AIM: Liver fibrosis is a common pathological process of chronic liver diseases. Activation of hepatic stellate cells(HSCs) is the key issue in the occurrence of liver fibrosis. In this study, we observed the inhibitor...AIM: Liver fibrosis is a common pathological process of chronic liver diseases. Activation of hepatic stellate cells(HSCs) is the key issue in the occurrence of liver fibrosis. In this study, we observed the inhibitory action of rat serum containing Biejiajian oral liquid (BOL), a decoction of turtle shell, on proliferation of rat HSCs, and to explore the antihepatofibrotic mechanisms of BOL.METHODS: A rat model of hepatic fibrosis was induced by subcutaneous injection of CC14. Serum containing low,medium and high dosages of BOL was prepared respectively.Normal and fibrotic HSCs were isolated and cultured. The effect of sera containing BOL on proliferation of HSCs was determined by 3H-TdR incorporation.RESULTS: The inhibitory rate of normal rat HSC proliferation caused by 100 mL/mL sera containing medium and high dosages of BOL showed a remarkable difference as compared with that caused by colchicine (medium dosage group:34.56±4.21% vs29.12±2.85%, P<0.01; high dosage group:37.82±1.32% vs29.12±2.85%, P<0.01). The inhibitory rate of fibrotic rat HSC proliferation caused by 100 mL/L serum containing medium and high dosages of BOL showed a remarkable difference as compared with that caused by colchicine (medium dosage group: 51.31_+3.14% vs 38.32_+2.65%,P<0.01; high dosage group: 60.15_+5.36% vs38.32_+2.65%,P<0.01). The inhibitory rate of normal rat HSC proliferation caused by 100 mL/L and 200 mL/L sera containing a medium dosage of BOL showed a significant difference as compared with that caused by 50 mL/L (100 mL/L group: 69.02±9.96%vs 50.82±9.28%, P<0.05; 200 mL/L group: 81.78±8.92%vs50.82±9.28%, P<0.01). The inhibitory rate of fibrotic rat HSC proliferation caused by 100 mL/L and 200 mL/L sera containing a medium dosage of BOL showed a significant difference as compared with that caused by 50 mL/L (100 mL/L group:72.19±10.96% vs 61.38±7.16%, P<0.05; 200 mL/L group:87.16±8.54% vs 61.38±7.16%, P<0.01).CONCLUSION: Rat serum containing BOL can inhibit proliferation of rat HSCs, and the inhibition depends 展开更多
为解决小麦粉加工过程追溯质量安全信息交叉、单位个体追溯困难等问题,该研究在分析小麦粉加工流程和追溯关键信息的基础上,研究基于批次清单的信息追溯方法,以加工时间为依据结合高津托图(Gozintograph)数据结构构建批次清单(bill of l...为解决小麦粉加工过程追溯质量安全信息交叉、单位个体追溯困难等问题,该研究在分析小麦粉加工流程和追溯关键信息的基础上,研究基于批次清单的信息追溯方法,以加工时间为依据结合高津托图(Gozintograph)数据结构构建批次清单(bill of lots,BOL),实现小麦粉产品信息和关键节点活动信息的精确追溯;在BOL的基础上,利用鱼骨图和Petri网分别描述小麦粉质量追溯点的位置和危害指标;结合山东某面粉厂实际生产参数对追溯模型进行验证,实现小麦粉产品与原料的批次关联和其质量危害传播路径的预测。分析结果表明,通过使用BOL和Petri网追溯模型与传统方法相比实现召回批次数量由7个减少到4个、危害因素查找数量由6个减少到5个。该研究提高了小麦粉追溯精度和缺陷召回效率,为粮食等小颗粒产品加工过程的追溯提供了理论支持。展开更多
Dear Friends,Our learning process is complicated.It takes many forms.Welearn from our family and from our friends.We learn from ourreadings and from our teachers.We learn from our experiences,and we learn from the exp...Dear Friends,Our learning process is complicated.It takes many forms.Welearn from our family and from our friends.We learn from ourreadings and from our teachers.We learn from our experiences,and we learn from the experiences of others.In my many years oflife,I have learned from all of these sources.In this column let me share with you a few of the"learnings"that I remember most at this moment.These are presented in nological order.They are merely bits of wisdom and how I interpretthem.展开更多
Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro- apoptosis member...Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro- apoptosis members that regulate apoptosis, mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events. However, death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly, bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins. Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated Bid is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.展开更多
Apoptosis manifests in two major execution programs downstream of the death signal: the caspase pathway and organelle dysfunction. An important antiapoptosis factor, Bcl-2 protein, contributes in caspase pathway of ap...Apoptosis manifests in two major execution programs downstream of the death signal: the caspase pathway and organelle dysfunction. An important antiapoptosis factor, Bcl-2 protein, contributes in caspase pathway of apoptosis. Calcium, an important intracellular signal element in cells, is also observed to have changes during apoptosis, which maybe affected by Bcl-2 protein. We have previously reported that in Harringtonine (HT) induced apoptosis of HL-60 cells, there’s a change of intracellular calcium distribution, moving from cytoplast especially Golgi’s apparatus to nucleus and accumulating there with the highest concentration. We report here that caspase-3 becomes activated in HT-induced apoptosis of HL-60 cells, which can be inhibited by overexpression of Bcl-2 protein. No sign of apoptosis or intracellular calcium movement from Golgi’s apparatus to nucleus in HL-60 cells overexpressing Bcl-2 or treated with Ac-DEVD-CHO, a specific inhibitor of caspase-3. The results indicate that activated caspase-3 can promote the movement of intracellular calcium from Golgi’s apparatus to nucleus, and the process is inhibited by Ac-DEVD-CHO (inhibitor of caspase-3), and that Bcl-2 can inhibit the movement and accumulation of intracellular calcium in nucleus through its inhibition on caspase3. Calcium relocalization in apoptosis seems to be irreversible, which is different from the intracellular calcium changes caused by growth factor.展开更多
基金Supported by the Natural Science Foundation of Zhejiang Province,No.398402
文摘AIM: Liver fibrosis is a common pathological process of chronic liver diseases. Activation of hepatic stellate cells(HSCs) is the key issue in the occurrence of liver fibrosis. In this study, we observed the inhibitory action of rat serum containing Biejiajian oral liquid (BOL), a decoction of turtle shell, on proliferation of rat HSCs, and to explore the antihepatofibrotic mechanisms of BOL.METHODS: A rat model of hepatic fibrosis was induced by subcutaneous injection of CC14. Serum containing low,medium and high dosages of BOL was prepared respectively.Normal and fibrotic HSCs were isolated and cultured. The effect of sera containing BOL on proliferation of HSCs was determined by 3H-TdR incorporation.RESULTS: The inhibitory rate of normal rat HSC proliferation caused by 100 mL/mL sera containing medium and high dosages of BOL showed a remarkable difference as compared with that caused by colchicine (medium dosage group:34.56±4.21% vs29.12±2.85%, P<0.01; high dosage group:37.82±1.32% vs29.12±2.85%, P<0.01). The inhibitory rate of fibrotic rat HSC proliferation caused by 100 mL/L serum containing medium and high dosages of BOL showed a remarkable difference as compared with that caused by colchicine (medium dosage group: 51.31_+3.14% vs 38.32_+2.65%,P<0.01; high dosage group: 60.15_+5.36% vs38.32_+2.65%,P<0.01). The inhibitory rate of normal rat HSC proliferation caused by 100 mL/L and 200 mL/L sera containing a medium dosage of BOL showed a significant difference as compared with that caused by 50 mL/L (100 mL/L group: 69.02±9.96%vs 50.82±9.28%, P<0.05; 200 mL/L group: 81.78±8.92%vs50.82±9.28%, P<0.01). The inhibitory rate of fibrotic rat HSC proliferation caused by 100 mL/L and 200 mL/L sera containing a medium dosage of BOL showed a significant difference as compared with that caused by 50 mL/L (100 mL/L group:72.19±10.96% vs 61.38±7.16%, P<0.05; 200 mL/L group:87.16±8.54% vs 61.38±7.16%, P<0.01).CONCLUSION: Rat serum containing BOL can inhibit proliferation of rat HSCs, and the inhibition depends
文摘为解决小麦粉加工过程追溯质量安全信息交叉、单位个体追溯困难等问题,该研究在分析小麦粉加工流程和追溯关键信息的基础上,研究基于批次清单的信息追溯方法,以加工时间为依据结合高津托图(Gozintograph)数据结构构建批次清单(bill of lots,BOL),实现小麦粉产品信息和关键节点活动信息的精确追溯;在BOL的基础上,利用鱼骨图和Petri网分别描述小麦粉质量追溯点的位置和危害指标;结合山东某面粉厂实际生产参数对追溯模型进行验证,实现小麦粉产品与原料的批次关联和其质量危害传播路径的预测。分析结果表明,通过使用BOL和Petri网追溯模型与传统方法相比实现召回批次数量由7个减少到4个、危害因素查找数量由6个减少到5个。该研究提高了小麦粉追溯精度和缺陷召回效率,为粮食等小颗粒产品加工过程的追溯提供了理论支持。
文摘Dear Friends,Our learning process is complicated.It takes many forms.Welearn from our family and from our friends.We learn from ourreadings and from our teachers.We learn from our experiences,and we learn from the experiences of others.In my many years oflife,I have learned from all of these sources.In this column let me share with you a few of the"learnings"that I remember most at this moment.These are presented in nological order.They are merely bits of wisdom and how I interpretthem.
文摘Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro- apoptosis members that regulate apoptosis, mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events. However, death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly, bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins. Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated Bid is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.
基金the National Natural Science Foundation of China(Grant No. 39730160).
文摘Apoptosis manifests in two major execution programs downstream of the death signal: the caspase pathway and organelle dysfunction. An important antiapoptosis factor, Bcl-2 protein, contributes in caspase pathway of apoptosis. Calcium, an important intracellular signal element in cells, is also observed to have changes during apoptosis, which maybe affected by Bcl-2 protein. We have previously reported that in Harringtonine (HT) induced apoptosis of HL-60 cells, there’s a change of intracellular calcium distribution, moving from cytoplast especially Golgi’s apparatus to nucleus and accumulating there with the highest concentration. We report here that caspase-3 becomes activated in HT-induced apoptosis of HL-60 cells, which can be inhibited by overexpression of Bcl-2 protein. No sign of apoptosis or intracellular calcium movement from Golgi’s apparatus to nucleus in HL-60 cells overexpressing Bcl-2 or treated with Ac-DEVD-CHO, a specific inhibitor of caspase-3. The results indicate that activated caspase-3 can promote the movement of intracellular calcium from Golgi’s apparatus to nucleus, and the process is inhibited by Ac-DEVD-CHO (inhibitor of caspase-3), and that Bcl-2 can inhibit the movement and accumulation of intracellular calcium in nucleus through its inhibition on caspase3. Calcium relocalization in apoptosis seems to be irreversible, which is different from the intracellular calcium changes caused by growth factor.
