Objective:To scan the common differentially expressed genes in mice liver tissue following subacute exposure to hepatotoxicants,including alcohol,carbon tetrachloride,BCG & LPS,the alcohol extracts of Rhizoma Dioscoreae Bulbiferae and Senecio scandens Buch.-Ham.,and apply to the rapid toxic evaluation of TCM and other xenobiotics.Methods:The gene expression profiles of mice liver tissue,after respective administration of alcohol,CCl4,BCG associated with LPS,the alcohol extracts of Rhizoma Dioscoreae Bulbiferae and Senecio scandens Buch.-Ham.to healthy mice,were analyzed by use of mouse genome cDNA microarray.The correlations between the common differential expressed genes and the liver injury were analyzed based on the biological functions of those differentially expressed genes.Results:Among all of the five drug administration groups,there were 7 known function genes(BC05200,NM-019410,NM-173019,AB028272,AK088925,AK030862 and AK088816)and 1 unknown function gene(BC069871)differentially expressed.Beside AK088816,the other 7 genes were all down-regulate expressed.Conclusion:The common differentially expressed genes participate in the process of saccharometabolism,apoptosis,cell growth cycle,cytoskeleton and signal transmission,protein folding and protein ubiquitin.The abnormal expression of the common genes were closely correlated to the liver,and might be important for rapid hepatoxicity elucidation of traditional Chinese medicine and other xenobiotics.

Objective To investigate the prognostic factors for chronic heart failure and the prognostic ability of copeptin,big endothelin-1(Big ET-1)and N-terminal pro-brain natriuretic peptide (NT-proBNP)in patients with chronic heart failure. Methods To study 1 5 9 consecutive patients hospitalized for chronic heart failure.Serum concentration of copeptin,NT-proBNP,cTnI,CKMB and plasma Big ET-1 as well as left ventricular ejection fraction (LVEF)and NYHA classⅠtoⅣ on admission were measured.Cardiac events were found by patients to discharge after 360~490 days,prospectively.Results During a median follow-up period of 385 days,the endpoint of recurrence for cardiac events was reached in 65 patients with 159 heart failure.Multivarlate canonical correlation analysis shows the older and the higher NYHA classification as well as the lower LVEF in patients with heart failure.There were higher concentration of copeptin,Big ET-1 and NT-proBNP.On a Cox proportional hazards regression models analyses,age,copeptin,Big ET-1 and NT-proBNP were found to be the inde-pendent predictors of cardiac events.Risk ratio (RR)were 1.215,1.236,4.031 and 13.052,respectively.Logistic regression models analyses,copeptin,Big ET-1 and NT-proBNP were found independent predictors of death.Odd ratio (OR)were 4.003,2.477 and 1.235,respectively.Conclusion Measurement of copeptin,Big ET-1 and NT-proBNP in patients with chronic heart failure can help to identify patients at higher risk for cardiac events and patients for prognosis.

Diabetic neuropathic pain (DNP) is the most common disabling complication of diabetes. Emerging evidence has linked the pathogenesis of DNP to the aberrant sprouting of sensory axons into the epidermal area; however, the underlying molecular events remain poorly understood. Here we found that an axon guidance molecule, Netrin-3 (Ntn-3), was expressed in the sensory neurons of mouse dorsal root ganglia (DRGs), and downregulation of Ntn-3 expression was highly correlated with the severity of DNP in a diabetic mouse model. Genetic ablation of Ntn-3 increased the intra-epidermal sprouting of sensory axons and worsened the DNP in diabetic mice. In contrast, the elevation of Ntn-3 levels in DRGs significantly inhibited the intra-epidermal axon sprouting and alleviated DNP in diabetic mice. In conclusion, our studies identified Ntn-3 as an important regulator of DNP pathogenesis by gating the aberrant sprouting of sensory axons, indicating that Ntn-3 is a potential druggable target for DNP treatment.
Mice ; Animals ; Diabetes Mellitus, Experimental/metabolism* ; Axons/physiology* ; Diabetic Neuropathies ; Sensory Receptor Cells/metabolism* ; Neuralgia/metabolism*