颈外静脉瓣膜窦段及其临床应用

经研究表明颈外静脉的瓣膜、缩窄环、瓣膜窦及窦段静脉壁共同组成一个灵敏地、高强度地抗逆流装置。本文称之为瓣膜窦段并报道189段的尸体解剖和光镜观察结果;测定尸体、活体和手术中瓣膜窦段的抗逆流功能,表明颈外静脉适于用无瓣导管作脑积水等分流途径。初步探明颈外静脉怒张的原因和消除怒张的简便方法以及术前鉴定瓣膜窦段位置和功能的方法。对2例脑积水用无瓣导管作侧脑室颈外静脉分流取得初步疗效。     

戊二醛交联提高胶原/壳聚糖真皮支架抗细胞收缩能力的研究

目的 应用交联处理的胶原支架,来减缓其降解过多、易收缩变形、机械性能不足等缺点.方法 采用冷冻-冻干法构建胶原/壳聚糖多孔支架,并通过戊二醛交联构建具有良好抗细胞收缩稳定性和细胞相容性的胶原支架.通过测定不同培养时间各类支架的尺寸变化,研究了戊二醛交联对支架抗细胞收缩能力的影响.结果 戊二醛交联后的胶原/壳聚糖支架未见明显收缩,其细胞活性也始终高于干热交联支架.结论 戊二醛能有效地提高胶原基支架的抗细胞收缩能力,并保持其良好的生物相容性.     

Similar motion of a hand-held object may trigger nonsimilar grip force adjustments.

The tight coupling between load (L) and grip (G) forces during voluntary manipulation of a hand-held object is well established. The current study is to examine grip-load force coupling when motion of the hand with an object was either self-generated (voluntary) or externally generated. Subjects performed similar cyclic movements of different loads at various frequencies with three types of manipulations: 1) voluntary oscillation, 2) oscillating the right arm via the pulley system by the left leg (self-driven oscillation), and 3) oscillating the arm via the pulley system by another person (other-driven oscillation). During the self-generated movements: 1) the grip forces were larger and 2) grip-load force modulation was more pronounced than in the externally generated movements. The G-L adjustments are not completely determined by the mechanics of object motion; nonmechanical factors related to movement performance, for instance perceptual factors, may affect the G-L coupling.     

实验性隐睾术后大鼠附睾的反应性变化

本研究描述了实验性隐睾术后大鼠附睾的形态学变化。结果表明,隐睾术后由于腹温作用和附皋管管腔内容物的改变,附睾管上皮细胞的形态和功能明显改变。术后早期上皮细胞出现无丝分裂相,上皮细胞的分泌和吞噬功能加强,胞质内含PAS阳性颗粒的细胞增多。随术后时间的延长,附睾上皮细胞变化逐渐趋于稳定。[     

乳管镜对乳腺导管内疾病的诊断及介入治疗--附100例临床分析

目的:探讨乳管镜在乳腺疾病诊断和治疗中的作用.方法:应用乳腺纤维导管内视镜对100例伴乳头溢液的乳腺导管性疾病进行诊断或介入治疗.结果:13例导管内占位性疾病得到了正确诊断,87例渗出性导管病经治疗后治愈.结论:乳管镜对乳管内病变的正确诊断及手术方式可提供依据,并可对渗出性病变进行介入治疗.     

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.