Id1 interacts and stabilizes the Epstein-Barr virus latent membrane protein 1 (LMP1) in nasopharyngeal epithelial cells

The EBV-encoded latent membrane protein 1 (LMP1) functions as a constitutive active form of tumor necrosis factor receptor (TNFR) and activates multiple downstream signaling pathways similar to CD40 signaling in a ligand-independent manner. LMP1 expression in EBV-infected cells has been postulated to play an important role in pathogenesis of nasopharyngeal carcinoma. However, variable levels of LMP1 expression were detected in nasopharyngeal carcinoma. At present, the regulation of LMP1 levels in nasopharyngeal carcinoma is poorly understood. Here we show that LMP1 mRNAs are transcribed in an EBV-positive nasopharyngeal carcinoma (NPC) cell line (C666-1) and other EBV-negative nasopharyngeal carcinoma cells stably re-infected with EBV. The protein levels of LMP1 could readily be detected after incubation with proteasome inhibitor, MG132 suggesting that LMP1 protein is rapidly degraded via proteasome-mediated proteolysis. Interestingly, we observed that Id1 overexpression could stabilize LMP1 protein in EBV-infected cells. In contrary, Id1 knockdown significantly reduced LMP1 levels in cells. Co-immunoprecipitation studies revealed that Id1 interacts with LMP1 by binding to the CTAR1 domain of LMP1. N-terminal region of Id1 is required for the interaction with LMP1. Furthermore, binding of Id1 to LMP1 suppressed polyubiquitination of LMP1 and may be involved in stabilization of LMP1 in EBV-infected nasopharyngeal epithelial cells.     

植物防御反应中活性氧的产生和作用

活性氧在植物抗病性中起着重要的作用。本文将对其在防御反应中的产生和作用进行简要的论述。     

高脂饲料诱导的肥胖大鼠网膜素水平的实验研究

人群调查发现肥胖人群网膜素水平较正常人群低,而正常及肥胖大鼠血清网膜素水平及其基因表达情况尚不清楚.将SD大鼠随机分为正常组(n=10)和高脂组(n=30),分别喂养普通饲料和高脂饲料.6 w后从高脂组选取体重增长最快的20只,再从中随机抽取10只继续喂养高脂饲料,12 w后两组各剩9只,采用全自动生化仪ADVIA2400测定血糖及血脂、ELISA检测血清胰岛素及网膜素水平、RT-PCR检测网膜脂肪组织网膜素mRNA表达水平.结果显示高脂组大鼠体重、体重增加值、肥胖指数、低密度脂蛋白、胰岛素、血清网膜素水平及网膜脂肪组织网膜素mRNA表达水平均高于正常组(P<0.05).首次发现肥胖大鼠血清网膜素水平及网膜脂肪组织中网膜素mRNA表达水平较正常大鼠显著增高,与人群调查结果不一致.     

Overexpression of fucosyltransferase IV in A431 cell line increases cell proliferation

Fucosyltransferase IV is an essential enzyme that catalyzes the synthesis of fucosylated oligosaccharides by transferring GDP-fucose to the terminal N-acetylglucosamine with the alpha1,3-linkage. Lewis Y oligosaccharide has a terminal alpha1,3-linked fucose residue and elevation of Lewis Y level is seen in many epithelial cancers. The mechanism of Lewis Y elevation in neoplastic cells is still largely unknown. To study the impact of fucosyltransferase IV on Lewis Y expression and its role on neoplastic cell proliferation, a pEGFP-N1-FUT4 recombinant plasmid was developed and stably transfected into A431 cells. We found that fucosyltransferase IV overexpression promoted cell proliferation and increased the expression of proliferating cell nuclear antigen that correlated with Lewis Y augmentation. Cell cycle analysis demonstrated that fucosyltransferase IV overexpression facilitated cell cycle progression. In conclusion, fucosyltransferase IV overexpression augments Lewis Y expression to trigger neoplastic cell proliferation. These studies suggest that fucosyltransferase IV may serve as a potential therapeutic target for the treatment of Lewis Y-positive epithelial cancers.     

准噶尔盆地荒漠灌丛对融雪水空间分布的反馈初探

温带荒漠的积雪沿灌丛始融,并以灌丛为中心形成融雪漏斗,导致融雪水向灌丛基部汇集。观测资料表明:通过灌丛对融雪水分布的反馈,使灌丛周围的沙层含水量明显增加,为裸沙区的152.1-228.9％,从而提高融雪水的利用率并改善灌丛自身的供水条件,对荒漠植被的分布格局亦起一定影响。     

颧颞部骨折术后并发颞部凹陷的临床回顾性研究

目的：分析不同颧颞部骨折性质与颞部凹陷的相关性,评价颧颞部骨折术后并发颞部凹陷的防治效果。方法：对105例颧颞部骨折病例进行回顾性分析,52例患者行颞部凹陷修复术,采用头皮冠状切口,应用钛网修复颞部凹陷,术后通过长期随访评价治疗效果。结果：陈旧性骨折颞部凹陷的发生率显著高于新鲜骨折,但治疗后颞部外形均有明显改善。结论：钛网植入能有效地修复颧颞部骨折术后并发的颞部凹陷,但应把握手术时机及治疗方法。     

妊娠肝内胆汁淤积症发生的分子机制研究进展

妊娠肝内胆汁淤积症（Intrahepatic cholestasis of pregnancy, ICP）是发生在妊娠中晚期,以皮肤瘙瘁、黄疸、血清胆汁酸升高,伴轻度肝功能损害为特征的妊娠并发症,严重影响母儿健康。ICP的发病机制尚未完全阐明,但有研究表明在遗传易感性妇女中,性激素及其代谢产物导致胆汁酸代谢异常与本病的发生密切相关。现就目前国内外有关ICP发病机制的研究进展做一综述,一方面为探寻更深层次的机制提供理论基础,另一方面为临床治疗ICP提供思路和方法。     

ELK-1/JNK/c-Fos对左归降糖解郁方(ZGJTJYF)体外培养的模拟糖尿病并发抑郁症(DD)大鼠海马神经元凋亡中的作用

目的:研究信号通路ELK-1/JNK/c-Fos在左归降糖解郁方(ZGJTJYF)对模拟糖尿病并发抑郁症(DD)环境下抗海马神经元凋亡中的作用。方法:原代培养海马神经元,加入高糖(150 mmol/L)+皮质酮(200μmol/L),构建DD体外细胞模型;将培养的海马神经元细胞随机分为5组:空白血清组、正常组、左归降糖解郁方含药血清组、阳性药(二甲双胍+氟西汀)含药血清组和模型组(每组3个复孔)。模型组和正常组给予等量培养液,其余组加入相应体积分数10%的相应血清,均干预18 h。分别采用Hoechst染色、高内涵细胞成像分析技术和RT-PCR技术分别检测海马神经元凋亡情况及检测凋亡相关ELK-1、JNK和c-Fos蛋白和基因的表达。结果:与空白组比较,模型组细胞凋亡明显,其海马神经元凋亡数量明显增多,ELK-1、JNK和c-Fos的mRNA及蛋白表达水平均显著升高(P<0.05);与模型组比较,左归降糖解郁方含药血清组和阳性药含药血清组大鼠海马神经元可见局部亮点明显减少,凋亡细胞数显著减少,ELK-1、JNK和c-Fos蛋白及mRNA表达均明显下调(P<0.05),且神经网络及树突连接情况得到明显改善。结论:左归降糖解郁方可以减低DD环境下海马神经元中Elk-1、JNK、c-fos表达而起到抗凋亡的效果。     

Quantitative determination of helicid in rat biosamples by liquid chromatography electrospray ionization mass spectrometry

A simple liquid chromatography electrospray ionization mass spectrometry (LC–ESI–MS) method with highly improved sensitivities for the determination of helicid in rat bile, urine, feces and most tissues was developed. The tissues and feces were firstly homogenized mechanically using deionized water as the media. Bile, urine, tissues and feces homogenates were extracted by liquid–liquid extraction with n-butyl alcohol for sample preparation. The subsequent analysis procedures were performed on a Shimadzu LCMS2010A system (electrospray ionization single quadrupole mass analyzer). A Luna C₁₈ column (150 mm × 2.00 mm, 5 μm) was used as the analytical column, while a mixture of acetonitrile and ammonium chloride water solution was used as the mobile phase. The proportions of mobile phase were changed timely according to gradient programs. Chlorinated adducts of molecular ions [M+Cl]^? at m/z 319.00 and 363.05 were used to quantify helicid and bergeninum (internal standard), respectively. The method was validated to be accurate, precise and rugged with good linearity. The proposed method was successfully applied to the preclinical tissue distribution and excretion studies of helicid in rats.     

Neuroprotective and nootropic drug noopept rescues α-synuclein amyloid cytotoxicity

Parkinson's disease is a common neurodegenerative disorder characterized by α-synuclein (α-Syn)-containing Lewy body formation and selective loss of dopaminergic neurons in the substantia nigra. We have demonstrated the modulating effect of noopept, a novel proline-containing dipeptide drug with nootropic and neuroprotective properties, on α-Syn oligomerization and fibrillation by using thioflavin T fluorescence, far-UV CD, and atomic force microscopy techniques. Noopept does not bind to a sterically specific site in the α-Syn molecule as revealed by heteronuclear two-dimensional NMR analysis, but due to hydrophobic interactions with toxic amyloid oligomers, it prompts their rapid sequestration into larger fibrillar amyloid aggregates. Consequently, this process rescues the cytotoxic effect of amyloid oligomers on neuroblastoma SH-SY5Y cells as demonstrated by using cell viability assays and fluorescent staining of apoptotic and necrotic cells and by assessing the level of intracellular oxidative stress. The mitigating effect of noopept against amyloid oligomeric cytotoxicity may offer additional benefits to the already well-established therapeutic functions of this new pharmaceutical.