真皮下血管网岛状皮瓣抗菌力的实验研究

为研究真皮下血管网薄皮瓣用于感染创面的可行性，在家猪臀部两侧分别形成以旋髂深血管主干分支为蒂的传统岛状皮瓣和远侧５０％修薄的真皮下血管网岛状皮瓣。用细菌计数、吖啶橙荧光染色测定白细胞吞噬指数和白细胞内杀菌率，应用激光多普勒、墨汁灌注、透明标本等方法，对两种皮瓣的抗菌力作自身对照研究。结果表明，真皮下血管网岛状皮瓣的抗菌力明显降低，可能与皮瓣修薄后血供减少，白细胞功能相应降低有关。     

Thrombin regulates components of the fibrinolytic system in human mesangial cells

Besides its procoagulant activity, thrombin has been shown to stimulate cell proliferation and to regulate the fibrinolytic pathway. We report here the effect of purified human alpha thrombin on the synthesis of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) by cultured human mesangial cells. Thrombin (0 to 2.5 U/ml) increased in a time- and dose-dependent manner the production of t-PA and PAI-1 (2- to 3-fold increase of secreted t-PA and PAI-1 release during a 24 hour incubation). This effect was associated with a twofold increase in DNA synthesis measured by 3H-thymidine incorporation. Zymographic analysis and reverse fibrin autography showed that thrombin also increased the level of the 110 Kd t-PA-PAI-1 complex, whereas PAI-1 was present as a free 50 Kd form in the culture medium conditioned by unstimulated and thrombin-stimulated cells. Free t-PA was never observed. Both membrane binding and catalytic activity of thrombin were required since the effects of 1 U/ml thrombin were inhibited by addition 2 U/ml hirudin, which inhibits the membrane binding and catalytic activity of thrombin, and since DFP-inactivated thrombin, which has the ability to bind but which has no enzymatic activity, did not induce t-PA or PAI-1. Gamma thrombin, which does not bind to thrombin receptor, did not increase t-PA and PAI-1 releases. The effects of thrombin were probably mediated by protein kinase C activation since H7, an inhibitor of protein kinases, inhibited significantly thrombin effects on t-PA and PAI-1 production, and since addition of an activator of protein kinase A, 8-bromocyclic AMP (100 microM), induced a significant inhibition of the thrombin effect. The effects of thrombin were also suppressed by 1.25 micrograms/ml alpha amanitin, suggesting a requirement of de novo RNA synthesis. Northern blot analysis indicated that thrombin induced an increase in the mRNA levels of t-PA and of PAI-1. We conclude that thrombin increases DNA synthesis in human mesangial cells and enhances the synthesis of both t-PA and PAI-1. The latter is released in a large excess as compared to t-PA. Hence, thrombin may have a role in provoking a localized hypofibrinolytic state and may contribute to the persistence of glomerular fibrin deposits during proliferative glomerulonephritis.     

Sideropenic Dysphagia综合征膜性蹼26例分析

目的 :研究SideropenicDysphagla (S -D)综合征膜性蹼产生的机制。方法 :回顾分析S -D综合征2 6例的临床资料。结果 :影像学检查显示膜性蹼在颈段食道前壁呈 2mm深的模样陷凹。血液学检查为缺铁性低血红蛋白性贫血改变。结论 :缺铁性贫血是S -D综合征的原因 ,铁剂治疗有效     

Deletion of aldose reductase leads to protection against cerebral ischemic injury.

Previously, we reported that transgenic mice overexpressing endothelin-1 in astrocytes showed more severe neurological deficits and increased infarct after transient focal ischemia. In those studies, we also observed increased level of aldose reductase (AR), the first and rate-limiting enzyme of the polyol pathway, which has been implicated in osmotic and oxidative stress. To further understand the involvement of the polyol pathway, the mice with deletion of enzymes in the polyol pathway, AR, and sorbitol dehydrogenase (SD), which is the second enzyme in this pathway, were challenged with similar cerebral ischemic injury. Deletion of AR-protected animals from severe neurological deficits and large infarct, whereas similar protection was not observed in mice with SD deficiency. Most interestingly, AR(-/-) brains showed lowered expression of transferrin and transferrin receptor with less iron deposition and nitrotyrosine accumulation. The protection against oxidative stress in AR(-/-) brain was also associated with less poly(adenosine diphosphate-ribose) polymerase (PARP) and caspase-3 activation. Pharmacological inhibition of AR by Fidarestat also protected animals against cerebral ischemic injury. These findings are the first to show that AR contributes to iron- and transferrin-related oxidative stress associated with cerebral ischemic injury, suggesting that inhibition of AR but not SD may have therapeutic potential against cerebral ischemic injury.     

经皮椎体成形术治疗脊柱疾病

目的评价经皮椎体成形术治疗脊柱疾病的临床应用价值.方法 56例多发骨髓瘤、溶骨性脊柱转移瘤、骨质疏松性椎体压缩性骨折患者应用经皮椎体成形术后,分24 h、3个月两阶段评估患者疼痛、术后X线片检查结果、椎体高度等指标.结果术后止痛效果良好,尤以骨质疏松性椎体压缩性骨折患者的止痛效果最好.无严重并发症. 结论经皮椎体成形术对骨质疏松性椎体压缩性骨折等脊柱疾病的止痛、稳固椎体等效果明显,可以谨慎开展.     

老年人肱骨近端二部分和三部分移位骨折19例临床分析

目的 探讨老年人肱骨近端二部分和三部分移位骨折的手术治疗方法。方法 回顾性分析19例老年肱骨近端二部分和三部分移位骨折患者的临床资料，其中二部分骨折13例、三部分骨折6例，采用切开复位，肱骨近端解剖钢板固定治疗。结果 二部分骨折术后优良率为76．9％，未出现骨折不愈合及肱骨头坏死；三部分骨折术后优良率为66．7％，肱骨头坏死率16．7％。结论 老年人肱骨近端二部分和三部分骨折应尽量采用有限切开复位，选择肱骨近端解剖钢板固定。     

受体介导内吞和自噬同凋亡的关系

目的 观察刀豆素A(ConA)与小鼠腹腔巨噬细胞表面ConA受体结合、内吞、转运及巨噬细胞自噬、凋亡的形态学变化，以探讨受体介导内吞与自噬体形成和细胞凋亡之间的关系。方法 用辣根过氧化物酶(HRP)标记ConA(ConA-HRP)与小鼠腹腔巨噬细胞共孵育，不同时间取出部分巨噬细胞，制备电镜标本，观察。结果透射电镜观察表明：ConA的内吞属于受体介导内吞；形成的内吞体有泡状、管状及双层膜的线状等形式；双层膜的线状结构包裹部分胞质和细胞器，形成自噬体；自噬体与溶酶体融合，而后巨噬细胞凋亡。结论受体介导内吞和自噬同凋亡之间存在一定的关系。     

夜来香根茎水提取液局部麻醉作用的研究

目的：研究夜来香(CN)根茎水提取液的局部麻醉作用及其作用机制。方法：采用蟾蜍离体坐骨神经动作电位法、豚鼠皮丘法、椎管麻醉法、表面麻醉法。结果：20％的CN水提取液对蟾蜍离体坐骨神经动作电位可完全消失，但较1％的普鲁卡因稍弱。豚鼠皮丘实验表明，20％CN提取液有浸润麻醉作用，其浸润麻醉效果与1％的普鲁卡因相似，而且盐酸肾上腺素可增强其麻醉强度和明显延长局麻作用时间；家兔椎管麻醉实验表明CN提取液有明显的椎管麻醉作用；CN提取液对家兔角膜也有一定的表麻作用，只是作用强度及持续时间比1％的普鲁卡因稍弱或稍短。结论：CN提取液有明显的局部麻醉作用。     

口服谷氨酰胺颗粒对烧创伤患者的疗效及安全性分析

目的观察口服谷氨酰胺(Gln)颗粒对烧(创)伤及大手术患者的疗效及可能发生的不良反应.方法采用随机双盲、安慰剂对照法,将受试患者分为Gln组和对照组,每组60例,两组患者采用等氮、等热量的营养支持.Gln组口服或管饲Gln 0.5 g·kg-1·d-1,对照组使用同等剂量的安慰剂甘氨酸,疗程均为7 d.比较用药前后两组患者肠黏膜屏障功能、蛋白代谢、免疫功能、肝和肾功能的变化及不良反应等. 结果伤后两组患者血浆Gln浓度明显低于正常值,而血浆二胺氧化酶(DAO)活性、内毒素含量、肠黏膜通透性[尿乳果糖/甘露醇(L/M)]及尿氮排量均明显增高;但Gln组用药7 d后血浆Gln浓度与用药前比较增加38.04%(P＜0.01).Gln组血浆前白蛋白、转铁蛋白及白细胞介素2(IL-2)含量均显著高于对照组(P＜0.01),升幅分别为21.19%、51.11%、57.54%.血浆DAO活性、L/M比值、内毒素含量及尿氮排量明显低于对照组,降幅分别为47.26%、52.18%、22.22%、27.78%(P＜0.05或0.01).两组患者的血浆总蛋白、白蛋白、血尿常规及肝、肾功能在用约前后变化不明显(P＞0.05).用药后有少数患者出现轻微不良反应如恶心、腹泻和便秘等,2～3 d后自行缓解,两组间比较,差异无显著性意义(P＞0.05).结论口服Gln能显著提高患者血浆Gln浓度,明显减轻伤后肠黏膜受损程度,并能促进机体蛋白合成,降低蛋白分解,提高机体免疫功能,且临床应用无明显不良反应.     

神经生长因子基因转染联合强化铁营养防治豚鼠爆震性聋的实验研究

Objective To study the protective effects of adenovirus-mediated human beta-nerve growth factor gene (hNGFβ) transfer combined with iron fortified nutrition on blast hearing damage in guinea pigs. Methods Deafness was induced by blast (172dB SPL) in 35 healthy guinea pigs. Seven days after noise exposure, 10 guinea pigs were inoculated with adenovirus-mediated hNGFβ (Ad-hNGFβ) into the perilymphatic space (the gene group), another 10 guinea pigs were given hNGFβ combined with iron fortified nutritional diet (the combination group), still another 10 guinea pigs were inoculated with artificial perilymphatic fluid (APF), and 5 guinea pigs served as control, given neither medicine nor noise exposure. Auditory brainstem response (ABR) threshold shifts were monitored in the guinea pigs before blast exposure and after gene transfer. Changes in cochlear morphology were examined with immunohistochemical and HE staining. Results One week after successful inoculation of hNGFβ, it was noted that Ad-hNGFβ protein was expressed in each turn of the cochlea, and its intensity was almost equal. After gene transfer in the combination group and the gene group, ABR threshold shifts at week 1 and 4 were significantly smaller than those of the APF group. HE staining showed that the number of the spiral ganglion cells in the combination group and the Ad-hNGFβ group was significantly higher than that of the control group after 4 weeks (P<0.01). Conclusions Ad-hNGFβ combined with iron fortified nutritional diet was effective in the prevention and treatment of blast hearing damage of cochlear hair cells.