替罗非班联合丁苯酞治疗超时间窗急性脑梗死患者对血清HO-1、NO、VEGF、Ang-1的影响

摘要 目的：探讨替罗非班联合丁苯酞治疗超时间窗急性脑梗死患者对血清血红素加氧酶-1（HO-1）、一氧化氮（NO）、血管生成素-1（Ang-1）、血管内皮生长因子（VEGF）的影响。方法：选择2018年1月到2020年1月在我院接受治疗的141例超时间窗急性脑梗死患者,采用随机数表法分为联合组（n=71）和单药组（n=70）。单药组给予丁苯酞治疗,联合组在单药组的基础上给予替罗非班治疗。比较两组临床疗效、HO-1、NO、VEGF、Ang-1、美国国立卫生研究院卒中量表（NIHSS）、Barthel指数（Barthel）、凝血酶时间(TT)、凝血酶原时间(PT)、纤维蛋白原（FIB）水平变化情况及药物并发症发生情况。结果：治疗后,两组总有效率比较差异显著（P<0.05）;治疗前,联合组和单药组血清HO-1、NO、VEGF、Ang-1比较无显著差异;治疗后联合组和单药组血清HO-1、NO、VEGF随着时间的推移而降低,且联合组均低于单药组,Ang-1随着时间的推移而升高,且联合组均高于单药组,差异显著（P<0.05）;治疗前,联合组和单药组NIHSS、Barthel比较无显著差异;治疗后联合组和单药组NIHSS随着时间的推移而降低,且联合组均低于单药组,Barthel随着时间的推移而升高,且联合组均高于单药组,差异显著（P<0.05）。结论：在超时间窗急性脑梗死患者中应用替罗非班联合丁苯酞效果显著,可能与其可有效改善血清HO-1、NO、VEGF、Ang-1水平有关,且不增加不良反应。     

丙戊酸钠联合奥卡西平治疗小儿癫痫的疗效及对患儿脑电图、认知功能和血清神经因子的影响

摘要 目的：评价丙戊酸钠联合奥卡西平治疗小儿癫痫的疗效及对患儿脑电图、认知功能和血清神经因子的影响。方法：选入2019年1月~2022年12月收治的癫痫患儿104例,根据治疗方法不同分为单药组（丙戊酸钠治疗）和联合组（丙戊酸钠+奥卡西平治疗）,各52例。评价两组的临床疗效、脑电图、认知功能、血清神经因子等指标,并进行统计比较。结果：联合组治疗后癫痫发作频率及每次持续时间显著低于单药组（P<0.05）,EEG显示痫样放电率、总异常亦明显低于单药组（P＜0.05）;联合组治疗总有效率94.23%,明显高于单药组的71.15%（P<0.05）;两组治疗后WISC-CR量表VIQ、PIQ和FIQ评分均较治疗前明显升高（P<0.05）,而联合组升高幅度更大,与单药组差异显著（P<0.05）;治疗前,两组血清BDNF、NSE和S-100β蛋白无明显差异（P＞0.05）,而治疗后,联合组血清BDNF水平明显高于单药组、NSE和S-100β水平显著低于单药组（P＜0.05）;两组不良反应总发生率无差异（P＞0.05）。结论：丙戊酸钠联合奥卡西平治疗小儿癫痫疗效较好,可有效缓解临床症状,控制脑部异常放电,改善认知功能,调节血清神经因子水平,且安全性良好。     

罗沙司他治疗肾性贫血的效果观察及对TSAT、Cys C及NOX2的作用分析

摘要 目的：探讨罗沙司他治疗肾性贫血的效果观察及对转铁蛋白饱和度（TSAT）、胱抑素C（Cys C）及NADPH氧化酶2（NOX2）的作用。方法：选择2019年12月到2020年12月在我院接受治疗的125例肾性贫血患者,采用随机数表法分为试验组（n=63）和对照组（n=62）。对照组给予重组人促红素治疗,试验组给予罗沙司他治疗。比较两组临床疗效、TSAT、Cys C、NOX2、红细胞计数（RBC）、血红蛋白（Hb）、血细胞比容（Hct）、铁蛋白（SF）、转铁蛋白（TRF）及铁调素（Hepc）水平变化情况及药物不良反应发生情况。结果：治疗后,两组总有效率比较差异显著（P<0.05）;治疗前,试验组和对照组血清TSAT、Cys C及NOX2比较无显著差异;治疗后,试验组和对照组血清TSAT随着时间的推移而升高,且试验组高于对照组,Cys C及NOX2随着时间的推移而升减降低,且试验组低于对照组,差异显著（P<0.05）;治疗前,试验组和对照组RBC、Hb、Hct检验结果比较无显著差异;治疗后,试验组和对照组RBC、Hb、Hct均随着时间的推移而升高,且试验组高于对照组,差异显著（P<0.05）;治疗前,试验组和对照组SF、TRF及Hepc检验结果比较无显著差异;治疗后,试验组和对照组血清SF、TRF均随着时间的推移而升高,且试验组高于对照组,Hepc随着时间的推移而下降,且试验组低于对照组,差异显著（P<0.05）;两组不良反应总发生率分别为4.76%、8.06%（P>0.05）。结论：在肾性贫血患者中应用罗沙司他效果显著,可能与其可有效改善血清TSAT、Cys C及NOX2水平有关,且不增加不良反应。     

硫酸镁联合小剂量阿司匹林治疗子痫前期效果及子宫动脉血流、胎盘VEGF、MMP-9表达影响研究

摘要 目的：探讨硫酸镁联合小剂量阿司匹林治疗子痫前期效果及子宫动脉血流、胎盘血管内皮生长因子（VEGF）、基质金属蛋白酶-9（MMP-9）表达影响研究。方法：选择2019年6月-2021年1月在我院接受治疗的125例子痫前期患者,采用随机数表法分为试验组（n=63）和对照组（n=62）。对照组给硫酸镁治疗,试验组在对照组的基础上联合小剂量阿司匹林治疗。比较两组临床疗效、子宫动脉血流、胎盘VEGF、MMP-9、血压水平变化情况及妊娠不良结局发生情况。结果：治疗后,两组总有效率比较差异显著（P<0.05）;治疗前,试验组和对照组子宫动脉指标水平比较无显著差异;治疗后,试验组和对照组RI、PI及S/D水平均随着时间的推移而升高,且试验组均高于对照组,差异显著（P<0.05）;治疗前,试验组和对照组胎盘VEGF、MMP-9水平比较无显著差异;治疗后,试验组和对照组胎盘VEGF、MMP-9水平均随着时间的推移而升高,且试验组均高于对照组,差异显著（P<0.05）;治疗前,试验组和对照组血压水平比较无显著差异;治疗后,试验组和对照组血压水平均随着时间的推移而降低,且试验组均低于对照组,差异显著（P<0.05）;试验组胎儿窘迫、宫缩乏力及新生儿窒息发生率均显著低于对照组,差异显著（P<0.05）。结论：在子痫前期中应用硫酸镁联合小剂量阿司匹林治疗疗效显著,可有效改善患者子宫动脉血流、胎盘VEGF、MMP-9水平。     

不同营养支持对急性重症胰腺炎的效果对比及对血清钙离子、hs-CRP、AMS、PCT的影响

摘要 目的：探讨不同营养支持对急性重症胰腺炎的效果对比及对血清钙离子、超敏C反应蛋白（hs-CRP）、淀粉酶（AMS）、降钙素原（PCT）的影响。方法：选择2015年1月到2020年12月在我院接受治疗的131例急性重症胰腺炎患者,采用随机数表法分为试验组（n=66）和对照组（n=65）。对照组给予肠外营养支持治疗,试验组给予肠内营养支持治疗。比较两组临床疗效、钙离子、hs-CRP、AMS、PCT、D-乳酸、二胺氧化酶（DAO）、内毒素、临床症状改善情况及不良反应发生情况。结果：治疗后,两组总有效率比较差异显著（P<0.05）;治疗前,试验组和对照组血清抑钙离子、hs-CRP、AMS、PCT比较无显著差异;治疗后,试验组和对照组血清hs-CRP、AMS、PCT随着时间的推移而降低,且试验组均低于对照组,血清钙离子随着时间的推移而升高,且试验组高于对照组,差异显著（P<0.05）;治疗前,试验组和对照组血清D-乳酸、DAO、内毒素比较无显著差异;治疗后试验组和对照组血清D-乳酸、DAO、内毒素随着时间的推移而降低,且试验组均低于对照组,差异显著（P<0.05）;试验组腹痛缓解、肠鸣音恢复、血淀粉酶恢复及尿淀粉酶恢复时间均显著低于对照组,差异显著（P<0.05）;两组不良反应总发生率分别为9.09%、15.38%（P>0.05）。结论：在急性重症胰腺炎患者中应用肠内营养支持效果显著,可有效改善血清钙离子、hs-CRP、AMS、PCT水平,且不良反应较低。     

医用保湿霜对湿疹患者皮肤屏障、皮损状况及炎症因子的影响

摘要 目的：探究医用护肤品对湿疹患者皮肤屏障损伤、免疫指标和血清因子的影响。方法：选取2020年12月~2021年3月来我院皮肤科就诊治疗的115例慢性湿疹的患者,按照其治疗不同分为单药组（n=66）与联合组（n=49）,其中单药组外涂糠酸莫米松乳膏,联合组外涂糠酸莫米松乳膏加用护肤品（保湿霜）。观察并记录治疗前后两组患者血清白细胞介素（IL）-2、IL-4、IL-5、Th细胞群、IgE水平及嗜酸性粒细胞（EOS）数目变化。对比两组患者湿疹病情严重程度评分差异。分析两组患者皮肤屏障功能[经表皮水分流失（TEWL）、皮肤油脂（SC）和角质层含水量（WCSC）]差异,并对比两组患者的临床疗效。结果：治疗后,联合组总有效率显著高于单药组（P<0.05）。两组患者血清IL-2水平与治疗前相比明显升高,而IL-4、IL-5水平显著降低,且联合组较单药组变化更为明显（P<0.05）。两组患者Th1、Th2与治疗前相比均显著下降,但联合组Th1/Th2比值较单药组显著升高（P<0.05）。两组患者外周血IgE、EOS与治疗前相比明显降低,且联合组更为明显（P<0.05）。两组患者瘙痒、皮损面积评分及EASI评分与治疗前相比下降明显,且联合组优于单药组（P<0.05）。两组患者TEWL指标与治疗前相比明显降低,而WCSC和SC指标显著升高,且联合组较单药组变化更为明显（P<0.05）。治疗后,两组患者皮损处TLR4,MyD88及NF-κB mRNA表达量与治疗前相比明显降低,且联合组更为明显,差异均有统计学意义（P<0.05）。结论：糠酸莫米松乳膏联合医用护肤品能够修复湿疹患者皮肤屏障损伤,调节免疫指标和血清因子的变化,改善湿疹患者临床症状。其机制可能与抑制TLR4/MyD88/NF-κB信号通路有关。     

系统性红斑狼疮患者血小板参数、血脂、补体C3、C4水平与病情活动度的关系分析

摘要 目的：研究系统性红斑狼疮（SLE）患者血小板参数、血脂、补体C3、C4水平与病情活动度的关系。方法：将从2011年1月～2018年1月我院收治的100例SLE患者纳入研究,将其按照SEL疾病活动指数（SLEDAI）评分的不同分成活动组（SLEDAI评分≥10分）36例,非活动组（SLEDAI评分<10分）64例,另取同期于我院进行体检的健康志愿者100例作为对照组。比较三组各项血小板参数、血脂指标以及补体C3、C4水平,采用Pearson相关性分析SLE患者SLEDAI评分与各项指标的相关性。结果：活动组、非活动组血小板计数（PLT）、血小板压积、大血小板百分率低于对照组,且活动组PLT、大血小板百分率低于非活动组（P<0.05）。活动组、非活动组血小板平均容积（MPV）、血小板体积分布宽度（PDW）高于对照组,且活动组高于非活动组（P<0.05）。活动组、非活动组低密度脂蛋白胆固醇（LDL-C）均高于对照组,高密度脂蛋白胆固醇（HDL-C）均低于对照组（P<0.05）,活动组HDL-C低于非活动组（P<0.05）。活动组、非活动组补体C3、C4水平均低于对照组,且活动组补体C3、C4水平均低于非活动组（P<0.05）。经Pearson相关性分析发现：SLE患者SLEDAI评分与PLT、大血小板百分率、HDL-C以及补体C3、C4水平呈负相关,与MPV、PDW呈正相关（P<0.05）。结论：SLE患者血小板参数PLT、大血小板百分率、血脂指标HDL-C以及补体C3、C4水平与SLEDAI评分密切相关,可能作为SLE患者疾病活动性的评估指标。     

西比灵联合NGF对脑出血患者的NIHSS、ADL评分及血肿体积改善效果

摘要 目的：研究西比灵联合神经生长因子(NGF)对脑出血患者的NIHSS、ADL评分及血肿体积影响。方法：研究对象选取我院2015年9月到2016年10月间收治的脑出血98例,采用随机数字法分为2组,每组各49例。对照组接受常规基础性治疗,在此基础上,研究组患者口服西比灵联合肌肉注射NGF治疗。比较两组患者的治疗总有效率,同时比较血肿、水肿带体积、神经功能缺损量表(NIHSS)、日常生活能力量表(ADL)评分、神经源性营养因子（BDNF）、单核细胞趋化蛋白-1（MCP-1）、神经元特异性烯醇化酶（NSE）水平变化情况及不良反应发生情况。结果：治疗后,两组总有效率比较差异显著（P<0.05）;治疗前,研究组和对照组血肿体积、水肿带体积比较无显著差异;治疗后,研究组和对照组血肿体积、水肿带体积随着时间的推移而降低,且研究组均低于对照组,差异显著（P<0.05）;治疗前,研究组和对照组NIHSS、ADL评分比较无显著差异;治疗后,研究组和对照组NIHSS随着时间的推移而降低,且研究组均低于对照组,ADL评分随着时间的推移而升高,且研究组高于对照组,差异显著（P<0.05）;治疗前,研究组和对照组BDNF、MCP-1、NSE比较无显著差异;治疗后,研究组和对照组MCP-1、NSE随着时间的推移而降低,且研究组均低于对照组,BDNF随着时间的推移而升高,且研究组高于对照组,差异显著（P<0.05）;两组不良反应比较无效显著差异（P>0.05）。结论：脑出血患者应用西比灵联合NGF效果可靠,可明显减少继发性损伤,且治疗安全性较高,值得在临床推广。     

桂枝芍药知母汤联合甲氨蝶呤对类风湿性关节炎患者中医证候评分、血清炎性因子及免疫球蛋白的影响

摘要 目的：探讨桂枝芍药知母汤联合甲氨蝶呤对类风湿性关节炎（RA）患者血清炎性因子、中医证候评分及免疫球蛋白的影响。方法：选取2018年1月~2019年10月期间我院接收的RA患者136例。根据随机数字表法分为对照组（n=68）和研究组（n=68）。对照组给予甲氨蝶呤治疗，研究组在对照组基础上联合桂枝芍药知母汤治疗。比较两组患者的疗效、中医证候评分、血清炎性因子[肿瘤坏死因子-α（TNF-α）、白介素-17（IL-17）、白介素-1β（IL-1β）]水平、风湿四项检查指标[类风湿因子（RF）、C反应蛋白（CRP）、抗链球菌溶血素"O"(ASO)、血沉（ESR）]水平及免疫球蛋白[免疫球蛋白A（IgA）、免疫球蛋白G（IgG）、免疫球蛋白M（IgM）]水平。结果：研究组治疗2个月后的临床总有效率91.18%（62/68）高于对照组的77.94%（53/68）（P<0.05）。两组治疗2个月后关节肿胀程度、关节屈伸不利程度、畏恶风寒、晨僵证候评分均下降，且研究组低于对照组（P<0.05）。两组治疗2个月后血清TNF-α、IL-1β、IL-17水平均下降，且研究组低于对照组（P<0.05）。两组治疗2个月后IgA、IgM、IgG水平均下降，且研究组低于对照组（P<0.05）。两组治疗2个月后RF、ESR、CRP、ASO水平均下降，且研究组低于对照组（P<0.05）。结论：RA患者在甲氨蝶呤的基础上联合桂枝芍药知母汤治疗，可有效降低患者血清炎性因子、风湿四项检查指标、免疫球蛋白水平，改善患者临床症状，疗效显著。     

硫酸羟氯喹口服辅助治疗糜烂型口腔扁平苔癣的效果及对AT-Ⅲ、ZAG的影响

摘要 目的：探讨硫酸羟氯喹口服辅助治疗糜烂型口腔扁平苔癣的效果及对人抗凝血酶Ⅲ（AT-Ⅲ）、锌α2糖蛋白（ZAG）的影响。方法：选择2018年12月-2021年1月在我院接受治疗的115例糜烂型口腔扁平苔癣患者,采用随机数表法分为治疗组（n=58）和对照组（n=57）。对照组给复方倍他米松治疗,治疗组在对照组的基础上联合硫酸羟氯喹口服治疗。比较两组临床疗效、AT-Ⅲ、ZAG、白细胞介素4（IL-4）、白细胞介素17（IL-17）、干扰素γ（IFN-γ）、糜烂面积、疼痛评分水平变化情况及不良反应发生情况。结果：治疗后,两组总有效率比较差异显著（P<0.05）;治疗前,治疗组和对照组血清AT-Ⅲ、ZAG比较无显著差异;治疗后,治疗组和对照组血清AT-Ⅲ、ZAG均随着时间的推移而降低,且治疗组均低于对照组,差异显著（P<0.05）;治疗前,治疗组和对照组实验室指标水平比较无显著差异;治疗后,治疗组和对照组IL-4、IL-17均随着时间的推移而降低,且治疗组均低于对照组,IFN-γ均随着时间的推移而升高,且治疗组均高于对照组,差异显著（P<0.05）;治疗前,治疗组和对照组糜烂面积、疼痛评分比较无显著差异;治疗后,治疗组和对照组糜烂面积、疼痛评分均随着时间的推移而降低,且治疗组均低于对照组,差异显著（P<0.05）;两组不良反应总发生率为3.45%、8.77%,无显著差异（P>0.05）。结论：在糜烂型口腔扁平苔癣中应用硫酸羟氯喹口服辅助治疗疗效显著,可有效改善患者AT-Ⅲ、ZAG水平。     

Generation of an antibody with a designed specificity difference for protein C and activated protein C

Rabbit polyclonal antibodies to a synthetic peptide, NH₂-Asp-Thr-Asn-Gln-Val-Asp-Gln-Lys-Asp-Gln-Leu-Asp-Phe-Arg-CONH₂ (APep), have been produced. This sequence is identical to that contained in the tetradecapeptide released from bovine protein C (PC) as a result of its conversion to its activated form (APC), except that Phe₁₃ replaced the normal Pro₁₃, in order to discourage cross-reactivity of antibodies to the carboxylterminal portion of APep with PC. The antibody pool obtained reacted with PC and showed virtually no cross-reactivity toward either APC or several typical plasma proteins. This general approach should serve well as a means of production of antibodies with a designed specificity capable of distinguishing between forms of the same protein that arise by release of peptide material.     

Zinc Modulates the Interaction of Protein C and Activated Protein C with Endothelial Cell Protein C Receptor

Zinc is an essential trace element for human nutrition and is critical to the structure, stability, and function of many proteins. Zinc ions were shown to enhance activation of the intrinsic pathway of coagulation but down-regulate the extrinsic pathway of coagulation. The protein C pathway plays a key role in blood coagulation and inflammation. At present there is no information on whether zinc modulates the protein C pathway. In the present study we found that Zn²⁺ enhanced the binding of protein C/activated protein C (APC) to endothelial cell protein C receptor (EPCR) on endothelial cells. Binding kinetics revealed that Zn²⁺ increased the binding affinities of protein C/APC to EPCR. Equilibrium dialysis with ⁶⁵Zn²⁺ revealed that Zn²⁺ bound to the Gla domain as well as sites outside of the Gla domain of protein C/APC. Intrinsic fluorescence measurements suggested that Zn²⁺ binding induces conformational changes in protein C/APC. Zn²⁺ binding to APC inhibited the amidolytic activity of APC, but the inhibition was reversed by Ca²⁺. Zn²⁺ increased the rate of APC generation on endothelial cells in the presence of physiological concentrations of Ca²⁺ but did not further enhance increased APC generation obtained in the presence of physiological concentrations of Mg²⁺ with Ca²⁺. Zn²⁺ had no effect on the anticoagulant activity of APC. Zn²⁺ enhanced APC-mediated activation of protease activated receptor 1 and p44/42 MAPK. Overall, our data show that Zn²⁺ binds to protein C/APC, which results in conformational changes in protein C/APC that favor their binding to EPCR.     

ZnO nanoparticles augment ALT,AST, ALP and LDH expressions in C2C12 cells

The present study aimed to investigate the effect of ZnO nanoparticles on alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzyme expressions in C2C12 cells. ZnO nanoparticles are widely used in the several cosmetic lotions and other biomedical products. Several studies report on ZnO nanoparticle mediated cytotoxicity. However, there are no reports on the effect of ZnO nanoparticles on ALT, AST, ALP and LDH enzyme expressions in C2C12 cells. A cytotoxicity assay was carried out to determine the effect of ZnO nanoparticles (1–5 mg/ml) on C2C12 cell viability at 48 and 72 h. ZnO nanoparticles increased ALT, AST, ALP and LDH enzyme mRNA expression and their activities in C2C12 cells. In conclusion, the present study showed that ZnO nanoparticles increased these enzyme activities and its mRNA expression in C2C12 cells in a dose-dependent manner.     

Neutraligands of C5a can potentially occlude the interaction of C5a with the complement receptors C5aR1 and C5aR2

The complement system is central to the rapid immune response witnessed in vertebrates and invertebrates, which plays a crucial role in physiology and pathophysiology. Complement activation fuels the proteolytic cascade, which produces several complement fragments that interacts with a distinct set of complement receptors. Among all the complement fragments, C5a is one of the most potent anaphylatoxins, which exerts solid pro-inflammatory responses in a myriad of tissues by binding to the complement receptors such as C5aR1 (CD88, C5aR) and C5aR2 (GPR77, C5L2), which are part of the rhodopsin subfamily of G-protein coupled receptors. In terms of signaling cascade, recruitment of C5aR1 or C5aR2 by C5a triggers the association of either G-proteins or β-arrestins, providing a protective response under normal physiological conditions and a destructive response under pathophysiological conditions. As a result, both deficiency and unregulated activation of the complement lead to clinical conditions that require therapeutic intervention. Indeed, complement therapeutics targeting either the complement fragments or the complement receptors are being actively pursued by both industry and academia. In this context, the model structural complex of C5a–C5aR1 interactions, followed by a biophysical evaluation of the model complex, has been elaborated on earlier. In addition, through the drug repurposing strategy, we have shown that small molecule drugs such as raloxifene and prednisone may act as neutraligands of C5a by effectively binding to C5a and altering its biologically active molecular conformation. Very recently, structural models illustrating the intermolecular interaction of C5a with C5aR2 have also been elaborated by our group. In the current study, we provide the biophysical validation of the C5a-C5aR2 model complex by recruiting major synthetic peptide fragments of C5aR2 against C5a. In addition, the ability of the selected neutraligands to hinder the interaction of C5a with the peptide fragments derived from both C5aR1 and C5aR2 has also been explored. Overall, the computational and experimental data provided in the current study supports the idea that small molecule drugs targeting C5a can potentially neutralize C5a's ability to interact effectively with its cognate complement receptors, which can be beneficial in modulating the destructive signaling response of C5a under pathological conditions.     

Constant expression of mouse calpastatin isoforms during differentiation in myoblast cell line, C2C12

C2C12 is a myoblast cell line which is used to studydifferentiation into multinucleated cells in vitro. Addition of calpain inhibitors, calpeptin orE-64d, to the culture medium prevented the myoblasticfusion of C2C12 cells. Immunoblot studies usingaffinity-purified antibody, revealed that the expressedlevels of mouse calpastatin remained unaltered duringC2C12 cell fusion. The detected calpastatin migratedas a protein of 130 kDa on SDS-polyacrylamide gelelectrophoresis. The estimated molecular mass wassomewhat greater than that in mouse liver anderythrocytes, and much greater than that reported inrat myoblasts. The 130 kDa isoform may contain anadditional N-terminal region designated XL domainfound in bovine calpastatin.     

孢素联合糖皮质激素对IgA肾病患者IgA、C3及IgA/C3影响研究

目的:探讨孢素联合糖皮质激素对IgA肾病患者IgA、C3及IgA/C3的影响。方法:我院收治的IgA肾病住院患者90例,按用药不同分为对照组与实验组。对照组予以醋酸泼尼松片口服,实验组在对照组基础上予以予环孢素软胶囊口服,治疗结束后对患者的血肌酐、血尿酸、24 h尿蛋白定量及IgA、C3、IgA/C3进行检测。结果:与对照组相比,实验组24 h尿蛋白定量水平较低,P0.05;IgA水平及IgA/C3水平较低,P0.05,差异具有统计学意义;两组患者的C3、血肌酐、血尿酸水平无显著差异,无统计学意义(P0.05)。结论:孢素联合糖皮质激素能够显著降低Ig A肾病患者Ig A水平及IgA/C3,对C3水平无影响,对临床有指导意义。     

Interaction of Axl receptor tyrosine kinase with C1-TEN,a novel C1 domain-containing protein with homology to tensin

Axl receptor tyrosine kinase is implicated in several malignancies and is the receptor for the vitamin K-dependent growth factor Gas6. From a yeast two-hybrid screen of protein-protein interactions with the Axl cytoplasmic domain, we detected a previously uncharacterised SH2 domain-containing protein. We cloned two novel splice variants of this protein that give rise to 1409- and 1419-amino acid proteins, differing only in their N-terminal residues and yielding a 150-kDa protein product by in vitro translation. The Axl-interacting C-terminus contains a tandem SH2 and PTB domain combination homologous to the focal adhesion protein tensin. We detected interaction of Axl with both domains in mammalian cells by co-immunoprecipitation and two-hybrid analyses. In addition, the protein possesses an N-terminal putative phorbol ester-binding C1 domain as well as a central tyrosine phosphatase motif. Thus, we have named the protein C1 domain-containing phosphatase and TENsin homologue (C1-TEN). Northern blot analysis of C1-TEN in human tissues revealed highest expression in heart, kidney, and liver. In summary, we have identified a novel multi-domain intracellular protein that interacts with Axl and which may furthermore be involved in other signal transduction pathways.     

Role of CYP2C9 and CYP2C19 polymorphisms in patients with atherosclerosis

The arachidonic acid metabolizing CYP enzymes with prominent roles in vascular regulation are epoxygenases of the two gene family which generate epoxyeicosatrienoic acids. Carriers of CYP2C9 mutant alleles exhibit a diminished CYP2C9 metabolic capacity leading to decreased endothelium-derived hyperpolarizing factors (EDHF) synthesis and an increased risk for atherosclerosis. We investigated whether the polymorphisms of CYP2C9/19 are related with atherosclerosis. We examined 108 patients having angioraphically > or =70 coronary artery narrowing and 90 healthy controls. CYPC2C9/19*2 and CYP2C9/19*3 alleles were investigated in both patients and controls by a real time PCR instrument. There was no significant difference in the distribution of the CYP2C9*2/*3 alleles between cases and the controls. We found that smoker patients having CYP2C9*2 heterozygote genotype have 3.7-fold risk of developing atherosclerosis. CYP2C19*3 heterozygote alleles are more frequent in patients than in controls (10.2%, 5.6% respectively) and it is related with a three-fold risk of atherosclerosis (odds ratio (OR) = 3.75, confidence interval (CI) = 0.75-18.65). It becomes clear that cigarette smoking can cause almost all major diseases prevalent today, such as cancer or heart disease. This inter-subject variability in cigarette-induced pathologies is partly mediated by genetic variants of genes that may participate in detoxification processes, e.g., cytochrome P450 (CYP), cellular susceptibility to toxins, such as p53, or disease development such as atherosclerosis.