UB-I粘结剂粘结面的微形态观察

目的：研究UB-Ⅰ粘结剂的粘结界面和粘结表面的微形态特点。方法：用扫描电子显微镜观察UB-Ⅰ和牙本质的粘结界面和粘结表面。结果：UB-Ⅰ粘结剂在牙本质小管内可聚合形成树脂突，在牙本质小管内的树脂突表面有树脂侧枝呈树枝状横行排列，并且和相邻的树脂突相连接，在牙本质和复合树脂之间有杂合层形成。结论：UB-Ⅰ粘合剂具有良好的渗透性，与牙本质之间可以形成良好的机械嵌合。     

Foley尿管气囊压迫治疗骶前静脉丛大出血的评价(附6例报告)

目的:评价直肠癌根治术中用Foley尿管气囊压迫治疗骶前静脉丛大出血(MPVP)的临床价值。方法:分析1995~2005年用Foley尿管气囊压迫治疗骶前静脉丛大出血6例的临床资料。结果:6例骶前大出血中全部用Foley尿管气囊压迫控制出血,术中出血量为800~1700mL,Foley尿管于术后4d拔除3例,5d1例,6d2例,均无再出血,会阴切口均一期愈合。结论:Foley尿管气囊压迫治疗骶前静脉丛大出血是一种简单安全有效的治疗方法。     

处女膜修补手术及麻醉方法的改进

目的；增大处女膜粘膜瓣的接触面，减少因麻醉造成的处女膜粘膜水肿，提高修复手术的成功率。方法：手术全部采用1％的卡因行粘膜表面麻醉。53例采用瓦合粘膜瓣法，3例用瓦合粘膜瓣联合阴道粘膜瓣修复法。结果：56例术后一月随访，53例处女膜孔径为一指，成功率94．64％。结论：采用1％的卡因粘膜表面麻醉，瓦合粘膜瓣法及瓦合粘膜联合阴道粘膜瓣修复法对处女膜修复是行之有效的。     

The CLDN5 locus may be involved in the vulnerability to schizophrenia.

The present study was designed to detect three single nucleotide polymorphisms (SNPs) located on 22q11 that was thought as being of particularly importance for genetic research into schizophrenia. We recruited a total of 176 Chinese family trios of Han descent, consisting of mothers, fathers and affected offspring with schizophrenia for the genetic analysis. The transmission disequilibrium test (TDT) showed that of three SNPs, rs10314 in the 3'-untranslated region of the CLDN5 locus was associated with schizophrenia (chi(2) = 4.75, P = 0.029). The other two SNPs, rs1548359 present in the CDC45L locus centromeric of rs10314 and rs739371 in the 5'-flanking region of the CLDN5 locus, did not show such an association. The global chi-square (chi(2)) test showed that the 3-SNP haplotype system was not associated with schizophrenia although the 1-df test for individual haplotypes showed that the rs1548359(C)-rs10314(G)-rs739371(C) haplotype was excessively non-transmitted (chi(2) = 5.32, P = 0.02). Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.     

6186例脑卒中患者发病时间的季节性分析

目的探讨青岛市区脑出血(CH)、脑梗死(CI)、蛛网膜下腔出血(SAH)发病时间的季节规律。方法收集青岛市1998年～2002年脑卒中患者6186例,其中CH1179人,CI4821人,SAH186人。圆分布分析探讨脑卒中患者发病时间的季节规律。结果CH冬季高发,平均角在1月份(P<0.05),男性患者的平均角在2月份(P<0.05),女性患者的平均角在1月份(P<0.05);CI秋季高发,男、女间无差别,平均角在10月份(P<0.05);SAH秋季高发,平均角在10月份(P<0.05),男性患者的平均角在9月份(P<0.05),女性患者的平均角在10月份(P<0.05)。结论青岛市的脑卒中发病具有季节性,在脑卒中预防工作中要充分考虑其发病的季节特点,并采取相应的措施。     

嗜铬细胞瘤患者围手术期处理的改进

目的：探讨提高嗜铬细胞瘤患者围手术期安全性的措施。方法：对15例嗜铬细胞瘤患者、术前采用选择性α1受体阻滞剂多沙唑嗪控释片(可多华)控制高血压；11例患者采用3D DCEMRA进行肿瘤定位；术中均采用联合高容量血液稀释(AHH)和术中患者自体血回输纠正血容量。结果：除1例持续性高血压患者需联合钙离子拮抗剂和ACEI药物降压外．其余患者血压控制均为满意；根据3D DCEMRA定位选择手术径路者均顺利完成手术；AHH联合术中自体血回输使14例患者避免了异体输血。结论：本文围手术期处理改进．可多华可明显减少药物的不良反应；采用3D DCEMRA进行肿瘤定位，可增加手术安全性；AHH联合术中自体血回输可减少医疗成本和异体输血，以及由此而引起的并发症。     

加热及增加细胞内氧自由基水平对恶性胶质瘤细胞生物学特性的影响

本文就加热及同时增加细胞内氧自由基水平对恶性胶质瘤细胞存活、增殖和细胞间隙连结通讯的影响做初步观察。用Ｍ．Ｔ．Ｔ法测定胶质瘤细胞存活率；用Ｋｉ－６７抗增殖细胞核抗原单克隆抗体，通过免疫组织化学ＡＢＣ染色分析胶质瘤细胞的增殖活性；用划痕染料示踪技术观察胶质瘤细胞的细胞间隙连结通讯。结果表明，Ｈ２Ｏ２和３ＡＴ能增强加热对胶质瘤细胞存活与增殖的抑制作用，促进胶质瘤细胞间隙连结通讯的改善，存在着明显的剂量和时间效应。实验结果提示，通过内外源性增加胶质瘤细胞内的氧自由基水平，将有助于强化加热治疗胶质瘤效果，并可以减少加热的剂且，降低副作用。     

角膜损伤后神经再生的实验研究

应用神经组织化学技术观察了兔角膜NA能神经及AchE阳性神经在角膜损伤后的再生,证实术后1月,两种神经均有再生轴突进入植片;术后3月可见交界区和植床内神经密度明显增加;同时,对术后两种神经再生的功能意义进行了讨论。     

Transient Brain Ischaemia Provokes Ca2+, PIP2 and Calpain Responses Prior to Delayed Neuronal Death in Monkeys

To clarify the mechanism of postischaemic delayed cornu Ammonis (CA)-1 neuronal death, we studied correlations among calpain activation and its subcellular localization, the immunoreactivity of phosphatidylinositol 4,5-bisphosphate (PIP₂) and Ca²⁺ mobilization in the monkey hippocampus by two independent experimental approaches: in vivo transient brain ischaemia and in vitro hypoxia-hypoglycaemia of hippocampal acute slices. The CA-1 sector undergoing 20 min of ischaemia in vivo showed microscopically a small number of neuronal deaths on day 1 and almost global neuronal loss on day 5 after ischaemia. Immediately after ischaemia, CA-1 neurons ultrastructurally showed vacuolation and/or disruption of the lysosomes. Western blotting using antibodies against inactivated or activated μ-calpain demonstrated μ-calpain activation specifically in the CA-1 sector immediately after ischaemia. This finding was confirmed in the perikarya of CA-1 neurons by immunohistochemistry. CA-1 neurons on day 1 showed sustained activation of μ-calpain, and increased immunostaining for inactivated and activated forms of μ- and m-calpains and for PIP₂. Activated μ-calpain and PIP₂ were found to be localized at the vacuolated lysosomal membrane or endoplasmic reticulum and mitochondrial membrane respectively, by immunoelectron microscopy. Calcium imaging data using hippocampal acute slices showed that hypoxia-hypoglycaemia in vitro provoked intense Ca²⁺ mobilization with increased PIP₂ immunostaining specifically in CA-1 neurons. These data suggest that transient brain ischaemia increases intracellular Ca²⁺ and PIP₂ breakdown, which will activate calpain proteolytic activity. Therefore, we suggest that activated calpain at the lysosomal membrane, with the possible release of biodegrading enzyme, will cause postischaemic CA-1 neuronal death.