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<p><b>OBJECTIVE</b>To study the impacts of pre-pregnancy maternal BMI and gestational weight gain(GWG) on pregnancy outcomes.</p><p><b>METHODS</b>We adopted a prospective cohort study with cluster sampling in single pregnant women, who were not with hypertension, diabetes, hyperlipidemia or other diseases in the previous history, neither did they have diseases of heart, liver, kidney, thyroid etc. related to current pregnancy. Those pregnant women who visited the prenatal nutrition clinic under 'informed consent' were surveyed with questionnaire to track their peri-natal complications, delivery mode and neonate birth outcomes etc. Pearson and partial correlations, chi-square test and binary logistic regression were used to study the association between pre-pregnancy maternal BMI, GWG and pregnancy outcomes.</p><p><b>RESULTS</b>A total of 623 pregnant women were recruited in the cohort, with 592 (95%) of them eligible for analysis. Results from the Multivariate Logistic Regression analysis indicated that, after controlling the potential confounding factors, when compared to women with pre-pregnancy BMI between 18.5 and 24.0, the odds ratios (ORs) for low birth ponderal index (PI) were 2.34 [95% confidence interval (CI), 1.24-4.42)]among those with BMI<18.5, respectively, while 2.73 (1.12-6.68) for high birth PI among those with BMI > 24.0. Similarly, when compared to pregnant women with normal GWG(defined as weight gain range from P15 to P85 by stratification of pre-pregnancy BMI), low GWG (<P15) seemed to be the risk factor for preterm birth, low birth weight, gestational diabetes mellitus, with low birth PI [ORs as 4.85(1.35-17.51), 10.30 (2.29-46.35), 2.29 (1.07-4.93) and 2.65(1.24-5.68), respectively. High GWG (>P 85)appeared the risk factor for high birth weight, high birth PI, and gestational diabetes mellitus, with ORs as 3.83(1.74-8.44), 2.39(1.14-5.01)and 2.21(1.07-4.55), respectively.</p><p><b>CONCLUSION</b>Low or high pre-pregnancy maternal BMI and GWG were associated with adverse pregnancy outcomes.</p>
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Adolescent , Adult , Female , Humans , Infant, Newborn , Pregnancy , Young Adult , Birth Weight , Body Weight , Follow-Up Studies , Pregnancy Outcome , Prospective Studies , Risk Factors , Weight GainABSTRACT
Objective To study the impacts of pre-pregnancy maternal BMI and gestational weight gain(GWG)on pregnancy outcomes. Methods We adopted a prospective cohort study with cluster sampling in single pregnant women,who were not with hypertension,diabetes,hyperlipidemia or other diseases in the previous history,neither did they have diseases of heart,liver,kidney,thyroid etc. related to current pregnancy. Those pregnant women who visited the prenatal nutrition clinic under‘informed consent’were surveyed with questionnaire to track their peri-natal complications,delivery mode and neonate birth outcomes etc. Pearson and partial correlations,chi-square test and binary logistic regression were used to study the association between pre-pregnancy maternal BMI,GWG and pregnancy outcomes. Results A total of 623 pregnant women were recruited in the cohort,with 592(95%)of them eligible for analysis. Results from the Multivariate Logistic Regression analysis indicated that,after controlling the potential confounding factors,when compared to women with pre-pregnancy BMI between 18.5 and 24.0,the odds ratios(ORs)for low birth ponderal index(PI) were 2.34[95%confidence interval(CI),1.24-4.42)]among those with BMI<18.5,respectively,while 2.73(1.12-6.68)for high birth PI among those with BMI>24.0. Similarly,when compared to pregnant women with normal GWG(defined as weight gain range from P15 to P85 by stratification of pre-pregnancy BMI),low GWG(<P15)seemed to be the risk factor for preterm birth,low birth weight,gestational diabetes mellitus,with low birth PI [ORs as 4.85(1.35-17.51),10.30 (2.29-46.35),2.29(1.07-4.93) and 2.65(1.24-5.68),respectively. High GWG(>P85)appeared the risk factor for high birth weight,high birth PI,and gestational diabetes mellitus,with ORs as 3.83(1.74-8.44),2.39(1.14-5.01) and 2.21(1.07-4.55),respectively. Conclusion Low or high pre-pregnancy maternal BMI and GWG were associated with adverse pregnancy outcomes.
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Objective To study the impacts of pre-pregnancy maternal BMI and gestational weight gain(GWG)on pregnancy outcomes. Methods We adopted a prospective cohort study with cluster sampling in single pregnant women,who were not with hypertension,diabetes,hyperlipidemia or other diseases in the previous history,neither did they have diseases of heart,liver,kidney,thyroid etc. related to current pregnancy. Those pregnant women who visited the prenatal nutrition clinic under‘informed consent’were surveyed with questionnaire to track their peri-natal complications,delivery mode and neonate birth outcomes etc. Pearson and partial correlations,chi-square test and binary logistic regression were used to study the association between pre-pregnancy maternal BMI,GWG and pregnancy outcomes. Results A total of 623 pregnant women were recruited in the cohort,with 592(95%)of them eligible for analysis. Results from the Multivariate Logistic Regression analysis indicated that,after controlling the potential confounding factors,when compared to women with pre-pregnancy BMI between 18.5 and 24.0,the odds ratios(ORs)for low birth ponderal index(PI) were 2.34[95%confidence interval(CI),1.24-4.42)]among those with BMI<18.5,respectively,while 2.73(1.12-6.68)for high birth PI among those with BMI>24.0. Similarly,when compared to pregnant women with normal GWG(defined as weight gain range from P15 to P85 by stratification of pre-pregnancy BMI),low GWG(<P15)seemed to be the risk factor for preterm birth,low birth weight,gestational diabetes mellitus,with low birth PI [ORs as 4.85(1.35-17.51),10.30 (2.29-46.35),2.29(1.07-4.93) and 2.65(1.24-5.68),respectively. High GWG(>P85)appeared the risk factor for high birth weight,high birth PI,and gestational diabetes mellitus,with ORs as 3.83(1.74-8.44),2.39(1.14-5.01) and 2.21(1.07-4.55),respectively. Conclusion Low or high pre-pregnancy maternal BMI and GWG were associated with adverse pregnancy outcomes.
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Objective: Medical therapy to prevent persistent ectopic pregnancy (PEP) after conservative laparoscopic operation was investigated. Methods:236 patients with ectopic pregnancy were divided into three groups according to the time of hospitalization. 83 cases were in group A, hyperosmolar glucose was injected into the fallopian tube lumen after laparoscopic salpingostomy. 81 cases were in group B, MTX was injected in the same way, 72 cases were in group C as control group. Serum β-HCG was tested for four times, before the operation, the first, third and a week after the operation respectively. Results:There were 6 patients of PEP in this study. One patient in group A, one patient in group B, the rest four patients in group C. The incidence of PEP was not statistically significant between group A and B( P>0. 05), while the difference was significant between group A and C ( P<0. 05). Serum β-HCG in three groups descended significantly in the first 24 hours after operation, but there were no differences among these groups. As for the descending of β-HCG in day 3 and 7, there was no difference between group A and B, but the difference was magnificent between group A and C( P < 0.05). Conclusions: Compared with the MTX, hyperosmolar glucose is an effective and safer method to prevent PEP.
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Objective To study the change of TLR4 on peripheral blood monoeytes (PBMCs) and its role in the pathogenesis of chronic severe hepatitis B. Methods The expression of TLR4 on 10000 CDI4 + PBMCs was determined by flow eytometer in 30 healthy control,31 patients with chronic hepatitis B and 30 patients with chronic severe hepatitis B. The level of serum tumor necrosis factor α(TNF- α) was determined by ELISA. Results The values of TLR4 on PBMCs and serum TNF-αof the groups of healthy control, patients with chronic hepatitis B and patients with chronic severe hepatitis B were 2.3±1.1,3.7±2.3, (6.9±4.1 ) mean fluorescence intensity (MFI) and (53.8±38.1 ), ( 164.3±89.9) and (359.8±140.0) ng/L. The TLR4 value in patients with chronic severe hepatitis B was signifi- cant higher than those in healthy control and the patients with chronic hepatitis B ( P <0.05). However, there was no significant difference between the patients with chronic hepatitis B and healthy control ( P > O. 05 ). TNF-α increased gradually and significantly from the healthy control to the patients with chronic hepatitis B and patients with chronic severe hepatitis B. There was a significant positive correlation be- tween the value of TLR4 and the value of serum TNF-αin the patients with chronic severe hepatitis B( r=0.666, P <0.01). Conclusion There may be a role of TLR4 in the pathogenesis of chronic severe hepatitis B.
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Objective To observe the effects of 5-fluorouraeil(5-FU)and eisplatin(DDP)on the expression of Toll-like receptor 2 (TLR2)and Toll-like receptor4(TLR4)in hepatocellular carcinoma cell lines HepG2 and HepG2.2.15.Methods Direct immanotlaorescenee flow cytometry was used to detect mean flubrescence intensity(MFI)of TLR2 and TLR4,and TLR2 and TLR4 positive cell percentage in HepG2 and HepG2.2.15 cells before and after treated with 5-FU.and DDP at various concentrations for 24h,48h and 72h.Results MFI of TLR2 and TLR4.and TLR2 and 11LR4 positive cell percentage in HepG2.2.15 cells were significantly higher than those in HepG2(P＜0.01).After HepG2 and HepG2.2.15 cells were treated with different concentration of 5-FU and DDP,MFI of TLR2 and TLR4,TLR2 and TLR4 positive cell percentage in HepG2 and HepG2.2.15 cells almost had no change.only MFI of TLR2 in HepG2.2.15 cells decreased after cells were treated with 5-FU at the concentrations of 100,200μg/ml and DDP at the concentrations of 20μg/ml for 72h(P＜0.05 for all).Conclusions 5-FU and DDP can not activate TLR2 and TLR4 signal pathway in hepatocellular carcinoma cell lines HepG2 and HepG2.2.15.To find the activated pathway in TLR2 and TLR4 signal pathway,some other methods should be used,and this will be helpful in antieancer therapy.
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Objective To investigate the role of TLR4 in the pathogenesis of chronic hepatitis B(CHB) by study the expression of TLR4 in liver tissues in patients with CHB, and the relationship among TLR4 and serum HBV DNA level, clinical severity degrees and histo-logical grades and stages. Methods Expression of TLR4 in liver tissues was semi-quantitatively determined by immunohistochemistry and e-valuated by a scoring system in 75 patients with CHB and 10 health controls. Results The positive staining of TLR4 mainly located in the cytoplasm and some on cell membrane of bepatocytes. Expression of TLR4 in the liver tissues of patients with CHB was stronger than that of health controls. The scores of TLR4 expression in patients with mild, moderate and severe CHB were 1.0±0.5,2.3±0.5 and 2.9±0.4. The scores increased gradually and significantly along with the increase of clinical severity degrees( F = 104.8, P<0.01). The scores of TLR4 expression in the liver tissues of patients with CHB were positively correlated with the clinical severity degrees (r=0.838, P<0.01) and histological grades (r=0.579, P<0.05), but not correlated with Lg (serum HBV DNA) or histological stages. Conclusion TLR4 was up-regulated in the hepatocytes of patients with CHB. There may be a role of TLR4 in the pathogenesis of CHB.
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Objective To study the effect of matrine on the expression of a proliferation-inducing ligand (APRIL) in colorectal cancer cell line (SW480 cell). Methods MTT assay was used to evaluate the inhibitory effect of matrine on SW480 cells. The protein and mRNA levels of APRIL in SW480 cells were determined by immunohistochemistry and real-time fluorescence quantitative PCR (RFQ-PCR). SW480 cells were treated with 0.5,1.0,2.0 mg/ml of matrine for 24 h, 48 h and 72 h. FU and blank were served as drug control and blank control groups, respectively. Results Matrine had obviously inhibitory effect on proliferation of SW480 cells in a time- and dose-dependant manner. The expression of APRIL was strong in SW480 cells. When treated with 50,100,200 ug/ml of FU, the APRIL mRNA levels in SW480 cells raised gradually and reached the highest levels at 72 h after treatment, which were significantly higher than those in blank control group (all P value<0.001). When treated with 0. 5,1.0, 2.0 mg/ml of matrine, the APRIL mRNA levels in SW480 cells increased at 24 h after treatment, which were significantly higher than those in blank control group (all P value<0. 001), and then decreased gradually and almost equal to level of blank control group at 72 h. Conclusion In treatment with FU, the survival cells.may have stronger ability of proliferation due to higher expression of APRIL in SW480 cells. Anti-APRIL therapy might be an important assistant treatment to counter the impact of APRIL. Matrine will not cause persistent increase of APRIL mRNA levels in SW480 cells, so it might be a helpful drug in anti-tumor theraphy.
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AIM:To investigate the expression of TLR2 and TLR4 in hepatocellular carcinoma(HCC),and to analyze their correlations to clinicopathologic features of HCC.METHODS:The protein and mRNA levels of TLR2 and TLR4 in HCC and para-tumor tissue were determined by immunohistochemistry and real-time fluorescence quantitative PCR(RFQ-PCR).RESULTS:The protein and mRNA levels of TLR2 and TLR4 in HCC were lower than those in para-tumor tissue(P