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Objective To investigate the effects of narrow-band ultraviolet B (NB-UVB) therapy on the levels of plasmin and CC chemokine ligand 20 (CCL20) in peripheral blood of patients with psoriasis vulgaris.Methods A total of 60 patients with psoriasis vulgaris in progressive stage were treated with NB-UVB radiation thrice a week for 8 weeks.Enzyme-linked immunosorbent assay (ELISA) was performed to detect the levels of plasmin and CCL20 in the peripheral blood of the patients before and after the treatment,as well as in the peripheral blood of 50 healthy controls.Results After the treatment,psoriasis area and severity index (PASI) scores in patients were significantly decreased compared with those before the treatment (2.54 ± 1.64 vs.10.26 ± 3.14,t =17.40,P ＜ 0.05),and the response rate was up to 87％ (52/60).Before the treatment,levels of plasmin and CCL20 were both significantly higher in the patient group than in the control group (plasmin:180.07 ± 40.62 μg/L vs.76.30 ± 26.92 μg/L,t =15.45,P ＜ 0.05;CCL20:422.41 ± 129.87 pg/L vs.205.33 ± 49.89 pg/L,t =11.15,P ＜ 0.05).After the treatment,levels of plasmin (148.22 ± 40.05 μg/L) and CCL20 (329.67 ± 100.73 pg/L) in patients were significantly decreased compared with those before the treatment (t =4.97,6.44,P ＜ 0.05),but still significantly higher than those in controls (t =10.82,7.95,P ＜ 0.05).Before the treatment,the level of plasmin was positively correlated with the level of CCL20 in peripheral blood of the patients (r =0.57,P ＜ 0.05),and the levels of plasmin and CCL20 were both positively correlated with the PASI score (r =0.49,0.62,respectively,both P ＜ 0.05).Conclusion NB-UVB radiation may exert a therapeutic effect on psoriasis vulgaris by reducing levels of plasmin and CCL20 in peripheral blood of patients.
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Objective To detect the expression of Livin,an apoptosis-inhibiting protein,and Smac,an apoptosis-promoting protein,in basal cell carcinoma (BCC) lesions.Methods Skin specimens were obtained from the lesions of 80 patients with BCC and normal skin of 30 human controls.Immunohistochemical SP method was used to detect the pmtein expression of Livin and Smac in these specimens.Chi-square test was conducted to compare the expression rate of Livin and Smac protein between the lesional and control specimens.The relationship between the protein expression of Livin and Smac in BCC was analyzed by Spearman correlation coefficients.Results The expression rate of Livin protein was significandy higher (77.50％ vs.3.33％,x2 =49.04,P ＜ 0.001),while that of Smac protein was statistically lower (46.25％ vs.100％,x2 =26.47,P ＜ 0.001),in BCC than in the control specimens.No significant difference was observed in the expression rate of Livin or Smac protein between nodular ulcerative and pigmented BCC specimens (75.41％ vs.80.00％,x2 =0.001,P ＞ 0.05; 47.54％ vs.40.00％,x2 =0.28,P＞ 0.05) or between nodulocystic and pigmented BCC specimens (73.58％ vs.80.00％,x2 =0.03,P ＞ 0.05; 45.28％ vs.40.00％,x2 =0.13,P ＞ 0.05).There was a negative relationship between the protein expression of Livin and Smac in BCC lesions (r =-0.432,P ＜ 0.01).Conclusion The upregulated expression of Livin and downregulated expression of Smac may be invoved in the occurrence and development of BCC.
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Objective To evaluate the influence of amphetamine-type stimulants on serum rapid plasma reagent (RPR) tiler and negative conversion rate of RPR in patients with syphilis. Methods Thirty-six patients with syphilis who took amphetamine-type stimulants (ATS) were recruited in this study together with 44 patients with syphilis who never took ATS and 30 normal human controls. Benzathine benzylpenicillin was given intramuscularly to all patients at a dose of 2 400 000 unit per week for 3 weeks. RPR and treponema pallidum particle agglutination (TPPA) assay were performed before treatment, 3, 6, 9 and 12 months after the therapy. Radioimmune assay and ncphelometry were used to detect the serum level of IgG, lgM and IgA. The capability of peripheral blood mononuclear cells (PBMCs) to product interferon-T (IFN-γ) and interleukin-4 (IL-4) was evaluated with ELISA. Results Before treatment, RPR titcr was significantly lower in the stimulant-taking group than in the non-taking group (χ2 = 14.93, P < 0.05). The negative conversion rates were 5.56%, 16.67% and 52.78% in stimulant-taking group 6, 9 and 12 months after the treatment, respectively, significantly lower than those in the control group (all P < 0.05). As for the serum level of IgG, IgM and IgA, there was no significant difference among the stimulant-taking group, non-taking group and normal control group (all P > 0.05). The capability of PBMCs to product IFN-γ was highest in the stimulant-taking group, followed by the non-taking group and normal control group (all P < 0.05). No significant difference was observed in the capability of PBMCs to produce IL-4 between the stimulant-taking group and non-taking group, but a significant increment was noted in these patients compared with the normal human controls (all P < 0.01). Conclusion Amphetamine-type stimulants could reduce serum RPR titer and negative conversion rate of RPR in patients with syphilis, likely by impairing cellular immunity of patients.
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Objective To investigate the role of the expression of p27 and cyclin E in the pathogenesis of Bowen's disease and squamous cell carcinoma (SCC). Methods The expression of p27 and cyclin E was assessed by immunohistochemical method in 16 patients with Bowen's disease, 53 patients with SCC and 25 normal controls. Results The expression of p27 was lower in Bowen's disease and SCC compared to that in the normal skin, and the expression level decreased with a decline in the differentiation of tumors, i.e. the lowest expression was observed in poorly differentiated SCC, followed by highly differentiated SCC and Bowen's disease. The expression of cyclin E was higher in Bowen's disease and SCC than that in the normal skin, and the expression level increased with a decline in the differentiation of tumors. The expression of p27 was inversely correlated with that of cyclin E among all the cases of Bowen's disease and SCC. Conclusion The abnormal expression of p27 and cyclin E may contribute to the pathogenesis of Bowen's disease and SCC.