小脑和脑干梗塞致突发性耳聋

目的:了解小脑和脑干梗塞引起的突发性耳聋的临床特点.探讨其发病机制.方法:回顾性分析12例小脑和脑干梗塞所致突发性耳聋的临床资料.结果:该组患者主要临床表现为耳聋、眩晕、耳鸣、眼震、同侧颜面麻木感.头颅CT或MRI发现小脑或脑干有小于2 cm的梗塞灶.结论:发病机制主要为小脑前下动脉(AlCA)供血不足使小脑脑桥角或脑干缺血,损伤该区域的耳蜗神经和听神经传导通路,导致耳聋.小脑和脑干梗塞的诊断主要依据临床表现、CT或MRI检查.     

不同地区妇女产褥期卫生行为研究

目的 了解江苏、陕西和贵州三省妇女产褥期卫生行为和保健的一般情况;比较 不同地区间产褥期各种卫生行为的发生率;了解影响产褥期卫生行为的相关因素。方法 用问卷调查的形式对三者１２个县的２３５２例２岁以下儿童母亲进行入户访问。结果 江苏、陕西、贵州三者产褥期各卫生行为的发和衣次为：洗头２６．４％,３８．８％,１９．８％, 下身（指外阴部,下同）８３．３％,２６．９％,６４．０％,正常活动７６．９％,７     

应用酵母双向杂交系统筛选和鉴定P75NGFR作用的蛋白

目的：探讨Ｐ７５ＮＧＦＲ介导神经细胞凋亡的分子机制。方法;以转染了Ｐ７５ＮＧＦＲ的大鼠小脑神经细胞株Ｒ２Ｌ２为细胞模型,应用酵母双向杂交系统（ｔｗｏ－ｈｙｂｒｉｄ ｓｙｓｔｅｍ）筛选和鉴定Ｐ７５ＮＧＦＲ胞内区Ｐ７５ＩＣＤ作用的蛋白。结果：和Ｐ７５ＮＧＦＲ作用的蛋白由一个６００ｂｐ大小的ＣＤＮＡ片段编码。结论：该工作将有助于探讨Ｐ７５ＮＧＦＲ介导细胞凋亡的分子机制和信号,为勃勃系统退行性病变的病因、     

大鼠局灶性脑缺血模型及其与C反应蛋白变化的关系

目的 改进大鼠大脑中动脉梗塞法,建立更接近于临床缺血性脑卒中及其再扩灌注的可靠模型,并观察其与血甭Ｃ反应蛋白变化的。方法沿大鼠右颈内动脉插入长２．１￣２．３ｃｍ直径０．２０５ｍｍ的单股尼龙丝,直达大脑中动脉起始部开口,阻断其血流,观察大鼠神经病学改变及脑组织形态学变化,并测定血清Ｃ反应蛋白含量。结果 术后大鼠表现特殊体态及典型追尾征,６ｈ大脑中动脉供血区出现缺血性外观（ＴＴＣ染色）及相应组织学变化     

Computerized analysis of lesions in US images of the breast

RATIONALE AND OBJECTIVES: Breast sonography is not routinely used to distinguish benign from malignant solid masses because of considerable overlap in their sonographic appearances. The purpose of this study was to investigate the computerized analyses of breast lesions in ultrasonographic (US) images in order to ultimately aid in the task of discriminating between malignant and benign lesions. MATERIALS AND METHODS: Features related to lesion margin, shape, homogeneity (texture), and posterior acoustic attenuation pattern in US images of the breast were extracted and calculated. The study database contained 184 digitized US images from 58 patients with 78 lesions. Benign lesions were confirmed at biopsy or cyst aspiration or with image interpretation alone; malignant lesions were confirmed at biopsy. Performance of the various individual features and output from linear discriminant analysis in distinguishing benign from malignant lesions was studied by using receiver operating characteristic (ROC) analysis. RESULTS: At ROC analysis, the feature characterizing the margin yielded Az values (area under the ROC curve) of 0.85 and 0.75 in distinguishing between benign and malignant lesions for the entire database and for an "equivocal" database, respectively. The equivocal database contained lesions that had been proved to be benign or malignant at cyst aspiration or biopsy. Linear discriminant analysis round-robin runs yielded Az values of 0.94 and 0.87 in distinguishing benign from malignant lesions for the entire database and for the equivocal database, respectively. CONCLUSION: Computerized analysis of US images has the potential to increase the specificity of breast sonography.     

Satellite-cell-derived nerve growth factor and neurotrophin-3 are involved in noradrenergic sprouting in the dorsal root ganglia following peripheral nerve injury in the rat

Injury to a peripheral nerve induces in the dorsal root ganglia (DRG) sprouting of sympathetic and peptidergic terminals around large-diameter sensory neurons that project in the damaged nerve. This pathological change may be implicated in the chronic pain syndromes seen in some patients with peripheral nerve injury. The mechanisms underlying the sprouting are not known. Using in situ hybridization and immunohistochemical techniques, we have now found that nerve growth factor (NGF) and neurotrophin-3 (NT3) synthesis is upregulated in satellite cells surrounding neurons in lesioned DRG as early as 48 h after nerve injury. This response lasts for at least 2 months. Quantitative analysis showed that the levels of mRNAs for NT3 and NGF increased in ipsilateral but not contralateral DRG after nerve injury. Noradrenergic sprouting around the axotomized neurons was associated with p75-immunoreactive satellite cells. Further, antibodies specific to NGF or NT3, delivered by an osmotic mini-pump to the DRG via the lesioned L5 spinal nerve, significantly reduced noradrenergic sprouting. These results implicate satellite cell-derived neurotrophins in the induction of sympathetic sprouting following peripheral nerve injury.     

Bone marrow transplantation attenuates murine IgA nephropathy: role of a stem cell disorder

BACKGROUND: The pathogenesis of IgA nephropathy is still obscure. The aim of this study was to investigate whether the fundamental pathogenesis of IgA nephropathy lies in bone marrow stem cells (BMCs). METHODS: We used donors of two different strains for bone marrow transplantation (BMT) into mice with a high content of serum IgA (ddY strain, HIGA mice), a murine model of IgA nephropathy. One group (B6-->HIGA, N = 5) received BMCs of C57BL/6j (B6) mice, and the other (HIGA-->HIGA, N = 8) were reconstituted with BMCs of HIGA mice. RESULTS: Twenty-six weeks after BMT, in B6-->HIGA mice, mesangial deposits of IgA and C3 were statistically milder than those in HIGA-->HIGA mice. Light microscopic observations disclosed that glomerular sclerosis and mesangial matrix expansion in B6-->HIGA mice were decreased compared with those in HIGA-->HIGA mice. These B6-->HIGA mice also excreted less urinary albumin than HIGA-->HIGA mice. Furthermore, serum levels of IgA in B6-->HIGA mice were markedly lower than those in HIGA-->HIGA mice. Size analysis of serum IgA revealed that macromolecular IgA were notably lower in B6-->HIGA mice than in HIGA-->HIGA mice. CONCLUSIONS: Our results suggest that qualitative and quantitative changes of serum IgA are determined at the level of stem cells, and that BMT from normal donors can attenuate glomerular lesions in HIGA mice. This approach may offer a new avenue to study the pathogenesis of IgA nephropathy.     

Organ transplantation in mice: current status and future prospects

With the development of microsurgery and molecular biology in the 1990s, the mouse model for organ transplants has become increasingly popular. In the past 10 years, the number of studies using the mouse model has increased three-fold. All the organ transplants, originally done in the rat model, can now be performed in mice with high success rates. This article reviews the development, advantages, limitations, and unique immunology of the mouse model as well as future prospects.