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Effect of IL-4 on altered expression of complement activation regulators in rat pancreatic cells during severe acute pancreatitis 被引量:14
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作者 Cheng Zhang Chun-Lin Ge Ren-Xuan Guo San-Guang He 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第43期6770-6774,共5页
AIM: To investigate the effect of IL-4 on the altered expression of complement activation regulators in pancreas and pancreatic necrosis during experimental severe acute pancreatitis (SAP). METHODS: SAP model of r... AIM: To investigate the effect of IL-4 on the altered expression of complement activation regulators in pancreas and pancreatic necrosis during experimental severe acute pancreatitis (SAP). METHODS: SAP model of rats was established by retrograde injection of 5% sodium taurocholate (1 mL/kg) into the pancreatic duct. We immunohistochemically assayed the expression of three complement activation regulators: decay accelerating factor (DAF; CD55), 20 ku homologous restriction factor (HRF20; CD59) and membrane cofactor protein (MCP; CEH6), in the pancreatic acinar cells of rats at 0, 3, 6, 12, and 24 h after the induction of SAP model. Meanwhile the levels of amylase and lipase were determined, and morphological examination was performed. Then, 61 rats were randomly divided into three groups. Group A (n = 21) received no treatment after the SAP model was established; group B (n = 20) was given IL-4 (8 IJg/animal) intraperitoneally 0.5 h before the SAP model was established; group C (n = 20) was given IL-4 (8 μg/animal) intraperitoneaUy 0.5 h after the SAP model was established. Plasma amylase and lipase, extent of pancreatic necrosis and expression of complement activation regulators were investigated 6 h after the induction of SAP model. RESULTS: Three complement activation regulators were all expressed in pancreatic acinar cells. MCP was not found on the basolateral surface as reported. Contrary to the gradually increasing plasma level of amylase and lipase, expression of complement activation regulators decreased after SAP model was set up. At the same time, the severity of pancreatic necrosis was enhanced. A strong negative correlation was found between the expression of MCP, DAF, CD59 in pancreatic acinar cells and the severity of pancreatic necrosis (r = -0.748, -0.827, -0.723; P〈0.01). In the second series of experiments, no matter when the treatment of IL-4 was given (before or after the induction of SAP model), the serum level of amylase or lipase was decreased and the extent of pancreatic necrosis was ameliorated significantly. Compared to SAP control group, the expression of DAF and CD59 in pancreas was reinforced when IL-4 was given before the induction of SAP model (P〈0.01, P〈0.05), but the expression of MCP was not influenced (P〉0.05). The expression of DAF was enhanced, when IL-4 was given after the induction of SAP model (P〈0.05), but the expression of CD59 and MCP did not change (P〉0.05). CONCLUSION: Complement activation regulators may participate in the pathogenesis of pancreatic inflammation. Downregulation of complement activation regulators expression may be one of the causes of pancreatic necrosis. IL-4 treatment may control SAP aggravation by enhancing expression of DAF and CD59 in pancreas and decreasing pancreatic necrosis. Moreover, DAF and CD59 may play an important role in the regulation of complement activation regulators during SAP. 展开更多
关键词 Severe acute pancreatitis complement activation regulators INTERLEUKIN-4
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面向电网最大频率偏差的风电机组短时频率支撑最优策略与机理 被引量:3
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作者 李阳 李群 +2 位作者 陈载宇 殷明慧 邹云 《中国电机工程学报》 EI CSCD 北大核心 2024年第3期1020-1034,I0014,共16页
当电网出现有功缺额并导致频率跌落时,风电机组可以通过释放自身轴系动能为电网提供短时频率支撑(short-term frequency support,STFS)。如何利用有限的风电机组轴系动能最大限度地支撑电网频率,是当前研究的热点问题。针对风电机组可... 当电网出现有功缺额并导致频率跌落时,风电机组可以通过释放自身轴系动能为电网提供短时频率支撑(short-term frequency support,STFS)。如何利用有限的风电机组轴系动能最大限度地支撑电网频率,是当前研究的热点问题。针对风电机组可释放动能和电网频率变化率约束下的电网最大频率偏差最小化问题,该文提出一种基于有功功率互补控制(active-power complementation control,ACC)的风电机组STFS策略,揭示STFS过程中风电机组的最小动能释放机理,并证明采用ACC释放全部轴系动能的STFS策略为上述问题的最优解。最后,基于含风电的电网动模实验平台的实验结果验证该文提出STFS策略的可行性与频率支撑效果。 展开更多
关键词 风电机组 一次调频 短时频率支撑 轴系动能 有功功率互补控制
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衰变加速因子结构及其功能研究进展 被引量:3
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作者 周绪霞 李卫芬 +1 位作者 余颂东 许梓荣 《免疫学杂志》 CAS CSCD 北大核心 2003年第S1期110-113,117,共5页
衰变加速因子为体内补体调控蛋白家族中的一种重要的同源限制因子,它对于防止同源补体对自身组织细胞的溶破有重要意义,并参与机体多种病理生理过程,如肿瘤免疫、生殖免疫、微生物感染等。本文综述了DAF的结构及其功能研究进展,并指出... 衰变加速因子为体内补体调控蛋白家族中的一种重要的同源限制因子,它对于防止同源补体对自身组织细胞的溶破有重要意义,并参与机体多种病理生理过程,如肿瘤免疫、生殖免疫、微生物感染等。本文综述了DAF的结构及其功能研究进展,并指出了其在免疫学,尤其在异种器官移植方面的应用前景及存在的问题。 展开更多
关键词 衰变加速因子(DAF) rca 免疫调节因子 器官移植
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补体相关性肾病 被引量:1
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作者 杨柳 谢红浪 《肾脏病与透析肾移植杂志》 CAS CSCD 北大核心 2014年第5期482-485,490,共5页
补体级联反应是一种免疫防御机制,能够有效诱导细胞凋亡、增强细胞免疫。补体的过度活化或调节异常参与多种慢性肾脏病及移植排斥反应的发生发展。补体在肾组织内活化、沉积与肾脏病临床及病理特点密切相关,亦在移植肾缺血再灌注损伤、... 补体级联反应是一种免疫防御机制,能够有效诱导细胞凋亡、增强细胞免疫。补体的过度活化或调节异常参与多种慢性肾脏病及移植排斥反应的发生发展。补体在肾组织内活化、沉积与肾脏病临床及病理特点密切相关,亦在移植肾缺血再灌注损伤、细胞介导的排斥反应和抗体介导的排斥反应中发挥重要作用。近年来,针对补体的靶向性治疗已成肾脏病领域内新的研究热点,与肾脏病相关的抗补体治疗聚焦于抗C5单克隆抗体、C5受体拮抗剂、C1抑制剂和补体受体1等针对补体不同环节的药物。本文对补体相关性肾病及靶向抗补体治疗肾脏病的最新研究进展加以综述。 展开更多
关键词 补体活化 补体调节 肾脏病
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CR2-Crry预处理诱导神经干细胞在颅脑损伤中发挥神经保护作用
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作者 高谋 徐如祥 +1 位作者 董勤 郭莉丽 《中华脑科疾病与康复杂志(电子版)》 2021年第4期215-220,共6页
目的探讨CR2-Crry预处理诱导神经干细胞(iNSCs)对颅脑损伤的神经保护作用。方法18只雄性成年C57BL/6小鼠制备颅脑损伤模型,神经功能缺损评分(NSS)4-8分的小鼠为颅脑损伤组,按照随机数字表法分为:CR2-Crry预处理iNSCs(CR2-Crry-iNSCs)组(... 目的探讨CR2-Crry预处理诱导神经干细胞(iNSCs)对颅脑损伤的神经保护作用。方法18只雄性成年C57BL/6小鼠制备颅脑损伤模型,神经功能缺损评分(NSS)4-8分的小鼠为颅脑损伤组,按照随机数字表法分为:CR2-Crry预处理iNSCs(CR2-Crry-iNSCs)组(6只)、磷酸盐缓冲液(PBS)预处理iNSCs(PBS-iNSCs)组(6只)和PBS组(6只)。于颅脑损伤后12 h分别将1×106个CR2-Crry-iNSCs、PBS-iNSCs或等体积PBS经立体定向移植到颅脑损伤小鼠脑内。于颅脑损伤后14 d处死小鼠,制备脑组织冰冻切片,并行双重免疫荧光和原位末端标记(TUNEL)染色,观察CR2-Crry-iNSCs和PBS-iNSCs对颅脑损伤小鼠脑内Crry、NeuN和TUNEL阳性细胞数量的影响。结果双重免疫荧光染色:与PBS组比较,PBS-iNSCs组和CR2-Crry-iNSCs组颅脑损伤小鼠脑内Crry和NeuN双阳性的神经细胞数量明显增加,差异具有统计学意义(P<0.05)。此外,与PBS-iNSCs组比较,CR2-Crry-iNSCs组颅脑损伤小鼠脑内Crry和NeuN双阳性的神经细胞数量明显增加,差异具有统计学意义(P<0.05)。TUNEL染色:与PBS组比较,PBS-iNSCs组和CR2-Crry-iNSCs组颅脑损伤小鼠脑内TUNEL和NeuN双阳性的神经细胞数量明显下降,差异具有统计学意义(P<0.05)。此外,与PBS-iNSCs组比较,CR2-Crry-iNSCs组颅脑损伤小鼠脑内TUNEL和NeuN双阳性的神经细胞数量明显下降,差异具有统计学意义(P<0.05)。结论CR2-Crry预处理iNSCs移植可增加颅脑损伤小鼠脑内神经细胞Crry表达,减轻补体介导的神经损伤。 展开更多
关键词 颅脑损伤 诱导神经干细胞 补体活化 补体调节 移植
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