OBJECTIVE:To study the mycoplasma infection and the drug susceptibility of mycoplasma in cervical secretions from female genital tract in our hospital.METHODS:Ureaplasma urealyticum(Uu)and mycoplasma hominis(Mh)in cervical secretions sampled from 3 416 female genital tract inflammation cases in our hospital were identified by cultivation,and the antibiotic resistance was also detected.RESULTS:The total positive rate of mycoplasma was 43.7%;Uu infection accounted for 40.0%,which was sensitive to Cycloate erythromycin,Minocycline,Deoxycycline,Josamycin;Mh infection accounted for 0.7%,which was sensitive to Deoxycycline,Minocycline and Josamycin;Uu+Mh infection accounted for 3.0%,which was sensitive to Deoxycycline,Josamycin and Minocycline.CONCLUSION:Rational use of drugs based on drug susceptibility test is of importance to prevent the production of persister of mycoplasma.

Aim To study the inhibitory effect of ginkgolide B (BN52021) on the PAF induced changes of chemotaxis of murine peritoneal macrophages and the related polymerization of F-actin.Methods Chemotaxis assays were performed using a modified 48-well Boyden chamber. Actin polymerization of murine peritoneal macrophages was analyzed by flow cytometry using a specific fluorescent stain. Results Peritoneal macrophages significantly migrated toward platelet-activating factor(PAF) through a micropore filter; however, in the presence of PAF receptor antagonist BN52021 (0. 01the actin polymerization of murine peritoneal macrophages induced by PAF in the presence of Ca2+ , but not in Ca2+ -free medium. Conclusion The results suggested that preventing polymerization of F-actin may be a pathway by BN52021 to inhibit the chemotaxis of macrophages, and this effect seems to be Ca2+dependent. The data further indicated that inhibition of PAF induced macrophage chemotaxis is an important mechanism underlying the anti-inflammatory action of BN52021.

Objective To investigate the anti carcinoma role of integrin targeted photodynamic therapy (PDT) on pancreatic carcinoma cells in vitro.Methods Pancreatic carcinoma cells SW1990 were divided into four groups:cells without quantum dots (QDs) and light-treated as blank control group,pure light-treated group,photosensitizer group and PDT group.The targeting of QDs-arginine,glycine,aspartic acid (RGD) and integrin probe was confirmed by laser confocal microscopy.And as a photosensitizer for photodynamic therapy,after treated for 48 hours the morphology changes of pancreatic carcinoma cells of each group were observed.After 48 hours,the cell proliferation,apoptosis and cell cycle changes were detected by methyl thiazolyl tetrazolium (MTT) assay and flow cytometry (FCM).The expressions of myeloid cell leukemia-1 (Mcl-1),protein kinase B(Akt) and tumor necrosis factor-related apoptosis inducing ligand (TRAIL) were detected by reverse transcriptase polymerase chain reaction(RT-PCR).The amount of reactive oxygen species (ROS) of each group were evaluated by fluorescence probe.One-way ANOVA was performed for comparison between groups to analyze the treatment effects of PDT group.Results The QDs RGD probe could effectively targeting pancreatic carcinoma cells.The MTT results indicated that the relative inhibition rate of pancreatic carcinoma cells proliferation of PDT group was statistically higher than that of the other groups at 24,48,72 h (F=73.00,85.10,126.58; all P＜0.01).The FCM results revealed that the cell apoptosis rate of PDT group (17.860％ ±1.230％) was higher than that of the other groups (F=130.617,P＜0.01) and cell cycle G0/G1 phase (69.14％±2.63％) and S phase (24.41％ ± 2.67 ％) retardance was also significant (all P＜0.05).The expression of proliferation and apoptosis related gene Mcl-1 and Akt at mRNA level was lower than that of the other groups however the expression of apoptosis-inducing ligand TRAIL at mRNA level was higher than that of the other groups (F=567.456,446.817,145.238; all P＜0.05).The ROS level of PDT group was higher than that of the other groups (F=3262.559,P＜0.01).Conclusion PDT with a QDs-RGD probe could significantly inhibit pancreatic carcinoma cell proliferation and promote cell apoptosis.

Objective To investigate the glycosidic linkage and immunomodulating activities of crude polysaccharides from the seeds of Zea mays. Methods Extraction, isolation and purification of polysaccharides were carried out with boiling-water extraction plus resolving deposit repeatedly. The structure was elucidated on basis of physicochemical properties and spectral data, and the biological activities were evaluated by means of Immunopharmacological examination. Results The structure of polysaccharides from the seeds of Z. mays exhibited identical structure with rice bran polysaccharides, i.e., a kind of glucan withα-1,4 andα-1,6 glucosidic bonds as the main frame. Conclusion Polysaccharides was obtained from the seeds of Z. mays for the first time, and it showed significant immunomodulating activity in mice.

This study is to explore the effect of ginkgolide B (BN52021) on the production of nitric oxide (NO), interleukin (IL)-6 and regulated upon activation normal T cell expressed and secreted (RANTES) from astrocytes induced by stimulators. Primary cultured rat astrocytes were stimulated with lipopolysaccharides (LPS), the production of NO was assayed using Griess reaction; U251 cells were stimulated with IL-1 beta, the contents of IL-6 and RANTES in the supernatant were measured using ELISA. The mRNA expressions of IL-6 and RANTES were detected using RT-PCR. LPS (10 ng mL(-1) to 10 microg mL(-1)) could stimulate rat astrocytes to produce NO in a dose-dependent manner. Ginkgolide B at the concentrations of 0.1-10 micromol L(-1) were shown to decrease NO production significantly. IL-1 beta could induce the mRNA expression and protein secretion of IL-6 from U251 cells, as well as RANTES. Ginkgolide B at concentrations of 0.1-10 micromol L(-1) were shown to inhibit RANTES secretion, and to inhibit mRNA expression of IL-6 and RANTES at concentration of 10 micromol L(-1). Ginkgolide B has inhibitory effect on the production of NO, IL-6 and RANTES from astrocytes treated with inflammatory stimulators.

Objective To compare the efficacy and safety of three regiments of transient intensive insulin therapy for type 2 diabetes mellitns: thrice preprandial injection of premixed insulin aspart 30, thrice preprandial injection of insulin aspart and injection of glargine at bedtime, thrice preprandial injection of regular insulin and injection of NPH at bedtime. Methods Patients were randomly divided into 3 groups, treated with 3 kinds of intensive insulin therapy. After achieving the target goal, continuous glucose monitoring system was used to compare the blood glucose level, therapeutic time, dosage of insulin, occurrence of hypoglycemia. Results Detected by continuous glucose monitoring system, there was no statistical difference in average blood glucose [(8.3±2.1,7.5±1.9, 6.8±0.8) mmol/L, P > 0.05], blood glucose area under curve 3 hours (AUC1-3) after breakfast, therapeutic time [ (8.3±2.5, 9.1±3.8, 8.4±1.7)d, P > 0.05], dosage of insulin [(0.63± 80%, P > 0.05) among three kinds of transient intensive insulin therapy. There were no patients complaining of hypoglycemic symptom. Conclusion The short-term efficacy and safety among three intensive insulin therapeutic methods are similar. More attention should be paid to monitor the blood glucose during sleep.

Objective To investigate the modulation of ET-3 on the nuclear factor (NF)-κB/Bfl-1 antiapoptotic pathway in a malignant melanoma cell line A375. Methods Flow cytometry was performed to detect the apoptosis in cultured A375 cells after treatment with ET-3 of 100 nmol/L for 24 hours. ET-3 of various concentrations (0, 1, 10, 100 nmol/L) was used to treat some A375 cells with or without the pretreatment with the ETRB antagonist BQ788; after another 24-hour culture, RT-PCR and Western blot were conducted to examine the mRNA expression of Bfl-1 and protein expressions of Bfl-1 and ETRB, respectively. Results The 24-hour treatment with ET-3 of 100 nmol/L significantly reduced the apoptosis rate of A375 cells (F = 10.68, P ＜0.05). The mRNA and protein expressions of Bfl-1 were up-regulated by ET-3 in a concentration dependent manner (both P ＜ 0.01 ), while BQ788 significantly blocked the ET-3-induced up-regulation (F = 420.38,229.49, both P ＜ 0.01 ). The protein expression of pNF-κB in A375 cells was also enhanced by ET-3 of different concentrations (all P ＜ 0.05), but the enhancement was suppressed by BQ788, and there was a significant difference in the protein expression of pNF-κB between cells treated with ET-3 of 100 nmol/L and those treated with the combination of ET-3 of 100 nmol/L and BQ788 (F = 255.46, P ＜ 0.01 ). Conclusion ET-3/ETRB inhibits the apoptosis in A375 cells likely by activating the NF-κB/Bfl-1 anti-apoptotic pathway.