Notch signaling pathway is a highly conserved signaling pathway ,and plays an important role in the individual growth and development process in the vertebrate .Many studies have demonstrated Notch 3 re-ceptor expression is aberrant in a variety of tumors .Recent studies show that aberrant Notch 3 mediated signaling pathway is closely related with the progression of diverse types of tumors .Notch3 plays a vital role in apoptosis , proliferation and differentiation of tumor cells .To promote the studies of Notch 3 as a drug development targets ,the molecular mechanisms of abnormal Notch 3 expression and its role on tumorgenesis ,progression and treatment re-sistance are reviewed in this paper .

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.

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.

Objective To investigate the inhibitory effect of bromfenac sodium hydrate ophthalmic solution on corneal neovascularization (CNV) induced by alkali burn.Methods A total of 192 specific pathogen free (SPF) degree adult male Sprague-Dawley (SD) rats were used in this study.One hundred and seventy-two rats were chosen to establish CNV model with alkali burn in the right eyes.Following alkali burn,rats were randomly divided into CNV group,model control group,bromfenac sodium group and fluorometholone group,with 43 rats (43 eyes) in each group.Another 20 rats (40 eyes) served as normal control group.One day after modeling,the model control group,bromfenac sodium group and fluorometholone group received phosphate buffer saline (PBS),bromfenac sodium hydrate ophthalmic solution and 0.1％ fluorometholone eye drops,respectively.The state of cornea and anterior chamber and the growth of CNV of rats in each group were observed by slit-lamp microscope every day after modeling.At 1,3,7,14,21 and 28 days after modeling,the anterior segment photos of the experimental eyes were captured,and the percent of cornea areas covered by CNV was calculated.At 7,14 and 28 days after modeling,the eye tissue sections were stained with hematoxylin and eosin staining and immunohistochemistry staining to evaluate the expressions of CD45 and VEGF-A.Real-time quantitative PCR and enzyme-linked immunosorbent assay (ELISA)were used to detect the expression of COX-2 and VEGF mRNA and protein level.The use and care of the animals complied with the Statement of the Association for Research in Vision and Ophthalmology(ARVO).Results Each model group showed corneal edema and opacification 1 day after modeling.The corneal edema was aggravated 7 days after modeling.On the 14th day after modeling,the degree of corneal opacity and edema decreased gradually.On the 28th day after modeling,leucoma was observed in CNV group and model control group,and nebula was observed in bromfenac sodium group and fluorometholone group.At 7,14,21 and 28 days after modeling,the percentages of CNV areas in bromfenac sodium group and fluorometholone group were significantly lower than those in CNV group and model control group (all at P＜0.05).No significant difference was found in the percentage of CNV areas between bromfenac sodium group and fluorometholone group at various time points (all at P＞0.05).On the 7th day after modeling,the thinning of corneal epithelial layer,edema and arrangement disorder of stroma layer were observed,and the expression of VEGF-A was positive in all model groups;a small amount of CD45 positive inflammatory cell infiltrations were observed in CNV group and model control group.On the 14th and 28th day after modeling,CNV was seen in the center of cornea in CNV group and model control group;the epithelial keratosis and reduction of corneal edema were seen in each group,and no inflammatory cell infiltration was observed in each group.On the 7th day after modeling,the expressions of COX-2 and VEGF mRNA in CNV group and model control group were significantly higher than those in normal control group,bromfenac sodium group and fluorometholone group (all at P ＜ 0.05),the expressions of COX-2 and VEGF protein in bromfenac sodium group were significantly lower than those in CNV group (all at P＜0.05).The corneal peroration rate in model control group and bromfenac sodium group was 10％ (1 case in 10 rats).The corneal perforation rate in fluorometholone group was 30％ (3 cases in 10 rats).In each model group,10％ to 30％ rats had hyphema.Conclusions Bromfenac sodium hydrate ophthalmic solution can inhibit the formation and growth of CNV after alkali burn in rats.This effect may be mediated by regulating COX-2 expression,reducing inflammation and inhibiting VEGF production.