attenuated after inhibition of CD34+CXCR4+ cells in the intima.