Objective:To analyze the clinical effect and safety of Lingdan tablets and Wuling capsules in the treatment of alopecia areate. Methods:Totally 84 patients with alopecia areate were divided into the observation group and the control group with 42 ones in each. Minoxidil tincture was used for external in the two groups. The control group were treated with 0. 9 g Lindan tablets, tid, for 4 months and the treatment group was additionally treated with 0. 99 g Wuling capsules,po,tid, for 4 months. The changes in the area and position of trichomadesis, light pull test, the tissue growth score and Pittsburgh Sleep Quality Index ( PSQI) score were compared before and after the treatment. Results:The efficacy of the observation group was better than that of the control group(P<0. 05). Af-ter the treatment, the evaluated indices in the two groups were lower than those before the treatment(P<0. 01), and the reduction of the observation group was more significant than that of the control group(P<0. 01) . There was no notable adverse reaction appeared in the observation group. Conclusion:Lingdan tablets and Wuling capsules can improve sleeping quality, promote the growth of halr and enhance the curative effect.

BACKGROUND: Both animal experiments and clinical practice have confirmed that mild or moderate hypothermia is effective in reducing secondary brain injury, but its effect on homeostasis is not very clear.OBJECTIVE: To investigate the effect of a combined therapy of mild hypothermia and hibernation on the homeostasis of patients with severe brain injury.DESIGN: A randomized controlled study.SETTING: Neurosurgical Institute of Beijing; Neurosurgical Department of the First Clinical Medical College Affiliated to Harbin Medical University;and Neurological Department of the Second Clinical Medical College Affiliated to Harbin Medical University.PARTICIPANTS: The study was conducted at the Department of Neurosurgery, the First Affiliated Hospital of Harbin Medical University, from June to December 2002. Totally 24 patients (aged 35-60 years) with severe cerebral hemorrhage or brain injury were randomly divided into combined therapy group and normothermia group. Their Glasgow Coma Scale scores ranged from 3 to 8. The subjects signed the informed consent.METHODS: Within 10 hours of their injury, patients in hypothermia and hibernation combination group were given half dosage of No. 1 hibernation cocktail (chlorpromazine 25 mg, pethidine hydrochloride 50 mg, and promethazine 25 mg), and were cooled by cooling blankets to make their body temperature dropped to 32-34 ℃ (rectal temperature). Their temperature was kept within this range for 5 days, at 35 ℃ for 24 hours, and then was slowly increased to their normal level. The body temperature of patients in normothermia group was maintained at 37-38 ℃. The mean arterial pressure and heart rate of all patients were measured continuously by HP monitor. On the 3"d and 7th days of hospitalization, intracranial pressure and creatine phosphate kinase were measured via lumbar puncture.Femoral artery puncture was performed to check the partial pressure of arterial O2 and CO2. Platelets count and blood electrolytes K+ and Na+ concentration of each patient were measured, too. On the 7th day Glasgow Outcome Scale scores of each patient and mortality of each group were recorded.activity of creatine phosphokinase, platelets count, blood K+ and Na+ conand CO2 of patients in combined therapy group on the 3rd and 7th days of hospitalization.intracranial pressure, creatine phosphokinase and platelets count: The decreased values of intracranial pressure, creatine phosphokinase and platelet number in combined therapy group were all significantly higher than those in normothermia group [(104.09±54.90), (58.75±25.33) mm H2O; (26.95±19.22), (10.17±7.18) μkat/L; (89.82±46.36)×109/L, (48.83±44.59)×109/L,the mean arterial pressure, blood electrolytes, and partial pressure of artewas significantly lower than that of normothermia group (25.0%, 66.6%,P ＜0.05).CONCLUSION: This combined therapy of hypothermia and hibernation can effectively decrease intracranial pressure and creatine phosphokinase,but has no significant effects on the mean arterial pressure, blood electrolytes concentration, and partial pressure of arterial O2 and CO2. It has the risk of disturbing the patients' hematopoiesis.

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.

Aim To investigate effects of ZX-5 on the expression and activity of nitric oxide synthase ( NOS) in endothelial cells,and to confirm which kind of NOS increases NO production and promote choroidal blood flow in ZX-5 -induced HUVECs. Methods HUVECs ( human umbilical vein endothelial cells) were used to determine the expression of eNOS,iNOS and nNOS by Western blot; the activities of NOS were investigated by the corresponding kit. Results ( R,R) ZX-5 upregulated eNOS expression and increased NO production; ( S,S) ZX-5 upregulated iNOS expression and slightly increased NO release. Conclusions ( R,R) ZX-5 promotes choroidal blood flow via upregulating eNOS expression and activity and promoting NO production; the compound may be used for the prevention and treatment of age-related macular degeneration in the elderly.

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.

Objective To study the activation of alveolar macrophage β (AM) and the expression of co-stimulatory molecule CD40 in transfusion-related acute lung injury (TRALI) model in order to illustrate the pathogenesis of TRALI.Methods Sixty SD rats were randomly (random number) divided into normal control group (n =15) with sham operation using normal saline instead of LPS and plasma,positive control group (n =15) with ALI induced by intravenous infusion of 5 mg/kg lipopolysaccharide (LPS) in equivalent volume of whole blood drawn out),and TRALI group (n =15) treated by intra-peritoneal injection of 2 mg/kg LPS 2 h before the transfusion of human plasma (1 mL whole blood about 10％ of total blood volume drawn out and replaced with 1 mL plasma),LPS control group (n =15) treated by intra-peritoneal injection of 2 mg/kg LPS 2 h before saline infusion in equivalent volume of blood drawn out.The pathologic changes of rat lung tissue were observed by HE staining.The expression of TLR4 was examined by RT-PCR.The activation of NF-κB in AM was measured by electrophoresis mobility shift assay (EMSA).The expression of CD40 mRNA and CD40 molecule were analyzed by Northern blot and flow cytometry respectively.ELISA was performed to detect the concentration of TNF-α,MIP-2 and IL-1 β in broncho-alveolar lavage fluid (BALF).Results Broken alveolar septa,hyperemia,and massive infiltration of inflammatory cells including the neutrophils were observed in lung tissues of TRALI group.The expression of TLR4 gene was detected in activated macrophage phi (AMφ) of TRALI group rats.The activation of NF-κB was increased in TRALI group rats.The expression of CD40 in AMφ was higher in rats of TRALI group than that in rats of control group and LPS control group.The concentration of TNF-αt,MIP-2 and IL-1β were enhanced significantly in BALF of TRALI group rats.Conclusion The activation of AM and up-regulation of costimulatory molecule CD40 induced release of some inflammatory cytokines.It suggested that AM activation may play an important role in the pathogenesis of TRALI.

Phthaloyl dichloride (1)was reacted with LiAlSeH2 to give benzo[c]selenophene-1;3-dione (2);which was treated with the Grignard reagents to generate hydroxyl compounds 3a-3h.These compounds were finally converted to target products 4a-4h by treatment with hydriodic acid.The structures of 4a-4h were confirmed by MS and 1 H NMR.Their inhibitory activity against adenosine diphosphate (ADP)-induced platelet aggregation was evaluated by Born′s turbidimetric assay;free radical scavenging activity was assayed by xanthine oxidasemethod and 1;10-phenanthroline spectrophotometric method.It was found that compound 4 f displayed more potent inhibi-tory effect on platelet aggregation than 3-n-butylphthalide and comparable hydroxyl free radical scavenging activity in vitro to that of edaravone.Therefore;compound 4 f might be the candidate for further investigation.

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 .

Objective To investigate the function of the hypothalamic-pituitary-adrenal (HPA) axis in postmenopausal women with type 2 diabetes and visceral obesity. Methods Subjects were divided into three groups:control group(group C),type 2 diabetes mellitus with non-obesity group (group DM) and type 2 diabetes mellitus with visceral obesity group (group DM + OB). General clinical characteristics, morning blood cortisol concentrations and 24 h urine free cortisol of three groups were compared. Serum cortisol levels were also compared after 0.25 mg dexamethasone suppression test and followed by oral intake of 25 mg cortisone acetate. Results (1) There were no significant differences in basal cortisol levels, but after inhibition with dexamethasone the group DM + OB showed significantly higher cortisol level than that in the control group (P < 0.01). (2) Conversion of oral cortisone to plasma cortisol differed significantly between the group C (lower) and group DM + OB (P < 0.05). (3) Plasma LH and FSH concerntrations were significantly lower in group DM + OB compared with group C (P < 0.01). Conclusion In the postmenopausal women with type 2 diabetes mellitus, the negative feedback mechanism and hepatic 11β-HSD-1 activity were impaired, especially in those with visceral obesity.

The plasma level and the regulation of cortisol in type 2 diabetic patients were invesligated.Plasma and urinary cortisol levels were measured, and dexamethasonc suppression test and oral cortisone test in vivo were performed. Compared with controls, diabetic patients had higher urinary cortisol level. The activity of hepatic 11 β-hydroxy-steroid dehydrogenase-1 (11β-HSD1) in type 2 diabetic patients was decreased, suggesting that the elevated basal cortisol in type 2 diabetic patiens may due to impaired hepatic degradation of cortisol.