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。     

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。     

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。     

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。     

痹祺胶囊联合依那西普对强直性脊柱炎患者急性时相反应物指标、血清疼痛介质和骨代谢指标的影响

摘要 目的：探讨痹祺胶囊联合依那西普对强直性脊柱炎（AS）患者急性时相反应物指标、血清疼痛介质和骨代谢指标的影响。方法：纳入西安市第五医院2020年4月~2022年3月期间收治的96例AS患者。按照随机数字表法分为对照组（n=48）和研究组（n=48）,对照组接受依那西普治疗,研究组接受痹祺胶囊联合依那西普治疗。对比两组疗效、临床症状指标[Bath强直性脊柱炎活动指数（BASDAI）、Bath强直性脊柱炎功能指数（BASFI）、Bath强直性脊柱炎计量学指数（BASMI）、视觉疼痛模拟（VAS）评分]、急性时相反应物指标[红细胞沉降率（ESR）、C反应蛋白（CRP）]、血清疼痛介质指标[前列腺素E₂ (PGE₂) 、P物质( SP)、多巴胺（DA）,五羟色胺（5-HT）]和骨代谢指标[骨形态发生蛋白-2（BMP-2）、骨钙素（BGP）],观察两组不良反应发生情况。结果：研究组（95.83%）的临床总有效率高于对照组（79.17%）,差异有统计学意义（P<0.05）。两组治疗后PGE₂、SP、DA、5-HT下降,且研究组的下降程度更大（P<0.05）。两组治疗后CRP、ESR下降,且研究组的下降程度更大（P<0.05）。两组治疗后BMP-2、BGP升高,且研究组的升高程度更大（P<0.05）。两组治疗后BASDAI、BASFI、BASMI、VAS评分下降,且研究组的下降程度更大（P<0.05）。两组不良反应发生率对比无差异（P>0.05）。结论：痹祺胶囊联合依那西普治疗AS患者,疗效较好,可改善临床症状,调节急性时相反应物指标、血清疼痛介质和骨代谢指标水平,安全性较高。     

金乌骨通胶囊联合塞来昔布胶囊治疗强直性脊柱炎的临床研究

摘要 目的：观察金乌骨通胶囊联合塞来昔布胶囊治疗强直性脊柱炎（AS）的临床疗效。方法：选取天津中医药大学第一附属医院2017年4月~2020年4月期间收治的126例AS患者。采用双色球法（红色、绿色）将患者分为对照组（红色）和研究组（绿色）,各63例。对照组接受塞来昔布胶囊治疗,研究组接受金乌骨通胶囊联合塞来昔布胶囊治疗,两组均治疗3个月。治疗3个月后,观察两组疗效,记录治疗期间不良反应发生率,对比两组治疗前、治疗3个月后的临床症状缓解情况、生存质量及实验室指标变化。结果：研究组的临床总有效率高于对照组（P<0.05）。治疗3个月后,研究组巴氏强直性脊柱炎疾病活动指数（BASDAI）、巴氏强直性脊柱炎功能指数（BASFI）评分低于对照组,枕墙距小于对照组,腰椎活动度、胸廓活动度大于对照组（P<0.05）。治疗3个月后,研究组世界卫生组织生存质量简表（WHOQOL-BRIEF）各维度评分高于对照组（P<0.05）。治疗3个月后,研究组血沉（ESR）、C-反应蛋白（CRP）、白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）低于对照组（P<0.05）。两组不良反应发生率组间比较无统计学差异（P>0.05）。结论：金乌骨通胶囊联合塞来昔布胶囊治疗AS患者,可促进其临床症状及生存质量改善,降低ESR及炎性因子水平,是一种安全有效的治疗方案。     

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。     

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。     

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。     

艾拉莫德增强丝裂霉素C诱导的人食管癌Eca109细胞凋亡

目的探讨艾拉莫德增强丝裂霉素C（MMC）诱导的人食管癌Eca109细胞凋亡的作用及其机制。 方法将人食管癌Eca109细胞分为五组：对照组、MMC组、25,50,100 μg/ml浓度艾拉莫德+MMC组;通过CCK-8和DCFH-DA染色法分别检测25,50,100 μg/ml浓度艾拉莫德联合MMC对人食管癌Eca109细胞活力和细胞活性氧（ROS）生成的影响,流式细胞术检测艾拉莫德联合MMC对人食管癌Eca109细胞凋亡的影响,并通过Western Blot检测艾拉莫德联合MMC对TNF-α和cleaved caspase3蛋白表达的影响。采用单因素方差分析和t检验进行统计学分析。 结果CCK-8结果显示,与0 μg/ml T-614+MMC组A450值（0.85±0.03）比较,25、50、100 μg/ml T-614+MMC组A450值（0.73±0.02,0.52±0.02,0.33±0.02）均降低,差异具有统计学意义（F = 127.60, P < 0.01）;DCFH-DA染色检测结果显示,与0 μg/ml T-614+MMC组DCFH荧光值（130.00±10.00）比较,25、50、100 μg/ml T-614+MMC组DCFH值（219.67±9.50,280.33±10.50,338.33±16.07）均升高,差异具有统计学意义（F = 170.20,P < 0.01）;流式细胞术检测结果显示,与对照组的细胞凋亡率（5.33±0.35）﹪比较,T-614和MMC组的凋亡率（20.30±2.00）﹪,（25.60±3.00）﹪均升高。与MMC组细胞凋亡率（25.60±3.00）﹪比较,艾拉莫德与MMC联用组（T-614+MMC）食管癌Eca109细胞的细胞凋亡率（56.20±3.00）﹪升高,差异均具有统计学意义（F = 247.50,P < 0.01）;Western Blot结果显示,与MMC组细胞TNF-α和cleaved caspase3蛋白表达（0.87±0.06,0.25±0.03）比较,艾拉莫德与MMC联用组（T-614+MMC）食管癌Eca109细胞的TNF-α和cleaved caspase3蛋白表达（1.28±0.08,0.59±0.03）升高,差异均具有统计学意义（F = 96.90,P < 0.01）。 结论艾拉莫德能够增强MMC对食管癌Eca109细胞活力的抑制作用,其机制可能通过促进ROS的生成,激活线粒体凋亡通路,最终导致食管癌Eca109细胞凋亡。     

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.     

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.     

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.     

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。     

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.     

鲎C因子的性质、结构、功能及应用

鲎C因子是一种分子量为123kD的丝氨酸蛋白酶原,主要由六种结构域构成,能特异地结合内毒素分子而被激活。在内毒素的检测,抗内毒素治疗,去除生物制品中污染的内毒素,以及在抗微生物作用中有多种潜在的应用价值 。