介入治疗34例膜部室间隔缺损

目的：评价介入治疗膜部室间隔缺损的临床效果。方法：经胸超声心动图及临床表现诊断为膜部室间隔缺损的患者34例，在局部或全身麻醉下行经导管室间隔缺损的介入治疗，其中31例应用Amplatzer不对称型膜部室间隔缺损封堵器，3例应用国产室间隔缺损封堵器。术中连续经胸超声心动图和X线监测，术后1天、1月、3月、6月行心电图及超声心动图复查。结果：超声测定膜部室间隔缺损直径为3．0～11．6mm(平均4．5mm)，距离主动脉右冠瓣2．7～7．8mm(平均3．6mm)，左心室造影测定膜部室间隔缺损的直径为3．0～8．8mm(平均5．4mm)，所选膜部室间隔缺损封堵器直径为4．0～16mm(平均7．9mm)。技术成功率100％。超声心动图示术后即刻残余分流为17．6％(6／34)，24h后残余分流为8．8％(3／34)，1个月后残余分流为5．9％(2／34)。34例患者术中均有一过性室性心律失常，1例发生一过性心跳骤停。术后1例出现股静脉血栓形成，3例出现了一过性Ⅲ度房室传导阻滞，2例于术后24h内发生溶血，经内科治疗后完全恢复，未见封堵器脱落、主动脉瓣返流等并发症。结论：经导管关闭膜部室间隔缺损的操作简单、方便、并发症少，残余分流少见，值得在临床全面推广。     

颅内出血性椎动脉夹层的治疗

目的探讨颅内出血性椎动脉夹层的治疗方法。方法回顾分析了2000-2005年40例出血性颅内段椎动脉夹层的治疗。其中支架辅助的弹簧圈栓塞33例,夹层段动脉闭塞6例,夹层近端主干动脉闭塞1例。结果手术无死亡病例。术后随访1-46个月,平均16.3个月。发现夹层动脉通畅,无夹层再出血,无新发后循环梗死。1例支架辅助弹簧圈栓塞患者夹层复发,行补充填塞弹簧圈。结论血管内夹层近端闭塞以及夹层段动脉闭塞是治疗颅内出血性椎动脉夹层的经典术式。支架辅助的弹簧圈栓塞治疗保留了载瘤动脉,避免了术后对侧椎动脉血流负荷量的增加;减少了后循环缺血的危险,扩大了血管内治疗出血性椎动脉夹层的手术适应证。本组结果显示支架辅助弹簧圈栓塞术并未增加夹层再通以及穿支动脉闭塞。本组经验初步表明支架辅助的弹簧圈栓塞是治疗出血性颅内椎动脉夹层的合理选择之一。     

人钠/二羧酸协同转运蛋白3基因调控肾小管上皮细胞线粒体膜电位的研究

目的 观察人钠／二羧酸协同转运蛋白3(hNaDC3，)对人肾脏近曲小管上皮细胞(HKC)线粒体膜电位的变化及其对细胞能量代谢的影响。方法 应用亚克隆技术构建正义pcDNA3-hNaDC3和反义pcDNA3-AhNaDC3两个真核表达载体，通过脂质体LipofectAMINE将pcDNA3-hNaDC3及pcDNA3-AhNaDC3转染至HKC细胞。克隆筛选后，用RT—PCR、Northern印迹及Western印迹鉴定外源基因的整合和表达。荧光探针JC-1观察各细胞系线粒体膜电位的变化。结果 外源hNaDC3基因稳定整合到HKC细胞基因组中，并获得高、低表达。转染正义hNaDC3cDNA的HKC细胞线粒体膜电位降低，JC-1在线粒体内形成单体，发出绿色荧光；而转染反义hNaDC3cDNA的HKC细胞线粒体膜电位略微升高，JC-1形成聚合体，发出红色荧光。结论 hNaDC3过表达引起线粒体膜电位降低，反义hNaDC3则使线粒体膜电位略微升高。提示NaDC3可能通过使线粒体膜电位下降，参与了细胞能量代谢。     

小红参滴丸的制备工艺研究

目的 :研究小红参滴丸的最佳成型工艺条件。方法 :采用正交试验法 ,考察了提取物与基质配比、滴制温度、滴头口径大小等因素TLC定性鉴别。结果 :药物提取物 :基质 (1:1.4 ) ,滴制温度 85℃ ,滴头口径 1/ 2mm (内径 /外径 )。滴速 (8± 2 )滴 /min ,滴距 8cm ,冷却剂温度 (4± 2 )℃ ,柱高 6 0cm进行滴制 ,滴丸的成型率最高。结论 :证明此工艺可行 ,成品得率高 ,符合滴丸剂的质量标准。     

胃癌患者胃液可溶性白细胞介素-2受体初步研究

应用双抗体夹心ELISA法对87例消化道疾病患者胃液可溶性白细胞介素-2受体(sIL-2R)水平进行测定。结果表明,胃癌患者胃液sIL-2R水平明显高于慢性浅表性胃炎及十二指肠溃疡患者(P相似文献   

新兵基础训练期间过劳性损伤的前瞻性研究

目的：查明我军基础训练中过劳性损伤的发病情况及分布特征。     

Reduction mammaplasty by central pedicle flap with short submammary scar

Reduction mammaplasty was performed in 30 patients by combining the central pedicle flap method with the short submammary scar (3-S) technique to avoid the common drawbacks of currently popular dermoglandular procedures. Reduction was accomplished by using perforating vascular branches from the pectoralis major muscle and its fascia supplying the nipple and breast parenchyme instead of the subdermal plexus. The central vascular pedicle supplying the nipple-areola complex was preserved. Only the periphery of the breast parenchyme was resected circumferentially, with the exception of the inferolateral portion, so as not to injure the sensory nerve. The remaining breast parenchyme was preserved in an inverted cone shape. The nipple-areola complex was safely transposed with great freedom, and the amount of resection was accurately adjusted for symmetry. No cases of nipple-areola complex sensory change occurred postoperatively, and lactation is possible because of preservation of the lactiferous ducts. The length of postoperative scars was reduced by using the short submammary scar technique. We believe this combined method is ideal in patients requiring resections ranging from 200 to 600 g per breast with good skin elasticity and moderate degree of ptosis.Presented at the Sixth Asian Pacific Congress of the International Confederation for Plastic and Reconstructive Surgery, in Seoul, Korea, October 1993.     

Lewis Histo-Blood Group System and Associated Secretory Phenotypes

This review summarises present knowledge of the chemistry, immunology, genetics and clinical significance of antibodies in the Lewis and secretor histoblood group systems. Although red cell serology has laid the foundations for these systems, more recent advances have been made by studying Lewis and related glycoconjugates with monoclonal antibodies, determining structures by mass spectrometry and NMR spectroscopy, identifying enzymes and their specificities, and identifying the genes by molecular biology. The expression of Lewis system antigens is dependent on Lewis and secretor loci. Fucosyltransferases coded by genes at these loci compete and interact with each other and with other transferases to determine an individual's Lewis and secretor phenotype. Exocrine epithelial cells, mostly of endodermal origin, synthesise the Lewis antigens which, as plasma glycolipids, are secondarily acquired by cells of the peripheral circulation. Phenotyping red cells is often regarded as a simple way of determining the Lewis and sometimes the secretor status of an individual; however, the red cell phenotype is influenced by many factors and may not necessarily reflect someone's Lewis and secretor genotypes. Two main red cell Lewis groups are usually found, Lewis negative and Lewis positive. In Lewis-negative individuals, the secretor genotype does not affect the Lewis phenotype, but in Lewis-positive individuals, the non-secretor genotype generates the Le(a+b–) phenotype, the secretor genotype causes the Le(a–b+) phenotype, and the partial secretor genotype gives rise to the Le(a+b+) phenotype.     

Amadori糖化白蛋白对牛视网膜血管二酯酰甘油--蛋白激酶C级联的影响

目的 :探讨Amadori糖化血清白蛋白对牛视网膜血管二酯酰甘油 (DAG)———蛋白激酶C(PKC)信号级联的影响及d-α-生育酚的干预作用。方法 :体外制备的Amadori糖化的牛血清白蛋白 (AGSA)分别在生理浓度葡萄糖 (5 .5mmol/L)和高浓度葡萄糖 (2 0mmol/L)培养液中作用于新鲜牛视网膜血管。采用薄层层析和放射自显影法测定DAG含量和PKC活性 ;并检测d -α-生育酚预处理后DAG、PKC改变。结果 :在生理葡萄糖浓度下 ,牛视网膜血管暴露于AGSA2 4h或 72h后细胞内DAG含量、PKC活性均较对照组显著增加 ,当AGSA和高葡萄糖同时作用于牛视网膜血管时 ,DAG -PKC级联显著激活 ,分别为正常葡萄糖组的 3.4 7倍和 4 .5 4倍 ;在正常血清培养液中 ,与 5 .5mmol/L的葡萄糖相比 ,2 0mmol/L高糖在 2 4h时并不刺激DAG含量增加 (P >0 .0 5 ) ,而 72h时则较对照组增加 4 5 % ,PKC活性较对照增加 5 6 % ,而d -α -生育酚可逆转上述生化改变。结论 :Amadori糖化血清白蛋白可在生理葡萄糖浓度下刺激DAG -PKC途径活化 ,从而影响血管一系列生理功能 ,而d -α-生育酚对血管生化改变有保护作用。