补肾活血方对大鼠卵巢局部VEGFmRNA表达的影响

目的探讨补肾活血方对大鼠多束卵巢形成中血管内皮生长因子的基因表达(VEGFmRNA)的影响。方法选用未成年24 d龄SD雌性大鼠60只,随机分为模型对照组、西药对照组、补肾活血方高剂量组、补肾活血方低剂量组、正常对照组5组。用Bogovich法建立大鼠多囊卵巢病理模型。以克罗米酚为对照,用原位杂交法观察补肾活血方对多囊卵巢大鼠局部VEGFmRNA的影响。结果模型组卵巢局部VEGFmRNA存在颗粒细胞、卵泡膜细胞、间质细胞及血管内皮细胞表达的显著增高。用补肾活血方高、低剂量和西药对照治疗后,卵巢局部VEGFmRNA的表达明显降低,差异具有统计学意义(P<0.05,P<0.01),说明补肾活血方高、低剂量组与西药组对VEGFmRNA的表达具有抑制作用。补肾活血方高、低剂量组与西药组比较,高剂量组抑制作用优于西药组,差异具有显著统计学意义(P<0.01);低剂量组与西药组比较差异无统计学意义(P>0.05),补肾活血方高、低剂量组比较,高剂量组抑制作用优于低剂量组,差异具有显著统计学意义(P<0.05)。结论VEGFmRNA可能参与多囊卵巢综合征的发病机制有关。以补肾活血立法的补肾活血方能降低多囊卵巢大鼠局部VEGFmRNA的显著增高表达,降低VEGFmRNA在卵巢局部的作用。提示补肾活血方可能通过VEGFmRNA途径切入卵泡发育、促卵泡优势化、卵泡成熟、基质降解、诱发局部类炎症反应,使排卵成功。     

补肾活血方对PCO大鼠卵巢COX-1mRNA表达的影响

目的探讨环氧化酶（COX—1）的表达在多囊卵巢卵泡破裂中的作用及补肾活血方治疗多囊卵巢排卵障碍的作用机制。方法选用未成年24d龄SD雌性大鼠60只。随机分为模型组、克罗米酚对照组、补肾活血方高剂量组、补肾活血方低剂量组、正常对照组5组,每组12只。用Bogovieh法建立大鼠多囊卵巢病理模型。以克罗米酚为对照,采用原位杂交法检测各组卵巢组织中环氧化酶COX-1基因的表达水平。结果模型组与正常组比较,卵泡内膜细胞COX—1 mRNA表达明显增加,两者比较差异有统计学意义（P〈0．01）;补肾活血方高剂量组与正常组相比。差异无统计学意义（P〉0.05）。结论COX—1 mRNA在卵巢卵泡内膜细胞水平升高可能是PCOS发病的重要因素或环节。补肾活血方可能通过影响COX—1mRNA水平。从而发挥治疗多囊卵巢排卵障碍的作用．这可能是其促进卵巢排卵的作用机制之一。     

补肾活血方对多囊卵巢大鼠卵巢MMP-2，9的表达干预

目的观察补肾活血方对多囊卵巢（PCO）大鼠基质金属蛋白酶-2，9（MMP-2，9）表达的影响，探讨补肾活血方治疗PCO排卵障碍的机理。方法选用未成年24日龄SD雌性大鼠60只，随机分为模型对照组、西药对照组、补肾活血方高剂量组、补肾活血方低剂量组、正常对照组共5组，每组12只。建立大鼠PCO病理模型，采用原位杂交法检测各组卵巢组织中MMP-2，9基因的表达水平。结果经图象分析和统计处理，各组大鼠卵巢中卵泡的颗粒细胞和发育良好的卵泡膜细胞中均可检测到MMP-2和MMP-9的杂交信号。模型组MMP-2与MMP-9表达强度明显超过正常组、补肾活血方高剂量组、补肾活血方低剂量组及西药对照组（P〈0．05）；补肾活血方高剂量组MMP-2与MMP-9的表达接近正常组（P〉0．05）；补肾活血方低剂量组、，西药对照组与正常组相比，MMP-2与MMP-9的表达均较正常组高（P〈0．05）；补肾活血方低剂量组与西药对照组MMP-2与MMP-9的表达强度相似，但均超过补肾活血方高剂量组的表达强度（P〈0．01）。结论MMPs的过度表达可能是卵巢排卵障碍的关键因素，提示MMPs参与了卵巢排卵过程；大鼠PCO动物模型卵巢局部MMP-2，9异常高表达与PCO大鼠卵巢排卵障碍有关，补肾活血方通过抑制MMP-2，9的异常高表达，从而发挥治疗多囊卵巢排卵障碍的作用，这可能是其促进卵巢排卵的机制之-。     

补肾活血方对多囊卵巢大鼠卵巢MMP-2、9的表达干预研究

目的 观察补肾活血方对多囊卵巢(PCO)大鼠基质金属蛋白晦-2,9(MMP-2、9)表达的影响,探讨补肾活血方治疗PCO排卵障碍的机制.方法选用未成年24日龄SD雌性大鼠60只,随机分为模型对照组、西药对照组、补肾活血方高剂量组、补肾活血方低剂量组、正常对照组共5组.建立大鼠PCO病理模型,采用原位杂交法检潮各组卵巢组织中MMP-2、9基因的表达水平.结果 各组大鼠卵巢中卵泡的颗粒细胞和发育良好的卵泡膜细胞中均可检潮到MMP-2和MMP-9的杂交信号.模型组MMP-2与MMP-9表达强度明显超过正常组、补肾活血方高剂量组、低剂量组及西药对照组,差异具有统计学意义(P<0.05);补肾活血方高剂量组MMP-2与MMP-9的表达接近正常组,差异无统计学意义(P>0.05);补肾活血方低剂量组、西药对照组与正常组相比,MMP-2与MMP-9的表达均较正常组高,差异具有统计学意义(P<0.05);补肾活血方低剂量组与西药对照组MMP-2与MMP-9的表达强度相似,但均超过补肾活血方高剂量组的表达强度,差异具有统计学意义(P<0.01).结论 MMPs的过度表达可能是卵巢排卵障碍的关键因素,提示MMPs参与了卵巢排卵过程;大鼠PCO动物模型卵巢局部MMP-2、9异常高表达与PCO大鼠卵巢排卵障碍有关,补肾活血方通过抑制MMP-2、-9的异常高表达,从而发挥治疗多囊卵巢排卵障碍的作用,这可能是其促进卵巢排卵的机制之一.     

自拟补肾化痰方与补肾活血方对PCO大鼠性激素和P450arom及PAI-1的影响

目的观察自拟补肾化痰方与补肾活血方对多囊卵巢（PCO）大鼠血清性激素水平及卵巢局部因子P450arom和PAI-1表达的影响，探讨其对PCO模型大鼠的不同治疗作用并分析可能的作用机制。方法采用胰岛素联合人绒毛膜促性腺激素（HCG）造模法制备PCO模型大鼠。随机分为PCO模型组、补肾化痰组、补肾活血组、西药组（二甲双胍）和对照组。运用放射免疫法测定血清性激素、胰岛素（INS）水平；免疫组化法测定卵巢组织中P450amm和PAI-1的表达。结果补肾化痰方可以降低PCO模型大鼠血清睾酮（T）水平，升高E2、FSH水平。可上调P450arom的表达，而补肾活血方可以降低PCO模型大鼠血清T、LH和胰岛素（INS）水平，可下调PAI-1的表达。结论卵巢局部因子P450arom和PAI-1在多囊卵巢的发生、发展中起重要作用，自拟补肾化痰方与补肾活血方从不同途径调整内分泌和卵巢局部因子的表达，从而促进卵泡的发育、成熟及排卵。     

卵巢癌组织中uPA与PAI-1 mRNA表达及意义

目的 探讨尿激酶型纤溶酶原激活剂（uPA）和纤溶酶原激活剂抑制物-1（PAI—1）mRNA在卵巢癌组织中的表达及其临床意义。方法 采用逆转录-聚合酶链反应技术，检测38例卵巢癌、21例卵巢良性上皮性肿瘤及17例正常卵巢组织中uPA及PAI-1 mRNA的表达，并分析其与病理分化程度的相关性。结果 uPA及PAI—1 mRNA在卵巢癌中的表达水平均较卵巢良性上皮性肿瘤、正常卵巢组织显著升高（F=184．51、51．00，q=11．34～26．69，P〈0．05）。在不同分化程度的卵巢癌组织中uPA及PAI-1 mRNA的表达量随肿瘤分化程度的降低而增加（F=110．62、38．43，q=3．10～6．86，P〈0．05）。结论 卵巢癌组织中uPA及PAI—1 mRNA呈高表达，且与卵巢癌的病理分化程度相关。     

补肾活血法对多囊卵巢综合征大鼠的防治作用及机制初步研究

目的观察补肾活血法治疗多囊卵巢综合征(PCOS)的疗效并探讨其作用机制。方法 60只大鼠分为正常对照组、模型组、补肾活血法高、中、低剂量及罗格列酮组,每组10只。除正常对照组外,其余各组均制备PCOS模型。除正常对照组采用正常饮水外,其余大鼠造模结束后每日仍用5%葡萄糖溶液替代日常饮水。补肾活血方高、中、低剂量组通过人与大鼠体表面积比率换算法计算出灌胃给药量分别为68. 66 g/kg,34. 33 g/kg,17. 17 g/kg。正常对照组和模型组大鼠每日按照体质量灌胃蒸馏水1 ml/100 g,1次/d,连续28 d;罗格列酮组灌胃罗格列酮3 mg/(kg·d),1次/d,连续28 d。检测各组大鼠体质量、卵巢重量和子宫重量,血清激素(LH、FSH和T)、炎症因子(HMGB1和TNF-α)、基因和蛋白(HMGB1、TLR4、NF-KBP65)的表达水平变化。结果与正常对照组比较,模型组、低剂量组和中剂量组的体质量、卵巢质量显著增加(P 0. 05,P 0. 01);模型组、补肾活血法低剂量组和中剂量组体质量、卵巢质量高于高剂量组和罗格列酮组,但组间比较差异无统计学意义(P 0. 05);而模型组、低剂量组和中剂量组子宫质量显著低于正常对照组(P 0. 05)。与正常对照组比较,各组LH、FSH和T含量均显著增加(P 0. 05,P 0. 01);模型组LH、FSH和T含量均高于高剂量组和罗格列酮组(P 0. 05,P 0. 01);高剂量组和罗格列酮组LH、FSH和T含量显著低于补肾活血法低、中剂量组(P 0. 05)。与正常对照组比较,其余各组HMGB1和TNF-α含量均显著增加(P 0. 05);模型组HMGB1和TNF-a含量均高于高剂量组和罗格列酮组(P 0. 05);高剂量组和罗格列酮组HMGB1和TNF-α含量显著低于低、中剂量组(P 0. 05)。与正常对照组比较,其余各组HMGB1、TLR4和NF-κB-P65基因的表达水平均显著增加(P 0. 05);模型组HMGB1、TLR4和NF-κB-P65基因表达水平均高于高剂量组和罗格列酮组(P 0. 05);补肾活血法高剂量组和罗格列酮组HMGB1、TLR4和NF-κB-P65基因表达水平显著低于低、中剂量组(P 0. 01)。结论补肾活血法具有显著的降低PCOS大鼠体质量、卵巢质量、激素水平和炎症因子的作用,且对卵巢组织功能损伤具有保护作用,其作用机制可能与HMGB1/TLR4/NF-k BP65直接相关。     

补肾健脾活血方对大鼠悬尾试验性骨质疏松和肌萎缩影响的实验研究

目的:探讨补肾活血健脾方对悬尾大鼠骨密度和肌萎缩的影响。方法:采用SPF级健康SD大鼠48只,随机平均分为健脾活血方高剂量组,低剂量组,造模组和空白对照组,每组12只。除空白对照组外,其余各组均选用大鼠悬尾实验作为废用性骨质疏松和肌萎缩模型的建立动物模型造模共计28 d,造模期间,补肾健脾活血方高剂量组给予补肾健脾活血方提取物2.50 g/(kg·d)灌胃,补肾健脾活血方低剂量组给予补肾健脾活血方提取物1.25 g/(kg·d)灌胃,造模组和空白对照组给予等剂量饮用水灌胃,每天1次。28 d后,全部大鼠腹腔采血后处死,取右侧股骨以及L1~4椎骨和完整分离左右侧比目鱼肌。采用酶联免疫吸附法(ELISA)检测血清成骨标记物血清骨形成蛋白2(BMP-2)、骨钙素(OCN)及破骨标记物抗酒石酸酸性磷酸酶(TRAP)进行测定,应用实时荧光定量聚合酶链式反应(Real-time PCR)测定大鼠股骨成骨相关基因OCN,Runx-2的表达,双能X线检测各组椎体和股骨骨密度的表达,并测量比目鱼肌湿重与横截面积测量。结果:与造模组相比,健脾活血方高剂量组大鼠右侧股骨和椎体BMD显著性增高(P<0.05);健脾活血方高剂量和低剂量组血清TRAP呈显著性降低(P<0.01,P<0.05);健脾活血方高剂量和低剂量组大鼠股骨OCN和Runx-2 mRNA的表达显著性增高(P<0.05);健脾活血方高剂量组和低剂量组左侧和右侧比目鱼肌平均湿重显著性增高(P<0.05);健脾活血方高剂量组左侧和右侧比目鱼肌I型和II型纤维横截面积显著性增高(P<0.05),健脾活血方低剂量组左侧和右侧比目鱼肌I型纤维横截面积相比造模组呈显著性增高(P<0.05)。结论:补肾活血健脾方可以防止失重引起的骨密度降低和肌萎缩,为临床用于治疗废用性骨质疏松和肌萎缩奠定了理论基础。     

补肾活血中药加克罗米芬治疗多囊卵巢综合征的临床观察

目的探讨补肾活血中药加克罗米芬治疗多囊卵巢综合征的疗效。方法将我院2010年8月～2011年2月收治的60例多囊卵巢综合征的患者分为治疗组和对照组,每组各30例。对照组采用克罗米芬治疗,治疗组在对照组的基础上采用补肾活血的中药治疗,比较两组患者的临床疗效、血清性激素结合球蛋白（SHBG）、排卵情况、月经量化评分及性激素血清睾酮（T）、黄体生成素（LH）的水平。结果治疗组显效17例,有效8例,总有效率为83．3％显著高于对照组的66．7％（P〈0．05）。治疗组治疗后的SHBG、总排卵率、月经量化评分显著优于对照组（P〈0．05）。治疗组治疗后的T、LH显著低于对照组（P〈0．05）。结论补肾活血中药加克罗米芬能够显著提高多囊卵巢综合征的疗效,改善患者的激素水平。促进患者排卵,值得临床推广。     

补肾活血方治疗大鼠糖尿病性勃起功能障碍的机理

目的研究补肾活血方对糖尿病(DM)性勃起功能障碍(ED)大鼠勃起功能的疗效及其作用机理。方法将40只雄性SD大鼠随机分为正常组、糖尿病模型组、补肾活血方低剂量组、补肾活血方高剂量组,每组10只。糖尿病模型组、补肾活血方低剂量组、补肾活血方高剂量组3组大鼠腹腔注射链脲佐菌素(STZ),构建糖尿病大鼠模型。正常组和糖尿病模型组进行生理盐水灌胃,补肾活血方低剂量组(3 g/kg)和高剂量组(6 g/kg)进行补肾活血方灌胃,疗程8周,8周后取材测定阴茎脏器指数和一抗、二抗浓度,采用Biopack电生理仪检测阴茎海绵体内压(ICP),蛋白印迹法检测蛋白激酶B(AKT)、磷酸化蛋白激酶B(p AKT)表达,TUNEL法检测阴茎组织凋亡,Masson三色染色观察阴茎组织病理改变。结果与糖尿病模型组比较,补肾活血方低、高剂量组阴茎脏器指数无明显差异(P0.05),补肾活血方高剂量组ICP和ICP与平均动脉压(MAP)的比值明显升高(P0.05)。与糖尿病模型组比较,补肾活血方低、高剂量组p AKT、AKT表达显著增加(P0.05),并且阴茎海绵体平滑肌凋亡率均有所下降,但差异无显著性意义(P0.05)。补肾活血方低剂量组与糖尿病模型组相比,胶原纤维比例显著下降(P0.05)。结论补肾活血方可增加糖尿病大鼠阴茎ICP,其机理与提高p AKT表达、抑制阴茎海绵体平滑肌细胞凋亡、降低胶原纤维的生成有关。     

益气活血消臌汤治疗难治性乙型肝炎肝硬化腹水的临床观察

目的观察益气活血消臌汤治疗难治性乙型肝炎肝硬化腹水的临床疗效。方法将60例乙型肝炎肝硬化腹水患者随机分为治疗组（益气活血消臌汤结合西药常规治疗）和对照组（西药常规治疗）各30例,治疗1个月后,观察症状和体征、肝功能指标、血钠、尿钠与尿钾、尿素氮、血肌酐、腹水的变化。结果治疗组能明显的退黄、降酶和升高白蛋白（P〈0．05,P（0．01）,能明显的升高血钠、尿钠,尿钾（P〈0．05）,降低尿素氮、血肌酐（P〈0．05）;治疗组总疗效优于对照组（P〈0．05）。结论益气活血消臌汤治疗难治性乙型肝炎肝硬化腹水有较好的临床疗效。     

A clinical trial of premedication for unscheduled laser in situ keratomileusis surgeries and a related bacteriological analysis of conjunctival sacs

Laser in situ keratomileusis （LASIK） is a quick and effective approach for treating ametropia. It is used to treat relatively healthy corneas, and patients usually have high expectations and requirements for postoperative visual results. Therefore, the prevention of severe postoperative complications, such as corneal infections, is important.~ In China, some individuals require a rapid improvement in uncorrected visual acuity through surgery. There are also individuals from other cities seeking better medical services. Because of time limitations, the preoperative preparation time may be too short to complete a 3-day eye drop treatment with antibiotics. In this case study, we compared the bacterial eliminating effects and adverse reactions of levofloxacin eye drops （Santen Corp., Japan） and 0.5% Povidone-iodine （PVI, Nanda Pharmaceutical Corp., China） irrigation, for different time periods before unscheduled LASIK surgery.     

Efficacy of miacalcic in treating a hypercalcemia crisis caused by Williams-Beuren syndrome

Williams-Beuren syndrome （WBS） is a hereditary disease involving multiple systems due to microdeletion of chromosome 7q11.23. The deleted region in most patients is approximately 1.55 Mb, including 26-28 genes. The incidence of WBS in liveborn children is roughly 1/7 500-1/25 000.1     

子宫颈上皮内瘤变或原位腺癌的处理(2006年版)

2006年9月18—19日,146名代表29个组织和专业学会的专家在Bethesda聚会,修改制订了有关如何处理宫颈癌筛查异常结果妇女的以循证医学为依据的共识指南。有关低度宫颈上皮内瘤变（cervical intraepithelial neoplasia,CIN）的处理,变化较大。以往,需要根据阴道镜检查结果是否满意进行处理,对所有的CIN1妇女均可以采用破坏或者切除疗法。在新的指南中,不论阴道镜检查满意与否,对因低度宫颈细胞学结果转诊而明确的CIN1,细胞学随访是唯一的处理建议。     

Microvascular protective role of pericytes in melatonin-treated spinal cord injury in the C57BL/6 mice

Background Pericytes,located on microvessels,help to maintain vascular stability and blood-brain barrier integrity.The influence of pericytes on microvessels after spinal cord injury （SCI） is less clear.Therefore,the aim of this study was to investigate whether pericytes took a protective effect on microvessels in melatonin-treated SCI.Methods C57BL/6 mice were randomly divided into three groups：sham group,SCI group,and melatonin group （n=27per group）.Functional recovery was evaluated using the Basso Mouse Scale.Motor neurons were observed using hematoxylin and eosin staining.Pericyte coverage was analyzed using immunofluorescence.Permeability of blood-spinal cord barrier （BSCB） was assessed by administration of Evan＇s Blue.Protein levels of occludin,aquaporin-4 （AQP4）,angiopoietin-1 （Ang1）,intercellular cell adhesion molecule-1 （ICAM-1）,Bcl-2,and Bax were determined using Western blotting.Mimicking the pathological conditions of SCI,melatonin-treated primary pericytes were subjected to oxygenglucose deprivation/reperfusion （OGD/R）.Secretion of Ang1 was analyzed using an enzyme-linked immunosorbent assay,and the expression of ICAM-1 was detected by immunofluorescence.Results Melatonin treatment improved locomotor functional outcome and rescued motor neurons.Pericyte coverage was significantly reduced after SCI; melatonin treatment alleviated the loss of pericyte coverage and rescued perfused microvessels 7 days after injury.The permeability of BSCB and loss of occludin were attenuated,and edema formation and upregulation of AQP4 were inhibited,after melatonin treatment.The expression of Ang1 and Bcl-2 was improved,while the expression of ICAM-1 and Bax was inhibited,in melatonin-treated SCl mice.Furthermore,the secretion of Ang1 was increased and the expression of ICAM-1 was inhibited in melatonin-treated pericytes after OGD/R.Conclusions Melatonin ameliorated the loss of blood vessels and disruption of BSCB to exert a protective effect on SCI,which might be mediated by increased p     

Sphingosine Kinase-1/sphingosine 1-phosphate pathway in diabetic nephropathy

Objective Diabetic nephropathy （DN） is the major cause of end-stage renal disease worldwide and its prevalence continues to increase.Currently,therapies for DN provide only partial renoprotection; hence new targets for therapeutic intervention need to be identified.In this review,we summarized the new target,sphingosine kinase-1/sphingosine 1-phosphate （SphK1/S1P） pathway,explored its potential therapeutic role in the prevention and treatment of DN.Data sources Most relevant articles were mainly identified by searching PubMed in English.Study selection Mainly original articles and critical review articles by major pioneer investigators in this field were selected to be reviewed.Results SphK1/S1P pathway can be activated by hyperglycemia,advanced glycation end products,and many proinflammatory cytokines,which leads to fibronectin,transforming growth factor-31 up-regulation and AP-1 activation.And then it could promote glomerular mesangial cells proliferation and extracellular matrix accumulation,mediating the initiation and progression of diabetic renal fibrosis.Conclusions SphK1/S1P pathway is closely correlated with the pathogenesis of DN.The results suggest that SphK1/ S1P pathway as a new target for clinically improving DN in future is of great prospect.     

Association between interferon gamma receptor 1 -56C/T gene polymorphism and tuberculosis susceptibility: a meta-analysis

Background Genetic variations in the interferon-gamma （IFN-γ） receptor 1 gene （IFNGR1） may contribute to tuberculosis （TB） risk in different populations.Many studies have investigated the relationship between IFNGR1 56C/T polymorphism and the susceptibility to TB,but have yielded conflicting results.A comprehensive meta-analysis is needed to provide a more accurate estimation of the relationship between them.Methods A literature search based on a combination of manual and computer-based methods was conducted on four English databases （PubMed,Science Direct,SpringerLink,and EBSCO） and three Chinese databases （Wanfang,CQVIP,and Chinese National Knowledge Infrastructure databases）.Pooled odds ratios （ORs） and 95％ confidence intervals （95％ Cls） were calculated using either the fixed-effects model or the random-effects model for different genetic models based on the heterogeneity examination.Results A total of six studies comprising 1 497 confirmed TB cases and 1 802 controls were included in this meta-analysis.Overall,no significant association was observed between IFNGR1-56C/T polymorphism and TB susceptibility （C vs.T,OR=0.90,95％ Cl 0.69-1.17; CC vs.TT,OR=0.87,95％ Cl 0.65-1.18; TC vs.TT,OR=-1.031,95％ Cl 0.872-1.219; CC＋TC vs.TT,OR=0.89,95％ Cl 0.64-1.26; CC vs.TC＋TT,OR=0.92,95％ Cl 0.66-1.29）.In subgroup analysis,a significant association was found in the dominant model （CC＋TC vs.TT,OR=1.24,95％ Cl 1.02-1.51） in Africans,but not in Asians or Caucasians.Conclusions Our meta-analysis did not provide enough powerful evidence to identify a significant association between IFNGR1-56C/T polymorphism and TB susceptibility in the overall population.In subgroup analysis,it indicates that IFNGR1-56C/T is possibly associated with increased TB risk in Africans,but not in Asians or Caucasians.However,larger sample size and better-designed case-control studies are needed to validate these findings.     

糖络方联合弥可保治疗2型糖尿病周围神经病变的临床观察

目的观察益气养阴活血通络之糖络方联合弥可保治疗2型糖尿病周围神经病变的疗效。方法将65例患者随机分成治疗组（中西药组）和对照组（西药组）,均在西药降血糖基本达标的同时,对照组单纯口服弥可保,治疗组口服弥可保的基础上加用糖络方内服,治疗8周。结果总有效率及治疗后证候积分比较,治疗组优于对照组,差异有统计学意义（P〈0．05）;治疗后肌电图比较,治疗组优于对照组,差异有统计学意义（P〈0．01）。结论益气养阴活血通络之糖络方联合弥可保治疗2型糖尿病周围神经病变疗效优于单用弥可保,是治疗该病的有效方剂之一。     

程丑夫教授论治情志病验案举隅

程丑夫是国家级名老中医,湖南中医药大学第一附属医院主任医师、教授、博士生导师,享受政府特殊津贴专家,出身于中医世家,从医40余年,经验丰富,对于内科系统及疑难杂症的治疗颇有心得,笔者有幸跟师学习,聆听教诲,受益匪浅,现将程师论治情志病的经典验案略陈一二。1思虑伤脾案患者肖某,女,27岁。初诊：2014年5月20日。半年前因婚变后出现忧心忡忡,多思多虑,近1月来反复腹部胀满,刻诊：腹胀,食后为甚,呃逆,无反酸,通气后可减轻,无腹痛,不欲食,夜寐不安,二便调。舌红苔厚白腻,脉弦,BP：110／70mmHg。     

Depressant effect and mechanism of atorvastatin on the chronic rejection of aortic allograft in rats

Objective To investigate the depressant effect and mechanism of atorvastatin on the chronic rejection of aortic allograft in rats. Methods： The models of abdominal aorta transplantation were made with micro-surgery in rats. The recipients were divided into three groups： allograft control group, atorvastatin-treated group and isograft control group. Vascular intimal thickness in all of the groups were observed by histological examination. The expression of PCNA and α-SMA were determined by immunohistochemistry. The content of nitric oxide was determined by nitrate reductase chromatometry. Results： The vascular intimal thickness in rats of atorvastatin-treated group （11.60% ± 2.40% ） were lower than those in allograft control group （34.60 % ± 6.40 % ; P 〈 0.05） and higher than those in isograft control group （1.15 % ± 0.65 %; P〈 0.05 ）. The expression level of PCNA was decreased in atorvastatin-treated group （4.80% ± 0.80% ） than allograft control group （18.40% ± 1.80% ; P〈0.05） and higher than isograft group （1.20% ± 0.40% ; P〈0.05）. Conclusion： The expression of PCNA in the transplant aorta could be suppressed by atorvastatin, which resalted in relief of chronic rejection of aortic allograft.