刺激视上核对大鼠痛阈及电针镇痛的影响

以钾离子透引起的大鼠甩尾反应为痛指标，观察了电和化学刺激视上核（ＳＯＮ）对大鼠痛阈（ＰＴ）和电针（ＥＡ）镇痛的影响。电刺激ＳＯＮ后，ＰＴ明显高于假刺激组（Ｐ＜０．０５～０．００１），电刺激ＳＯＮ后电针足三里，镇痛效应明显提高，并有明显的量效关系。电刺激ＳＯＮ的近旁部位（０．５—１ｍｍ）对ＰＴ及电针镇痛无明显影响。ＳＯＮ内注射Ｌ－谷氨酸（Ｌ－Ｇｌｕ）后痛阈和电针镇痛效应都明显对照组，也有明显的量效关     

Alterations of G-protein Coupling Function in Phosphoinositide Signalling Pathways of Rat Hippocampus by Ischaemic Brain Injury

The activation of membrane-associated phospholipase C is rapidly and transiently induced in the central nervous system by a variety of stimuli. Ischaemic brain injury is one of the situations that leads to a dramatic increase in polyphosphoinositide (PPI) turnover. In this study, stimulation of PPI hydrolysis by glutamate (500 μM) was measured in hippocampal slices from rats up to 21 days after an ischaemic insult of 30 min. Ischaemia was induced using the four-vessel occlusion method. PPI hydrolysis elicited by glutamate was significantly increased in the slices prepared from ischaemic rats 24 h after reperfusion, the accumulation of inositol phosphates (InsP_s) and inositol 1,4,5-trisphosphate (InsP₃) was 614±74% ( n = 8) and 182±11% ( n = 9) of the basal level respectively. This potentiation was also observed 21 days after ischaemia. Hyper-responsiveness to glutamate was also accompanied by an increase in AIF⁻₄-stimulated formation of [³H]inositol phosphates. In addition, global ischaemia did not change either high-affinity [³H]glutamate binding in hippocampal membranes or the stimulation of PPI hydrolysis by carbachol or noradrenaline in hippocampal slices. The present results suggest that the increased responsiveness to glutamate is the result, at least in part, of functional changes at the G-protein level, and may contribute to the pathophysiology of ischaemic brain injury or to the regenerative phenomena that accompany ischaemic damage.     

白细胞介素—2新的功能位点及其中枢镇痛作用

白细胞介素－２（ＩＬ－２）不仅是重要的免疫调节因子，而且还具有重要的中枢调节作用。本实验以钾离子透入引起大鼠甩尾反应为指标，发现侧脑室注射ＩＬ—２能显著提高动物痛阈，并能被纳洛酮所阻断，表示ＩＬ－２的中枢镇痛作用可能与阿片受体有关。利用基因定位突变技术获得的无免疫活性ＩＬ－２实查体仍具有中枢镇痛作用，表明ＩＬ—２分子上发挥镇痛和免疫调节作用的功能位点是相互独立的。纳洛酮能够阻断ＩＬ—２的中枢镇痛作用，而不能影响ＩＬ—２增殖ＣＴＬＬ－２细胞的作用，提示ＩＬ－２发挥镇痛和免疫调节作用可能通过不同的受体途径。ＩＬ－２分子中第４５位Ｔｙｒ残基突变为Ｖａｌ后，虽仍保留了免疫活性，但丧失了镇痛功能，表示４５位Ｔｙｒ残基是ＩＬ—２发挥中枢镇痛功能的关键残基之一。我们推测ＩＬ—２的镇痛功能位点可能在ＩＬ—２分子中第４５位Ｔｙｒ残基附近区域。     

赖型钩体flaB2与VR1012中的CpG基序分析

目的：对问号赖型钩端螺旋体（赖型钩体）DNA疫苗[包括内鞭毛蛋白基因（flaB2)和质粒DNA表达载体（VR1012）]的CpG基序（CpG motifs)进行分析，为DNA疫苗免疫机制的阐明和提高DNA疫苗的效能奠定基础。方法：以flaB2与VR1012构建重组DNA的免疫原，对flaB2及VR1012全核苷酸序列进行计算机分析（分类、计数和定位）。结果：CpG的“C”的侧翼为两个嘌呤，“G”的侧翼为两个嘧啶，在flaB2中共3个，分别为GACGCT，GACGTC和GACGCC；在VR1012中共11个，分别为GACGTC1个，GACGCT2个，GACGCC1个，GACGTT1个，GGCGTT2个，GGCGCT2个，GGCGCC1个，AACGCT1个，其中特别重要的TGACGTCA4个和TAACGCCA有1个，位于5'端456－463；509－516；592－599；778－785和486－493；4个TGACGTCA和1个TAACGCCA均位于5'端且相对集中。结论：赖型钩体flaB2与VR1012构成的DNA疫苗含有TGACGTCA等CpG，这些基序又称免疫刺激序列，构成了DNA疫苗中的佐剂。     

早期肠道营养对烧伤后肠源性高代谢的影响

从８０年代末起，通过对６００只大（豚）鼠、６０只兔和６０头小香猪所建立的４种烧伤后早期营养的动物模型，以及２１例严重烧伤病人对比分析，发现烧伤后早期肠道喂养可改善胃肠道血流供应，减轻肠道缺血再灌流损伤；可维护肠粘膜结构以及吸收、分泌、运动功能，降低门脉、中心静脉血内毒素水平，减少肠道内毒素易位；可降低伤后枯否细胞获得数、吞噬墨汁枯否细胞数和面积，以及其培养上清中肿瘤坏死因子（ＴＮＦ）量，对伤后枯否细胞的活化有刺激作用；可降低血胰高糖素、皮质醇、儿茶酚胺、ＴＮＦ、ＩＬ－８前列腺素Ｅ２（ＰＧＥ２）等递质的水平，降低高代谢，使烧伤４５％成人静息能量消耗（ＲＥＥ）在烧伤后４、８、１４ｄ的均值降低２８．６％。通过相关分析发现ＲＥＥ与血丙二醛（ＭＤＡ）、内毒素、分解激素、ＴＮＦ均呈显著正相关（ｒ＝０．７３８６～０．９９２２，Ｐ＜０．０５～０．０１）。     

阴茎海绵体折叠术治疗单纯阴茎下弯

对１９例先天性单纯阴茎下弯采用阴茎海绵体折叠术矫治，即在弯曲的凸面白膜折叠缝合以拉直阴茎，为减少并发症，同时加以改进措施。所有病例随访１０～７１个月，手术效果满意     

组织胺诱导胸腺细胞凋亡的研究

用苔盼蓝及吖啶橙染色，ＤＮＡ片段检定与ＤＮＡ电泳等方法进行组织胺诱导胸腺细胞凋亡的研究，旨在探讨其可能机制及其在胸腺细胞负选择中的作用。结果表明，组织胺诱导使体外培养的胸腺细胞出现典型的细胞调亡。雷尼替丁可阻断上述作用，提示胸腺细胞存在Ｈ＿２受体，活化该受体可能在胸腺细胞的负选择中起重要作用。     

脑干梗死的MRI和MRA征象

目的：探讨脑干梗死的MRI和MRA征象特点。方法：搜集我院1998年～2002年49例经MRI和MRA检查并经临床治疗证实的脑干梗死病例，其中21例行Gd-DTPA增强扫描，对比临床症状进行分析。结果：中脑梗死11例，桥脑梗死32例，延髓梗死6例。病灶直径以6～15mm为主，病灶形态主要因为不规则斑片状。病灶信号为长T1、长T2信号，行Gd—DTPA增强扫描，大部分呈斑片状或环状强化。MRA检查异常发现主要为椎动脉、基底动脉的狭窄或闭塞，基底动脉纡曲扩张。结论：脑干梗死主要因为椎-基底动脉异常，病灶部位可提示其临床意义。     

心脏移植术后肾功能衰竭的围手术期处理(附2例报告)

目的报告2例原位心脏移植术后肾功能衰竭的发生及治疗经过,探讨其围手术期处理的初步经验和要点.方法我院自2000年12月一2002年12月共对4例终末期心脏病患者施行同种异体原位心脏移植术,4例均为男性,采用标准原位心脏移植术,术后应用三联免疫治疗的方法抗排异.结果4例患者均获得手术成功,术后未发现超急性排斥反应或急性排斥反应,2例术后1周左右并发急性肾功能衰竭,应用床边连续肾脏替代(CRRT)治疗后,1例存活22d,1例完全康复,随访半年患者心功能恢复Ⅰ～Ⅱ级(NYHA),生活质量良好.结论心脏移植手术后肾功能损害较常见,围手术期的肾功能保护非常重要,如符合手术指征,及早手术治疗是抢救成功的关键.     

TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice.

Tumor necrosis factor-alpha (TNFalpha) and Fas are induced after traumatic brain injury (TBI); however, their functional roles are incompletely understood. Using controlled cortical impact (CCI) and mice deficient in TNFalpha, Fas, or both (TNFalpha/Fas-/-), we hypothesized that TNFalpha and Fas receptor mediate secondary TBI in a redundant manner. Compared with wild type (WT), TNFalpha/Fas-/- mice had improved motor performance from 1 to 4 days (P<0.05), improved spatial memory acquisition at 8 to 14 days (P<0.05), and decreased brain lesion size at 2 and 6 weeks after CCI (P<0.05). Protection in TNFalpha/Fas-/- mice from histopathological and motor deficits was reversed by reconstitution with recombinant TNFalpha before CCI, and TNFalpha-/- mice administered anti-Fas ligand antibodies had improved spatial memory acquisition versus similarly treated WT mice (P<0.05). Tumor necrosis factor-alpha/Fas-/- mice had decreased the numbers of cortical cells with plasmalemma damage at 6 h (P<0.05 versus WT), and reduced matrix metalloproteinase-9 activity in injured brain at 48 and 72 h after CCI. In immature mice subjected to CCI, genetic inhibition of TNFalpha and Fas conferred beneficial effects on histopathology and spatial memory acquisition in adulthood (both P<0.05 versus WT), suggesting that the beneficial effects of TNFalpha/Fas inhibition may be permanent. The data suggest that redundant signaling pathways initiated by TNFalpha and Fas play pivotal roles in the pathogenesis of TBI, and that biochemical mechanisms downstream of TNFalpha/Fas may be novel therapeutic targets to limit neurological sequelae in children and adults with severe TBI.