Objective To better understand the regulation of the soluble receptor of vascular endothelial growth factor (VEGF), s-VEGFR-1 (or soluble fms-like tyrosine kinase, SFlt-1), in angiogenetic process in endometriosis. Methods Levels of free VEGF and s-VEGFR-1 were measured by enzyme-linked immunosorbent assay (ELISA) in peritoneal fluid from 28 subjects with surgically confirmed endometriosis, and 10 controls with no clinical evidence of the disease and other diseases. Meanwhile, we calculated a VEGF activity index by means of the ratio VEGF/s-VEGFR-1. Results We found higher VEGF concentration in endometriotic lesions than controls (P0.05). VEGF activity index in controls, stage Ⅰ-Ⅱ and stages Ⅲ-Ⅳ of endometriosis was 0.310, 0.276 and 0.273, respectively. VEGF and s-VEGFR-1 concentration were also higher in proliferative phase than in secretory phase in endometriotic lesions (P

Objective:In order to explore the anti inflammatory mechanisms of ? melanocyte stimulating hormone (? MSH), the effects of ? MSH on the production of NO and proinflammatory cytokines in astrocytes induced by LPS were investigated Methods:Rat brain astrocytes cultured in vitro were stimulated with LPS or given ? MSH with LPS stimulation NO produced in astrocytes was tested with Griess reagent IL 1, IL 6 and TNF ? secreted from astrocytes were examined by MTT assay The expression of macrophage migration inhibitory factor (MIF) mRNA was examined with semiquantitative RT PCR analysis Results:The production of NO, IL 1, IL 6, TNF ? and the expression of MIF mRNA were significantly increased in astrocytes stimulated with LPS If giving ? MSH with LPS stimulation, the production of NO, IL 1, IL 6, TNF ? and the expression of MIF mRNA were markedly decreased Conclusion:[WT5”,6BZ]It is suggested that the inhibitory actions of ? MSH on the production of NO and proinflammatory cytokines in astrocytes are related to the inhibitory effects of ? MSH on inflammation in central nervous system

Objective To investigate the association among cerebral lesions, mild cognitive impairment and artery stenosis.Methods In 685 cases which seek medical care in our hospital in recent years, we studied the cortical infarction lesions in this study, analysis of subcortical infarction in patients with cognitive impairment as well as the composition of the artery stenosis conditions were conducted .Results in this study, subcortical infarct patients with mild disturbance of consciousness accounted for 9.20%, while blood supply stenosis cases accounted for 49.34%.Elder than 70 years, long course of subcortical infarction, family history of alcohol consumption and dementia were associated with cortical (P <0.05), the incidence of subcortical infarct and mild cognitive disturbance were 2.138 times for infarct and mild disturbance of consciousness patients.Multivariate regression analysis showed that family history of hypertension and cerebrovascular disease were also risk factors.In addition, mild cognitive impairment can increase the risk of subcortical infarct and the incidence of vascular stenosis, OR was 2.077;elder than 70 years of age, subcortical infarct length, hypertension and family history of cerebrovascular disease were risk factors for subcortical infarction and stenosis of blood supply.In multivariate regression analysis, mild cognitive impairment, long duration of subcortical infarct, overweight and obesity, and hypertension showed to be risk factors of subcortical infarct and blood supply stenosis.Conclusion The artery stenosis and subcortical infarction with mild cognitive impairment show a positive correlation, while the presence of mild cognitive impairment and subcortical infarction and artery stenosis and an increased risk of an association, are related to each while age, duration and associated subcortical infarcts family history and other factors also affect the potential relationship between them .

For medical student, diagnostic practice is the first step of clinical study. To penetrate the humanities education in diagnostic teaching,the combination with practice from the following steps as physical examination, laboratory examination and interrogation, would cultivate medical students' humane quality imperceptibly and play an important role in creating noble medical ethics of them.

[Objective] To explore the risk factors for mortality of bloodstream infections in the patients with hematologic diseases,so as to provide evidence for reasonable and effective application of treatments.[Methods] The clinical data of 242 cases of bloodstream infections who were hospitalized from Jan 2012 to Jun 2016 were analyzed retrospectively,then the analysis was performed for risk factors.The statistical analysis was processed by SPSS 19.0.[Results] A total of 266 strains of pathogens were isolated,including 99 strains of gram-positive bacteria,accounting for 37.2％,and 164 strains of gram-negative bacteria,accounting for 61.7％.Multivariate analysis showed that the significant independent risk factors for mortality were active states of hematologic diseases (P =0.007,OR =5.622,95％ CI 1.586 ～ 19.924),presentation with septic shock(P =0.007,OR =4.978,95％ CI 1.560 ～15.884),cardiac insufficiency (P =0.001,OR =11.878,95％ CI 2.760 ～ 51.120),level of albumin less than 35 g/L (P =0.036,OR =3.468,95％ CI 1.087 ～ 11.066),polymicrobial infection (P =0.010,OR =6.024,95％ CI 1.540 ～ 23.563),and Staphylococcus haemolyticus (P =0.001,OR =19.308,95％ CI 3.392 ～ 109.888)/Enterococcus (P =0.002,OR =15.266,95％ CI 2.817 ～82.728) infection.The survival curves show that the inappropriate initial antimicrobial therapy group or presentation with any one of the independent risk factors had a lower probability of survival than the control group.[Conclusions] Bloodstream infections in patients may cause high mortality rate,so it is necessary that we use antibiotic reasonably and spare no effort to reduce the mortality rate by appropriate application of antimicrobial therapy and effective intervention of the risk factors.

Objective To detect the expression of VEGF in NHL and analyze the relation of the expression levels with malignant aggressiveness,treatment response,and prognosis.Methods The expression of VEGF in lymph nodes taken from 39 NHL patients Wag measured by immunohistochemical-staining method.9 patients with benign lymphadenopathy were acted as control.Results The expression of VEGF in NHL(79.5%)was higher than that in the contrel(44.4%)(P=0.048＜0.05).In NHL,the VEGF level was higher in aggressive lympboma than that in indolent lymphoma(x2=5.284,P=0.044＜0.05).The patients had the higher-level expression as the Ann Arbor stage Wag higher,and the patients who had the higher-level expression of VEGF had higher serum LDH level,lower chemotherapy remission,unfavorable prognosis and lower 3-year survival (P＜0.05).Conclusion The expression of VEGF in NHL was increased.It was correlated with histopathological grade,Ann Arbor stage,chemotherapy response and prognosis.

Objective To investigate the effect of membrane-bound prostaglandin E2 synthase 1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60/A cells.Methods Flow cytometry,Western blot and ELISA were used to measure the difference of cell cycle,expression of cyclin D1, mPGES-1 among HL-60/A cells,MNC and HL-60 cells.The effect of MK886 on cell cycle,cyclin D1,mPGES-1,PGE2,P-Akt and c-myc of HL-60/A cells were observed.Results Compared with MNC and HL-60 cells,the expression of cyclin D1 and mPGES-1 were higher in HL-60/A cells,the percentage of G0-G1 phase was decreased [MNC (62.63±6.58) ％,HL-60 (38.86±2.25) ％,HL-60/A (30.53±2.15) ％]and S phase increased[MNC (12.18±4.43) ％,HL-60 (47.70±1.88）％,HL-60/A (57.56±1.54) ％](all P＜ 0.05).After treated with MK886,cell cycle was arrested in G0-G1 phase.The expression of mPGES-1,cyclin D1,P-Akt and c-myc and synthesis of PGE2 were decreased.Conclusion MK886 can arrest HL-60/A cell cycles in G0-G1 phase,which possibly through down-regulation of mPGES-1/PGE2,reduction cyclin D1,P-Akt and c-myc expression.

Objectiye To investigate the effect of selective COX-2 inhibitor, nimesulide, on inhibiting proliferation of the human acute myeloid leukemia HL-60 cells. Methods HL-60 cells were treated with different concentration of nimesulide. HL-60 cell proliferation was examined by CCK-8 method. Flow cytometry, Western blotting and ELISA were used to measure the effect of nimesulide on apoptosis, cell cycle,COX-2, PGE2, bax, bcl-2 and c-myc. Results Nimesulide inhibited HL-60 cells proliferation in a dose and time dependence manner. Nimesulide induced cell apoptosis and arrested cell cycle in G0-G1 phase. The expression of COX-2 protein declined after treated with nimesulide 48 h, the total apoptosis in 100, 200,400 μmol/L nimesulide-treated group and control group were (24.97 ± 6.36) %, (34.22 ± 5.76) %, (44.59 ±6.69) % and (4.11 ± 1.26) %, there were significant differences (P ＜ 0.05). Nimesulide inhibited the synthesis of PGE2, the expressions of bcl-2 and c-myc protein and upregulated the expression of bax protein simultaneity.Conclusion Nimesulide significantly inhibited the proliferation of HL-60 cells and induced cell apoptosis,which may be associated with the downregulation of COX-2 expression, reduction of PGE2 synthesis, arrest of cell cycle and regulation bcl-2, c-myc and bax protein expression.

Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.

Objective Our preliminary study demonstrates that quercetin can inhibit the proliferation of HL-60 cells. This sudy aimed to find some drugs which could have synergistic effects with quercetin on apoptosis of HL-60 cells. Methods HL-60 cells were cultured with bortezomib at different concentrations (1, 2, 4, 8, 16, and 32μmol/L) alone or combined with quercetin at different concentrations for 48 h. HL-60 cells were cultured with lenalidomide at different concentrations (5, 10, 20, 40, 80, 160, and 320 μmol/L) alone or in combination with quercetin at different concentrations for 48 h. The CCK-8 assay was used to determine the effects on proliferation of HL-60 cells. Results Bortezomib significantly inhibited the proliferation of HL-60 cells (P<0.01). IC50 of quercetin was 49.24μmol/L after cells treated by quercetin combined with bortezomib, which was 13.44μmol/L lower than that treated by quercetin alone. Isobolographic analysis revealed the two drugs had synergistic effect. The results of cell viability of HL-60 cells treated by lenalidomide at lower concentrations (5, 10, 20, 40, and 80μmol/L)were not different from those of the control group (P > 0.05). The results of cell viability of HL-60 cells treated by lenalidomide at higher concentrations (160 and 320μmol/L) were lower than those of the control group (P<0.05). IC50 of quercetin after cells treated by quercetin combined with bortezomib was not different from that treated by quercetin alone. Isobolographic analysis revealed the two drugs had no synergistic effect. Conclusions Bortezomib can inhibit the proliferation of HL-60 cells and it has a synergistic effect with quercetin on HL-60 cells. Lenalidomide has a weaker role in inhibition of the proliferation of HL-60 cells, and it has no synergistic effect with quercetin on HL-60 cells.