高糖对体外培养Schwann细胞生长及细胞外信号调节激酶1／2磷酸化的影响

目的:探讨高糖对体外培养Schwann细胞生长及细胞外信号调节激酶(ERK)磷酸化的影响.方法:按照培养液中葡萄糖浓度的小同,分为对照组与高糖组.用MTT法检测Schwann细胞生长情况;用ELISA法检测对照组与高糖组ERK1/2磷酸化的程度,以及加入神经源性一氧化氮合成酶(nNOS)抑制剂后ERK1/2磷酸化的程度.结果:高糖浓度下,细胞虽有增殖但幅度及时程明显低于对照组,高糖抑制Schwann细胞生长;随着精浓度的升高.ERK1/2磷酸化的程度逐渐增加,并与加入nNOS抑制剂有相似的表现.结论:高糖抑制Schwann细胞生长,并且降低nNOS的量,减弱一氧化氮(NO)对ERK1/2的抑制作用,导致ERK1/2磷酸化水平升高.     

Bednar tumor (pigmented dermatofibrosarcoma protuberans). An analysis of six cases

Six cases of Bednar tumor were analyzed clinicopathologically along with a review of 39 published cases. The findings were then compared with data on 44 cases of ordinary dermatofibrosarcoma protuberans (DFSP) obtained from our files. The clinical manifestations of the patients and the anatomic locations of the tumors were similar between the two categories, but the rate of recurrence was lower in cases of Bednar tumor. The histologic pattern of Bednar tumor was indistinguishable from ordinary DFSP except for scattered melanosome-containing cells. Ultrastructural and immunohistochemical examinations showed no evidence of neuroectodermal differentiation of dominant spindle-shaped cells in Bednar tumor, supporting a fibroblastic line of differentiation. The origin and pathogenesis of the melanosome-containing cells were considered. These cells failed to react with HMB-45, a melanoma-specific antibody, and the large majority of melanosomes present were mature or at Stage IV, plus a few immature ones at Stage II. These pigmented cells do not appear to be neoplastic, and cannot be used as proof to indicate that Bednar tumor is a neuroectodermal neoplasm.     

Study on structure-property relationship of polyimide blends, 2. Structure and miscibility of polyimide PBPI-E/PTI-E blends

The structure and miscibility of polyimide PBPI-E/PTI-E blends were studied by wide- and small-angle X-ray scattering and dynamic mechanical analysis, where PBPI-E is a biphenyldianhydride-based polyimide, and PTI-E is a polyimide from 4,4′-thiodiphthalic anhydride and 4,4′-oxydianiline. The results obtained show that there exists a paracrystalline structure in the blends with high content of PBPI-E, but this does not affect the miscibility of the blends. The blends are miscible over the entire composition range, since only one T_g was observed for each blend. Meanwhile, the segregation of PTI-E during crystallization of PBPI-E in the blends is interlamellar.     

经皮穿刺椎间盘髓核摘除术入路的研究

为提供椎间盘髓核摘除术形态学依据，在7具成人横断面标本上观察测量了L1～L5椎间盘平面经皮穿刺椎间盘髓核摘除术的进针点、角度和深度。发现在L1～L3、L4～L5椎间盘髓核的穿刺点以距后正中线8～10cm，9～11cm，穿刺角度以46．7°～59．5°，穿刺深度为110．2～128．9mm为最宜。     

Regulation of the association between PSTPIP and CD2 in murine T cells

Prominent in T cells and natural killer cells, CD2 binding protein 1 (CD2BP1) plays an important role in CD2-mediated adhesion and signal transduction. In the current study, we investigated CD2 and PSTPIP (proline, serine, threonine phosphatase interacting protein, murine homologue of CD2BP1) interactions in purified mouse splenic T cells. PSTPIP associated with CD2 in both resting and activated T cells. Following various stimuli, such as concanavalin A, anti-TCRbeta, anti-CD3epsilon, anti-CD3epsilon/phorbol myristate acetate (PMA), IL-2, or PMA/ionomycin, PSTPIP and CD2 expression, as well as their association, increased in a time-dependent fashion. While PSTPIP expression and CD2 expression were comparable across most groups, the PSTPIP-CD2 association stimulated by anti-CD3epsilon alone was significantly greater than with other stimuli. Stimulation by anti-CD3epsilon plus anti-CD28 induced even greater PSTPIP-CD2 association than anti-CD3epsilon treatment alone, indicating that CD28 initiated signals are involved in regulating this interaction. There was no direct association between CD3epsilon or CD28 and PSTPIP. Tyrosine phosphorylated PSTPIP bound poorly to CD2 compared to dephosphorylated PSTPIP, and protein tyrosine phosphatase was shown to affect both phosphorylation of PSTPIP and the CD2-PSTPIP association. In addition to CD2, PSTPIP associated with CD4, CD8, CD54, and CD62L. CD2 and CD4 ligation reciprocally regulated their association with PSTPIP. These findings indicate that T cell activation, particularly through the CD3 and CD28 signal transduction pathways, regulates PSTPIP-CD2 interactions. PSTPIP likely has additional broader effects through interactions with CD4, CD8, CD54, and CD62L, and this may influence T cell responses to antigen.     

Identification of a novel mutation in patients with medium-chain acyl-CoA dehydrogenase deficiency

A novel mutation was identified in two unrelated patients with medium-chain acyl-CoA dehydrogenase deficiency. First, a 19-year-old Caucasian female presented with a devastating illness, resulting in sudden death in adulthood which is unusual. The second patient, now a 3.5-year-old male, presented at 17 months of age with a hypoglycemic seizure and dehydration. Sequence analysis revealed a novel mutation G617T in exon 8 resulting in an arginine to leucine substitution at codon 206 (R206L). Both patients were compound heterozygous for this G617T and the common mutation A985G.     

大鼠再生肝对二乙基亚硝胺启动作用的敏感性

目的比较再生肝和正常肝对二乙基亚硝胺（ＤＥＮ）启动作用的敏感性。方法以２／３肝叶切除后８周末的大鼠为实验组,正常大鼠为对照组,作如下比较：肝重、常规组织学检查及３Ｈ－ＴｄＲ掺入试验;用修改的Ｓｏｌｔ－Ｆａｒｂｅｒ模型,通过对ＧＧＴ阳性癌前病灶的体视学测量,观察肝脏对ＤＥＮ的启动效应;在体内和体外（无血清原代培养肝细胞）经ＤＥＮ攻击后,以核酸原位缺口标记方法观察肝细胞ＤＮＡ的损伤程度。结果２／３肝叶切除后８周末的实验组肝脏的修复过程已完成,未见肝细胞继续增生的表现;经ＤＥＮ攻击后,实验组肝癌前病灶在数密度和体积密度上都显著高于对照组;无论在体内或体外接受ＤＥＮ攻击后,实验组肝细胞ＤＮＡ的损伤程度都显著大于对照组。结论即使再生过程已经完成,再生肝仍比正常肝具有较高的致癌敏感性,这与再生肝肝细胞在ＤＥＮ攻击后其ＤＮＡ损伤较重相关。     

弯曲血管内血流与动脉粥样硬化斑块的相互影响与作用

作为文章[1]的继续,本文在文章[1]的分析结果基础上,针对壁面对称和非对称狭窄的两种不同情况,通过数值计算给出弯曲狭窄血管内血流的轴向和周向切应力的分布曲线,并讨论其随管壁面几何参数的变化情况。同时,还讨论壁面几何参数对平均血流量和压力降影响的规律。从中发现,当狭窄较轻时(λ<0.2),壁面切应力、平均流量和压力降受狭窄度(λ)的影响不大,而在狭窄较严重时(λ>0.7),狭窄度微小的变化会引起它们急剧变化。此外,在讨论狭窄的非对称性对上述血流动力学参数的影响时还发现,非对称性只对轴向切应力有明显的影响,而对其它参量的影响并不十分显著。     

Matcha Green Tea Alleviates Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice by Regulating Lipid Metabolism and Inflammatory Responses

Lately, matcha green tea has gained popularity as a beverage and food additive. It has proved to be effective in preventing obesity and related metabolic syndromes. However, the underlying mechanisms of its control effects against non-alcoholic fatty liver disease (NAFLD) are complicated and remain elusive. In the present study, we performed an in vivo experiment using male C57BL/6 mice fed with a high-fat diet and simultaneously treated with matcha for six weeks. Serum biochemical parameters, histological changes, lipid accumulation, inflammatory cytokines, and relevant indicators were examined. Dietary supplementation of matcha effectively prevented excessive accumulation of visceral and hepatic lipid, elevated blood glucose, dyslipidemia, abnormal liver function, and steatosis hepatitis. RNA sequencing analyses of differentially expressed genes in liver samples indicated that matcha treatment decreased the activity of lipid droplet-associated proteins and increased the activity of cytochrome P450 enzymes, suggesting improved metabolic capacity and liver function. The current study provided evidence for new dietary strategies based on matcha supplementation to ameliorate lipotoxicity-induced obesity and NALFD.