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1. The xylanase product used in this study was derived from a genetically modified isolate of Aspergillus niger. Two trials were conducted to investigate the effects of xylanase supplementation on growth, digestion, circulating hormone and metabolite levels, immune parameters and composition of the gut microflora in cockerels fed on wheat-based diets. 2. The experimental diets consisted of a wheat-based control diet supplemented with 0 or 0.1% enzyme preparation. The diets were fed between 7 and 21 d of age. 3. Enzyme supplementation improved growth and feed conversion efficiency. The addition of enzyme to wheat-based diet increased the apparent total digestibility of dry matter (DM), crude protein and fat. 4. Enzyme supplementation reduced the relative weight of digestive organs to a certain extent, but there was no significant difference. Enzyme supplementation reduced digesta viscosity in the jejunum. There was no significant difference between the two experimental groups in counts of lactobacillus and coliform bacteria in the caeca. 5. Enzyme supplementation increased the concentration of blood thyroxine (T(4)), insulin-like growth factor I (IGF-I) and insulin, reduced the concentrations of blood uric acid, but had no significant effect on the concentrations of blood glucose and triiodothyronine (T(3)). 6. Enzyme supplementation increased the relative weight of spleen of cockerels, serum antibody titres to Newcastle disease virus (NDV), lymphocyte proliferation in response to phytohaemagglutinin (PHA) and the natural killer (NK) cell activity. 7. It is concluded that supplementation with an enzyme preparation (xylanase), which hydrolyses non-starch polysaccharides can improve growth in cockerels fed on wheat-based diets. This improvement is achieved through enzyme effects on digestion, absorption, metabolism and immunity of cockerels.

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Background: Although inflammatory cell adhesion molecules (CAMs) and anti-inflammation factor Kruppel-like transcription factor (KLF) 4 have all been reported to be induced after cerebral ischemic stroke (CIS), the close temporal and spatial relationship between expressions of CAMs and KLF4 following CIS and whether and how CAMs and KLF-4 contribute to the development of CIS-induced vascular injury are still unclear. Methods: Here, we first examined the correlation between serum levels of CAMs/KLF4 and infarct volume in acute CIS patients. Then, we determined the relationship between CAMs and KLF4 in mice after focal cerebral ischemia. Finally, we investigated the mechanism of KLF4 in protecting against oxygen-glucose deprivation-induced brain endothelial cell injury.

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Dietary phytoestrogens have been implicated in infertility among ruminants and may relate to human breast cancer risk. Formononetin is an isoflavonoid phytoestrogen found in animal fodder and in certain human foodstuffs. To investigate a possible mechanism by which phytoestrogens might influence mammary carcinogenesis, this study examined the capacity of formononetin to stimulate mammary gland proliferation. Formononetin was administered to castrated female BALB/c mice by daily subcutaneous injection; then mammary gland proliferation and estrogen receptor expression were quantified, and plasma prolactin levels were measured. A preliminary dose-finding study demonstrated an estrogenic effect on vaginal cytology when formononetin was injected at 40 mg/kg sc. Peak plasma concentrations of 2.5 +/- 0.8 (SD) micrograms/ml at two hours and peak mammary tissue concentrations of 2.0 +/- 0.2 ng/mg tissue at four hours were noted after a single injection at this minimally bioactive dose. Among animals treated with formononetin at 40 mg/kg/day for five days, mammary gland proliferation was enhanced 3.3-fold over saline-treated controls and was comparable to that of animals treated with estradiol-17 beta at 1 microgram/kg/day for five days. Mammary tissue estrogen receptor expression was 2-fold higher among the formononetin-treated animals (P < 0.01 vs. saline-treated controls), and plasma prolactin concentrations were increased 1.7-fold (P < 0.001 vs. saline-treated controls). In subsequent in vitro binding studies, formononetin competitively bound murine mammary estrogen receptors, but with a relative binding affinity 15,000 times less potent than that of estradiol-17 beta. The results demonstrate an ability of formononetin to support mammary gland proliferation. However, the estrogenic potency of formononetin appears extremely weak compared with that of estradiol-17 beta and is roughly proportional to estrogen receptor-binding capacity.

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