A 9-week feeding experiment was conducted to determine the dietary biotin requirement of Japanese seabass, Lateolabrax japonicus C. Six isonitrogenous and isoenergetic purified diets (Diets 1-6) containing 0, 0.01, 0.049, 0.247, 1.238 and 6.222 mg biotin kg )1 diet were fed twice daily to triplicate groups (30 fish per group) of fish (initial average weight 2.26 ± 0.03 g) in 18 fibreglass tanks (300 L) filled with 250 L of water in a flow-through system. Water flow rate through each tank was 2 L min )1 . Water temperature ranged from 25.0 to 28.0°C, salinity from 28.0 to 29.5 g L )1 , pH from 8.0 to 8.1 and dissolved oxygen content was approximately 7 mg L )1 during the experiment. After the feeding experiment, fish fed Diet 1 developed severe biotin deficiency syndromes characterized by anorexia, poor growth, dark skin colour, atrophy and high mortality. Significant lower survival (73.3%) was observed in the treatment of deficient biotin. The final weight and weight gain of fish significantly increased with increasing dietary biotin up to 0.049 mg kg )1 diet (P < 0.05), and then slightly decreased. Both feed efficiency ratio and protein efficiency ratio showed a very similar change pattern to that of weight gain. Dietary treatments did not significantly affect carcass crude protein, crude lipid, moisture and ash content. However, liver biotin concentration (0-6.1 lg g )1) significantly increased with the supplementation of dietary biotin (P < 0.05), and no tissue saturation was found within the supplementation scope of biotin. Broken-line regression analysis of weight gain showed that juvenile Japanese seabass require a minimum of 0.046 mg kg )1 biotin for maximal growth.
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The present study was undertaken to determine the effect of tetramethylpyrazine administered intraperitoneally on gastric lesions, gastric acid secretion, gastric barrier mucus secretion, and gastric contraction in reserpine-treated rats. The results of this study demonstrated that tetramethylpyrazine at doses of 0.5, 1, 10, and 20 mg/kg significantly inhibited the formation of gastric lesions induced by reserpine, with suppressive rates of 57.5%, 64.0%, 94.1%, and 96.0%, respectively. Tetramethylpyrazine (1 and 20 mg/kg) significantly prompted the secretion of gastric barrier mucus but had no effect on the secretion of gastric acid. Our findings also showed that tetramethylpyrazine (1 and 20 mg/kg) significantly suppressed the frequency of gastric contractions, but had no effect on the amplitude of gastric contraction. These results indicate that the protection of tetramethylpyrazine results, in part, from promoting gastric barrier mucus secretion and suppressing the frequency of gastric contraction, but not from suppressing the secretion of gastric acid and the amplitude of gastric contraction.
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