Objective To estimate the curative effect and cost-effectiveness of moxifloxacin and gatifloxacin for treatment of urinary traet infection. Methods Eighty patients with urinary tract infection were randomly divided into treatment group (40 cases) and control group (40 cases). The patients in treatment group were given 400 mg moxifloxacin once a day for 7 d, while in control group were given 400 mg gatifloxacin once a day for 7d. Results The total clinical effective rate of treatment group and control group were 95.0%(38/40) and 92.5%(37/40) respectively, and the bacterial eliminating rate were 77.50% (31/40) and 76.92% (30/39), and the rate of adverse reaction were 5.0% ( 2/40 ) and 7.5% (3/40) respectively. There was no significant difference between two groups (P>0.05). The cost-effectiveness ratio of moxifloxacin was 2296 and 779 for gatifloxacin (P<0.01). Conclusion The therapeutic scheme of gatifloxacin seems to be the best one for treating urinary tract infection.

BACKGROUND: Human β-defensin is mainly located in various tissues epidermis or epithelium, also exists in ocular surface, but its ocular surface and its role of ocular surface diseases remain poorly understood.OBJECTIVE: To observe the distribution of human β-defensins in ocular surface tissue, and to analyze their potential effects on ocular surface disease. DESIGN, TIME AND SETTING: In vitro controlled observation with regard to ocular surface tissue was performed at the Central Laboratory, Xinhua Hospital, Medical College of Shanghai Jiao Tong University and Cell Biochemistry Institute, Chinese Academy of Sciences Shanghai Branch, between October 2006 and December 2007.MATERIALS: A total of 18 inflammatory conjunctival specimens consisted of 6 pterygium surface bulbar conjunctiva, 4 bulbar conjunctival cysts, 4 acid burn conjunctiva, 2 thermal burn conjunctiva and 2 conjunctival granuloma; 15 inflammatory corneal specimens included 6 viral keratitis, 4 fungal keratitis, 3 bacterial keratitis and 2 eye removal following corneal perforation; 9 cadaver normal bulbar conjunctiva samples, 8 cadaver normal corneal samples. METHODS: RT-PCR method and immunohistochemistry were applied to detect human β-defensin expression in 50 samples. MAIN OUTCOME MEASURES: Distribution and location of human β-defensin proteins in normal and inflammatory ocular surface tissues. RESULTS: RT-PCR showed that human β-defensin 1 and human β-defensin 3 were positive in all of the tested samples, whereas human β-defensin 2 existed in a majority of inflammatory ocular surface tissues and no expression was observed in normal ocular surface tissues. Immunohistochemistry analysis revealed most of inflammatory ocular surface tissues expressed human β-defensins 1 and 2, distributing in epithelial cell layer and predominantly in basal lamina, occasionally infiltration of stromal cells was observed, only a small number of human β-defensin 2 expression was absent; normal cornea and conjunctiva samples presented with human β-defensin 1 expression, distributing in epithelial cells and predominantly in basal lamina, only few expressed human β-defensin 2.CONCLUSION: Human β-defensin 1 and 3 appear to be constitutively expressed in surface epithelial cells and basal lamina of normal and inflammatory ocular surface tissues, while human β-defensin 2 may be induced to express in the majority of inflammatory ocular surface tissues. Three human β-defensins expression plays a pivotal role in preventing ocular surface infection and promoting ocular surface injury repair.

Objective To investigate the relationship between promoter hypermethylation of secreted frizzled-related protein (SFRP) gene and acute leukemia (AL). Methods We examined the promoter methylation starus of SFRP1, 2, 4 and 5 in primary or relapsed AL patients, cell lines ( HL60,NB4, Molt-4 and Jurkat) and peripheral blood mononuclear cells from healthy people with methylationspecific PCR (MSP). Results None of the normal mononuclear cells showed methylation of any SFRP genes. The frequencies of aberrant methylation among the samples were 33.9% (20/59) for SFRP1,23.7%(14/59) for SFRP2, 6. 8% (4/59) for SFRP4 and 10. 2% (6/59) for SFRP5 in acute myelocytic leukemia (AML), and 39.3% (11/28) for SFRP1, 28.6% (8/28) for SFRP2, 25.0% (7/28) for SFRP4 and 32. 1% (9/28) for SFRP5 in acute lymphoblastic leukemia (ALL). Hypermethylation of SFRP1, 2, 5genes were present in the 4 AL cell lines. SFRP4 was methylated in NB4, Molt-4 and Jurkat cell lines.However, methylation and unmethylation of SFRP4 were both detected in HL60. Conclusions Hypermethylation of SFRP genes is a common event in the evolution of AL. Methylation of SFRP genes might serve as potential independent biomarkers for early detection of AL.

Objective To investigate the inhibition of proliferation and the regulation of histone acetylation modification in Jurkat cells treated by sodium valproate(VPA). Methods Jurkat cells were treated with VPA.Cell proliferation was determined by CCK-8 assay, and cell cycle were analyzed by flow cytometry (FCM). mRNA of HDAC1 was detected by semi-quantitative RT-PCR, and protein expression of HDAC1 and acetylation of histone H3, H4 was examined by Western blotting. Results VPA inhibited the proliferation of Jurkat cells in concentration-and time-dependent manners. After exposure to VPA in different concentrations for 48h,cell cycle was arrested obviously at G0/G1 phase (P <0.05), and with increasing concentration, the percentage of G0/G1 phase cells was increased and that of S phase were decreased. HDAC1 mRNA expression were inhibited with the increasing concentration of VPA. The protein level of HDAC1 was down-regulated, while acetylation of histone H3、H4 was up-regulated in Jurkat cells by VPA. Conclusion VPA can inhibit proliferation of Jurkat cells and induce G0/G1 phase arrest. The mechanism may be that VPA increase acetylation of histone H3/H4 by inhibiting expressions of HDAC1 gene.

Detailed knowledge on tissue-specific metabolic reprogramming in diabetic nephropathy (DN) is vital for more accurate understanding the molecular pathological signature and developing novel therapeutic strategies. In the present study, a spatial-resolved metabolomics approach based on air flow-assisted desorption electrospray ionization (AFADESI) and matrix-assisted laser desorption ionization (MALDI) integrated mass spectrometry imaging (MSI) was proposed to investigate tissue-specific metabolic alterations in the kidneys of high-fat diet-fed and streptozotocin (STZ)-treated DN rats and the therapeutic effect of astragaloside IV, a potential anti-diabetic drug, against DN. As a result, a wide range of functional metabolites including sugars, amino acids, nucleotides and their derivatives, fatty acids, phospholipids, sphingolipids, glycerides, carnitine and its derivatives, vitamins, peptides, and metal ions associated with DN were identified and their unique distribution patterns in the rat kidney were visualized with high chemical specificity and high spatial resolution. These region-specific metabolic disturbances were ameliorated by repeated oral administration of astragaloside IV (100 mg/kg) for 12 weeks. This study provided more comprehensive and detailed information about the tissue-specific metabolic reprogramming and molecular pathological signature in the kidney of diabetic rats. These findings highlighted the promising potential of AFADESI and MALDI integrated MSI based metabolomics approach for application in metabolic kidney diseases.