出土文献与彭祖养生学术研究

彭祖是我国古代的"寿星",随着一系列的考古发现,如汉早期马王堆墓《十问》篇、张家山汉墓《引书》篇,尤其是上海博物馆藏竹简(三)有《彭祖》篇,改变了我们对彭祖学术的认识,不仅为证明楚国产生并流传黄老学派思想提供了佐证,而且在学术史领域提供了新的课题,进一步廓清了彭祖养生学术之源乃是古代巫术,其流是在春秋战国秦汉时期被诸子传诵,与道家等流派结合,具有神仙色彩,最终被汉末魏晋道家改造为神仙方术。     

红景天对高原去势大鼠骨质疏松症的血清IL-6、TNF-α和尿DPD影响

目的:探讨高原高寒地区低氧环境去势大鼠骨质疏松症与血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和尿脱氧吡啶酚(DPD)的关系及红景天预防骨质疏松的作用。方法:选用Wistar雌性大白鼠75只,分别摘除卵巢或假性去卵巢。分为A组(假手术组),B组(切除卵巢组),C组(切除卵巢 尼尔雌醇组),D组(切除卵巢 红景天混合饲料组),E组(切除卵巢 红景天浸液组)。每组15只,术后在海拔3100m青海海北州地区饲养,术后3个月处死,应用放免方法测定血清IL-6、TNF-α和化学发光法测定尿中DPD含量。结果:B组血清IL-6、TNF-α和尿DPD含量显著高于A、C、D、E组。C、D、E组血清IL-6、TNF-α和尿DPD含量与A组比较差异无显著性统计学意义。结论:红景天的抗高原骨质疏松症的作用可能与降低血清IL-6、TNF-α含量和尿中DPD浓度有关。     

Flavonoids modulate monocarboxylate transporter-1-mediated transport of gamma-hydroxybutyrate in vitro and in vivo.

The objective of this study was to determine the effects of flavonoids on the in vitro monocarboxylate transporter 1 (MCT1)-mediated transport and in vivo disposition of the drug of abuse, gamma-hydroxybutyrate (GHB). The uptake of GHB in rat MCT1 gene-transfected MDA-MB231 cells was significantly decreased in the presence of the flavonoids apigenin, biochanin A, chrysin, diosemin, fisetin, genistein, hesperitin, kaempferol, luteolin, morin, narigenin, phloretin, and quercetin, but was not affected by the flavonoid glycosides phloridzin and rutin. The IC(50) values for luteolin, morin, and phloretin were 0.41 +/- 0.14, 6.41 +/- 2.01, and 2.57 +/- 0.48 microM, with the inhibition mechanism for luteolin being competitive. [(3)H]Kaempferol and [(3)H]biochanin A did not exhibit MCT1-mediated uptake, suggesting that these flavonoids are not substrates for MCT1. The combination of luteolin and phloretin inhibited the uptake of GHB in a synergistic manner; however, the combination of luteolin and morin was antagonistic. GHB 1000 mg/kg was administered to rats by i.v. bolus, with or without the concomitant administration of luteolin 10 mg/kg i.v. After luteolin treatment, the renal and total clearances of GHB were significantly increased, probably because of inhibition of the MCT1-mediated renal reabsorption of GHB, and the sleep time significantly decreased (121 +/- 5 min versus 165 +/- 10 min) compared with control rats. Overall, the results of this study indicate that flavonoids from food or herbal products may significantly alter the pharmacokinetics and pharmacodynamics of MCT substrates.     

先天性胃壁肌层缺损诊治体会

目的 探讨提高新生儿先天性胃壁肌层缺损治愈率的方法。方法 总结分析近年来收治的本症11例患儿(均经过病理检验证实)的临床及相关资料。结果 11例患儿中，8例存活，其中7例为近十年的病例。1例死亡，2例放弃治疗，均为十年以前的病例。在存活者中，经追踪观察及消化道造影检查，残胃有明显代偿性生长，患儿生长发育未受到明显的影响。结论 早期发现、及时手术、控制感染、术后营养、支持治疗，其预后良好。     

孕妇血清AFP、uE3和β-hCG水平与严重胎儿缺陷的关系

①目的 探讨孕中期血清甲胎球蛋白（AFP），游离雌三醇（uF3)和β绒毛膜促性腺激素（β-HCG）水平与严重胎儿缺陷的关系。②方法 用ELISA方法对832例16-21周妊娠妇女血清AFP、UE3和β-hCG进行检测，以筛查阳性病人。③结果 14例胎儿被确诊为异常，其中唐氏综征2例，无脑儿3例，脊柱裂3例，唇腭裂1例，腹裂肠外翻1例，孕中期自然流产2例，死胎1例，葡萄胎1例，总检出率为1.68%，假阳性15例，占被检人数的1.80%。④结论 以上3种生化指标联合检测可作为产前诊断严重胎儿缺陷的有效方法。     

星形胶质细胞瘤伽玛刀治疗的疗效与影响因素

目的分析星形胶质细胞瘤伽玛刀(γ-刀)治疗的疗效与影响因素.方法回顾性分析48例星形胶质细胞瘤病人的γ-刀治疗结果.以性别、有无普通放疗经过、有无化疗经过、边缘剂量、病灶的平均直径、病变的病理等级、影像学上有无相对较清楚的边界为治疗结果影响因素,判定标准以病灶缩小为有效,采用logistic回归模型,确定多因素条件下治疗结果的影响因素.结果有效32例(66.7%),logistic回归模型分析表明:病理等级和病灶平均直径为与肿瘤控制有关的影响因素.结论γ-刀对星形胶质细胞瘤的治疗有一定的意义.     

微创经皮肾镜取石术治疗上尿路结石

目的 探讨微创经皮肾镜取石术治疗上尿路结石的有效性和安全性.方法上尿路结石患者368例,平均年龄57岁.其中输尿管上段结石116例,结石大小(2.1±0.8)cm;肾结石252例,结石大小(4.6±1.4)cm,其中非鹿角形结石190例,结石大小(3.2±1.1)cm,鹿角形结石62例,结石大小(7.6±1.6)cm.均采用微创经皮肾穿刺,输尿管镜下气压弹道或联合钬激光碎石治疗,对结石清除率和并发症等进行统计分析.结果 368例患者中单通道取石356例(96.7%),双通道12例(3.3%).一期取石344例(93.5%),二期取石24例(6.5%).总结石取净率为88.6%(326/368).平均手术时间73 min.一期取净结石者住院时间4～8 d,平均6 d.术后发热14例(3.8%);输血5例(1.4%);2例肾结石术后出血严重者经输血及超选择性肾动脉栓塞后治愈.结论 微创经皮肾镜取石术损伤小、住院时间短、术中出血及并发症少、结石清除率高、可重复取石,是治疗上尿路结石有效的微创手段.     

首例中国可视化人体心脏三维重建及临床意义

目的 对首例中国数字化可视人体的心脏进行三维重建，为心脏疾病的影像学诊断和外科手术提供三维解剖学依据。方法 将首例中国数字化可视人体心脏部分的薄层断面(层厚1．0mm)输入SGI工作站，经数据分割、对位重建、平滑处理和三维显示等步骤，完成对心脏结构的三维重建。结果 本研究完整地重建出了心脏结构，重建的结构能够以多结构、多彩色实体模型方式显示，可显示心脏内部各结构的空间位置和毗邻关系，可在三维空间伴置上绕任意轴旋转任意角度。结论 重建出的三维图像清晰地显示了心脏内部和整体的结构，实现了心脏的二维可视化。     

Angiopoietin1/Tie2 and VEGF/Flk1 induced by MSC treatment amplifies angiogenesis and vascular stabilization after stroke.

Bone marrow stromal cells (MSCs) increase vascular endothelial growth factor (VEGF) expression and promote angiogenesis after stroke. Angiopoietin-1 (Ang1) and its receptor Tie2 mediate vascular integrity and angiogenesis as does VEGF and its receptors. In this study, we tested whether MSC treatment of stroke increases Ang1/Tie2 expression, and whether Ang1/Tie2 with VEGF/ vascular endothelial growth factor receptor 2 (VEGFR2) (Flk1), in combination, induced by MSCs enhances angiogenesis and vascular integrity. Male Wistar rats were subjected to middle cerebral artery occlusion (MCAo) and treated with or without MSCs. Marrow stromal cell treatment significantly decreased blood-brain barrier (BBB) leakage and increased Ang1, Tie2, and occludin (a tight junction protein) expression in the ischemic border compared with MCAo control. To further test the mechanisms of MSC-induced angiogenesis and vascular stabilization, cocultures of MSCs with mouse brain endothelial cells (MBECs) or astrocytes were performed. Supernatant derived from MSCs cocultured with MBECs significantly increased MBEC expression of Ang1/Tie2 and Flk1 compared with MBEC alone. Marrow stromal cells cocultured with astrocytes also significantly increased astrocyte VEGF and Ang1/Tie2 expression compared with astrocyte culture alone. Conditioned media from MSCs alone, and media from cocultures of MSCs with astrocytes or MBECs, all significantly increased capillary tube-like formation of MBEC compared with control Dulbecco's modified Eagle's medium media. Inhibition of Flk1 and/or Ang1 significantly decreased MSC-induced MBEC tube formation. Knockdown of Tie2 expression in MBECs significantly inhibited MSC-induced tube formation. Our data indicate MSC treatment of stroke promotes angiogenesis and vascular stabilization, which is at least partially mediated by VEGF/Flk1 and Ang1/Tie2.     

The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.