Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.

Tutorial System is beneficial to improving the general disposition of undergraduate students,forming better learning atmosphere,enhancing the scientific research ability,broadening the pathway of contacting society,developing students' cognitive ability,and strengthening employment instructive work.Tutorial system for undergraduate students has been carried out for 4 years in our military medical university.After finding some problems of the work,making a summary of the beneficial experience and analyzing the cause of problems,we try to put forward some suggestions and take some optimization measures.

Objective To investigate the influence of recombinant human parathyroid hormone [rhPTH (1-34)]on the proliferation of HaCaT cells induced by tumor necrosis factor-α (TNF-α) in vitro.Methods Cultured HaCaT cells were treated with various concentrations of rhPTH (1-34) for different durations after incubation with recombinant human TNF-α of 10 g/L for 24 hours.MTT assay and flow cytometry were performed to detect the proliferation and cell cycle of HaCaT cells,respectively.Results As contrast phase microscopy showed,the growth of HaCaT cells was inhibited by rhPTH (1-34) along with a decrease in the growth speed.MTT assay showed a suppressed proliferation of HaCaT cells after being treated with rhPTH (1-34) of 0.05,0.2,0.8,3.2 and 12.8 pmol/L for 36 and 48 hours (P＜ 0.01 or 0.05).The percentage of cells at G1 phase in HaCaT cells markedly increased (all P ＜ 0.01 ),while that at S phase declined (all P ＜ 0.01 )after 48-hour treatment with rhPTH(1-34) of 0.2,0.8,3.2 and 12.8 μ mol/L.Conclusions rhPTH(1-34) has an obvious inhibitive effect on the proliferation of HaCaT cells induced by TNF-α in vitro,and the effect is in a dose-dependent manner.

Objective To investigate the effects of trivalent arsenicals on ce ll proliferation and induction of apoptosis in human epidermal keratinocytes. Me thods Human benign epidermal keratinocytes (cell line HaCaT), human epidermal ca rcinoma cells(cell line A431) were cultured. After treatment with arsenous acid, inhibition of cellular growth was determined by measuring MTT dye absorption of living cells.Apoptosis was assessed with respect to morphological changes by li ght and electron microscopy and to cell cycle distribution by flow cytometry. An nexin-ⅴbinding assay was used to detect the early stage of apoptosis. Results With concentrations ranging from 0.5 to 10 ?mol/L, arsenous acid significantly inhibited the proliferation of HaCaT cells in a dose-and time-dependent manner . By light and electron microscopy, morphological changes revealed characteristi cs of apoptosis. But A431 cells showed no obvious change. DNA flow cytometric an alysis indicated that arsenous acid induced an arrest in G2M phase and sub-G1 p hase in HaCaT compared with A431 cells. The green flurorescence indicated early stage of apoptosis in HaCaT cells by annexin-V binding assay. Conclusion Arseno us acid may inhibit the proliferation of HaCaT cells and induce apoptosis, but d oes not affect A431 cell line obviously, which suggests that HaCaT cells are mor e sensitive to arsenous acid compared with A431 cells.

Objective To investigate the effect of tacrolimus on Langerhans cell migration in order to understand the therapeutic mechanism of tacrolimus. Methods C57BL/6 mouse injected with different doses of tacrolimus was stimulated by FITC at ear back. After twelve hours, the number of Langerhans cells which took antigen and migrated to lymph nodes was measured by flow cytometry. The number of Langerhans cells which took antigen and resided in epidermis was examined by immunohistochemical staining. Results After injection with tacrolimus, the number of Langerhans cells which took antigen and migrated to lymph nodes was reduced, especially at 12 hours before stimulation by FITC. The reduction was significantly different between the high dose and low dose injection groups. However,the number of Langerhans cells residing in epidermis was significantly higher in tacrolimus injection group than that in the control. Conclusions Tacrolimus, a new kind of immunosuppressive drug,may probably suppress Langerhans cell migration and therefore inhibit immune response in some diseases.

Objective To investigate the effect of the exogenous fragile hisdidine triad(FHIT) gene on the proliferation and the apoptosis of cutaneous carcinoma cell line A431,and to explore the mechanism of tumor suppression by the FHIT gene.Methods The plasmids pcDNA3-FHIT and pcDNA3-vector were transfected into the cutaneous carcinoma cell line A431 without FHIT gene expression,and then the transfected cells were screened by G418 and the expression of FHIT was determined by the immunocytochemical staining technique.The effect of FHIT on the growth characteristics of cutaneous carcinoma cell line A431 was observed by MTT,colony forming test and flow cytometry.Results Stable FHIT gene expressing A431 cells were produced,the proliferation activity and colony forming capability of A431FHIT were suppressed,whereas the apoptosis was increased.All these differences between A431-FHIT cells and the two control groups of cutaneous carcinoma cells had statistical significance.Conclusion Transfecting the exogenous FHIT gene into cutaneous carcinoma cells line A431can suppress the proliferation of tumor cells,and can also induce apoptosis and cell cycle arrest.

Objective To investigate the expressions and significance of IL-22 and related cytokines (IL-23pl9 and IL-6) in sera and PBMCs of patients with psoriasis. Methods Sera and PBMCs were obtained from the venous blood samples from 58 patients with psoriasis vulgaris and 20 normal human controls. The PBMCs were subjected to culture for 5 hours followed by the collection of cells and culture supernatant. Then,quantitative real-time RT-PCR was used to examine the mRNA expressions of IL-22, IL-23pl9 and IL-6 in PBMCs, enzyme-linked immunosorbent assay (ELJSA) to detect the level of IL-22 protein in the sera and culture supernatant of PBMCs. Results In the patients with psoriasis and controls, the relative expression level in PBMCs was 4.48 ± 2.64 and 2.35 ± 0.91 respectively for IL-22 mRNA, 6.07 ± 4.09 and 2.61 ± 1.46 respectively for IL-23pl9 mRNA, 3.87 ± 1.49 and 1.48 ± 0.62 respectively for IL-6 mRNA; significant differences were observed between the two groups in all the above parameters (all P < 0.01). ELISA revealed that the level of IL-22 protein in the patients and controls was (86.23 ± 25.58) ng/L and (43.67 ± 14.82) ng/L respectively in the sera (P< 0.01), (119.11 ± 21.51) ng/L and (57.70 ± 13.17) ng/L respectively in the culture supernatant of PBMCs (P< 0.01). Conclusion There is an overexpression of IL-22 in the PBMCs and sera of patients with psoriasis, implying that IL-22 is involved in the pathogenesis of psoriasis.

0.1). Plasma PAF-AH activity in the patients with psoriasis was significantly lower than that in the healthy controls(P

Objective To investigate the relationship between a mutation in the platelet-activating factor (PAF) acetylhydrolase gene (Arg92→His) and psoriasis. Methods Genomic DNA was analyzed in 47 patients with psoriasis and 52 healthy controls via polymerase chain reaction and restriction fragment length polymorphism. Results The frequency of the mutation in the PAF acetylhydrolase gene (Arg92→His) was significantly higher in patients with psoriasis than that in the controls (P

Objective To evaluate the efficacy and safety of 0.05% desonide cream in the treatment of patients with eczema. Methods A randomized, double-blind, multicenter, vehicle-controlled study was conducted. The patients of the study and control groups applied 0.05% desonide cream and vehicle respectively, twice daily for 3 consecutive weeks. The efficacy was determined by measuring the total scores of erythema, erosion, infiltration, papule, exudation/crust, pruritus and the extent of lesions. Results At the end of the 3 weeks study, the total clinical effective rate was 80.8% in the study group,compared to 41.1% in the control group, with a significant difference between the two groups (P