The effects of autonomic drugs on the activities of the upper urinary tract were studies with the ureteral perfusion pressure method.It was found that a-adrenergic and M-cholinergic receptors possess excitatory effect on the upper urinary tract while ?-adrenergic receptor possess inhibitory effect.It is likely that a-adrenergic receptor plays a certaion role in the maintenance of the normal activity of the upper urinary tract but both the M-and ?-receptors have a little effects.The effects of the autonomic nervous system and its receptors on the activities of the upper urinary tract were discussed.

Targeted therapeutic strategy for cancer stem cells (CSCs) is the key to prevent tumor relapse and metastasis. The im-portant roles of epigenetic regulation on the development of stem cells and gene reprogram of somatic cells suggest that this process may remarkably affect the occurrence and development of CSCs. The epigenome, which comprises DNA methylation, histone modifica-tions, chromatin structures, and non-coding RNAs, controls gene expression patterns. In renal cell carcinoma (RCC), aberrant changes occur in the epigenome. To date, cells with CSC properties from RCC have been successfully isolated using different methods, such as sorting using the Hoechst 33342 side population, forming tumor spheroid, and sorting CD105 cell surface biomarker. According to the progress in genetic studies on RCC, in addition to DNA sequence, the abnormality in the regulatory mechanism has considerable func-tions in tumor progression. Epigenetic changes may be integral to the behavior of cancer progenitor cells and their progeny. Knowledge on epigenetics in renal tumorigenesis process is beneficial in the development of new therapeutic modalities and may deliver new prog-nostic and early diagnostic markers. This paper reviews the latest development in the study of RCC stem cells and the underlying mech-anisms of epigenetic regulation on the development of CSCs in RCC.

AIM　To study the effects of dexamethasone on expressing monocyte chemoattractant protein-1(MCP-1 ) mRNA in the rats with pulmonary fibrosis, elaborate the molecular mechanism of dexamethasone (Dxs) in pulmonary fibrosis therapy. METHODS　The model of pulmonary fibrosis was established by instilling bleomycin intratracheally. After treating with Dxsip, the levels of MCP-1 mRNA were determined by RT-PCR. The histological changes were observed and the numbers of inflammatory cells were counted in optical microscopy field. RESULTS　The accumulation of inflammatory cells decreased markedly, and the symptom of pulmonary fibrosis was alleviated. Furthermore, Dxs evidently inhibited the expression of MCP-1 mRNA in lung tissues with pulmonary fibrosis. CONCLUSION　The molecular mechanism of Dxs in pulmonary fibrosis therapy was associated with inhibiting the expression of MCP-1 mRNA.

This article describes a method totransfer physiological data through carrier-current communication.The microcontroller measures the data of heartrate and body temperature and sends them through the serial port tothe carrier-current module implementing carrier-current communication.This method can be used totransfer physiological data through short distance less than200meters.

AIM To study the effects of dexamethasone on expressing monocyte chemoattractant protein 1(MCP 1 ) mRNA in the rats with pulmonary fibrosis, elaborate the molecular mechanism of dexamethasone (Dxs) in pulmonary fibrosis therapy. METHODS The model of pulmonary fibrosis was established by instilling bleomycin intratracheally. After treating with Dxs ip , the levels of MCP 1 mRNA were determined by RT PCR. The histological changes were observed and the numbers of inflammatory cells were counted in optical microscopy field. RESULTS The accumulation of inflammatory cells decreased markedly, and the symptom of pulmonary fibrosis was alleviated. Furthermore, Dxs evidently inhibited the expression of MCP 1 mRNA in lung tissues with pulmonary fibrosis. CONCLUSION The molecular mechanism of Dxs in pulmonary fibrosis therapy was associated with inhibiting the expression of MCP 1 mRNA.

To study the expression of HCV non-structure 5 antigen in vitro, a human HepG2 cell line was incubated with a HCV RNA positive serum. The S ABC i mmunological techniques and gold-labeled colloid electron microscopy method wer e employed to examine for the viral proteins in those cells. The HCV non-struct ure 5 antigen was first detected in the HepG2 cells at 72 hours post incubation. The antigen was continuously observed in the cytoplasm or on the membrane as we ll on the cell wall of the HepG2 cells even after 1, 2, 3 and 4 weeks post incub ation. The observation of HCV non-structure 5 antigen continuously expressed in the HepG2 cells strongly indicates that the cells may have been infected by HCV virus and the virus may have replicated in the cells. Therefore, the HepG2 cell line may be served as a potential host for establishment of HCV infection and p ropagation in vitro.

Objective To analysis the human cytomegalovirus (HCMV)and human T lymphotropic virus(HTLV)infection status in Beijing among voluntary blood donors.Methods Randomly selected 2 010 blood samples from five districts and counties of Beijing City to screen HCMV-IgG,HCMV-IgM and HTLV-Ⅰ/Ⅱ antibody by ELISA method.The positive samples were reexamined two times,two test results of samples were positive that were determined positive by ELISA. HTLV positive samples was confirmed by nested PCR.Results The HCMV-IgM and HCMV-IgG positive rates of Beijing blood donors were 2.19% and 92.59%,screened 1 case of anti-HTLV positive by ELISA method,then confirmed to be neg-ative result by nested PCR.The statistics showed that the HCMV-IgG positive rate female blood donors was higher than male (P <0.05).The positive rates of HCMV-IgM and HCMV-IgG among18~25 years old donors was lowest (P <0.05). Positive rate of HCMV-IgG in college students was lower than other occupation blood donars (P <0.05)and education de-gree was independent of HCMV-IgG,HCMV-IgM positive rates (P >0.05).Conclusion In this investigation,2 010 cases of voluntary blood donors from five districts of Beijing were not found in cases of HTLV infection,HCMV infection was prevalent.

OBJECTIVETo explore the distribution, combination and evolution of various syndromic etiologies of erectile dysfunction (ED) based on the syndrome etiology theory.

METHODSUsing the ED Syndromic Etiology Scale, we collected the clinical data on the Chinese medicine diagnoses of 297 cases of ED, extracted the core syndromic etiologies by analysis of principal components and factors, and analyzed the patterns of distribution, combination, and evolution of ED syndromic etiologies according to the general information of the patients.

RESULTSThrough analysis of principal components and factors, 9 core syndromic etiologies were extracted, i. e. , liver constraint with qi stagnation, kidney yin deficiency, damp-heat, liver constraint transforming into liver-fire, blood stasis, kidney yang deficiency, heart-spleen paired deficiency, qi-yin paired deficiency, and phlegm-damp. Each of these syndrome etiologies exhibited its own specific distribution patterns. Of the total number of cases studied, 51.52% had 2 or 3 core syndromic etiologies and 36.03% had only one.

CONCLUSIONIn the early stage of ED, its syndromic etiologies are usually liver constraint with qi stagnation, kidney yin deficiency, damp-heat, liver constraint transforming into liver-fire, and blood stasis. With the natural progres- sion of the disease, its syndromic etiologies gradually evolve into kidney yang deficiency, heart-spleen paired deficiency, qi-yin paired deficiency, phlegm-damp, and blood stasis, and finally into yin-yang deficiency of the heart, spleen and kidneys, combined with phlegm-damp and blood stasis.

Microscopy, Electron, Transmission ; methods ; Negative Staining ; methods ; Viruses ; ultrastructure

Background The pathogenesis and development of cataract is associated with oxidative stress-induced apoptosis of human lens epithelial cells(LECs).BH3-only protein is a factor that can initiate apoptosis,and thus the apoptotic process is probably related to the activation of the c-Jun N-terminal kinase(JNK).However,the relationship between oxidative stress-induced apoptosis of human LECs and the JNK pathway remains to be illuminated.Objective This study was to investigate the effects of the JNK/c-Jun pathway and its target gene,Bim (Bcl-2 interacting mediator of cell death)and PU M A(p53 up-regulated modulator of apoptosis),on oxidative stressinduced apoptosis of human LECs.Methods The human LECs cell line(HLEC-B3)was cultured and passaged in DMEM with 10％ fetal bovine serum in vitro.Confluent cells were incubated in 24 well plates and divided into 4 groups.Hydrogen peroxide(H2O2)(50 μmol/L)was used to treat the cells for 4,8 or 12 hours,and cells without H2O2 treatment served as the control group.Apoptosis was detected using Hoechst 33258 staining and quantified by counting the number of cells with pyknotic nuclei.In addition,confluent cells were seeded in 6 well plates,and Western blot and RT-PCR were used to detect the expression of the caspase-3,c-Jun,Bim and PUMA proteins and their mRNA in HLEC-B3,respectively.The JNK/c-Jun pathway inhibitors,CEP11004 or SP600125,were added into cultured media with H2O2,and cells treated with DMSO or H2O2 only served as negative and positive control groups.The expression of the p-JNK,JNK,p-c-Jun,c-Jun,Bim,PUMA proteins was detected by Western blot and apoptosis was assayed using Hoechst 33258 staining.200 pmoL/L of Bim or PUMA small interference RNA(siBim or siPUMA)fragments were transfected into the cells for 24 hours,respectively,and H2O2 was then used to treat the cells for 8 hours.The expression of the Bim and PUMA protein and their mRNA in the cells was detected by Western blot and RT-PCR,respectively.Results After H2O2 treatment in HLEC-B3 cells for 4,8,or 12 hours,the rates of apoptosis were 4.30％±1.15％,27.08％±0.74％ and 46.59％±0.91％,showing a significant difference among them (F=1909.433,P=0.000),and those of the 4,8,12 hour groups were significantly increased in comparison to the control group(P =0.049,0.000,0.000).Compared to untreated cells,the levels of expression of the JNK,Bim,PUMA proteins and their mRNA in HLEC-B3 cells were significantly elevated.After the addition of CEP11004 or SP600125,the expression of these protein and mRNA in HLEC-B3 cells in the presence of H2O2 was significantly weaker than that in the DMSO control group(P =0.000,0.000).After the tranfection of siBim or siPUMA,the apoptosis rates of the H2O2 treated groups were significantly higher than those in the Bim-/-or PIMA-/-group (P＜0.05).Conclusions H2O2 can activate the JNK/c-Jun pathway and up-regulate the expression of its target genes Bim and PUMA in human LECs in a time-dependent manner.Inhibiting the JNK/c-Jun pathway and interfering with the expression of Bim and PUMA can protect human LECs against oxidative stress-induced apoptosis.