Objective To cxplore the research and application of big data mining technology in clinical healthcare environment.Methods The characteristics of clinical heahhcare data mining methods were expounded and the current research status of healthcare data mining technology was analyzed in clinical task according to the literature mining.Meanwhile,the application of healthcare data mining in clinical environment was introduced from the following four aspects:medicine research,personalized diagnosis,risk prediction and process mining.Results The necessity and importance of research and application of clinical healthcare data mining were illustrated.Moreover,the achicvements of healthcare data mining in clinical application,as well as existing problems and technical difficulties were summarized.Furthermore,the development tendencies of healthcare data mining were predicted.Conclusion The research and application of clinical healthcare data mining have improved the healthcare quality and promoted the medical advances,which is the developmcnt direction of clinical healthcare research.

Objective To evaluate the clinical,pathological and imaging features of basal cell adenoma in the parotid. Methods The clinical,pathological and CT imaging data of 21 cases with parotid basal cell tumor confirmed by operation and pathology were retrospectively analyzed. Results All 21 patients(5 male,16 female ) had solitary BCA lesion,which located at the superficial lobe of parotid gland(n=17)and involved both the superficial and deep lobe(n=4). Twelve lesions were well-defined and cystic degeneration was displayed in 9 le-sions,3 lesions had punctate calcification at the edge of tumor. All lesions were significantly enhanced,the enhancement of BCA in the ve-nous phase was close to the arterial phase. Conclusion The CT features of BCA in parotid gland are characteristic,which is helpful to make qualitative diagnosis when in combination with clinical features.

Overexpression of multidrug resistance gene, (MDR1) is responsible for the resistance of anticancer agents in cancer cells. In this study, we designed three pairs of DNA primers to clone MDR, cDNA from human normal liver by polymerase chain reaction. The sites of these primers in MDR cDNA are (I)-64-46 (5') and 1680-1698 (3'); (II) 1471-1489 (5') and 2905-2923 (3'); (III)2729-2747 (5') and 3845-3863 (3). The three reactions were underwent after the human normal liver mRNA was reverse transcripted into single strand DNA. The lengths of PCR products are 1762bp, 1452 bp and 1134bp, respectively. The former two products were subcloned in pBluscript SK, respectively and the latter product was subcloned in pGEM7Z (named as pMDR1.7, pMDR1.4 and pMDRl.l, respectively). Cloned genes were certificated as MDR1 cDNA by sequence analysis. Full-length MDR, cDNA was obtained after further subcloning. Full-length MDR1 cDNA we obtained will be a very important tool in molecular diagnosis and gene therapy of anticancer drug resistance.

We have cloned full-length MDR1 cDNA from human normal liver tissue in previous study. Using this MDR1 cDNA as probe, we observed the MDR1 gene expression in human hepatocellular carcinoma treated with and without chemotherapy by Northern blot. The results showed that expression of MDR1 gene in hepatocellular carcinoma tissues was higher than that in their adjacent normal liver tissues; and enhanced MDR1 gene expression was also observed in hepatocellular carcinoma treated with chemotherapic agents. We also explored a method for quantitative analysis of MDR1 gene expression in hepatocellular carcinoma by polymerase chain reaction. This study suggests that overexpression of MDR1 gene may be responsible for the intrinsic and acquired drug resistance of human hepatocellular carcinoma, and PCR is a preferable method for quantitative analysis of MDR1 gene expression in hepatocellular carcinoma.

Objective To observe the effect of intrathecal injection of TRESK overexpression adenoviruson phosphorylation of JNK and apoptosis of neurons in neuropathic pain rats.Methods Seventy-two male SD rats were randomly divided into six groups:groups C,S,NP,T,V,and NS,12 for each group.SNI was administrated to rats in groups NP,T,V and NS.TRESK adenovirus and negative virus were intrathecally injected after use of SNI in groups T and V,while equal volume of NS was injected to rats in group NS.MWT and TWL were measured at 1 day before operation(baseline,BL)and at 1,3,7 and 14 days after operation (days 1,3,7,and 14).Six rats in each group were sacrificed at D7 to determinate the expression of TRESK protein of DRG.The other rats were sacrificed at D14 to determinate neural apoptosis and the expressions of caspase3 and p-JNK of DRG.Results As compared with groups C,S and T,the expression of TRESK protein was significantly decreased at D7 in groups NP,NS and V (P＜0.05).Compared with groups C and S,MWT was significantly decreased at days 1,3,7 and 14 (P＜0.05),phosphorylation of JNK in DRG was significantly increased at D14 (P＜0.05),neuronal apoptosis rate and expressions of Caspase3 of DRG were significantly increased at D14 (P＜0.05) in groups NP,T,NS and V.Compared with groups NP,V and NS,MWT was significantly increased at time points of days 1,3,7 and 14 in group T (P＜0.05),phosphorylation of JNK of in DRG was significantly decreased at D14 in group T (P＜0.05),neuronal apoptosis rate and expression of Caspase3 of DRG were significantly decreased at D14 in group T (P＜0.05).Intrathecal injection ofpAd/CMV/VS-DEST-TRESK obviously reduced mechanical hyperalgesia,upregulated TRESK expression,and lowered JNK phosphorylation and NP in SNI rat.Conclusions Intrathecal injection of TRESK over expression adenovirus relieves NP via inhibiting JNK activation and neuronal apoptosis.