俄歇电子发射体67Ga-EDTMP 对骨肉瘤细胞株辐射效应的形态学变化

目的　研究俄歇电子发射体67Ga-EDTMP对人骨肉瘤细胞株 (HOS - 86 0 3)的辐射效应 ,探讨67Ga作为原发肿瘤和骨转移癌内照射治疗核素的可能性。方法　用成集落实验和透射电镜研究受照细胞的形态变化。结果　发现67Ga-EDTMP对肿瘤细胞有明显的杀伤和抑制增殖作用 ,并随剂量的加大 ,抑制效率增加 ;倒置显微镜下细胞集落数量减少 ,集落偏小 ,细胞稀疏。电镜下胞浆中空泡形成 ,细胞溶解、坏死 ,细胞核固缩 ,出现典型的细胞凋亡改变 ,形成凋亡小体。结论　67Ga可能是一种有前途的骨肉瘤和骨转移癌的放射性治疗核素     

后半规管阻塞前后豚鼠前庭及耳蜗功能的动态变化

目的 探讨机械性后半规管阻塞前后豚鼠前庭和耳蜗功能的动态变化。方法 采用２０只豚鼠建立单侧后半规管阻塞的动物模型,观察手术前后眼震电图,听性脑干反应,耳声发射等变化。结果 术后第１天,第３天豚鼠正弦摆动刺激术侧眼震反应,明显减术,术后第５天起双侧眼震恢复正常。术后早期ＡＢＲ阈值一度升高,第５天达高峰,ＡＢＲ阈值平均升高４．５ｄＢ。ＤＰＯＡＥ反应幅度无明显改变。结论 后半规管阻塞能选择性地消除后半规     

门静脉高压症合并幽门螺杆菌感染患者胃粘膜的病理改变

目的：本文研究门静脉高压症合并幽门螺杆菌感染患者胃粘膜病理变化的特点,旨在探讨ＨＰ感染在ＰＨＧ发病机制中的意义。方法：对６０例门静脉高压症患者由内窥镜取胃粘膜活检证实有无ＨＰ感染;同时对门静脉高压性胃粘膜病变（ＰＨＧ）者,无论是否伴有幽门杆菌感染分别进行光镜、电镜观察。结果：（１）６０例门脉高压症（ＰＨ）患者有４８例为ＨＰ阳性（８０％）,其中ＰＨＧ患者ＨＰ阳性率为８７％,ＮＰＨＧ患者阳性率仅为６０％;（２）ＨＰ阳性和ＨＰ阴性的门脉高压症患者均合并有胃粘膜病变,且前者以重型为主,后者以轻型为主。结论：（１）ＨＰ感染是形成门脉高压性胃粘膜病变的促进因素;（２）门脉高压时胃粘膜变化包括细胞机制和免疫反应两方面。     

COEXISTENCE OF OSTEOARTHRITIS AND OSTEOPOROSIS INFEMORAL HEAD: A SCANNING ELECTRONMICROSCOPIC STUDY

ffeSUtn6 Objectif Detenniner ie cusistence d' ostdoarthrite et d' ostdope dans la tste du femur. liChen 12 femmes (age moron 56 ans )atteintes d' ortdoorthrite de la hanche, on a Prdlevd la tste du femur durant la substitutiontotale de l' articulation de leur hanche. APrds das traitements, Ies tstes du femur furent studioes sons ie microscope dlectroniqued belang (soon ). ~flats to lesions ostdcorthritiques de differents degrds (azractdrithe per ba digs~nce du cartilage articulaire et d' hyp…     

黑河上蔡段河水及饮用水的致突变性

目的：探讨黑河上蔡段癌症高发区河水及饮用水的致突变性。方法：采集严重污染的黑河河水及沿岸浅井水分别进行以下试验。①用ＸＡＤⅡ树脂提取各水样中的有机提取物作为待测样品,以呋喃基康酰胺和叠氮钠作阳性对照,以自发回变率为阴性对照,用鼠伤寒沙门氏菌属ＴＡ９８ 、ＴＡ１００ 菌株进行Ａｍｅｓ 试验。以突变比ＭＲ 值评价试验结果。②松滋青皮蚕豆温浸芽约２ ｃｍ ,分别取３ ～４ 粒放入不同水样中处理,同时以蒸馏水、郑州市自来水作阴性对照,环磷酰胺（１ ｍｇ／Ｌ） 作阳性对照进行微核试验。显微镜下观察根尖细胞微核数,统计微核千分率（ＭＣＮ‰） 。结果：①河水有机提取物对ＴＡ９８、ＴＡ１００ 菌株均可诱发阳性回变;②沿岸浅井水有机提取物能诱发ＴＡ９８菌株的阳性回变;③河水、井水均可致蚕豆根尖细胞微核率（ＭＣＮ‰） 明显增高。④浅井水和河水的致突变性及毒性（ 抑菌圈直径大小） 基本相同。结论：①由于浅井水和河水的致突变性及毒性基本相同,故浅井水中的致突变物质可能来源于河水的水平渗透;②沿岸居民癌症高发与河水污染的潜在致癌性有密切关系,应予以高度重视     

颈椎椎间盘与后部结构断层解剖及影像学研究

选用43具青年尸体,蛛网膜下腔注入铸型造影剂,低温冷冻,以椎间盘为中心制作断层标本,同时选取40例正常健康人进行超声、CT及MR扫描图像分析.发现同组中不同椎间盘水平测量数据的大小不同;解剖学与影像学各测量结果进行比较无显著性差异.     

Intracapsular Hip Fracture: Increased Cortical Remodeling in the Thinned and Porous Anterior Region of the Femoral Neck

It has been shown previously that the antero-inferior cortex is subjected to maximal tensile stress during a fall onto the greater trochanter. We have recently shown that in cases of femoral neck fracture, cortical thinning and porosity is greatest in the anterior and antero-inferior region of the femoral neck. To investigate whether this is due to increased remodeling, we have quantified surface-based parameters associated with Haversian remodeling in femoral neck biopsies from women with intracapsular hip fracture and post-mortem controls. Cryostat sections of chilled biopsies were reacted for either tartrate-resistant acid phosphatase (TRAP) or alkaline phosphatase (ALP) activity. Proportions of active canals were determined in each quadrant (inferior, anterior, superior, posterior) of the femoral neck. The biopsies were then embedded in methacrylate to permit histomorphometry using Goldner’s and Solochrome sections. In the cases there was no significant increase in the proportion of canals undergoing remodeling in the cortex as a whole (p = 0.846), but the regional distribution of remodeling was markedly different from that in the controls. In the anterior cortex, the proportion of canals undergoing remodeling was increased by 56% (p = 0.0087); in contrast there was a relative decrease of 35% in the superior region (p = 0.0047). In the anterior cortex of cases there were 76% and 42% increases in the proportions of eroded (p = 0.019) and osteoid-bearing (p = 0.041) canals, respectively. In the superior region, the decrease in the proportion of remodeling sites was due to a marked decrease in canals with an osteoid surface (51%; p = 0.0031). Covariance analysis with cortical porosity as the dependent variable showed that porosity was significantly dependent on the regional distribution of eroded (p = 0.033) but not on the distribution of forming (p = 0.153) canals (R ²adj = 0.51). Cellular levels of TRAP and ALP were significantly elevated in the anterior region of cases compared with the controls (TRAP 55%, p = 0.006; ALP 36%, p = 0.003). For the posterior and inferior regions there were no marked differences in cellular TRAP and ALP levels compared with control values. These data show that the increased cortical thinning and increased porosity we have previously observed in the anterior cortex in cases of hip fracture are associated with increased indices of Haversian remodeling. These findings are consistent with the hypothesis that, in cases of hip fracture, remodeling imbalance in the anterior cortex is a continuing process up to the time of fracture and is due to increased osteoclastic cellular activity associated with an osteoblastic response that is inadequate to prevent bone loss. Received: 16 November 1998 / Accepted: 17 February 1999     

Spatiotemporal distribution of dying neurons during early mouse development

Apoptosis is a critical cellular event during several stages of neuronal development. Recently, we have shown that biotinylated annexin V detects apoptosis in vivo in various cell lineages of a wide range of species by binding to phosphatidylserines that are exposed at the outer leaflet of the plasma membrane. In the present study, we tested the specificity by which annexin V binds apoptotic neurons, and subsequently investigated developmental cell death in the central and peripheral nervous system of early mouse embryos at both the cellular and histological level, and compared the phagocytic clearance of apoptotic neurons with that of apoptotic mesodermal cells. Our data indicate: (i) that biotinylated annexin V can be used as a sensitive marker that detects apoptotic neurons, including their extensions at an early stage during development; (ii) that apoptosis plays an important part during early morphogenesis of the central nervous system, and during early quantitative matching of brain-derived neurotrophic factor and neurotrophic factor 3 responsive postmitotic large clear neurons in the peripheral ganglia with their projection areas; and (iii) that apoptotic neurons are removed by a process that differs from classical phagocytosis of non-neuronal tissues.     

CAMs and FGF cause a local submembrane calcium signal promoting axon outgrowth without a rise in bulk calcium concentration

Binding of basic fibroblast growth factor (bFGF) and cell adhesion molecules to the nerve cell membrane promotes axon outgrowth. This response can be blocked by antagonists of voltage-gated calcium channels, yet no change of cytosolic calcium concentration in the growth cone can be detected upon binding of the growth factor bFGF or the cell adhesion molecule L1. Using barium as a charge carrier, we show that bFGF and L1 open a calcium influx pathway in growth cones of rat sensory neurons without changing the membrane voltage. L1 does not activate influx in cells expressing a dominant negative mutant of the fibroblast growth factor receptor (FGFR) tyrosine kinase. FGFR-activated influx is blocked by specific antagonists of L- and N-type voltage-gated calcium channels and by an inhibitor of diacylglycerol lipase. We propose that both L1 and bFGF act via the FGFR to generate polyunsaturated fatty acids which in turn cause calcium channels to flicker open and shut. Short-lived domains of raised calcium at the cytosolic mouth of open channels activate axon outgrowth without raising bulk cytosolic calcium concentration. In confirmation of this model, the rapidly-acting calcium buffer BAPTA is significantly more effective at blocking FGF-induced axon outgrowth when compared with the slower buffer EGTA. Generation of short-lived calcium domains may provide a crucial mechanism for axon guidance during development and for promoting regeneration of damaged axons.     

中毒剂量锌对大鼠小肠粘膜超微结构的影响

目的：阐明中毒剂量锌对肠粘膜免疫屏障结构的影响及其机理。方法：通过建立常锌（ＺＮ）、中毒剂量锌（ＺＰ）大鼠模型,应用病理形态学手段（电镜）对大鼠肠道粘膜的超微结构进行研究。结果：第４周末和第７周末血浆、红细胞膜和肠组织的锌含量ＺＰ组明显高于ＺＮ组（Ｐ＜０．０５）。第四周末和第七周末ＺＰ组光镜下肠粘膜未见异常改变;但是电镜下见肠道粘膜超微结构的严重损害。结论：中毒剂量锌可以引起肠道粘膜超微结构的严重损害;屏障功能削弱,大鼠小肠粘膜的免疫防御能力降低。