The aim of the present study was to optimize trypsin inhibitor degradation in soybean meal by solid-state fermentation （SSF） with Lactobacillus brevis and Aspergillus oryzae, and to determine the effect of SSF on ph...The aim of the present study was to optimize trypsin inhibitor degradation in soybean meal by solid-state fermentation （SSF） with Lactobacillus brevis and Aspergillus oryzae, and to determine the effect of SSF on phytic acid, crude protein, crude fat, and amino acid profile. Response surface methodology （RSM） with Box-Behnken design was used to optimize SSF. The optimal conditions derived from RSM for L. brevis fermentation were： pH=5. 1; inoculum size=10%; duration=72 h; substrate to water ratio=1.5. The minimum content of trypsin inhibitors was 6.4 mg g^-1 dry matter. The optimal conditions derived from RSM for A. oryzae fermentation were： substrate to water ratio= 0.8 1; inoculum size=4%; duration=120 h. The minimum content of trypsin inhibitors was 1.6 mg g^-1 dry matter. Both L. brevis and A. oryzae decreased trypsin inhibitors dramatically （57.1 and 89.2% respectively）. L. brevis fermentation did not affect phytic acid （0.4%） and crude fat （5.2%） considerably, whereas A. oryzae fermentation degraded phytic acid （34.8%） and crude fat （22.0%） contents to a certain extent. Crude protein content was increased after both fermentation （6.4 and 12.9% for L. brevis and A. oryzae respectively）. Urease activity was reduced greatly （83.3 and 58.3% for L. brevis and A. oryzae respectively）. In conclusion, SSF with A. oryzae and L. brevis reduced trypsin inhibitor content and modified major macronutrients in soybean meal.展开更多
目的研究兔胆道口括约肌(sphincter of Oddi,SO)平滑肌细胞在胆固醇脂质体作用后收缩性的变化,探讨高胆固醇血症兔SO 动力异常的机制方法取纯种新西兰兔 SO 段,用Ⅱ型胶原酶消化获得单个平滑肌细胞,与胆崮醇/卵磷脂摩尔比为2:1和0.5:1...目的研究兔胆道口括约肌(sphincter of Oddi,SO)平滑肌细胞在胆固醇脂质体作用后收缩性的变化,探讨高胆固醇血症兔SO 动力异常的机制方法取纯种新西兰兔 SO 段,用Ⅱ型胶原酶消化获得单个平滑肌细胞,与胆崮醇/卵磷脂摩尔比为2:1和0.5:1的胆固醇脂质体(1g/L)分别孵育2 h 后,用不同浓度 KCl(9-24)nmol/L,乙酰胆碱(10^(12)～10^(-6))mol/L 作用于平滑肌细胞,激动剂作用后30s,加入丙烯醛固定,分别测量各组细胞的收缩百分比.结果兔 SO 平滑肌细胞平均长度为(143.7±12.3)μm,经胆固醇脂质体作用后平均长度无明显变化,对 KCl 和乙酰胆碱呈浓度依赖性收缩.KCl(18mmol/L)诱导最大收缩比为22.2%±0.7%,而2:1的胆固醇脂质体作用后收缩比为16.5%±0.6%(P<0.01);乙酰胆碱(10^(-7)mol/L)诱导最大收缩比为20.3%±1.4%,2:1的胆固醇脂质体作用后收缩比为16.5%±1.3%(P<0.05).摩尔比为0.5:1胆固醇脂质体作用后最大收缩比分别为21.3%±1.4%和19.2%±1.1%,同对照组相比无显著下降.结论兔 SO 平滑肌细胞经摩尔比2:1的胆固醇脂质体后起收缩性下降,推测这是高胆固醇血症可以导致兔 SO 的动力异常的机制.展开更多
基金supported by a research project of the Science and Technology Key Group in Zhejiang Provincethe research projects from the Science and Technology Department of Zhejiang Province,China (2009C12068)
文摘The aim of the present study was to optimize trypsin inhibitor degradation in soybean meal by solid-state fermentation （SSF） with Lactobacillus brevis and Aspergillus oryzae, and to determine the effect of SSF on phytic acid, crude protein, crude fat, and amino acid profile. Response surface methodology （RSM） with Box-Behnken design was used to optimize SSF. The optimal conditions derived from RSM for L. brevis fermentation were： pH=5. 1; inoculum size=10%; duration=72 h; substrate to water ratio=1.5. The minimum content of trypsin inhibitors was 6.4 mg g^-1 dry matter. The optimal conditions derived from RSM for A. oryzae fermentation were： substrate to water ratio= 0.8 1; inoculum size=4%; duration=120 h. The minimum content of trypsin inhibitors was 1.6 mg g^-1 dry matter. Both L. brevis and A. oryzae decreased trypsin inhibitors dramatically （57.1 and 89.2% respectively）. L. brevis fermentation did not affect phytic acid （0.4%） and crude fat （5.2%） considerably, whereas A. oryzae fermentation degraded phytic acid （34.8%） and crude fat （22.0%） contents to a certain extent. Crude protein content was increased after both fermentation （6.4 and 12.9% for L. brevis and A. oryzae respectively）. Urease activity was reduced greatly （83.3 and 58.3% for L. brevis and A. oryzae respectively）. In conclusion, SSF with A. oryzae and L. brevis reduced trypsin inhibitor content and modified major macronutrients in soybean meal.
文摘目的研究乌司他丁对肝脏手术后炎症介质释放及氧化反应的影响,探讨其保护患者术后肝功能的机理。方法通过前瞻、随机、对照临床研究,将我院肝脏外科中心收治的肝切除患者30例分为治疗组和对照组,治疗组于手术当天和术后3 d静脉滴注乌司他丁;全部患者分别在术前及术后抽外周静脉血测定淋巴细胞亚群分类(CD4、CD8)、急性反应蛋白(CRP)水平以及白细胞介素-1(IL-1)和IL-6、肿瘤坏死因子(TNF-α)、一氧化氮合酶(iNOS)的基因表达。结果应用乌司他丁后,治疗组患者术后12 h TNF-α和iNOS均较对照组有明显下降(0．053±0．02和0．12±0．04 vs．0．084±0．01和0．21±0．02,P<0．05);IL-1的释放高峰被推后;但对CD4、CD8和CRP的变化却无明显作用。结论乌司他丁可能通过特异性抑制或调节某些促炎因子的水平来保护肝脏术后的肝功能;这种保护作用还可能同抗氧化作用有关。
文摘目的研究兔胆道口括约肌(sphincter of Oddi,SO)平滑肌细胞在胆固醇脂质体作用后收缩性的变化,探讨高胆固醇血症兔SO 动力异常的机制方法取纯种新西兰兔 SO 段,用Ⅱ型胶原酶消化获得单个平滑肌细胞,与胆崮醇/卵磷脂摩尔比为2:1和0.5:1的胆固醇脂质体(1g/L)分别孵育2 h 后,用不同浓度 KCl(9-24)nmol/L,乙酰胆碱(10^(12)～10^(-6))mol/L 作用于平滑肌细胞,激动剂作用后30s,加入丙烯醛固定,分别测量各组细胞的收缩百分比.结果兔 SO 平滑肌细胞平均长度为(143.7±12.3)μm,经胆固醇脂质体作用后平均长度无明显变化,对 KCl 和乙酰胆碱呈浓度依赖性收缩.KCl(18mmol/L)诱导最大收缩比为22.2%±0.7%,而2:1的胆固醇脂质体作用后收缩比为16.5%±0.6%(P<0.01);乙酰胆碱(10^(-7)mol/L)诱导最大收缩比为20.3%±1.4%,2:1的胆固醇脂质体作用后收缩比为16.5%±1.3%(P<0.05).摩尔比为0.5:1胆固醇脂质体作用后最大收缩比分别为21.3%±1.4%和19.2%±1.1%,同对照组相比无显著下降.结论兔 SO 平滑肌细胞经摩尔比2:1的胆固醇脂质体后起收缩性下降,推测这是高胆固醇血症可以导致兔 SO 的动力异常的机制.
