0.05 and P values in later four groups were

Objective To explore the effect of oxidative stress on human Wiskott-Aldrich syndrome related protein 2 (WAVE2) expression in placental trophoblasts in women with preeclampsia.Methods (1) Twenty women with preeclampsia and twenty-three normal term pregnant women,delivered from August 15,2011 to February 23,2012 in the First Affiliated Hospital of Chongqing Medical University,were recruited and divided into preeclampsia group and control group.Placenta samples were collected after cesarean section.The localization and distribution of WAVE2 in placenta was studied by immunohistochemistry.Quantitative real-time polymerase chain reaction and Western blot were employed to assay the WAVE2 mRNA and protein levels.Tissue homogenates was applied to determine the levels of reactive oxygen species (ROS).The correlation between ROS levels and WAVE2 was also analyzed.(2) An in vitro hypoxia/reoxygenation (H/R) model was utilized to simulate ischemia/reperfusion injury to placental trophoblasts.The HTR-8/ SVneo cells (immortalized human first trimester extravillous trophoblast cells) were pre-incubated overnight,after exposure to H/R or normoxic conditions for 48 hours.Flow cytometry was employed to analyze intracellular ROS level.Meanwhile,Transwell assay was utilized to analyze the invasion and migration of HTR-8/SVneo cells.The location and expression of WAVE2 in trophoblasts was evaluated by cell immunofluorescence and Western blot.Statistical differences between the two groups were evaluated by independent t-tests.Pearson's correlation coefficient test was used for correlation analysis.Results (1)Compared with the control group,preeclampsia group had significantly higher 24-hour proteinuria [(1.96±0.24) g vs (0.08±0.05) g,t=19.436,P＜0.05],systolic blood pressure [(154 ± 13) mm Hg vs (98 ±11) mm Hg,t=11.324,P＜0.05] and diastolic blood pressure [(105±14) mm Hgvs (69±8) mm Hg,t=9.612,P＜0.05].In addition,the placental weight and birth weight of infants in preeclampsia group were significantly reduced as compared to the control group [(432±53) g vs (536±67) g,(2446± 187) g vs (3207± 233) g,t=14.562 and 16.307,allP＜0.05)].The WAVE2 mRNA level (0.28±0.07 vs 1.01±0.02,t=12.747,P＜0.05) and the WAVE2 protein levels (0.63±0.08 vs 1.34±0.19,t=11.648,P＜0.05) were also significantly decreased in preeclampsia groups.The level of ROS in placenta in the preeclampsia group was significantly higher than in control group [(144.22 ± 12.32) nmol/(mg · prot) vs (75.17 ± 8.71) nmol/(mg · prot),t=20.467,P＜0.05].There was significant negative correlation between ROS level and WAVE2 protein expression in preeclamptic placenta (r =-0.726,P =0.000).(2) In vitro study showed that,the levels of ROS in normoxia group and H/R group was (82.9±5.8)％ and (155.6±8.1)％,(t=12.747,P＜0.05).Compared with normoxia condition,decreased cell invasion and migration were found in HTR-8/SVneo cells in H/R group [(51.9 ± 3.3)％ and (58.4 ±4.2)％ respectively,t=11.034 and 13.839,P＜0.05].Results from the cell immunofluorescence showed that WAVE2 protein located in the cytoplasm of HTR-8/SVneo cells,and the expression of WAVE2 protein was significant decreased in HTR-8/SVneo cells after exposure to H/R for 48 h (0.37±0.05 vs 0.76±0.06,t=8.631,P＜0.05).Conclusions Excessive oxidative stress in preeclamptic placentas was correlated with the decreased expression of WAVE2.H/R-induced oxidative stress could decrease WAVE2 expression,which may contribute to impaired trophoblast invasion and migration in preeclampsia.

Objective To explore the characters of behavioral inhibition/activation systems in clinical depressed adolescents.Methods According to CCMD-3 diagnostic criteria,46 depressed adolescents and 35 healthy adolescents were selected and assessed by Behavioral Inhibition/Activation System Scale,Beck Depression Inventory and Hospital Anxiety and Depression Scale.Results (1) Compared with subgroup of mixed depression-anxiety (15.84 ± 2.36),depression only subgroup (13.70 ± 1.72) and control group (12.71 ± 2.55) scored higher in BIS (P＜0.01).And the two depressed subgroups (34.00 ± 4.94,35.88 ± 6.80)scored lower than control group (39.11 ± 5.06) in BAS (P ＜ 0.05).(2) Compared with healthy controls (39.11 ± 5.06),depressed adolescents in first-episode(15.28 ± 1.56) and recurrent (14.96 ±2.63) scored higher in BIS(P＜0.01).Adolescents in recurrent (34.58 ± 6.63) scored lower in BAS(P ＜ 0.01).(3) Compared with healthy controls,medication (15.30 ±2.48) and unmedicated depressed adolescents(14.60 ± 1.82) scored higher in BIS(P ＜ 0.01).Medication adolescents (34.52 ± 5.78) scored lower in BAS (P ＜ 0.01).Conclusion The BIS/BAS of depressed adolescents have their characters.BIS reflects mixed depression and anxiety.BAS reflectsdepression and may be a vulnerable index of clinical depression.

Purpose:To study the efficacy and toxicity of VIDM regimen (vincristine,idarubicin,dexamethasone and melphalan) for refractory or relapsed multiple myeloma(MM).Methods:45 refractory or relapsed MM patients were randomized into two groups: VIDM group(treatment group) had 22 patients treated with VIDM regimen, VAD group(control group) had 23 patients with VAD regimen.Results:The effective rate with VIDM regimen (59.1%) was significantly higher than that of VAD regimen (26.1%) (P

Objective:To study the clinical pathologic,immunophenotypic and clinical and molecular biological characteristics of subcutaneous panniculitic T-cell lymphoma.Methods:The clinical and pathologic features were studied by clinical observation,laboratory test and clinical pathology.Immunophenotypic features were measured by paraffinnimmunoperoxidase with the antibodies of LCA?CD3?UCHL?L26,by freeze section immunoperoxidase with the antibodies of ??TCR???TCR and analysis of the subtype with the antibodies of V 1 ??V 2 ?.T cell receptor-? gene rearrangements were studied by polymerase chain reaction(PCR).Results:Cutaneous node,high fever,loss of body weight appeared in seven patients and hemophagocytic syndrome in five patients.Imbalance of dielectric,acid and basic,abnormality of the enzyme involvement of the subcutaneous fat in a lacelike pattern with neoplastic cells were seen in all patients.The expression of LCA?CD 3?UCHL occurred in all patients,but no L26.The expression of ??TCR was found in three patients whose ??TCR was V 2+ ? and the expression of ??TCR was found in one of four patients.T cell receptor-? gene rearrangements were seen in three patients.Conclusion:SPTCL is a critical disease.The tumor cells origin from V 2+ ? of T-lymphocyte relating to cutaneous lymphotissue.T cell receptor-? gene rearrangements may happened in SPTCL patient.

Objective To investigate colonization of multidrug-resistant organisms (MDROs)in neonatal intensive care unit (NICU)newborns on admission.Methods From April to November 2013,293 newborns who admitted to NICU of a hospital were screened for methicillin-resistant Staphylococcus aureus (MRSA)by nasal and throat swabs and for extended-spectrumβ-lactamases (ESBLs)bacteria and vancomycin-resistant Enterococcus (VRE)by anal swabs.Results Of 293 newborns,61 were detected MDROs (20.82%).The positive rate of MDROs screening in newborns aged <3 days(5.92%)was lower than those aged <3-6 days(37.74%)and 7-28 days (43.66%), the difference was significant (P =0.000).The major colonized MDROs were ESBLs-producing bacteria(83.60%), the major colonized site was anus(88.52%).Conclusion Neonatal anus and stool are important sources of MDROs in NICU;more attention should be paid to colonization screening for MDROs by anal swabs in newborns aged >3 days,and appropriate isolation measures should be taken for positive screening patients to prevent the transmission of MDROs.

AIM: Through detecting bone marrow angiogenic mediators and inhibitors in aplastic anemia(AA) patients,the value of angionesis in AA pathogenesis was elucidated.METHODS: The patients were divided into severe AA group(SAA,8 patients),non severe AA group(NSAA,10 patients),and normal control group(7 persons),5 patients were observed before treating(group beginning) and getting improvement(group improving).The angiogenic mediators vascular endothelial growth factor(VEGF) and bFGF were detected by ELISA,angiogenic inhibitors IFN? and TSP were detected by ELISA and flow cytometry,respectively.RESULTS: The levels of VEGF were lower in SAA group and NSAA group than those in control group significantly(P

Adult ; Aged ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Female ; Fibroblast Growth Factor 2 ; metabolism ; Humans ; Laryngeal Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Staging ; Receptors, Fibroblast Growth Factor ; metabolism

Objective:To study the influence and mechanism of thalidomide on bone marrow hematopoietic progenitor cells in multiple myeloma patients and in normal controls.Methods:Bone marrow GM CFU, E CFU and MK CFU from multiple myeloma patients and from normal controls were cultured in methylcellulose semisolid medium in vitro after being treated by different concentration of thalidomide. IFN ? and TNF ? concentration in cell suspension of bone marrow hematopoietic progenitor cells from multiple myeloma patients and from normal controls were measured by ELISA.Results:Thalidomide inhibited GM CFU in multiple myeloma patients and in normal controls at concentration higher than 200 and 100 ?g/ml, respectively, and inhibited MK CFU in multiple myeloma patients and in normal controls at concentration higher than 300 ?g/ml and 150 ?g/ml, respectively. However, there was no significantly influence of thalidomide on E CFU in multiple myeloma patients and in normal controls at concentration between 10 and 400 ?g/ml. Thalidomide increased IFN ? concentration in cell suspension of bone marrow hematopoietic progenitor cells from multiple myeloma patients and from normal controls at concentration greater than 100 and 200 ?g/ml, respectively. The level of thalidomide of higher than 300 ?g/ml reduced TNF ? concentration in cell suspension of bone marrow hematopoietic progenitor cells from multiple myeloma patients.Conclusion:Different concentrations of thalidomide have different influences on the hematopoietic function of bone marrow hematopoietic progenitor cells in multiple myeloma patients and in normal controls, probably mediated through increased IFN ? by thalidomide.

Objective:To investigate influence of Fludarabine to lupus activity of lupus mice and the effectiveness and safety of Fludarabine on the treatment of BXSB lupus mice and their possible methanism Methods:Fludarabine of 30 mg/(m 2?d) was injected into BXSB by tail vein,3 days continuously Results of treatment was observed through counting number of peripheral blood WBC Anti ds DNA and anti nuclear antibody in BXSB serum was measured by ELISA Pathologic transformation of kidney or urine protein was measured by immunofluorescence or urine protein test paper after treated by Fludarabine Expression of CD4 +Fas +?CD8 +Fas +?CD45RO + Fas + on T lymphocyte were measured by flowcytometry Results:The number of peripheral blood WBC of BXSB mice began to decline from the third day after treated by Fludarabine The lowest value 〔0 5?0 2)?10 9 L -1 〕of the number of peripheral blood WBC appeared on the seventh day and on the nineteenth day the number of peripheral blood WBC was up to 1 0?10 9 L -1 after treated by Fludarabine The falling of anti ds DNA and anti nuclear antibody in BXSB serum appeared on the fourteenth and twentieth one day after treated by Fludarabine, respectively Reduction of from +～++ turning?kindey immunofluorescence were 72 7% in group of Fludarabine Reduction of protein urine from ++～+++ turning ?～ - appeared on the twentieth one and twentieth eight days Reduction of expression of CD4 +Fas +?CD8 +Fas +?CD45RO + Fas + on T lymphocyte was obvious after treated by Fludarabine Conclusion:Fludarabine can evidently reduce the serum level of anti ds DNA and anti nuclear antibody of BXSB and reduce injury of kidney and formation of protein urine So Fludarabine may have good curative effect to severe SLE Fludarabine can reduce expression of CD4 +Fas +?CD8 +Fas +?CD45RO + Fas + on T lymphocyte,which may be one of methanism of Fludarabine to SLE