缺氧缺血性脑损伤新生大鼠海马突触体素的表达及当归调控作用

目的探讨脑缺氧缺血对新生大鼠海马齿状回突触体素表达的影响及当归注射对其表达的调控作用。方法取7日龄健康SD新生大鼠33只,随机分为对照组、缺氧组和当归组各11只。缺氧组和当归组新生大鼠在无菌环境下结扎左侧颈总动脉,术后护理2 h后置于三气培养箱持续缺氧2 h,制作新生鼠缺氧缺血性脑损伤（HIBD）模型,对照组仅行假手术,不结扎左侧颈总动脉、不缺氧。术后第8 d开始,缺氧组和对照组大鼠经腹腔注射生理盐水（8ml/kg）,连续7 d;当归组用等量当归注射液（250 g/L）代替生理盐水。于生后第22 d取大鼠脑组织,常规石蜡包埋、经海马切片,行突触体素（SY）免疫组化染色,图像分析海马齿状回SY阳性细胞的积分光密度（IOD）值。结果缺氧组大鼠海马齿状回SY阳性细胞的IOD值较对照组降低,而当归组SY阳性细胞的IOD值较缺氧组增高。结论脑缺氧缺血可降低新生大鼠海马齿状回SY的表达,而当归注射液对缺氧缺血性脑损伤新生大鼠可能具有保护作用。     

顶空气相色谱法测定醋酸烯诺孕酮埋植剂中环氧乙烷的残留量

用顶空气相色谱法测定醋酸烯诺孕酮埋植剂中环氧乙烷的残留量，结果表明，线性试验与精密度良好，平均回收率为99．8％，残留量为0．93％。样品在灭菌后，室温放置3天，其环氧乙烷残留量均在0．0001％以下，符合环氧乙烷残留量应不大于0．001％的规定。表明采用顶空气相色谱法测定醋酸烯诺孕酮理植剂中环氧乙烷残留量，方法简便，结果准确，适用于对该产品中环氧乙烷残留量的检测与控制。     

复合纳米人工骨的注射、凝固及其机械性能研究

目的 构建半水硫酸钙和纳米羟基磷灰石为主的复合人工骨材料并对其注射性能、凝固性能和机械强度的影响因素进行考察.方法 测试不同液固比条件下复合材料的注射特性,25℃和37℃时分别测试不同液固比、不同二水硫酸钙促凝剂条件下的材料初、终凝时间和压缩强度,均与纯硫酸钙作对比.结果 液固比0.50以上时注射性能满意.无论何种液/固比,复合材料的凝固时间均较硫酸钙延长,37℃下的凝固时间较25℃下延长.一定范围内促凝剂用量过大或过小均使凝固时间延长.液固比越大或促凝剂用量越高,材料压缩强度越低.纳米磷灰石含量增大则材料强度降低.结论 合理掌握纳米磷灰石的比例,液固比和促凝剂的用量,是开发可注射纳米人工骨的关键.     

Expression of FAK-related non-kinase (FRNK) coincides with morphological change in the early stage of cell adhesion

Focal adhesion kinase (FAK), a protein tyrosine kinase, has recently been suggested to play a role in signal transduction through integrins. In fact, FAK is involved in cell proliferation and cell motility by performing signal transduction through integrins. FAK-related non-kinase (FRNK) has been found to be an inhibitor of FAK. As the expression level of FRNK in the cell is very low, the study of FRNK has been preferentially performed by gene overexpression, up to the present, and the role of constitutive FRNK in cells remains unclear. We hypothesized that FRNK is involved in the adhesion of cells to the extracellular matrix (ECM) and investigated the expression of FRNK by time kinetic analysis shortly after cell seeding. We found that FRNK expression was significantly increased in the cells during the early stage of cell adhesion to the ECM. These data indicated that FRNK plays an important role in cell adhesion during the very early stages of cell culture.     

喉的应用解剖与临床意义

目的：为功能性喉手术提供解剖形态学数据。方法：对50例结构完整的喉标本进行解剖观察和测量。结果：提供了喉重建术相关的甲状软骨、环状软骨、甲状舌骨膜、环甲韧带、弹性圆锥和方形膜等共75项按性别分组的测量数据。结论：为临床功能性喉手术以及喉功能重建提供了形态学参考数据。     

Increased expression levels of E-cadherin,cytokeratin 18 and 19 observed in preeclampsia were not correlated with disease severity

Introduction

Preeclampsia is a pregnancy-specific disorder and placental factor(s) contribute to the pathogenesis of preeclampsia. Turnover of villous trophoblast is affected by impaired placental perfusion in preeclampsia. Expression and localisation of cadherins and cytokeratins are involved in the pathogenesis of preeclampsia. However, studies describing the associations between cadherins and cytokeratins in preeclampsia are limited. The aim of this study was to investigate the expression of E-cadherin, N-cadherin, cytokeratin 18 and cytokeratin 19 in placentae from women with preeclampsia in order to determine whether their expression differs with disease severity.

Methods

29 preeclamptic placentae and 25 normotensive placentae were included in this study. The expression of E-cadherin, cytokeratin 18, cytokeratin 19 andN-cadherin was quantified by immunohistochemistry and western blotting.

Results

E-cadherin, cytokeratin 18 and cytokeratin 19 were expressed predominantly in the syncytiotrophoblast of the placenta and the expression of E-cadherin, cytokeratin 18 and cytokeratin 19 was significantly increased in preeclampsia compared to normotensive pregnancies. However, there was no significant difference in expression between severe preeclampsia and mild preeclampsia. In addition, there was no difference in the expression of N-cadherin between preeclampsic and normotensive pregnancies.

Discussion

Our data demonstrated increased expression of E-cadherin, cytokeratin 18 and cytokeratin 19 in the syncytiotrophoblast of preeclamptic placentae, but this increase was not correlated with disease severity.

Conclusion

Our data suggests that E-cadherin and cytokeratins are involved in the pathogenesis of preeclampsia.     

神经生长因子对大鼠胫骨骨折愈合的影响

背景：临床中发现失神经可导致骨折断端骨痂过度生长甚至在肌肉中出现异位骨化 ,这一现象提示神经因素对骨折愈合有影响。 目的：探讨神经生长因子对大鼠胫骨骨折愈合的影响。 设计、时间及地点：随机对照动物实验，于2005-06/2006-03在解放军第二军大学动物实验中心完成。 材料：健康雄性3个月龄SD大鼠120只，体质量250~300 g，随机分为单纯左胫骨骨折组和神经生长因子治疗组，每组60只。注射用神经生长因子由厦门北大之路生物工程有限公司提供。 方法：两组大鼠制备单纯胫骨骨折，神经生长因子治疗组肌注2 000 AU(1.4 g)，1 次/ d,分别注射两侧腓肠肌，连续肌注2周。伤后第4周对2组大鼠骨折断端行断层CT，测量骨折断端最大横截面及计算骨痂灰度值，行生物力学3点折弯试验。 主要观察指标：①骨组织形态计量学、骨密度测定。②骨痂组织形态学的观察。③免疫组化法测定骨痂组织骨钙素的表达。④观察2组大鼠骨痂中成骨细胞的超微结构变化。⑤Western印迹检测Ⅰ、Ⅱ型胶原的表达。 结果：神经生长因子治疗组3点折弯试验各项生物力学参数均优于单纯左胫骨骨折组(P < 0.05)。形态学及超微结构观察见神经生长因子治疗组骨折愈合优于单纯左胫骨骨折组。神经生长因子治疗组Ⅰ型胶原蛋白表达明显高于单纯左胫骨骨折组(P < 0.05)；而单纯左胫骨骨折组骨痂Ⅱ型胶原蛋白的表达明显高于神经生长因子治疗组(P < 0.05)。 结论：生物力学测试及Ⅰ型胶原蛋白表达和成骨细胞微观结构均说明神经生长因子对骨折断端的骨化有促进作用，其途径有可能在骨痂生长的不同时期通过调节Ⅰ、Ⅱ型胶原的量来调控骨折的愈合。     

Low baseline and subsequent higher aortic abdominal aneurysm FDG uptake are associated with poor sac shrinkage post endovascular repair

Purpose

The growth phases of medically treated abdominal aortic aneurysms (AAA) are frequently associated with an ¹⁸F–fluorodesoxyglucose positron emission tomography (FDG-PET) pattern involving low baseline and subsequent higher FDG uptake. However, the FDG-PET patterns associated with the endovascular aneurysm repair (EVAR) of larger AAA are presently unknown. This study aimed to investigate the relationship between serial AAA FDG uptake measurements, obtained before EVAR and 1 and 6 months post-intervention and subsequent sac shrinkage at 6 months, a well-recognized indicator of successful repair.

Methods

Thirty-three AAA patients referred for EVAR (maximal diameter: 55.4?±?6.0 mm, total volume: 205.7?±?63.0 mL) underwent FDG-PET/computed tomography (CT) before EVAR and at 1 and 6 months thereafter, with the monitoring of AAA volume and of a maximal standardized FDG uptake [SUVmax] averaged between the axial slices encompassing the AAA.

Results

Sac shrinkage was highly variable and could be stratified into three terciles: a first tercile in which shrinkage was absent or very limited (0–29 mL) and a third tercile with pronounced shrinkage (56–165 mL). SUVmax values were relatively low at baseline in the 1st tercile (SUVmax: 1.69?±?0.33), but markedly increased at 6 months (2.42?±?0.69, p?=?0.02 vs. baseline). These SUV max values were by contrast much higher at baseline in the 3rd tercile (SUVmax: 2.53?±?0.83 p?=?0.009 vs. 1st tercile) and stable at 6 months (2.49?±?0.80), while intermediate results were documented in the 2nd tercile. Lastly, the amount of sac shrinkage, expressed in absolute values or in percentages of baseline AAA volumes, was positively correlated with baseline SUVmax (p?=?0.001 for both).

Conclusion

A low pre-EVAR FDG uptake and increased AAA FDG uptake at 6 months are associated with reduced sac shrinkage. This sequential FDG-PET pattern is similar to that already shown to accompany growth phases of medically treated AAA.

     

阿魏酸对小鼠骨髓造血功能辐射损伤的防护作用

目的 观察阿魏酸对小鼠外周血象和骨髓造血功能辐射损伤的防护作用,初步探讨阿魏酸的抗辐射作用机制。方法 6~8周ICR小鼠96只,随机数表法分为正常对照组、照射模型组、阳性药（408片）治疗组和阿魏酸10、30、90 mg ·kg^-1·d^-1治疗组,每组16只。小鼠初次给药后24 h接受3.5 Gy ⁶⁰Co γ单次全身照射,之后连续7 d给药。其中,每组10只用于观察照射前2 d及照射后3、7、10、15、22 d的外周血象;其余6只用于照射后7 d检测骨髓嗜多染红细胞的微核细胞率、造血祖细胞集落形成能力、以及Thbd和HMGB1蛋白的表达水平。结果 与照射模型组比较,90 mg ·kg^-1 ·d^-1的阿魏酸可有效提高小鼠3.5 Gy照射后3、10、15、22 d的外周血白细胞数（t=2.267、2.399、1.945、2.828,P<0.05）,显著降低骨髓嗜多染红细胞微核细胞率（t=4.013,P<0.05）,明显提高造血祖细胞红细胞集落生成单位（CFU-E）、红细胞爆裂型集落生成单位（BFU-E）和粒-单细胞集落生成单位（CFU-GM）的集落形成能力（t=2.366、2.953、3.115,P<0.05）,并提高骨髓细胞中Thbd和核内HMGB1蛋白表达水平（t=17.75、23.39,P<0.01）。结论 阿魏酸可通过调节Thbd和HMGB1蛋白表达,促进小鼠骨髓造血功能辐射损伤修复,加速外周血象恢复。