口腔鳞状细胞癌和癌旁组织的基因表达分析

目的利用来自美国国立生物信息技术中心(NCBI)基因表达数据库(GEO)的基因芯片数据,分析基因在口腔鳞状细胞癌(OSCC)中癌和癌旁组织的差异表达情况,为寻找癌和癌旁组织双边的抑癌靶标提供依据。方法选取来自NCBI-GEO数据库中OSCC患者的癌和癌旁组织,以及正常人口腔组织的基因芯片数据,分别计算得到前两者相对后者的差异表达基因,并进行功能聚类与特定基因的通路分析。结果大部分差异基因为癌与癌旁所共有,其中多数基因的差异表达方向在两者中一致,少部分方向不一致。如WIF1基因在癌组织中表达下调,但在癌旁组织中表达上调。这种差异表达行为的不同与基因的功能相关,因此,差异表达行为可能为抑癌靶标的发现提供线索。结论基因在癌和癌旁组织中的差异表达行为与基因的功能相关,具有特定差异表达行为的基因可能成为潜在的抑癌靶标。     

Wnt signaling pathway in aging-related tissue fibrosis and therapies

Fibrosis is the final hallmark of pathological remodeling, which is a major contributor to the pathogenesis of various chronic diseases and aging-related organ failure to fully control chronic wound-healing and restoring tissue function. The process of fibrosis is involved in the pathogenesis of the kidney, lung, liver, heart and other tissue disorders. Wnt is a highly conserved signaling in the aberrant wound repair and fibrogenesis, and sustained Wnt activation is correlated with the pathogenesis of fibrosis. In particular, mounting evidence has revealed that Wnt signaling played important roles in cell fate determination, proliferation and cell polarity establishment. The expression and distribution of Wnt signaling in different tissues vary with age, and these changes have key effects on maintaining tissue homeostasis. In this review, we first describe the major constituents of the Wnt signaling and their regulation functions. Subsequently, we summarize the dysregulation of Wnt signaling in aging-related fibrotic tissues such as kidney, liver, lung and cardiac fibrosis, followed by a detailed discussion of its involvement in organ fibrosis. In addition, the crosstalk between Wnt signaling and other pathways has the potential to profoundly add to the complexity of organ fibrosis. Increasing studies have demonstrated that a number of Wnt inhibitors had the potential role against tissue fibrosis, specifically in kidney fibrosis and the implications of Wnt signaling in aging-related diseases. Therefore, targeting Wnt signaling might be a novel and promising therapeutic strategy against aging-related tissue fibrosis.     

miRNA在冠心病中的作用机制

MicroRNA(miRNA)是一类新发现的非编码小RNA分子.近来研究表明,miRNA在冠心病的发病机制中都起到了重要的调控作用,有望成为新型的特异性心肌损伤标记物及药物治疗的新靶点.本文系统性总结了近年来miRNA在冠心病领域的相关研究成果,并对其在临床中的应用价值进行了探讨.     

精神分裂症发病机制及治疗靶点的研究现状

精神分裂症是一种严重的精神疾病,但确切的机制至今尚未研究透彻。近来,研究者们发现D1、D2受体的过度活化、多巴胺和环腺苷酸调节的磷蛋白的调节机制、受体磷酸化磷酸酶β/ζ的编码基因PTPRZ1(蛋白酪氨酸磷酸酶,受体类型,Z多肽1)与精神分裂症密切相关;γ氨基丁酸α受亚单位α5受体进行变构调节,能逆转多巴胺功能异常亢进,进而缓解精神分裂症的阳性症状。     

Cardiovascular therapy in patients with renal insufficiency

Chronic renal failure and arterial hypertension run in parallel. New goal blood pressure levels have been established in 130/85 mmHg and 125/75 mmHg depending on the level of proteinuria being below or above 1 g/day.New and lower threshold BP (>130/85 mmHg) to initiate pharmacologic therapy are required in the presence of renal failure in order to facilitate the strict BP control that is required.Renal insufficiency is accompanied since its initial stages by a marked increase in cardiovascular risk and serum creatinine, its estimated clearance and the presence of proteinuria are very powerful predictors of a bad cardiovascular outcome. Hence, the need to consider that both renal and cardiovascular protection are obtained with such a strict BP control which, otherwise seems to require blockade of angiotensin II effects when proteinuria above 1g/day is present.Prevention of renal failure related to elevated blood pressure requires of strict blood pressure control, usually obtained with combination of two or more antihypertensive agents, one of them capable of blocking angiotensin II. Besides this, strict control of associated cardiovascular risk factors is also required.     

Fasting insulin and uric acid levels but not indices of iron metabolism are independent predictors of non-alcoholic fatty liver disease. A case-control study

BACKGROUND: Non-alcoholic fatty liver disease is a common reason for hepatological consultation and may herald severe hepatic and extra-hepatic disease. The aetiopathogenesis of this condition is an area of increasing interest. AIM: To evaluate anthropometric and biochemical factors associated to non-alcoholic fatty liver disease in a case-control study. Methods. Demographic and biochemical data of 60 consecutive patients with bright liver absent-to-low alcohol consumption, no evidence of viral, genetic and autoimmune diseases, were compared to those of 60 age- and gender-matched historical controls without fatty liver by univariate and multiple logistic regression analysis. RESULTS: Patients were more often hypertriglyceridaemic, obese and diabetic than controls (p<.01). Mean values of alanine transaminase, gammaglutamyltranspeptidase, triglycerides, uric acid, fasting and log insulin, transferrin percent saturation and ferritin were significantly higher in the patients, while transferrin and quantitative insulin sensitivity check index, a quantitative insulin sensitivity index, were lower. No iron storage was found in those who underwent liver biopsy At univariate analysis the relative risk for non-alcoholic fatty liver disease significantly increased (p<0. 05) with increasing body mass index, fasting insulin, alanine transaminase, uric acid, triglycerides and gammaglutamyltranspeptidase; it decreased with increasing transferrin and quantitative insulin sensitivity check index. Multiple logistic regression analysis disclosed only fasting insulin and uric acid to be independent predictors of non-alcoholic fatty liver disease (p<0.05). CONCLUSIONS: Fasting insulin and serum uric acid levels indicating insulin resistance, but not indices of iron overload, are independent predictors of non-alcoholic fatty liver disease.