Obesity increases the risk of ovarian cancer,and it is associated with the poor prognosis of ovarian cancer.Its pathogenic mechanism may be associated with the increased level of serum estrogen,insulin and insulin-like growth factors-1 induced by obesity and a variety of adipocytokines,which has an impact on the therapeutic result and prognosis of ovarian cancer.Maintaining a proper weight may prevent the development of ovarian cancer.

Objective The impact of complement Clq on inflammation in beta amyloidstimulated microglia.Methods After the cultured BV-2 microglial cells were treated with 100mg/L beta-amyloid fibers (fAβs),some of them were given C1q,others wcrc given C1q and C1qA.Then,interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) in the supernatant and cell lysate were determined by the sandwich ELISA.Results A significant increase in TNF-α started at giving 50 nmol/L C1q after 100 mg/L fAβs (F =1177.27,P＜ 0.05),while the release of TNF-α was significantly suppressed by using 50 nmol/L C1qA on basis of this(P＜0.05).The level of IL-6 showed no above change.Conclusions C1q may enhance the inflammation of Aβ-induced BV-2 microglia cells and TNF-α may play important role in this effect.

Objective To investigate Monilia infection and adverse pregnancy outcomes of pregnant women in labor.Methods Before informed consent,542 cases of pregnant women in labor were collected in Obstetrics Department of Maternity and Child Healthcare of Maoming City from January 2013 to April 2014,and all of these cases were examined by Monilia inspec-tion of vaginal secretions.All of these cases were 20 to 30 years old,without vaginal pathogenic infection symptoms,but in-cluded in a few of formulation of clinical features of vaginal Candida infection.With the two methods of 10% potassium hy-droxide solution wet sheet and Gram staining,if blastospore or pseudohypha of Candida mycoderma were found out in the two methods under microscope,this case was diagnosed as positive result,otherwise as negative result.Respectively choosing positive cases as observation group,and negative cases as control group,the indexes of premature rupture of membranes,per-ineum wound infection,neonatal thrush and neonatal diaper rash of the two groups were recorded.The statistical method:e-numeration data by chi-square test,measurement data using analysis of varianc.Results The positive rate of Monilia was 23.1% (125/542),higher than 19.3% reported in domestic.The incidence rates of neonatal diaper rash,premature rupture of membranes,neonatal thrush and perineum wound infection of the observation group were respectively 19.2%,8.0%, 16.8% and 12.8%,all much higher than the control group respectively was 8.4%,1.2%,3.8% and 1.7%,(χ2 =12.578~29.273,all P <0.01).Conclusion Monilia infection of pregnant women in labor could increase the chance of adverse preg-nancy outcomes.Healthy or clinical doctors should suggest that pregnant women early carry out routine examination and ear-ly treatment,in order to prevent adverse pregnancy outcomes.

Objective:To evaluate association of peripheral blood brain-derived neurotrophic factor (BDNF) with Alzheimer's disease (AD) .Methods:Databases including Pubmed, Cochrane library, Web of science, Embase, China National Knowledge Infrastructure, CBM disc, VIP-CSTJ and Wanfang Data were used to collect case-control studies related to the concentration of BDNF in peripheral blood of dementia patients with Alzheimer's type(DAT) and mild cognitive impairment(MCI). After extracting data and appraising the quality of the included studies, meta-analysis were conducted using Review Manager 5.3 and CMA 3.0.Results:A total of 51 articles were included in the analysis, with a total subjects of 7 182, including 2 673 subjects in DAT group, 1 506 subjects in MCI group, and 3 003 subjects in control group.The Meta-analysis showed that the levels of peripheral blood BDNF in patients with DAT were significantly lower than normal control group(SMD=-0.71, 95% CI : -0.99--0.43, P<0.001) ( n=5 111), and there were no statistical differences in peripheral blood BDNF levels between MCI group and control group and between DAT group and MCI group.The subgroup analysis showed that the level of serum BDNF in patients with DAT (SMD=-0.85, 95% CI: -1.15--0.55, P<0.001)( n=4 425) and MCI(SMD=-0.38, 95% CI: -0.62--0.14, P=0.002)( n=2 476) was significantly lower than that in normal control group, and the level of serum BDNF (SMD=-0.76, 95% CI: -1.37--0.16), P=0.01)( n=1 630) in patients with DAT was lower than that in MCI; However, there were no statistical difference among DAT, MCI and control groups in the level of plasma BDNF( P>0.05). Conclusion:The patients with DAT and mild cognitive impairment have lower level of serum BDNF, which suggesting that serum BDNF level may be a potential biomarker for early diagnosis of AD.

Objective:To explore the protective effect and mechanism of Tongfu Lifei decoction (TFL) on human monocytic leukemia cell THP-1 induced by lipopolysaccharide (LPS).Methods:① THP-1 cells were cultured in vitro, and incubated with 1 mg/L LPS for 18 hours to construct an in vitro THP-1 cell inflammation model. Other THP-1 cells were taken as blank control group. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) secreted by cells. ② THP-1 cells were divided into seven groups and treated with 0, 0.005, 0.01, 0.02, 0.04, 0.08, and 0.16 mL/mL TFL for 24 hours (added different dosages of TFL solution per milliliter of culture medium, with a crude drug content of 1 kg/L). The cell survival rate was detected using methyl thiazolyl tetrazolium (MTT) colorimetric method, and the intervention dosage of TFL for its non-toxic effect on THP-1 cells was screened. ③ Another THP-1 cells were divide into inflammatory model group and 0.01, 0.02, and 0.04 mL/mL TFL groups according to the intervention dosage of TFL screened by MTT colorimetry. After 24 hours of intervention, the levels of TNF-α and IL-6 secreted by cells were measured using ELISA. Western blotting was used to detect the expressions of programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) signaling pathway proteins in cells. Real time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expressions of microRNAs (miR-146a, miR-146b, miR-155) in cells. ④ The maximum non-toxic concentration of TFL (0.04 mL/mL) on the THP-1 cell was selected as the intervention dose. THP-1 cells were divided into inflammation model group, TFL group, TFL+miR-146a inhibitor group, TFL+miR-146b inhibitor group, and TFL+miR-155 inhibitor group. The inflammation model group was not given any drug intervention. The other inhibitor groups were added 100 nmol/L corresponding inhibitor. After 24 hours of intervention, the levels of TNF-α and IL-6 secreted by cells were measured using ELISA. Western blotting was used to detect the expressions of PD-1/PD-L1 signaling pathway proteins in cells. Results:① Compared with the blank control group, the levels of TNF-α and IL-6 secreted by cells in the inflammatory model group were significantly increased, indicating the successful construction of the THP-1 inflammatory cell model in vitro. ② 0-0.04 mL/mL TFL had no toxic effect on THP-1 cells. However, the survival rates of cells in the 0.08 mL/mL and 0.16 mL/mL TFL groups were significantly lower than those in the inflammation model group, indicating that TFL dosages exceeding 0.04 mL/mL had toxic effects on THP-1 cells. ③ Compared with the inflammation model group, 0.01 mL/mL TFL had no significant effect on the levels of TNF-α and IL-6 secreted by THP-1 cells, while intervention with 0.02 mL/mL and 0.04 mL/mL TFL significantly reduced the levels of TNF-α and IL-6 secreted by cells [TNF-α(ng/L): 95.89±8.55, 70.73±11.70 vs. 137.10±7.19, IL-6 (ng/L): 23.03±2.55, 16.58±1.72 vs. 32.60±2.55, all P < 0.01]. Compared with the inflammation model group, the expressions of PD-1/PD-L1 signaling pathway proteins in THP-1 cells in different dosages of TFL groups were significantly reduced, and showed a certain dosage dependence. The expressions of the pathway proteins in the 0.04 mL/mL TFL group were significantly lower than those in the inflammation model group [PD-1 protein (PD-1/β-actin): 0.28±0.04 vs. 1.00±0.10, PD-L1 protein (PD-L1/β-actin): 0.54±0.05 vs. 1.00±0.08, phosphoinositide 3-kinase (PI3K) protein (PI3K/β-actin): 0.28±0.03 vs. 1.00±0.08, phosphorylated protein kinase B (p-Akt) protein (p-Akt/Akt): 0.38±0.04 vs. 1.00±0.10, all P < 0.01]. Compared with the inflammation model group, the expression of miR-146a in THP-1 cells in the 0.01, 0.02, and 0.04 mL/mL TFL groups was significantly reduced (2 -ΔΔCt: 0.46±0.11, 0.31±0.13, 0.23±0.14 vs. 1.01±0.18, all P < 0.01), while there was no significant change in the expressions of miR-146b and miR-155. ④ Compared with the inflammation model group, the TFL group showed a significant decrease in the levels of TNF-α and IL-6 secreted by THP-1 cells. The miR-146a inhibitor could significantly reverse the inhibitory effect of TFL on inflammatory factors, and the difference was statistically significant as compared with the TFL group [TNF-α (ng/L): 138.55±10.30 vs. 72.33±10.59, IL-6 (ng/L): 31.35±3.98 vs. 15.75±3.76, both P < 0.01]. Compared with the inflammation model group, the expressions of PD-1/PD-L1 signaling pathway proteins in THP-1 cells in the TFL group were significantly reduced. The expressions of pathway proteins in cells in the TFL+miR-146a inhibitor group were significantly higher than those in the TFL group [PD-1 protein (PD-1/β-actin): 0.85±0.09 vs. 0.37±0.04, PD-L1 protein (PD-L1/β-actin): 0.83±0.08 vs. 0.55±0.06, PI3K protein (PI3K/β-actin): 0.85±0.09 vs. 0.63±0.06, p-Akt protein (p-Akt/Akt): 0.98±0.10 vs. 0.75±0.07, all P < 0.05]. Conclusion:TFL regulates the expression of miR-146a to inhibit the PD-1/PD-L1 signaling pathway in THP-1 cells, regulates the immune barrier of sepsis induced in cell inflammation model in vitro, and thus protects LPS induced THP-1 cells.