脑胶质瘤中血脑屏障的超微结构特点

８例胶质瘤病例，标本分别取自同一病例的瘤体，瘤周水肿区和邻近脑组织。瘤体和瘤周水肿区血脑屏障超微结构变化无明显差异，内皮肿胀，毛细血管腔狭小，腔面有稀疏的绒毛样突起，内皮为无孔型，胞质内胞饮泡较多，内皮紧密连接增长，细胞连接间隙增宽，基膜完整，基膜完整，胶质膜缺损。     

Enhancement of murine IgE antibody detection by IgG removal

RATIONALE: Although animal models for the study of allergic reactions are desirable, the use of mice has been hindered by the lack of sufficiently sensitive in vitro immunoglobulin epsilon (IgE) antibody assays. The aim of this study was to enhance IgE antibody measurements by immunoglobulin gamma (IgG) depletion. METHODS: Seven- to eight-week-old female mice of four strains (C3H/HeJ, CBA/J, C57Bl/6J, and Balb/c) were immunized (20 mice/group) with shrimp or peanut extracts using Al(OH)(3) as adjuvant. Following immunization, animals were sacrificed by exsanguination and the sera of each group pooled. Initial measurements of IgE antibody levels by enzyme-linked immunosorbent assay (ELISA) were relatively low; IgG and IgE reactivity patterns by immunoblot were similar. Thus, sera from shrimp or peanut immunized mice were depleted of IgG (absorbed 3-6 times with immobilized protein G) and then tested for IgE antibody to shrimp or peanut allergen. RESULTS: A 3- to 5-fold increase in IgE antibody reactivity as measured by ELISA was demonstrated when >80-90% of the IgG was removed. This increase in detection of allergen-specific IgE occurred in sera from all mouse strains and to all allergens tested. In addition, reactivity of IgE antibodies to peanut or shrimp allergens by immunoblot increased visually approximately 4- to 10-fold. CONCLUSIONS: These studies indicate that allergen-specific IgG antibodies, which may be in more than 100-fold excess to IgE antibodies, interferes with detection of allergen-specific IgE, probably by competitive binding to allergenic epitopes. Substantial depletion of IgG antibodies (>80%) result in a significant increase in the sensitivity of the antibody measurements.     

耳蜗的扫描电镜观察

为研究柯替氏器的超微结构,用豚鼠、猫及4个月胎儿的耳蜗,在扫描电镜下观察。柯替氏器呈螺旋梯状,围绕在蜗轴周围。蜗尖部的柯替氏器较宽,蜗底部的较窄,其上方的前庭膜由单层扁平上皮组成,上皮表面有微绒毛。紧贴表面的盖膜由原纤维组成。大多数原纤维平行排列,表面与边缘的原纤维多交织成网。柯替氏器中有3排外毛细胞与1排内毛细胞,二者之间有柱细胞头板,外毛细胞上的听毛排列成W形,内毛细胞上的听毛排列成弧形。此外,所有细胞表面均有微绒毛。在轻度噪音刺激后,听毛减少并紊乱,微绒毛也减少或消失。 4月胎儿的柯替氏器有3～4排外毛细胞,其表面为绒球状听毛,后来发育为W形排列。内毛细胞为1排,表面为束状的原始听毛,后变为弧形排列。本文还观察到断裂的柯替氏器中,暴露出外毛细胞的柱状胞体及底部的杯状支持结构。外毛细胞由外指细胞所肩托。外指细胞的指突与外毛细胞均倾斜排列,交错成一定角度。当暴露出外柱细胞时,其胞体上细下粗,表面有传入神经纤维。当外毛细胞、外柱细胞等掀向上方后,可见隧道中纵行的神经纤维束及其分支,即螺旋隧道束与放线隧道纤维,它们系橄榄耳蜗束的传出纤维。     

Transformation of ψ − Saccharomyces cerevisiae to ψ + with DNA co-purified with 3 μm circles

Summary DNA enriched for supercoiled plasmids prepared from the 3 m plasmid-enriched, [ ⁺], [2 m°] strain 6-1G-P188 and from the [2 m⁺] [⁺] strain LL20 can be used to transform a ^– recipient strain to ⁺. Fractionation of the former preparation by electrophoresis showed that the 3 Mm plasmid band contained the transforming activity.     

Bile mediates intestinal pathology in endotoxemia in rats

Intestinal pathology frequently accompanies experimental endotoxic shock and is mediated by proinflammatory cytokines. Our hypotheses are that hepatobiliary factors operating from the luminal side of the gut make a major contribution to this damage and that tumor necrosis factor alpha (TNF-alpha) is involved in the pathology. We treated rats with lipopolysaccharide (LPS) intravenously and found that external drainage of bile totally protected the gastrointestinal tract, macroscopically and microscopically, 4 h after LPS administration and dramatically improved survival of the animals for 48 h after LPS administration. The concentration of TNF-alpha in bile increased markedly after LPS administration and was over 30 times higher in bile than in serum. Tissue damage and the biliary TNF-alpha response were abrogated when animals were pretreated with gadolinium chloride to eliminate Kupffer cells. TNF-alpha infusion into the duodenal lumen caused intestinal damage similar to that elicited by intravenous LPS. In rats treated with LPS, survival was significantly increased during the first 36 h in animals given an infusion of anti-TNF-alpha antibody into the duodenum. These results demonstrate that in endotoxemia, intestinal damage is mediated by factors derived from the bile. The findings indicate that luminally acting TNF-alpha contributes to the intestinal damage.     

The UDP-galactose translocator gene is mapped to band Xp11.23-p11.22 containing the Wiskott-Aldrich syndrome locus

We have cloned a segment of the human gene encoding UDP-galactose translocator by genetic complementation of its defective mutant in mouse FM3A cells. Chromosome mapping using fluorescentin situ hybridization revealed that the cloned gene hybridized to the Xp11.23-11.23 region of the X chromosome. This region is shared by the locus of Wiskott-Aldrich syndrome, an X-linked recessive immunodeficiency disorder, characterized by defective sugar chains on cell surface components. Genetic and phenotypic similarities suggest a possible link between UDP-galactose translocator and the Wiskott-Aldrich syndrome (WAS).     

虚拟咬合运动初步仿真模拟的研究与实现

我们试验了利用VR技术进行虚拟咬合仿真制作的全部过程。首先,采用光学三维测量仪对上下颌石膏模型进行数字化,通过预处理获取有效的三角网格曲面模型;其次,对咬合运动模型进行合理的简化,分解为一系列的平移运动和旋转运动;通过动态刷新完成开闭口运动、侧移运动的计算机运动仿真,可视化地观察咬合运动;然后利用模型碰撞检测算法动态地计算咬合接触位,并详细地分析了咬合接触时的咬合点位置分布和咬合剖切面上的咬合点接触关系;最后讨论了目前虚拟咬合仿真存在的问题和今后研究的方向。     

The kinase haspin is required for mitotic histone H3 Thr 3 phosphorylation and normal metaphase chromosome alignment

Post-translational modifications of conserved N-terminal tail residues in histones regulate many aspects of chromosome activity. Thr 3 of histone H3 is highly conserved, but the significance of its phosphorylation is unclear, and the identity of the corresponding kinase unknown. Immunostaining with phospho-specific antibodies in mammalian cells reveals mitotic phosphorylation of H3 Thr 3 in prophase and its dephosphorylation during anaphase. Furthermore we find that haspin, a member of a distinctive group of protein kinases present in diverse eukaryotes, phosphorylates H3 at Thr 3 in vitro. Importantly, depletion of haspin by RNA interference reveals that this kinase is required for H3 Thr 3 phosphorylation in mitotic cells. In addition to its chromosomal association, haspin is found at the centrosomes and spindle during mitosis. Haspin RNA interference causes misalignment of metaphase chromosomes, and overexpression delays progression through early mitosis. This work reveals a new kinase involved in composing the histone code and adds haspin to the select group of kinases that integrate regulation of chromosome and spindle function during mitosis and meiosis.     

STAT3 couples with 14-3-3σ to regulate BCR signaling,B-cell differentiation,and IgE production

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