30ml) undergoing minimally invasive evacuation of intracranial hematoma in our department were analyzed retrospectively.The chants of IL-1,IL-6 and IL-8 in hematoma fluid were observed continuously.The content of IL-1,IL-6 and IL-8 was determined by radioimmunassay.Results IL-1,IL-6 and IL-8 were observed at 6～12h after hypertensive cerebral hemorrhage,and showed different changes in acute stage.Conclusion Inflammatory cytokines are involved in the pathological process of cerebral hemorrhage.

Objective:To study the inhibition of astragaloside on the proliferation of human keloid fibroblasts. Methods: Com-pared with that of normal skin, the expression of transforming growth factor-β( TGF-β) and its transduction factors Smad in the human keloid fibroblasts was detected. The optimal concentration was screened by MTT after HFF-1 human skin fibroblast was infected with astragaloside at different concentrations. The mRNA expression of Smad2, Smad3, Smad4 and Smad7 in the fibroblasts was studied by using real-time. The protein expression of TGF-βRⅡ, Smad2, Smad3, Smad4 and Smad7 in the fibroblasts was detected by using Western blot. Results: Compared with that of normal skin tissue, the expression of Smad protein was significantly increased ( P <0. 05) in the human keloid fibroblasts, and there was no significant difference in the TGF-βRⅡ expression (P>0. 05). The optimal concentration of astragaloside was 0. 5μg·ml-1 . The expression level of Smad2 protein in the two groups was significantly increased, and the level of Smad3 expression was significantly decreased (P<0. 05). Conclusion:Astragaloside can inhibit the formation of fi-broblast possibly through Smad2 over-expression and Smad3 inhibition in the TGF-β/Smad signal transduction pathway.

Objective To estimate the activity of the phosphatidylinositol3-kinase (PI3K) signaling pathway in peripheral blood T cells from patients with atopic dermatitis (AD),and to investigate its clinical significance.Methods T cells were isolated by using the Rosettsep T cell purification kit from the peripheral blood of 38 patients with AD and 38 healthy human controls,and classified into several groups to be treated with anti-CD3 monoclonal antibody,anti-CD28 monoclonal antibody,and LY294002 (an inhibitor of PI3K) respectively.The activity of PI3K signaling pathway in T cells was estimated by immunoprecipitation and enzyme-linked immunosorbent assay (ELISA).Western blot was performed to measure the expressions of total Akt and phosphorylated Akt in T cells,methyl thiazolyl tetrazolium (MTT) assay to examine the proliferation of T cells,and ELISA to determine the levels of interleukin 6 (IL-6) and IL-10.Results The activity of PI3K and Akt was significantly higher in freshly isolated patient-derived T cells than in control-derived T cells (both P ＜ 0.05).However,the difference in the activity of PI3K and Akt between patient-derived and control-derived T cells disappeared (both P ＞ 0.05) after 24-hour in vitro culture.The activity of PI3K and Akt in control-derived T cells was significantly increased after 24-hour incubation with sera from the patients with AD (both P ＜ 0.05).In addition,compared with patient-derived T cells treated with patients' sera or anti-CD3/CD28 monoclonal antibody alone,those treated with the combination of LY294002 and patients' sera or anti-CD3/CD28 monoclonal antibody showed a significant decrease in the proliferative activity (63％ ± 11％ vs.123％ ± 25％,125％ ± 22％ vs.195％ ± 28％,both P＜ 0.05),supematant levels of IL-6 ((168 ± 33) vs.(265 ± 46) ng/L,(431 ± 64) vs.(823 ± 128) ng/L,both P＜ 0.05) and IL-10 ((56 ± 14) vs.(98 ± 25) ng/L,(120 ± 21) vs.(213 ± 35) ng/L,both P＜ 0.05).Eczema area and severity index (EASI) was unassociated with the activity of PI3K or Akt in fresh T cells from patients with AD (both P ＞ 0.05).Conclusions The PI3K signaling pathway is abnormally activated in peripheral blood T cells from patients with AD,which is associated with the proliferation of,as well as secretion of cytokines by,T cells,suggesting that there exist serum factors activating this pathway in peripheral blood of patients with AD.

0. 05]. After sublingual glycerytrinitrate administration,the diameter of the brachial artery dilated significantly [(4.26?0.54) mm vs (4.73?0.43) mm, P 0.05]. Sublingual glycerytrinitrate administration dilated the brachial artery significantly [(4. 37? 0.77) mm vs (4. 82?0. 60) mm, P

Objective To evaluate the efficacy of dural tenting suture and epidural drainage in craniotomy. Methods In 145 cases of intracranial lesions, dural tenting suture and epidural drainage were performed to prevent epidural hematoma. Results Postoperative computed tomography (CT) showed no epidural hematoma required surgery in both groups. Conclusion Both dural tenting suture and epidural drainage are effective in preventing epidural hematoma. Hemostasis is the key step. Dural tenting suture without epidural drainage relieves psychological stress. It decreases the risk of intracranial infection and avoids some unusual complications.

The histological and immunohistological features of two cases of cutaneous lymphadenoma was studied. A single, erythematous nodule with smooth surface developed on the face of both patients. The lesion slowly progressed. Histology revealed irregular epithelial lobules in the dermis which showed a peripheral palisaded border of basaioid-like cells as well as a center composed of clear cells. Some epithelial lobules and surrounding stroma were infiltrated by numerous small lymphocytes. Immunohistological study showed that the lymphocytic infiltration was predominantly composed of T cells (CD3 positive) along with a small number of B cells (CD20 positive). Within epithelial lobules and surrounded stroma, there were numerous dendritic cells that were positive for S-100 and CDia but negative for cytokeratin 7, cytokeratin 20 or carcino-embryonic antigen. In the center of epithelial lobules in one case, a few cells positive for epithe-lial membrane antigen and CD30 was observed. The diagnosis of cutaneous lymphadenoma was made according to the pathological and immunohistochemical findings, and the infiltration was predominated by CD3-positive lymphocytes in this uncommon epithelial neoplasm.

Objective To evaluate changes of Rho kinase (ROK)activity in peripheral blood T lymphocytes from patients with atopic dermatitis (AD), and to analyze their clinical significance. Methods Eight milliliters of heparin-anticoagulated blood samples were collected from 60 patients with AD and 60 healthy human controls followed by separation of T lymphocytes and sera from these blood samples as well as culture of isolated T lymphocytes with 10% fetal bovine serum for 24 hours. Both patient- and control-derived T lymphocytes were classified into two groups to be cultured with patient- or control-derived sera. In addition, some patient-derived T lymphocytes were classified into 4 groups:Y27632 group treated with the Rho kinase-specific inhibitor Y2763, CD3/CD28 group treated with anti-CD3/anti-CD28 monoclonal antibodies, Y27632 + CD3/CD28 group treated with Y27632 and anti-CD3/anti-CD28 monoclonal antibodies, and control group treated with patient-derived sera. Subsequently, Western-blot analysis was performed to evaluate ROK activity in cells, methyl thiazolyl tetrazolium(MTT)assay to evaluate proliferative activity of T lymphocytes, and ELISA to measure interleukin 6 (IL-6)and IL-10 levels in supernatants of T lymphocytes. Results ROK activity was significantly lower in fresh T lymphocytes from patients than in those from healthy controls (2.47% ± 0.89% vs. 0.65% ± 0.35%, t =2.729, P < 0.05). After 24-hour culture with 10% fetal bovine serum in vitro, ROK activity was significantly decreased in patient-derived T lymphocytes compared with those before culture (0.70% ± 0.38% vs. 2.47% ± 0.89%, t = 2.658, P <0.05), but no significant difference was observed between patient- and control-derived T lymphocytes(0.70% ± 0.38% vs. 0.63% ± 0.32%, t = 1.010, P > 0.05). Compared with T lymphocytes cultured with control-derived sera, those cultured with patient-derived sera showed significantly increased ROK activity (F = 8.22, P < 0.001). Concretely speaking, ROK activity was significantly higher in patient-derived T lymphocytes cultured with patient-derived sera than in those cultured with control-derived sera (2.41% ± 0.87% vs. 0.76% ± 0.41%, P < 0.05), and higher in control-derived T lymphocytes cultured with patient-derived sera than in those cultured with control-derived sera(2.17% ± 0.85% vs. 0.64% ± 0.33%, P< 0.05)at 24 hours. Y27632 could significantly inhibit the proliferation of as well as secretion of IL-6 (F = 18.68, 22.95, respectively, both P < 0.001)by patient-derived T lymphocytes, but had insignificant effects on secretion of IL-10. The cellular proliferative activity and IL-6 supernatant level were significantly lower in the Y27632 group than in the control group, and lower in the Y27632 + CD3/CD28 group than in the CD3/CD28 group (all P < 0.05). Conclusion Aberrant activation of ROK exists in T lymphocytes from patients with AD, which may play a certain role in the pathogenesis of AD.

Objective To evaluate regulatory effects of miRNA-146a on peripheral blood CD4 + T lymphocytes from patients with psoriasis vulgaris, and to investigate the role of miRNA-146a in the pathogenesis of psoriasis vulgaris. Methods Totally, 30 patients with psoriasis vulgaris and 30 healthy human controls were enrolled into this study. Venous blood samples were obtained from these subjects, and CD4 + T lymphocytes were isolated from these samples by using magnetic activated cell sorting (MACS). Real-time quantitative PCR (RT-PCR)was performed to measure the expression of miRNA-146a in peripheral blood CD4+ T lymphocytes, and enzyme-linked immunosorbent assay(ELISA)to determine plasma levels of interferon-γ(IFN-γ)and interleukin 4(IL-4). Some CD4+ T lymphocytes were divided into 3 groups to be transfected with 50 nmol/L negative control miRNA (control group), miRNA-146a mimics(miRNA-146a group)or miRNA-146a inhibitor (miRNA-146a inhibitor group). After 24-hour additional culture, flow cytometry was conducted to determine the number of Th1 and Th2 cells, Western-blot analysis and RT-PCR were performed to measure the protein and mRNA expressions of IFN-γ receptor α (IFN-γRα), T-box expressed in T cells (T-bet)and GATA-binding protein-3 (GATA-3)respectively, and ELISA was carried out to determine the levels of IFN-γ and IL-4 in supernatants of CD4 + T lymphocytes. Results Compared with the healthy control group, the patient group showed significantly increased miRNA-146a expression in peripheral blood CD4 + T lymphocytes (243.81% ± 94.32% vs. 105.74% ± 22.93%, t = 6.653, P < 0.01)and plasma IFN-γ level (27.69 ± 7.64 ng/L vs. 9.75 ± 2.81 ng/L, t = 4.237, P <0.01). Moreover, miRNA-146a expression was positively correlated with plasma IFN-γ level in the patients(r = 0.837, P <0.01). After 24-hour culture in vitro, there was a significant increase in the number of Th1 cells, protein and mRNA expressions of T-bet, and supernatant level of IFN-γ, but a significant decrease in the protein expression of IFN-γRα in the miRNA-146a group compared with the control group (all P < 0.01). However, no significant differences were observed in the number of Th2 cells, mRNA or protein expressions of GATA-3, or supernatant level of IL-4 among the control group,miRNA-146a group and miRNA-146a inhibitor group (all P > 0.05). Conclusion miRNA-146a may play an important role in the pathogenesis of psoriasis vulgaris by participating in the regulation of peripheral blood CD4+ T lymphocytes via affecting Th1 cell differentiation and function.

Objective To investigate the effects of miRNA-146a on the differentiations and functions of CD4+ T lymphocytes in patients with psoriasis vulgaris.Metbods Thirty patients with psoriasis vulgaris and twenty heathy subjects were enrolled in this study.Quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of miRNA-146a in CD4+ T lymphocytes isolated from the peripheral blood samples.The levels of IFN-γ and IL-4 in serum samples were determined by using enzyme-linked immunosorbent assay (ELISA).Mononuclear cells were isolated from human peripheral blood samples by using Ficoll-Hypaque density-gradients centrifugation,from which the CD4+ T lymphocytes were separated by magnetic-activated cell sorting.The CD4+ T cells (2× 106/ml) were seeded in culture plates with 6 wells.The CD4+ T lymphocytes were divided into 3 groups including the control group,miRNA-146a group and miRNA-146a inhibitor group.The numbers of Th1 and Th2 cells were measured by flow cytometry analysis (FACS).The expression of IFN-γRα,T-bet and GATA-3 at mRNA and protein levels were measured by using RT-PCR and Western blot assay,respectively.The levels of IFN-γ and IL-4 in culture supernatants of CD4+ T lymphocytes were detected by using ELISA.Results In comparison with the normal control group,there were significant increases in the expression of miRNA-146a in CD4+ T lymphocytes and the level of IFN-γin serum samples from patients with psoriasis vulgaris [(2.43±0.94) vs (1.05±0.23),(27.69±7.64) ng/L vs (9.75±2.81) ng/L,all P＜0.01].A positive correlation between the expression of miRNA-146a and the level of IFN-γ in serum was observed (r=0.837,P＜0.01).Results of the in vitro culture of CD4+ T lymphocytes showed that the number of Th1 cells,the expression of T-bet at mRNA and protein levels and the level of IFN-γin culture supernatant were significantly increased,while the expression of IFN-γRα protein was decreased in the miRNA-146a group in comparison with those of the control group (all P＜0.01).No significant differences in the number of Th2 cells,the expression of GATA-3 protein,the expression of GATA-3 and IFN-γRα at mRNA level and the level of IL-4 in culture supernatants were found between the control and miRNA-146a groups (all P＞0.05).The miRNA-146a inhibitor could effectively attenuate the effects of miRNA-146a on Th1 cells.Conclusion The miRNA-146a could promote the differentiation and enhance the function of Th1 cells.It might play an important role in the pathogenesis of psoriasis vulgaris.

Objective To study the quantity change and significance of myeloid‐derived suppressor cells(MDSCs) in patients withpost‐traumaticmultipleorgandysfunctionsyndrome(MODS).Methods 66patientswithMODS,34patientswithnon‐system‐ic inflammatory response syndrome(SIRS)and 37 healthy volunteers were enrolled in this study .Peripheral blood was collected and CD14-CD11b+ CD33+ were used as markers of MDSCs .The percentage of MDSCs was determined by flow cytometry and serum interleukin‐10(IL‐10) and tumor necrosis factor‐α(TNF‐α) levels were determined by ELISA .The MODS scoring system was used to assess patients′disease severity .The relationship was analyzed between MDSCs and TNF‐αand MODS score .Results The per‐centage of MDSCs in peripheral blood of healthy volunteers was(1 .18 ± 0 .22)% .after MODS ,the percentage of MDSCs in periph‐eral blood was(11 .84 ± 2 .18)% and(6 .52 ± 0 .37)% in patients with non‐MODS ,the percentages of MDSCs in three groups showed significant differences(P<0 .05) .Serum IL‐10 and TNF‐αin patients with MODS group and non‐MODS group were signif‐icant differences(P<0 .05) .The correlation was found between MDSCs percentage in peripheral blood and MODS score and TNF‐α(r=0 .342 6 ,0 .387 9 respectively ,P<0 .05) .Conclusion The increase proportion of MDSCs in peripheral blood correlates with the onset of infection in patients with MODS ,indicating that the expansion of MDSCs in peripheral blood may play important roles in immune dysfunction after MODS .