Effects of herbal compound 861 on human hepatic stellate cell proliferation and activation

AIM: To investigate the effects of herbal compound 861 (Cpd 861) on cell proliferation in human hepatic stellate cells (LX-2) and human hepatocellular liver carcinoma cells (HepG2), and expression of α-smooth muscle actin (α-SMA) in LX-2 cells.METHODS: LX-2 and HepG2 cells were incubated with various concentrations of Cpd 861 (0.1-0.003 mg/mL)for 1, 2, 3, 5 and 7 d. Cell proliferation was analyzed by 3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. Effects of Cpd861on the expression of cc-SMA mRNA in LX-2 cells weremeasured by real-time quantitative PCR method using SYBRGreen I technology.RESULTS: Cpd 861, at 0.1 mg/mL, significantly inhibitedLX-2 cell proliferation (15% decrease relative to control,P<0.05) after 3 d of incubation. The inhibitory effects seemedto increase with the treatment time (25% decrease after5 d of incubation and 35% decrease after 7 d of incubation,P<0.01). However, Cpd 861 did not affect HepG2 cellproliferation at the same concentration used for I_X-2 cells.The expression levels of ~-SMA mRNA decreased significantlywhen LX-2 cells were exposed to Cpd 861 for 48 h (59%decrease relative to control, P<0.05) or 72 h (60% decreaserelative to control, P<0.01).CONCLUSION: Cpd 861 can significantly inhibit LX-2 cellproliferation in a dose-dependant manner, and reduce theexpression levels of o~-SMA mRNA in LX-2 cells. Since hepaticcell proliferation and high level of ~-SMA are associatedwith liver fibrosis, the results suggest that Cpd 861 may beuseful in the treatment of this disease.     

自发性颈部动脉夹层与缺血性卒中

自发性颈部动脉夹层（spontaneous cervical artery dissection,SCAD）是青中年缺血性卒中的主要病因之一。SCAD是遗传、环境、感染等多因素疾病,其中,血管相关危险因素与SCAD的关系仍然存在争论。研究显示,SCAD引起的缺血性卒中以血栓栓塞机制为主,因此,抗凝、抗血小板治疗是SCAD的主要治疗方式,但目前尚缺乏随机对照试验对两种治疗方式的疗效进行对比。同时,多项单中心病例研究证实了血管内支架治疗SCAD的有效性和安全性。     

基于小波变换的膈肌肌电信号降噪方法研究

膈肌肌电信号是分析和诊断呼吸疾病最科学及有效的数据之一,该信号往往受到被测对象心电信号的严重干扰.利用小波变换的分析方法,在对原始信号小波分解的基础上,针对各尺度小波系数的特点提出一种新的阈值滤波算法.对来自临床食道电极采集的膈肌肌电信号进行降噪处理,处理前后的时域信号对比以及频域的功率谱分析均表明,心电干扰信号能够被有效地去除,而膈肌肌电信号的信号特征得到较好地保留,为膈肌肌电信号的进一步分析处理创造了良好的条件.     

结合QRS检测和小波阈值的膈肌肌电信号降噪方法

为了消去夹杂在膈肌肌电(EMGdi)信号中的心电干扰,在比例阈值算法的基础上,提出一种结合QRS检测和小波阈值的降噪方法.首先,根据小波系数的相关性构造QRS波群的检测方法,分析确定干扰的位置和范围;其次,将小波系数分为受干扰和未受干扰两部分,并构造相应的阈值算法,针对性地处理受干扰系数,以未受干扰部分系数作为阈值算法构造的依据;最后,重构处理后的小波系数,得到降噪后的EMGdi信号.对临床采集信号的处理对比表明,该方法能够更为有效地去除心电干扰,并更好地保留EMGdi的有用信号.     

Clearance of amyloid-beta in Alzheimer's disease: progress, problems and perspectives

Alzheimer's disease (AD) is the most common form of senile dementia and the fourth highest cause of disability and death in the elderly. Amyloid-beta (Abeta) has been widely implicated in the etiology of AD. Several mechanisms have been proposed for Abeta clearance, including receptor-mediated Abeta transport across the blood-brain barrier and enzyme-mediated Abeta degradation. Moreover, pre-existing immune responses to Abeta might also be involved in Abeta clearance. In AD, such mechanisms appear to have become impaired. Recently, therapeutic approaches for Abeta clearance, targeting immunotherapy and molecules binding Abeta, have been developed. In this review, we discuss recent progress and problems with respect to Abeta clearance mechanisms and propose strategies for the development of therapeutics targeting Abeta clearance.     

Peripheral Delivery of Ganglioside GM1 Exacerbates the Patho-genesis of Alzheimer's Disease in a Mouse Model

Dear Editor, Alzheimer's disease (AD) is the most common cause of dementia among the older population,and is characterized by amyloid-beta (Aβ) accumulation,hyp...     

Plasma Amyloid-Beta Levels in Patients with Different Types of Cancer

Several epidemiological investigations indicate that cancer survivors have a lower risk for Alzheimer’s disease (AD) and vice versa. However, the associations between plasma amyloid-beta (Aβ) levels with cancer remain largely unknown. In this case–control study, 110 cancer patients, 70 AD patients, and 70 age- and gender-matched normal controls were recruited. The cancer types include esophagus cancer, colorectal cancer, hepatic cancer, and lung cancer, all of which were reported to be associated with a lower risk for AD. Plasma levels of Aβ40, Aβ42, common pro-inflammatory cytokines, IL-1β, IL-6, TNF-α, IFN-γ, anti-inflammatory IL-4, chemokines, and cytokines MCP-1 were measured with enzyme-linked immunosorbent assay (ELISA) kits. Plasma levels of Aβ40 and Aβ42 in all cancer patients were higher than that in normal controls. More specifically, hepatic cancer patients exhibited significantly higher plasma Aβ levels. No significant difference in plasma Aβ levels was found between chemotherapy and no chemotherapy subgroups. Plasma Aβ levels were not significantly correlated with pro-inflammatory cytokines, anti-inflammatory, chemokines, and cytokines. Peripheral Aβ levels increased in cancer patients, especially in patients with hepatic cancer, independent of chemotherapy and inflammation. Further verification is required for the association between plasma Aβ and cancer.     

散发性脑淀粉样血管病的危险因素及治疗方法的研究进展

散发性脑淀粉样血管病（cerebral amyloid angiopathy,CAA）是一种老年人中常见的颅内微 血管病。CAA相关病变（如脑出血、认知功能下降等）的发生主要包括淀粉样蛋白沉积于脑血管壁、 继发血管损伤两个重要过程,其危险因素包括ApoE 基因多态性等遗传因素和高血压病等非遗传因素。 免疫治疗和一些天然多酚类物质可防止脑血管内的淀粉样蛋白沉积,而控制高血压等非遗传危险因 素或使用依达拉奉能减轻CAA继发血管损伤。这些方法有望成为今后散发性CAA治疗的发展方向。     

uPA、uPAR与尿路移行细胞癌侵袭行为的相关性研究

背景与目的:丝氨酸蛋白水解酶的uPA(urokinase-typeplasminogenactivator)uPAR(urokinase-typeplasminogenactivatorreceptor)作用系统被认为在细胞外基质和基底膜的降解、促进肿瘤侵袭转移过程中起核心作用,本研究旨在探讨uPA、uPAR在尿路移行细胞癌组织中的表达及其与肿瘤侵袭行为的关系。方法:应用免疫组织化学PicTureTM通用型二步法检测50例肾盂输尿管癌及40例膀胱癌组织中uPA和uPAR的表达水平及分布。结果:uPA和uPAR在正常肾盂、输尿管、膀胱组织中未见表达,在癌组织中的表达明显高于癌旁组织;G1级uPA和uPAR的阳性率分别为33.33%、50.00%,G3级分别为88.47%和96.15%;Ta～T1期的分别为37.50%和50.00%,T4期均为100.0%;在高分级、高分期肿瘤组织中,uPA和uPAR的阳性率明显升高(P<0.05),且uPA阳性与uPAR阳性高度相关(rs=0.979)。结论:uPA、uPAR的共同表达是尿路移行细胞癌的特征之一,且与分级和分期密切相关,在尿路移行细胞癌浸润和转移中可能具有重要作用。