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101.
Liver X receptors in cardiovascular and metabolic disease 总被引:5,自引:0,他引:5
Liver X receptors (LXRs) α and β are nuclear oxysterol receptors and metabolic sensors initially found to regulate cholesterol
metabolism and lipid biosynthesis. Recent studies have elucidated the importance of LXR in the development of cardiovascular
diseases and metabolic disorders. LXR agonists prevent development of atherosclerosis by modulation of metabolic as well as
inflammatory gene expression in rodent models. Moreover, LXR activation inhibits hepatic gluconeogenesis and lowers serum
glucose levels, indicating possible application of LXR activation in the treatment of diabetes mellitus. However, first-generation
LXR agonists elevate hepatic and serum trigylceride levels, making subtype-specific agonists and selective LXR modulators
rather than unselective LXR agonists a potential pharmacological strategy. This review summarizes the multiple physiological
and pathophysiological implications of LXRs and observations that identify LXRs as potential targets for therapeutic interventions
in human cardiovascular and metabolic disease.
Received 30 August 2005; received after revision 10 October 2005; accepted 4 November 2005 相似文献
102.
Phytanic acid is a branched-chain fatty acid that accumulates in a variety of metabolic disorders. High levels of phytanic
acid found in patients can exceed the millimolar range and lead to severe symptoms. Degradation of phytanic acid takes place
by α-oxidation inside the peroxisome. A deficiency of its breakdown, leading to elevated levels, can result from either a
general peroxisomal dysfunction or from a defect in one of the enzymes involved in α-oxidation. Research on Refsum disease,
belonging to the latter group of disorders and characterized by a deficiency of the first enzyme of α-oxidation, has extended
our knowledge of phytanic acid metabolism and pathology of the disease greatly over the past few decades. This review will
centre on this research on phytanic acid: its origin, the mechanism by which its α-oxidation takes place, its role in human
disease and the way it is produced from phytol.
Received 4 October 2005; received after revision 24 February 2006; accepted 26 April 2006 相似文献
103.
Anti-amyloidogenic therapies: strategies for prevention and treatment of Alzheimer’s disease 总被引:1,自引:1,他引:0
Deposition of amyloid β-protein (Aβ) in the brain is an early and invariant neuropathological feature of Alzheimer’s disease
(AD). The current search for anti-AD drugs is mainly focused on modification of the process of accumulation of Aβ in the brain.
Here, we review four anti-amyloidogenic strategies: (i) reduction of Aβ production, which has mainly been approached with
secretase inhibition, (ii) promotion of the Aβ degrading catabolic pathway, including an Aβ degrading enzyme, neprilysin,
(iii) immunotherapy for Aβ and (iv) inhibition of Aβ aggregation. We have reported that AD patients have a favorable molecular
environment for Aβ aggregation and that various compounds, such as polyphenols, interfere with Aβ aggregation and destabilize
preformed Aβ fibrils.
Received 21 December 2005; received after revision 14 February 2006; accepted 29 March 2006 相似文献
104.
Lehmann F Tiralongo E Tiralongo J 《Cellular and molecular life sciences : CMLS》2006,63(12):1331-1354
Sialic acids consist of a family of acidic ninecarbon sugars that are typically located at the terminal positions of a variety
of glycoconjugates. Naturally occurring sialic acids show an immense diversity of structure, and this reflects their involvement
in a variety of biologically important processes. One such process involves the direct participation of sialic acids in recognition
events through specific interactions with lectins, a family of proteins that recognise and bind sugars. This review will present
a detailed overview of our current knowledge regarding the occurrence, specificity and function of sialic acid-specific lectins,
particularly those that occur in viruses, bacteria and non-vertebrate eukaryotes.
Received 13 December 2005; received after revision 9 February 2006; accepted 15 February 2006 相似文献
105.
Glycogen synthase kinase 3β and Alzheimer’s disease: pathophysiological and therapeutic significance 总被引:3,自引:0,他引:3
Balaraman Y Limaye AR Levey AI Srinivasan S 《Cellular and molecular life sciences : CMLS》2006,63(11):1226-1235
Alzheimer’s disease (AD) is a neurodegenerative disorder associated with cognitive and behavioral dysfunction and is the leading
cause of dementia in the elderly. Several studies have implicated molecular and cellular signaling cascades involving the
serine-threonine kinase, glycogen synthase kinase β(GSK-3β) in the pathogenesis of AD. GSK-3β may play an important role in
the formation of neurofibrillary tangles and senile plaques, the two classical pathological hallmarks of AD. In this review,
we discuss the interaction between GSK-3β and several key molecules involved in AD, including the presenilins, amyloid precursor
protein, tau, and β-amyloid. We identify the signal transduction pathways involved in the pathogenesis of AD, including Wnt,
Notch, and the PI3 kinase/Akt pathway. These may be potential therapeutic targets in AD.
Received 19 December 2005; received after revision 24 January 2006; accepted 6 February 2006 相似文献
106.
目的探讨快速老化小鼠SAM-P/8的同向旋转现象与帕金森病动物模型的相关性。方法取发作旋转行为的7月龄雄性SAM-P/8和同源对照SAM-R/1小鼠各6只,分为旋转组和正常对照组两组,首先采用老化度评价标准对其老化度进行评定,其次根据帕金森病动物模型造模标准对其旋转行为进行评定。结果同月龄SAM-P/8的老化度高于SAM-R/1;SAM-P/8出现可重复的同向右侧旋转,频率为60 r/min,符合帕金森病动物模型造模成功的标准,SAM-R/1无旋转现象出现。结论初步认定SAM-P/8的同向旋转现象为类帕金森病现象,对帕金森病研究有重要意义。 相似文献
107.
108.
109.
阿托伐他汀对冠心病慢性心力衰竭患者的心功能和预后的影响 总被引:2,自引:0,他引:2
余信强 《江汉大学学报(自然科学版)》2009,37(3):75-77
目的:观察阿托伐他汀对冠心病慢性充血性心力衰竭患者的心功能和预后的影响.方法:选取2004年1月~2008年6月江汉大学附属医院心内科病区冠心病慢性充血性心力衰竭患者132例,随机分成治疗组(67例)和对照组(65例).两组患者均行冠心病慢性充血性心力衰竭的常规基础治疗.治疗组在常规治疗的基础上,加用阿托伐他汀10mg,每晚一次.总疗程26周.治疗前后检测血脂全套、左室射血分数(LVEF)、C反应蛋白(CRP),观察所有患者治疗后两年的住院次数、住院总日数和病死率.结果:治疗组与对照组比较,治疗6个月后,血清总胆固醇(TC),低密度脂蛋白胆固醇(LDL-C),CRP均有不同程度降低,LVEF明显提高,治疗后两年的住院次数和总日数相对减少,差异无显著性;病死率明显降低,差异有非常显著性(P<0.01).结论:阿托伐他汀治疗能改善冠心病慢性心衰患者的心功能和预后. 相似文献
110.
在小世界网络拓扑结构上,研究信息影响力、接种比例和个体间信息传播概率的变化,对传染病传播的影响。研究发现小世界强度减弱时,信息影响力对传染病爆发概率和爆发规模的影响作用发生了逆转;在个体间信息传播速率增加的过程中,传染病的爆发概率和爆发规模呈现上升的趋势。 相似文献