小鼠间质胶原和基膜成分在诱导排卵过程中的变化

目的　研究间质胶原和基膜成分在诱导排卵过程中的变化。　方法　苦味酸 -天狼星红偏振光法 ,生物素 -抗生物素蛋白间接免疫荧光 ,原位杂交。　结果　排卵前后 , 型胶原、 型胶原、层粘连蛋白的分布、数量 ,以及 型胶原和间质金属蛋白酶 - 2 m RNA的表达有一定改变。　结论　间质胶原和基膜成分对排卵过程有一定调控作用。     

缺血缺氧时新生大鼠脑微血管基膜细胞外基质与脑细胞线粒体钙的变化

本文用６０ 只新生大鼠随机分为空白对照组、假手术对照组、缺血缺氧组、复氧２４ ｈ 组和复氧４８ ｈ 组。对每组中的４ 例大脑用抗Ⅳ型胶原抗体和抗层粘连蛋白抗体进行免疫组织化学反应;每组中的８ 例测定脑细胞线粒体钙浓度。用方差分析Ｓｔｕ ｄｅｎ Ｎｅｗ ｍ ｅｎ Ｋｅｕｌｓ 法检验所得数值的差异显著性,Ｐ＜ ０．０５。缺血缺氧组、复氧２４ ｈ 组和复氧４８ ｈ 组Ⅳ型胶原和层粘连蛋白阳性反应平均单位面积分别比两对照组者小;三个实验组阳性反应呈不连续线状的微血管数比两对照组者多;同时三个实验组阳性反应呈连续线状的微血管数比两对照组者少。三个实验组之间的阳性反应呈不连续线状的微血管数或呈连续线状的微血管数也都存在着显著性差异。缺血缺氧组脑细胞线粒体钙含量比两对照组者高,缺血缺氧后复氧２４ ｈ 组继续升高,复氧４８ ｈ 组的脑细胞线粒体钙含量却下降。缺血缺氧可导致新生脑细胞线粒体的钙离子增多,并可能激活细胞外的蛋白酶,溶解微血管的基膜成分－ Ⅳ型胶原和层粘连蛋白等,损伤血脑屏障,渗透性增高,发生脑水肿。如果能够及时给予合理的治疗和处理,则应该可以得到一定程度的恢复。     

人卵母细胞体外成熟前后线粒体分布的变化

目的 研究人未成熟和成熟卵母细胞中线粒体的分布,进一步阐明卵母细胞成熟和线粒体分布的关系.方法 未成熟卵母细胞和成熟卵母细胞均用Mito Tracker Green FM染色,经多聚甲醛固定后在激光扫描共焦显微镜下观察线粒体的分布.结果 线粒体在细胞质中的分布方式可分为:周边分布、半周边分布和均匀分布.在64.10%(50/78)的GV期卵母细胞中,线粒体呈周边分布.45.16%(28/62)的MI期卵母细胞中,线粒体仍维持周边分布;呈均匀分布的卵母细胞的比例为38.71%(24/62).体外培养成熟以后,线粒体在75.47%(80/106)的卵母细胞中呈现均匀分布.与体外培养成熟的卵母细胞相比,体内成熟的卵母细胞中线粒体分布最明显的特点是胞质中央区域线粒体的浓集,荧光强度高于周边区域.结论 人卵母细胞成熟前后,线粒体出现明显的分布变化,由未成熟卵母细胞中以周边分布为主变为成熟卵母细胞中以均匀分布为主.     

DISTRIBUTION OF α1(IV) AND α3(IV) CHAINS OF TYPE IV COLLAGEN IN LUNG TUMOURS

Tumour invasion is associated with strong remodelling of the extracellular matrix, including the basement membrane (BM). The major structural component of BMs is type IV collagen, which is composed of an association of three α chains. In this study, the distribution of the α1 and α3 chains in both normal and neoplastic lung tissues has been examined by immunohistochemistry, using specific monoclonal antibodies. In normal tissues, the α1(IV) chain was found in all BMs, whereas the α3(IV) chain was only found in alveolar BMs. In 36 lung tumours, the α1(IV) chain was detected in all cases, with irregular positivity around tumour clusters and in the stroma. It was noteworthy that this stromal distribution was particularly associated with the presence of cancer cells, whatever their invasive properties. In contrast, in 22 tumours out of 36, the α3(IV) chain was only found at the interface between invasive tumour clusters and stroma, with a linear and disrupted pattern. These data show a distinctive distribution of type IV collagen chains in lung tumours, with expression of α1(IV) chain and likely neosynthesis of the α3(IV) chain around some invasive tumour clusters. The results suggest the involvement of these BM components in the process of tumour invasion. © 1997 John Wiley & Sons, Ltd.     

CD2相关蛋白在肾脏细胞中的分布及其在足细胞中的作用

目的 观察CD2相关蛋白(cD2AP)在肾脏不同细胞系中的表达分布,及其与足细胞裂孔隔膜分子nephrin和细胞骨架蛋白F-actin之间的联系.方法 以DMEM培养基培养人肾小球系膜细胞(HMC)和人肾小管上皮细胞系(HK-2),RPMI 1640培养基培养条件永生化小鼠足细胞系.以RT-PCR及Western blotting方法检测足细胞内CD2AP和nephrin的表达.间接免疫荧光结合激光共焦方法观察CD2AP在HMC、HK-2、未分化及已分化足细胞中的表达情况,及CD2AP与nephtin在足细胞中的共存.直接免疫荧光结合激光共焦方法观察F-actin在足细胞的表达及其与CD2AP的共存.结果 CD2AP均匀分布于HK-2及未分化足细胞的核周及胞浆,而不表达于HMC细胞.在足细胞分化过程中,CD2AP的分布发生了变化,出现向周边聚集的现象.CD2AP与足细胞裂孔隔膜分子nephrin及细胞骨架蛋白F-actin在足细胞中存在共定位关系.结论 CD2AP表达于上皮来源的肾脏固有细胞.CD2AP在足细胞中的分布特点,提示CD2AP可能参与足细胞的分化过程,并与裂孔隔膜分子功能及细胞骨架凋节有关.     

Epidermolysis bullosa acquisita: A comprehensive review

Epidermolysis bullosa acquisita is a rare autoimmune blistering disease which results in vesicle and bullae formation on the skin and erosions on the mucous membranes. EBA is mediated by autoantibodies to collagen VII. Clinically, it can present with numerous phenotypes, though the most common are the mechanobullous and inflammatory variants. Patients with mechanobullous EBA develop non-inflammatory bullae and erosions at sites of trauma while patients with the non-mechanobullous type develop inflammatory lesions which often mimic other blistering conditions including bullous pemphigoid, linear IgA bullous disease, and mucous membrane pemphigoid. Diagnosis is established by having a consistent clinical presentation, DIF, and autoantibodies against collagen VII. In apparent “seronegative” patients, the diagnosis is challenging due to the need for confirmatory tests which are often not routinely accessible outside of the specialized center. In light of EBA's rarity, and lack of any randomized controlled trials, treatment guidelines rely on the small case series presented in the literature. There has been variable success utilizing the arsenal of immunosuppressants and biologics. Development of experimental murine models has facilitated a deeper understanding of EBA's pathogenesis and allows for preclinical testing of numerous novel drug targets predominantly targeting inhibition of neutrophil activation. We herein review the presentation, diagnosis, treatments, and future avenues of research in EBA.