This paper made some reflections on the development of traditional Chinese medicine(TCM) nephrology in recent years. It analyzed the strategic position and importance of social development in the field of prevention and treatment of diseases by TCM. Problems and puzzles on this subject had been summarized and countermeasures had been put forward. Preliminary conceptions on development strategies, goals and direction of TCM nephrology had been made.

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Liver fibrosis can be classified as a wound-healing response to a variety of chronic stimuli,and is characterized by an excessive deposition of extracellular matrix(ECM)proteins.Hepatic stellate cells(HSCs)are presently regarded as one of the key cell types involved in the progression of liver fibrosis.Following a fibrogenic stimulus,HSC changes from a quiescent to an activated,collagen-producing cell.Each cellular response to extracelluar stimuli must be framed in a scenario.Along these lines,the identification and characterization of intracellular signaling pathways activated by different stimuli in HSCs represent a mandatory step.Drug targets which aim at the extra-cellular signals or intra-cellular cascades are required for ameliorating liver fibrosis.

Based on the "Grayscales average distribution" method which equally distributes the input gray levels to output gray levels, three improved methods named: "Reduce the gray range expressed by the less significant subfields", "Low levels preset" and "Modify the exponent of inverse-gamma function" are proposed in this paper. Using these methods, the inverse-gamma relation subfields code can be obtained easily which can improve the low level expressions of AC-PDP. And a program, "gray scales distribution validate program", which can enhance the expressions of the demanded gray levels range, is also proposed in this paper.

Hepatic fibrosis is a pathological process in which excessive deposition of extracellular matrix components, occurs due to an imbalance between the production and degradation of matrix. Fibrosis is the hallmark of most chronic liver diseases. It is also the major factor of the development of chronic hepatitis and cirrhosis. Therefore, in light of the regulative factors on different levels and mechanism of fiber synthesis and degradation, antifibrotic medicine can inhibit the synthesis of matrix or increase its degradation on different links. The present situation concerning the study of the therapeutic effect of traditional Chinese medicine and natural medicine on hepatic fibrosis is reviewed.

Objective: To explore the relationship between CDR1 and CDR2 expression and fluconazole-resistance in clinical Candida albicans strains, so as to explore the mechanism of drug-resistance in Candida albicans. Methods: The minimal inhibitory concentrations (MICs) of clinical Candida albicans strains to fluconazole were determined by broth microdilution method. The total RNA of fluconazole-susceptible and fluconazole-resistant Candida albicans strains were extracted, and the expression of the CDR1 and CDR2 genes was examined by real-time RT-PCR. The efflux of Rhodamine 6G was determined in the strains highly expressing CDR1 and CDR2 genes. Results: The incidences of CDR1 and (or) CDR2 overexpression in fluconazole-resistant strains were significantly higher than those in the fluconazole-sensitive stains. The efflux of Rhodamine 6G was significantly increased in the fluconazole-resistant strains when glucose was added, and overexpression of CDR1 and CDR2 were observed in theses strains. Some resistant strains showed no overexpression of CDR1 and CDR2. Conclusion: Fluconazole-resistance in clinical Candida albicans strains is related to the overexpression of ABC transporter proteins. Overexpression of ABC transporters can increase the efflux of drugs and therefore lead to drug-resistance. Other mechanisms may also participate in the development of drug resistance in the clinical Candida albicans strains.

ObjectiveTo measure levels of serum resistin in patients with nonalcoholic fatty liver disease (NAFLD) and explore the relationship between serum resistin and insulin resistance,and the role of serum resistin in the pathogenesis and progression of NAFLD.Methods 53 patients (including 30males and 23 females) with NAFLD and the 28 control subjects (including 16males and 12females) were enrolled in this study.The height,weight,waist circumstance,hip girth and blood pressure of all subjects were obtained by standard methods.To all the subjects,the parameters including fasting blood glucose (FBG),triglyceride ( TG),total cholesterol (TC),high-density lipoprotein cholesterol ( HDL-c ),lowdensity lipoprotein cholesterol ( LDL-c ),alanine aminotransferase ( ALT),aspartate aminotransferase (AST)and gamma glutamyl transferase (GGT) were measured.Serum resistin was measured by electrochemiluminescence immunoassay (ECLIA) and fasting serum insulin (FINS) were measured by enzymelinked immunosorbent assay (ELISA).Body mass indexes (BMI),waist hip ratio (WHR),body fat percentage ( BF％ ) were calculated with formula.Homeostasis model assessment was applied to assess the status of insulin resistance index (HOMA-IR).The relationships between serum resistin and various parameters in patients with NAFLD were observed and analyzed by statistical methods.ResultsThere were no significant differences in the number of cases,average age,compositions of sex and BF％ between the NAFLD group and the control group ( P ＞ 0.05).In the NAFLD group,systolic blood pressure ( SBP),diastolic blood pressure(DBP).The waist circumference,hip girth and BMI and WHR were higher than those of control group ( t =3.54,3.32,3.56,5.85,5.56,4.10,P =0.001).There were no significant differences on the level of TC,HDL-c,LDL-c between the NAFLD group and the control group ( P ＞0.05).In the NAFLD group,FBG,TG,AST were higher than those of control group ( P =0.001,P =0.004,P =0.001 ).The levels of serum resistin,FINS,HOMA-IR,ALT and GGT in NAFLD group were significantly higher than those of control group,and there was significant difference between two groups ( P =0.0005).There was no significant correlation between serum resistin and age,BMI,WHR,BF％,FBG,TG,TC,HDL-C,LDL-C,AST in NAFLD group ( P ＞ 0.05).The levels of serum resistin in patients with NAFLD were positively correlated with GGT,ALT,FINS,HOMA-IR ( r =0.354,0.391,0.875,0.881,P ＜0.05 or ＜0.01 ).After multiple stepwise regression analysis,the results showed that HOMA-IR was the most important factor for affecting the levels of serum resistin.The levels of serum resistin in male and female patients with NAFLD were higher than those of control group ( P ＜0.05).But no statistical difference was found between males and females in two groups ( P ＞ 0.05).ConclusionsThe levels of serum resistin in patients with NAFLD were significantly higher than those of controls.Serum resistin in patients with NAFLD was closely correlated with insulin resistance,and it may participate in the pathogenetic progress of NAFLD.Serum resistin in patients with NAFLD might be associated with hepatic insulin resistance,and it has no correlations with obesity-related insulin resistance.Serum resistin in patients with NAFLD may participate in the inflammation of fatty liver disease as inflammatory cytokines.

Objective To determine the effect of interleukin (IL)-17 on the proliferation of fibroblastlike synoviocytes (FLSs) from rheumatoid arthritis (RA)patients and to investigate whether signal transducer and activator of transcription 3 (STAT3) was implicated in this process.Methods FLSs were acquired by primary culturing from RA patients.STAT3,p-STAT3,Bcl-2 and Bax expression in FLSs were determined using western blotting analysis.The proliferation of FLSs was determined by MTT assay.Analysis of variance was used to determine the differences between two groups.Results IL-17 promoted the proliferation of FLSs from RA patients and inhibited their apoptosis.The pro-apoptotic Bax was decreased and anti-apoptotic Bcl-2 was increased in FLSs from RA (t=2.612,P＜0.05;t=2.723,P＜0.05).However,targeted silencing of STAT3 could inhibit the effect of IL-17 on FLSs (t=2.745,P＜0.05).[the control group:Bax (3.814±1.623),Bcl-2 (1.429± 0.311);IL-17 group:Bax (0.972±0.017),Bcl-2 (3.175±1.356);STAT3 silent group:Bax (5.729±1.236),Bcl-2 (0.637±0.006)].Conclusion STAT3 is critical in IL-17-induced proliferation of FLS from RA patients.IL-17/STAT3 pathway might be a good candidate for RA treatment modalities.