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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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.

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.

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.

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.

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.

Objective To explore the effect of out-hospital health education on quality of life of heart failure patients with dilated cardiomyopathy. Methods 60 cases of heart failure patients with dilated cardiomyopathy were selected and divided into follow-up group and control group with 30 cases in each group. The follow-up group accepted out-hospital health education, while the control group only accepted conventional in-hospital health education. Then World Health Organization Quality Of Life-Brief (WHOQOF-BRIEF) was used to evaluate their quality of life 6 months after discharge. Results The score of WHOQOF-BRIEF was higher in the follow-up group than in the control group (P<0.05). The satisfactory degree of nurse-patient relationship was better in the follow-up group than in the control group (P<0.05).Conclusion Out-hospital health education can improve the quality of life of heart failure patients with dilated cardiomyopathy.