慢性乙型肝炎患者血清sIL-2R和IGF-1与淋巴细胞凋亡的关系

目的 研究慢性乙型肝炎患者血清可溶性白细胞介素-2受体（sIL-2R）和胰岛素样生长因子-1（IGF-1）与外周血淋巴细胞凋亡的关系，并探讨其临床意义。方法 分别采用放射免疫分析法和流式细胞计数仪检测慢性乙型肝炎患者血清sIL-2R、IGF-1和外周血淋巴细胞凋亡率。结果 慢性乙型肝炎患者血清sIL-2R、IGF-1水平和外周血淋巴细胞凋亡率明显高于正常对照组。随着患者肝脏病变程度的加重，外周血淋巴细胞凋亡率和血清sIL-2R水平逐步升高，而IGF-1水平则逐步降低。慢性乙型肝炎患者外周血淋巴细胞凋亡率与血清sIL-2R水平呈正相关，与IGF-1水平呈负相关。结论 慢性乙型肝炎患者外周血淋巴细胞凋亡的异常与血清sIL-2R、IGF-1水平的异常有关，三者的变化与患者肝脏病变程度相关。     

“医药分开”政策对于临床医师服务行为的影响研究简

目的：了解“医药分开”政策对临床医师服务行为的影响。方法：以北京市试行“医药分开”政策的部分医院为研究现场,随机抽取800名临床医师进行问卷调查,分析该政策对临床医师服务行为的影响。结果：临床医师对“医药分开”政策的知晓率为99.5%;92.1%的临床医师更加重视规范诊疗;85.0%的临床医师提高了服务意识,服务更周到;86.8%的临床医师更加重视患者满意度。结论：试点医院临床医师对政策的知晓和掌握情况良好。大多数临床医师优化了服务行为,并对政策的进一步完善提出有益建议,如应加强宣传,正确舆论导向;提高医疗服务收费标准;提高医务人员待遇,建立完善激励机制和考核机制;提高医师积极性等。     

小鼠高迁移率族蛋白B1启动子的构建与转录活性检测

【目的】构建小鼠高迁移率族蛋白B1(high-mobility group box 1 protein,HMGB1)启动子全长序列的荧光素酶报告基因用于药物筛选。【方法】采用PCR技术扩增小鼠HMGB1基因启动子全长序列,用GV238载体构建报告质粒GV238-HMGB1-P-Luc,以pGL3-basic作为阴性对照质粒,与内参质粒pRL共转染Hela细胞,以内毒素(LPS,0.2μg/mL)作为激活剂,以正丁酸钠(SB,10 mmol/L)作为抑制剂,分组处理24 h后检测荧光素酶活性。【结果】经酶切、PCR及测序鉴定证实克隆的HMGB1基因启动子全长2 140 bp,DNA序列正确无突变。与pGL3-basic组比较,GV238-HMGB1-P-Luc组荧光素酶活性显著增强(P0.05);与GV238-HMGB1-P-Luc组比较,LPS组荧光素酶活性显著增强(P0.01);与LPS组比较,SB组荧光素酶活性显著降低(P0.01)。【结论】HMGB1基因启动子报告基因构建成功,LPS可以增强其表达,SB则可以抑制LPS刺激下的HMGB1启动子表达增强,可为下一步筛选具有调控HMGB1启动子活性的药物奠定基础。     

高压氧对脑损伤大鼠BDNF表达的影响

目的研究高压氧（HBO）治疗对侧位液压冲击脑损伤大鼠大脑皮层及海马区脑源性神经营养因子（BDNF）表达的影响。方法应用液压撞击仪制作侧位液压冲击脑损伤大鼠模型。Wistar雄性大鼠32只,随机分成脑损伤组及正常对照组,每组16只。各组再分别分为两组进行HBO暴露及常压空气暴露,每组8只。5 d后断头取脑,行脑组织切片,应用免疫组化方法检测BDNF在皮层及海马区的表达。结果正常对照组HBO暴露与常压空气暴露BDNF免疫阳性细胞数比较差异无统计学意义（P〉0.05）;脑损伤组中HBO暴露后皮层及海马BDNF免疫阳性细胞数多于常压空气暴露（P〈0.01）,脑损伤常压空气暴露组多于正常对照常压空气暴露组（P〈0.01）。结论大鼠脑损伤后可以提高损伤皮层及海马区BDNF的表达,HBO治疗可以进一步提高大鼠脑内BNDF的表达。     

组蛋白去乙酰化酶抑制剂联合芬维A胺诱导人肝癌细胞凋亡的研究

目的探讨组蛋白去乙酰化酶抑制剂Scdptaid、TSA分别联合芬维A胺诱导人肝癌细胞凋亡作用。方法组蛋白去乙酰化酶抑制剂Scriptaid（10／zM）合芬维A胺（10／zM）、TSA（1／zM）联合芬维A胺（10／zM）分别处理人肝癌细胞株（SNU475。SNU449,SNU398,sK—HEP-1,PLC／PRF／5）。通过Caspase-3／7检测试剂盒和CellTiter—Glo发光细胞活力检测试剂盒监测组蛋白乙酰化酶抑制剂联合芬维A胺对肝癌细胞的影响。结果组蛋白去乙酰化酶抑制剂Scriptaid（10／zM）、Ts（1／zM）联合芬维A胺（10肚M）处理细胞24h能显著诱导人肝癌细胞株SNU475、SNU449、SNU389、SK—HEP-1、PLC／PRF／5凋亡（P〈0．01）。结论组蛋白乙酰化酶抑制剂Scriptaid、TSA联合芬维A胺能诱导肝癌细胞凋亡。     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

2008年-2009年鞍山地区手足口病患儿粪便样本中肠道病毒的检测结果分析

目的:通过实时荧光RT-PCR法检测2008年-2009年手足口病患儿粪便样本,了解鞍山地区手足口病病原特征,为手足口病防治工作提供科学依据。方法:分别于2008年6月-9月收集657份手足口病患儿粪便样本及2009年5月-9月收集274份手足口病患儿粪便样本进行检测。结果:2008年EV71阳性31份,CA16阳性58份2,009年EV71阳性75份,CA16阳性55份。结论:鞍山地区手足口病病原体以EV71和CA16为主,2008年以CA16为主要病原,2009年以EV71为主要病原。重症手足口病患儿病原均为EV71。     

四维盆底超声在电刺激联合生物反馈结合盆底肌锻炼治疗压力性尿失禁疗效评估中的价值

目的:探讨四维盆底超声在电刺激联合生物反馈盆底肌锻炼治疗压力性尿失禁(SUI)疗效评估中的价值.方法:选择60例SUI患者,电刺激联合生物反馈盆底肌锻炼3个月后分析治疗效果;并于治疗前后采用经会阴四维盆底超声记录患者肛提肌裂孔面积、裂孔左右径、肛提肌厚度、膀胱颈移动度、膀胱尿道后角及尿道内口漏斗形成率.结果:治疗后,肛...     

急性肺损伤新生大鼠AQP5及CC16变化的临床意义

目的探讨肺组织水通道蛋白5（AQP5）、血及肺灌洗液Clara细胞蛋白（CC16）在急性肺损伤早期的动态改变及临床意义。方法将140只sD新生大鼠随机分两批（每批70只）,再随机分为正常对照组（NS组）及内毒素（LPS）组（LPS组,7个亚组）。LPS组予腹腔注射5mg／kgLPS制作新生大鼠急性肺损伤（ALI）模型。各亚组分别在注射后0．5、1、2、4、8、16h和24h处死后取材,第一批收集肺行组织病理和肺湿／干重比值检测,采集血清和支气管肺泡灌洗液（BALF）,用双抗体夹心ELISA法检测CC16含量。第二批取肺组织,用免疫印迹法测肺组织AQP5的表达,观察其动态改变。结果 ①LPS注射0．5h后在病理上动物出现点状肺出血,随时间推延渐发展为片状肺出血;LPS2h、4h组肺湿／干重比（W／D）明显增高,P〈0．01有统计学意义;②LPS0．5h组大鼠肺组织AQP5表达开始下调,1-2h组达到最低,继而AQP5表达渐上升,8h组与正常水平接近,之后再次下调至24h。③LPS致伤后大鼠BALF中CC16水平迅速下降,LPS组各组均较对照组有显著性差异（P〈0．01）;LPS组血清CC16水平较对照组上升,从注射LPS2h后开始有差异,4h达高峰,以后呈下降趋势,但8h、16h组仍明显高于对照组（P〈0．01）。结论①新生大鼠AQP5、CC16的改变反映了I型肺泡上皮细胞受损及Clara细胞损伤,三者可作为早期反映AU的敏感实验室指标。②LPS组AQP5、BALF及血清CC16与对照组有差异的时间点有差别,早期发现干预ALI对前两者监测更好。③AQP5表达变化提示可能存在治疗窗口期。     

Short-Term Visual Experience Leads to Potentiation of Spontaneous Activity in Mouse Superior Colliculus

Spontaneous activity in the brain maintains an internal structured pattern that reflects the external environment,which is essential for processing information and developing perception and cognition.An essential prerequisite of spontaneous activity for perception is the ability to reverberate external information,such as by potentiation.Yet its role in the processing of potentiation in mouse superior colliculus(SC)neurons is less studied.Here,we used electrophysiological recording,optogenetics,and drug infusion methods to investigate the mechanism of potentiation in SC neurons.We found that visual experience potentiated SC neurons several minutes later in different developmental stages,and the similarity between spontaneous and visually-evoked activity increased with age.Before eye-opening,activation of retinal ganglion cells that expressed ChR2 also induced the potentiation of spontaneous activity in the mouse SC.Potentiation was dependenton stimulus number and showed feature selectivity for direction and orientation.Optogenetic activation of parvalbumin neurons in the SC attenuated the potentiation induced by visual experience.Furthermore,potentiation in SC neurons was blocked by inhibiting the glutamate transporter GLT1.These results indicated that the potentiation induced by a visual stimulus might play a key role in shaping the internal representation of the environment,and serves as a carrier for short-term memory consolidation.