葛根素对急性水肿性胰腺炎血管内皮细胞血管内皮钙黏着蛋白表达的影响

目的探讨葛根素注射液对急性水肿性胰腺炎（AEP）动物模型的胰腺血管内皮细胞血管内皮钙黏着蛋白（VE-cadherin）的表达、分布及其调节作用。方法 18只Wistar大鼠按数字表法随机分为正常对照组、AEP治疗组和AEP自然病程组,每组各6只,后两组建AEP动物模型。AEP治疗组给予葛根素注射液100 mg/kg。应用荧光免疫组织化学染色,观察3组大鼠胰腺血管内皮VE-cadherin的表达。结果 3组血清淀粉酶比较差异有统计学意义（P〈0.05）,治疗组与自然病程组比较差异无统计学意义（P〉0.05）。正常对照组胰腺组织肉眼观察无明显改变;AEP自然病程组胰腺组织水肿较明显,AEP治疗组与AEP自然病程组胰腺外观相似。3组标本的平均荧光强度差异有统计学意义（P〈0.05）,AEP自然病程组的荧光强度为（1.04±0.05）,低于正常对照组的（1.41±0.06）,差异有统计学意义（P〈0.05）,而治疗组为（1.25±0.07）,较非治疗组明显改善,但与正常对照组比较仍低,差异有统计学意义（P〈0.05）。结论在AEP时VE-cadherin分布异常、表达水平下降,葛根素可改善其分布及表达水平。     

Transforming growth factor-β1 involved in urotensin II-induced phenotypic differentiation of adventitial fibroblasts from rat aorta

Background Urotensin Ⅱ （UⅡ） is a new vasoconstrictive peptide that may activate the adventitial fibroblasts.Transforming growth factor-β1 （TGF-β1） is an important factor that could induce the phenotypical transdifferentiation of adventitial fibroblasts. This study aimed to explore whether TGF-β1 is involved in UⅡ-induced phenotypic differentiation of adventitial fibroblasts from rat aorta.Methods Adventitial fibroblasts were prepared by the explant culture method. TGF-β1 protein secretion from the cells was determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expression of α-smooth nuscle actin （α-SM-actin）, the marker of phenotypic differentiation from fibroblasts to myofibroblasts, were determined using real-time quantitative RT-PCR （real-time RT-PCR） and Western blotting, respectively.Results UⅡ stimulated the secretion of TGF-β1 in cultured adventitial fibroblasts in a time-dependent manner. The secretion reached a peak at 24 hours, was higher by 69.8% （P ＜0.01）, than the control group. This effect was also concentration dependent. Maximal stimulation was reached at 10-8 mol/L of UⅡ （P ＜0.01）, which was increased by 59.9%,compared with in the control group （P ＜0.01）. The secretion of TGF-β1 induced by UⅡ was significantly blocked by SB-710411 （10-7 mol/L）, a specific antagonist of UⅡ receptor. In addition, both UⅡ （10-8 mol/L） and TGF-β1 significantly stimulated α-SM-actin mRNA and protein expression. Moreover, the α-SM-actin induced by UⅡ was inhibited by the specific neutralizing antibody （20 μg/ml） of TGF-β1, while the α-SM-actin expression stimulated by TGF-β1 （20 ng/ml）was inhibited by SB-710411 （10-7 mol/L）, the UⅡ receptor antagonist.Conclusion This study suggests that UⅡ could induce TGF-β1 secretion in adventitial fibroblasts via UT activation, and TGF-β1 might be involved in phenotypic differentiation from adventitial fibroblasts into myofibroblasts induced by UⅡ, and TGF-β1 signaling might be one of the important pathways by which UⅡ is involved in vascular fibrosis.     

临床医学本科毕业生择业基层的问题思考

临床医学本科生下基层就业将直接关系到基层卫生人力资源的配置和学生的出路问题。通过对部分到基层就业的临床医学本科毕业生的个性资料进行分析,以及对在校生基层就业意识的调查,发现：求学动机、择业价值取向、保障机制、地区经济状况、生源背景等是影响学生择业基层的关键因素。促进学生基层就业,要靠政府、社会、学校多方力量,形成合力共同推进。具体可从四个方面去尝试：找准思想引导切入点,提升学生基层就业意识;改善基层医疗现状,提升岗位吸引力;定向订单式培养乡镇临床医生,确保基层卫生人才的输出;激励政策规范化,创造学生岗位成长可能性。     

小剂量甲氨蝶呤治疗高甲状腺过氧化物酶抗体血症观察

目的：观察小剂量甲氨蝶呤（MTX）对高甲状腺过氧化物酶抗体（TPOAb）血症的疗效及安全性。方法：140例高TPOAb血症桥本甲状腺炎（HT）患者,分为治疗组110例和对照组30例。两组均给予小剂量、短期的抗甲亢和（或）补充左甲状腺素（L-T4）治疗。治疗组在此基础上加服甲氨蝶呤片（每周7.5～10mg）,观察时间3～24个月。比较两组治疗前后TPOAb水平变化、转阴率、甲减患者服用L-T4剂量的变化,及甲功正常者甲状腺功能的变化。结果：治疗后两组TPOAb水平持续明显下降,24个月后,治疗组TPOAb水平明显低于对照组,下降率则明显高于对照组（P〈0.01）;治疗组转阴率为19.1％,明显高于对照组（P〈0.01）。结论：小剂量MTX联合小剂量短期抗甲亢治疗,能显著降低HT患者TPOAb水平,延缓甚至终止TPOAb对甲状腺的破坏进程,优于常规抗甲亢治疗。     

脑出血的遗传因素

脑卒中是人类三大死因之一,具有发病率高、致残率高、死亡率高等特点。脑卒中分为出血性脑卒中和梗塞性脑卒中,出血性脑卒中又称脑出血,其死亡率及致残率更高。脑出血具有一定的家族遗传倾向,许多研究表明其与高血压、高脂血症、代谢综合征、凝血功能异常、动脉炎症等疾病有相关性。本文综述了近年来这些基础疾病研究中所发现与脑出血有关的遗传基因的研究进展。     

股骨近端防旋髓内钉内固定治疗老年股骨粗隆间骨折病人的护理

[目的]总结股骨近端防旋髓内钉（PFNA）内固定治疗老年股骨粗隆间骨折病人的护理.[方法]对39例老年人股骨粗隆间骨折行PFNA内固定术,加强术前护理,术后加强功能锻炼,预防内翻、下肢外旋、肺部感染、脂肪栓塞、深静脉血栓、压疮、骨折不愈合等并发症.[结果]39例病人均完成手术,参照Harris标准,术后髋关节功能优良36例,可3例.[结论]加强老年股骨粗隆间骨折行PFNA内固定的护理有利于术后康复.     

移动通讯工具物表微生物携带状况及消毒效果评价

目的了解人群中使用的移动通讯工具微生物携带状况,探讨消毒干预措施的效果。方法随机抽查受访人群中使用的移动通讯工具500部（实验组）及未使用对照移动通讯工具100部（对照组）,消毒前后采用棉拭子涂抹法对实验组手机经常接触部位采样,进行细菌总数、大肠菌群、致病菌、乙肝病毒及肠道病毒检测;对照组手机不作消毒处理,检测内容同实验组。同时对使用手机者作问卷调查。结果随机采集的500份移动通信工具消毒前表面样品细菌总数超标率为30．8％,大肠菌群超标率为28．4％,致病菌检出率为11．4％,HBV—DNA检出率为11．0％,肠道病毒检出率为9．8％,与对照组比较差异均有统计学意义（P〈0．05）;消毒后移动通信工具表面微生物检出率与消毒前比较差异有统计学意义（P〈0．05）。结论移动通讯工具表面污染比较严重,建议定期进行消毒。使用移动通信工具者要增强自我保护意识,养成勤洗手的习惯,减少因使用移动通信工具引起的致病微生物感染。     

心肌细胞肥大中番茄红素对自噬的作用

目的 探讨在血管紧张素Ⅱ（AngⅡ）诱导的心肌肥大中,番茄红素对自噬的影响.方法 原代培养的乳鼠心肌细胞,采用AngⅡ干预建立心肌肥大的模型;用番茄红素和自噬的阻断剂3-甲基腺嘌呤（3MA）干预.在光学显微镜下观察心肌细胞的形态;采用Western blot法检测自噬相关基因6（Atg6）Beclin1及自噬相关基因8（Atg8）LC3蛋白的表达;Real time PCR技术检测心肌细胞肥大标志物心房利钠多肽（ANP）的mRNA表达.结果 在AngⅡ诱导的心肌肥大中[细胞面积（517.19±52.31）;ANP相对含量（17.83±2.07）],番茄红素[细胞面积（355.82±40.45）;ANP相对含量（12.16±1.41）]缓解了心肌细胞面积的增加（F=56.518,P＜0.05）,下调了ANP的mRNA表达水平（F=157.048,P＜ 0.05）.番茄红素增加了心肌肥大时自噬相关基因Beclin1[蛋白相对含量（0.685±0.058）,F=202.873,P＜0.05]和LC3蛋白相对含量[（0.608±0.045）,F=177.114,P＜0.05]蛋白的表达.自噬阻断剂3MA降低了番茄红素对心肌细胞肥大的抑制作用（P＜0.01）.结论 番茄红素可能通过激活自噬来抑制心肌细胞肥大.     

Relationship between intracellular Ca2+ and ROS during fluoride‐induced injury in SH‐SY5Y cells

The mechanisms underlying the neurotoxicology of endemic fluorosis still remain obscure. To explore lactate dehydrogenase (LDH) leakage, intracellular Ca²⁺ concentration ([Ca²⁺]_i) and reactive oxygen species (ROS) production induced by fluoride, human neuroblastoma (SH‐SY5Y) cells were incubated with sodium fluoride (NaF, 20, 40, 80 mg/L) for 24 h, with 40 mg/L NaF for 3, 6, 12, 18, 24 h, and N‐acetyl‐L ‐cysteine (NAC), ethyleneglycol‐bis‐(β‐aminoethyl ether)‐N,N,N′,N′‐tetraacetic acid (EGTA), 1,2‐bis(O‐aminophenoxy)ethane‐N,N,N′,N′‐tetraacetic acid tetra(acetoxymethyl) ester (BAPTA‐AM) alone or combined with fluoride (40 mg/L) respectively for 12 h in vitro. The results showed that the LDH levels in the 40 and 80 mg/L fluoride‐treated groups were significantly higher than that of the control group (in the test level of 0.05, the difference were statistical significance). [Ca²⁺]_i and ROS reached a peak at 3 h and 12 h respectively after exposure to 40 mg/L fluoride. Fluoride coincubated with NAC (antioxidant) dramatically decreased ROS and LDH levels compared with the fluoride only group (in the test level of 0.05, the difference were statistical significance). However, fluoride‐induced increase in [Ca²⁺]_i was not affected by NAC. BAPTA‐AM (intracellular calcium chelator) markedly lowered fluoride‐induced increase of [Ca²⁺]_i, ROS and LDH levels while EGTA (extracellular calcium chelator) have no effects on them. These results indicate that fluoride‐related Ca²⁺ release from the site of intracellular calcium storage causes the elevation of ROS contributing to the cytotoxicity in SH‐SY5Y cells. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2013.     

碘化N-正丁基氟哌啶醇通过非外钙机制抗心肌细胞缺氧复氧损伤

目的研究碘化N-正丁基氟哌啶醇(F2)对大鼠心肌细胞无外钙缺氧/复氧(H/R)损伤的作用及其机制。方法建立无外钙(零钙液)的心肌细胞H/R模型,于缺氧液及复氧液中加入1×10-6mol/L的F2。倒置显微镜下观察细胞形态结构及搏动的变化;采用蛋白印迹法检测心肌细胞磷酸化ERK(p-ERK1/2)、总ERK1/2蛋白表达的变化。结果零钙液H/R可引起培养心肌细胞形态结构呈损伤性改变,包括胞体收缩、伪足减少和搏动无力;零钙液H/R可引起培养心肌细胞p-ERK1/2表达增加,但不影响总ERK表达,即可激活培养心肌细胞ERK1/2;F2可以改善零钙液H/R状态下心肌细胞形态结构的损伤。F2对零钙液H/R心肌细胞p-ERK1/2高表达具有抑制作用,但不影响总ERK的表达。结论 F2可通过非外钙依赖机制拮抗心肌细胞H/R损伤,这可能与其抑制零钙液H/R状态下ERK1/2的激活密切相关。