半导体激光穴位照射与药物治疗急慢性关节损伤的疗效比较

目的探讨低功率半导体激光对急慢性关节损伤的治疗作用.方法1999年至2004年急慢性关节损伤的患者240例,随机分为两组,各120例,激光组采用低功率半导体激光治疗仪照射痛点;对照组口服活血止痛胶囊,外用沈阳红药膏治疗.结果两周后的疗效比较.激光组有效率为85.0%,痊愈率为44.2%;对照组有效率为71.7%,痊愈率为20.8%;差异有显著意义.激光组中,急性关节损伤的患者痊愈率为52.9%,慢性关节损伤患者的痊愈率为32.7%,差异有显著意义(P＜0.05)有效率,差异无显著性意义.结论低功率半导体激光对急慢性关节损伤,尤其是急性小关节损伤有很好的疗效.     

家兔缺血与再灌流肾内脂质过氧化物含量的变化

本研究发现:家兔缺血60min(未再灌流)肾皮质和髓质内,脂质过氧化物含量均显著降低;缺血60min再灌流15min的肾皮质和髓质内,脂质过氧化物含量均显著增加。实验提示:缺血再灌流贤内氧自由基“爆发性”生成所引发的脂质过氧化可能是肾缺血性损伤的重要机制之一。     

SYBR Green荧光定量PCR检测外源ATP7B对于内源CP基因转录的影响

[目的]应用SYBR Green荧光定量PCR检测在正常BRL细胞中短暂转染人ATP7B cDNA后CP基因的转录情况.[方法]分为空质粒组(转染空质粒Kbpala/Alb)和处理组(转染野生型Kbpala/Alb-ATP7B),分别于转染后0、4、8、12、24、48、72、168 h提取mRNA,逆转录后行SYBR Green荧光PCR检测人ATP7B cDNA及大鼠CP基因的转录情况.SAS11.0统计软件进行数据处理和分析.[结果]人ATP7B cDNA在短暂转染后约48h转录达高峰,可持续至转染后7 d以上;经方差分析,空质粒组转染后各时间点CP基因的转录水平与t=0 h相比较P＞0.05;处理组亦是.[结论]外源ATP7B cDNA的转染及表达对于内源性CP基因的转录无影响.     

行气活血饮治疗慢性乙肝肝纤维化肝郁脾虚证34例

目的:观察利气活血类中药配伍组方对慢性乙肝纤维化肝郁脾虚证的影响。方法:65例患者随机分为2组,治疗组34例,用行气活血饮(桃仁、红花、赤芍、五灵脂、鳖甲、川楝子等)治疗;对照组用复方丹参片口服。结果:两组治疗后血清透明质酸酶、IV型胶原、血清铁、血清铁蛋白的水平较治疗前下降,两组相比具有显著性差异。治疗组总有效率为85.3%,显著高于对照组58.1%(P<0.05)。结论:行气活血饮有一定的抗肝纤维化作用,对血清铁、血清铁蛋白有显著抑制作用。     

新生儿血气分析标本采集方法的探讨

我院新生儿科自2001年元月起采用足底加温采血法采微量毛细血管血做血气分析,并与常规采血气方法相比较,发现在创伤小、失血少的情况下同样可以得到一个满意的血气结果,现报告如下.     

壮医药线点灸对大鼠肝纤维化组织学及血清学的影响

目的观察壮医药线点灸抑制肝纤维化作用。方法采用CCL4诱导大鼠肝纤维化模型,Wistar大鼠随机分正常对照组、模型组、药线组各10只,应用免疫组化及放射免疫等方法研究壮医药线对肝纤维化大鼠肝组织纤维化程度,肝星状细胞(HSC)凋亡率,超氧化物歧化酶(SOD)、丙二醛(MDA)、转化生长因子!1(TGF-"1)含量以及对血清中谷丙转氨酶(ALT)、透明质酸(HA)、III型前胶原(PCIII)、层粘蛋白(LN)含量的影响。结果与模型组相比,药线组能显著改善大鼠肝组织纤维化程度,促进活化HSC凋亡,提高SOD含量,降低MDA、TGF-#1的含量及血清中ALT、HA、PCIII、LN的水平(P<0.01)。结论壮医药线点灸具有一定的抑制肝纤维化作用。     

丹参对缺血—再灌流兔肾皮质过氧化脂质含量的影响

家兔静脉注射丹参(2g/kg)后,左肾缺血60min再灌流30min,其皮质内过氧化脂质(LPO)含量比注药前自身右肾的含量下降26.68％。丹参组缺血—再灌流肾LPO含量下降的幅度也显著大于葡萄糖组、提示丹参可能具有较强的抗氧化作用,对防治肾缺血—再灌流损害具有积极意义。     

交锁髓内针辅以小切口复位治疗股骨干骨折

目的 探讨交锁髓内针固定辅以小切口复位治疗股骨干骨折的临床疗效。方法 回顾性分析江西省九江市中医院2020年8月至2021年8月股骨干骨折48例患者,采用随机数字表法分为治疗组和对照组,每组各24例,治疗组使用髓内针辅助小切口辅助复位治疗,对照组使用髓内针闭合复位方式治疗,比较两组患者的骨折愈合情况、出血量及手术时间等。结果 两组患者的手术时间及出血量比较,差异有统计学意义（P<0.05）;两组患者的骨折愈合情况比较,差异无统计学意义（P>0.05）。结论 采用交锁髓内针固定辅以小切口复位治疗股骨干骨折,手术时间及出血量少,骨折愈合好,值得临床推广应用。     

Role of angiotensin Ⅱ and JAK2 signal pathway in transdifferentation of renal tubular cells in mice after acute ischemic followed by reperfusion

Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway.     

Role of angiotensin Ⅱ and JAK2 signal pathway in transdifferentation of renal tubular cells in mice after acute ischemic followed by reperfusion

Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway.