Fujian Provincial Maternal and Child Health Hospital

Fuzhou, China

Fujian Provincial Maternal and Child Health Hospital

Fuzhou, China

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PubMed | Centers for Disease Control and Prevention and Fujian Provincial Maternal and Child Health Hospital
Type: Journal Article | Journal: Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi | Year: 2014

To study the impacts of pre-pregnancy maternal BMI and gestational weight gain(GWG) on pregnancy outcomes.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.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 (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.Low or high pre-pregnancy maternal BMI and GWG were associated with adverse pregnancy outcomes.


Guo Q.,Maternal and Child Health Hospital | Lan F.,Fuzhou General Hospital | Xu L.,Fujian Provincial Maternal and Child Health Hospital | Jiang Y.,Maternal and Child Health Hospital | And 3 more authors.
Fertility and Sterility | Year: 2012

Objective: To develop a rapid and reliable method for molecular diagnosis of Y-chromosomal microdeletions. Design: Study of diagnostic accuracy. Setting: Molecular diagnostics laboratories in three hospitals. Patient(s): A total of 701 men with nonobstructive azoospermia or oligozoospermia from three hospitals. Intervention(s): We developed a quadruplex real-time polymerase chain reaction (PCR) assay and evaluated its performance in molecular diagnosis of Y-chromosomal microdeletions. Main Outcome Measure(s): Analytic sensitivity, analytic specificity, clinical sensitivity, and clinical specificity. Result(s): The limit of detection of quadruplex real-time PCR assay was 100 pg genomic DNA. The method attained 100% analytic specificity, 100% clinical sensitivity, and 100% clinical specificity. Conclusion(s): We have successfully upgraded the diagnostic method published by the European Academy of Andrology and the European Molecular Genetics Quality Network. Our method was validated to be fast, simple, contamination free, of high analytic sensitivity and specificity. Therefore, it is strongly suggested that such quadruplex real-time PCR assay can be readily applied as clinical routine in the near future. © 2012 by American Society for Reproductive Medicine.


Lu G.B.,Fujian Provincial Maternal and Child Health Hospital
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] | Year: 2012

To explore the relationship between gene polymorphism of GABAA receptors and childhood autism by detecting rs140682, rs2081648 and rs140679 site of single nucleotide polymorphism (SNP) in GABAA receptors gene. A total of 94 children with autism and 124 normal children were enrolled in a hospital from November 2010 to May 2011. Childhood autism rating scale (CARS) and autism behavior checklist (ABC) were used to evaluate or investigate the case group. After collecting venous blood and extracting the genome DNA, the allele and genotype of SNP rs140682, rs2081648 and rs140679 site in GABAA receptors gene were detected by PCR-RFLP. The allele and genotype of case group and control group were analyzed by χ(2) test, while the score of scales was analyzed by Spearman rank correlation analysis. The age of the case group was 5.12 ± 0.32, and it was 5.25 ± 0.27 in the control group (P < 0.05). In case group, the frequency of genotype CC, CT and TT of rs140682 site was 44, 41 and 9, while it was 48, 65, and 11 in control group (P > 0.05), respectively. The frequency of genotype AA, AG and GG of rs2081648 site was 8, 58 and 28 in case group, while it was 12, 49 and 63 in control group (P < 0.05), respectively. In case group, the frequency of genotype CC, CT and TT of rs140679 site was 15, 36 and 43, while it was 18, 59 and 47 in control group (P > 0.05), respectively. It was revealed by Spearman rank correlation analysis that of rs2081648 site, there was a positive correlation between genotype AG and sensation factor (S), social intercourse factor (R), and language factor (L) of autism behavior checklist (ABC) (r values were 0.149, 0.165 and 0.155, all P values < 0.05). A negative correlation between genotype GG and S, R, L and self-help factor (V) was proved (r values were -0.140, -0.173, -0.158 and -0.135, all P values < 0.05). There was a positive correlation between allele A and R and L factors (r values were 0.153 and 0.137, all P values < 0.05), while a negative correlation between allele G and R and L factors (r values were -0.153 and -0.137, all P values < 0.05). In case group, 42 children were diagnosed with mild-to-moderate autism, while 52 children were severe autism. There was no statistically significant correlation between allele or genotype of SNP rs140682 and rs140679 site and the degree of autism (P > 0.05). There was a positive correlation between allele A and genotype AG and the degree of autism (r values were 0.147 and 0.616, all P values < 0.05), while a negative correlation between allele G and genotype GG and the degree of autism (r values were -0.159 and -0.616, all P values < 0.05). The SNP rs2081648 site which located in GABAA receptors gene may be related to autism. No evidence for significant association between rs140682 and rs140679 site and autism was found.


Niu P.,Fujian Provincial Maternal and Child Health Hospital | Zhang Y.,Fujian Provincial Maternal and Child Health Hospital | Shi D.,Fujian Provincial Maternal and Child Health Hospital | Chen Y.,Fujian Provincial Maternal and Child Health Hospital | Deng J.,Fujian Provincial Maternal and Child Health Hospital
Planta Medica | Year: 2013

The mammalian target of rapamycin is crucial in the regulation of cell growth and metabolism. Recent studies suggest that the mammalian target of rapamycin and its downstream 70-kDa ribosomal S6 kinase 1 negatively modulate the insulin-signaling pathway, which is considered the main cause of insulin resistance. The aim of this study is to investigate the effects of cardamonin, a potential inhibitor of the mammalian target of the rapamycin, on insulin-resistant vascular smooth muscle cells and the molecular mechanisms involved. Vascular smooth muscle cells were cultured with high glucose and high insulin to induce insulin resistance. The mammalian target of rapamycin was overstimulated in cells that were incubated with high glucose and high insulin, as reflected by the excessive activation of S6 kinase 1. Insulin-resistant vascular smooth muscle cells displayed hyperphosphorylation of insulin receptor substrate-1 at Ser residues 636/639, which decreased the activity of insulin receptor substrate-1. Also, the activation of protein kinase B and phosphorylation of glycogen synthesis kinase-3β were inhibited. Cardamonin increased the 2-deoxyglucose uptake and glycogen concentration, which was reduced by insulin resistance. As with rapamycin, cardamonin inhibited the activity of the mammalian target of rapamycin and S6 kinase 1, decreased the Ser 636/639 phosphorylation of insulin receptor substrate-1 and increased the activation of protein kinase B. Both of them increased the Ser9 phosphorylation of glycogen synthesis kinase-3β and decreased the expression of glycogen synthesis kinase-3β. However, neither cardamonin nor rapamycin increased the expression of glucose transport 4 which decreased in insulin-resistant vascular smooth muscle cells. This study suggests that cardamonin inhibited the activity of the mammalian target of rapamycin and eliminated the negative feedback of the mammalian target of rapamycin and S6 kinase 1 on the insulin-signaling pathway. © Georg Thieme Verlag KG Stuttgart · New York.


Zhang R.L.,Fujian Provincial Maternal and Child Health Hospital
Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi | Year: 2010

To study the influence of HBV-DNA with different load levels of HBsAg-positive among fathers on the rate of neonatal cord blood HBV-DNA. Using HBsAg and HBV-DNA as screening indicators for pregnant women and their husbands from an obstetric clinic. 161 pregnant women whose HBsAg and HBV-DNA were negative, but HBsAg was positive among their husbands and their newborns, were selected. Blood samples from those pregnant women, their husbands and their newborns were collected to detect the related indicators. Using ELISA to detect hepatitis B virus markers (HBVM), and FQ-PCR to detect the levels of HBV-DNA load. According to neonatal cord blood HBV-DNA detection guideline, newborns with cord blood HBV-DNA positive were selected as cases, others as controls. (1) Result of the study showed that there was a dose-response relationship between paternal serum HBV-DNA load levels and neonatal cord blood HBV-DNA positive rates in newborns (trend χ(2) = 64.117, P = 0.000). The rate of vertical transmission of HBV from HBsAg-positive father to infant in the paternal serum HBV-DNA ≥ 1.0 × 10(7) copies/ml group was significantly higher than HBV-DNA < 1.0 × 10(7) copies/ml group (χ(2) = 71.539, P = 0.000). (2) There was a positive rank correlation between semen positive HBeAg and vertical transmission of HBV from HBsAg-positive father to infant (χ(2) = 6.892, P = 0.009). There was a dose-response relationship between paternal serum HBV-DNA load levels and neonatal cord blood HBV-DNA positive in newborns. Paternal serum HBV-DNA ≥ 1.0 × 10(7) copies/ml and with HBeAg positive status were risk factors of vertical transmission of HBV from HBsAg-positive father to infant.


Niu P.-G.,Fujian Provincial Maternal and Child Health Hospital | Zhang Y.-X.,Fujian Provincial Maternal and Child Health Hospital | Shi D.-H.,Fujian Provincial Maternal and Child Health Hospital | Liu Y.,Fujian Provincial Maternal and Child Health Hospital | And 2 more authors.
PLoS ONE | Year: 2015

The mammalian target of rapamycin (mTOR) regulates the motility and invasion of cancer cells. Cardamonin is a chalcone that exhibits anti-tumor activity. The previous study had proved that the anti-tumor effect of cardamonin was associated with mTOR inhibition. In the present study, the anti-metastatic effect of cardamonin and its underlying molecule mechanisms were investigated on the highly metastatic Lewis lung carcinoma (LLC) cells. The proliferation, invasion and migration of LLC cells were measured by MTT, transwell and wound healing assays, respectively. The expression and activation of mTOR- and adhesion-related proteins were assessed by Western blotting. The in vivo effect of cardamonin on the metastasis of the LLC cells was investigated by a mouse model. Treated with cardamonin, the proliferation, invasion and migration of LLC cells were significantly inhibited. The expression of Snail was decreased by cardamonin, while that of E-cadherin was increased. In addition, cardamonin inhibited the activation of mTOR and its downstream target ribosomal S6 kinase 1 (S6K1). Furthermore, the tumor growth and its lung metastasis were inhibited by cardamonin in C57BL/6 mice. It indicated that cardamonin inhibited the invasion and metastasis of LLC cells through inhibiting mTOR. The metastasis inhibitory effect of cardamonin was correlated with down-regulation of Snail and up-regulation of E-cadherin. © 2015 Niu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Tang Y.,Fujian Provincial Maternal and Child Health Hospital | Fang Q.,Fujian Provincial Maternal and Child Health Hospital | Shi D.,Fujian Provincial Maternal and Child Health Hospital | Niu P.,Fujian Provincial Maternal and Child Health Hospital | And 2 more authors.
Life Sciences | Year: 2014

Aims Cardamonin has previously demonstrated that it had an antiproliferative effect on vascular smooth muscle cells by inhibiting the activity of mammalian target of rapamycin (mTOR). The antiproliferative effect and the possible mechanism of combining with mTOR of cardamonin were investigated on A549 cells. Main methods Cell proliferation, cell cycle and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) and flow cytometry, respectively. mTOR and 12 kDa FK506 binding protein (FKBP12) were transfected into A549 cells by Lipofectamine. Western blots were used to examine the mTOR expressions and its activities, and the expressions of 70 kDa ribosomal S6 kinase (p70S6K), FKBP12 and Interleukin-2 (IL-2), respectively. Key findings Treated with cardamonin, the proliferation of A549 cells was inhibited. Meanwhile, cell cycle was blocked and DNA synthesis was decreased whereas cell apoptosis was promoted, and the activation of mTOR and p70S6K was decreased by cardamonin. Transfected with mTOR or FKBP12, proliferation of A549 cells was increased. Rapamycin had a similar degree of effect on antiproliferation of both transfected cells. However, the antiproliferative effect of cardamonin on mTOR transfected cells was stronger than that on FKBP12 transfected cells. Both rapamycin and cardamonin decreased the phosphorylation of mTOR and p70S6K in two kinds of transfected cells. Cardamonin had no effect on the expression of FKBP12 and IL-2, whereas the expressions were decreased by rapamycin. Significance Cardamonin inhibited proliferation and induced apoptosis of A549 cells via mTOR. It might directly interact with mTOR independently of binding with FKBP12. © 2014 Elsevier Inc.


PubMed | Fujian Provincial Maternal and Child Health Hospital
Type: Journal Article | Journal: Planta medica | Year: 2013

The mammalian target of rapamycin is crucial in the regulation of cell growth and metabolism. Recent studies suggest that the mammalian target of rapamycin and its downstream 70-kDa ribosomal S6 kinase 1 negatively modulate the insulin-signaling pathway, which is considered the main cause of insulin resistance. The aim of this study is to investigate the effects of cardamonin, a potential inhibitor of the mammalian target of the rapamycin, on insulin-resistant vascular smooth muscle cells and the molecular mechanisms involved. Vascular smooth muscle cells were cultured with high glucose and high insulin to induce insulin resistance. The mammalian target of rapamycin was overstimulated in cells that were incubated with high glucose and high insulin, as reflected by the excessive activation of S6 kinase 1. Insulin-resistant vascular smooth muscle cells displayed hyperphosphorylation of insulin receptor substrate-1 at Ser residues 636/639, which decreased the activity of insulin receptor substrate-1. Also, the activation of protein kinase B and phosphorylation of glycogen synthesis kinase-3 were inhibited. Cardamonin increased the 2-deoxyglucose uptake and glycogen concentration, which was reduced by insulin resistance. As with rapamycin, cardamonin inhibited the activity of the mammalian target of rapamycin and S6 kinase 1, decreased the Ser 636/639 phosphorylation of insulin receptor substrate-1 and increased the activation of protein kinase B. Both of them increased the Ser9 phosphorylation of glycogen synthesis kinase-3 and decreased the expression of glycogen synthesis kinase-3. However, neither cardamonin nor rapamycin increased the expression of glucose transport 4 which decreased in insulin-resistant vascular smooth muscle cells. This study suggests that cardamonin inhibited the activity of the mammalian target of rapamycin and eliminated the negative feedback of the mammalian target of rapamycin and S6 kinase 1 on the insulin-signaling pathway.


PubMed | Fujian Provincial Maternal and Child Health Hospital
Type: Journal Article | Journal: Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico | Year: 2015

This study is to evaluate the association of polymorphisms of glutathione S-transferase P1 (GSTP1), copper-transporting P-type adenosine triphosphatase A (ATP7A) and X-ray repair cross-complementing group 1 (XRCC1) with the efficacy and toxicity of cisplatin-based treatment in advanced non-small cell lung cancer (NSCLC) patients.The outcomes of 97 advanced non-small cell lung cancer patients treated with cisplatin-based chemotherapy were estimated. GSTP1, ATP7A, and XRCC1 genetic polymorphisms were determined via polymerase chain reaction of restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing. Association of the polymorphisms with the efficacy and toxicity of cisplatin was analyzed, respectively.Significant associations were observed between GSTP1 A313G and response rate (RR) (p=0.027), disease control rate (DCR) (p=0.019), and progression-free survival (PFS) (p=0.044), respectively. Patients with AG and GG of GSTP1 have notably lower risk of anemia (p=0.046). XRCC1 A1196G was associated with the incidence of lymphopenia (p=0.024) and diarrhea (p=0.020). ATP7A C2299G was not related with RR, DCR, PFS, and the risk of toxicity.Advanced NSCLC patients with AA genotype of GSTP1 would obtain better curative effect followed with more risk of anemia when treated by cisplatin-based chemotherapy. ATP7A C2299G does not impact the efficacy and toxicity of cisplatin-based chemotherapy. XRCC1 1196A allele could predict the incidence of lymphopenia and diarrhea.


PubMed | Fujian Provincial Maternal and Child Health Hospital
Type: Journal Article | Journal: Life sciences | Year: 2014

Cardamonin has previously demonstrated that it had an antiproliferative effect on vascular smooth muscle cells by inhibiting the activity of mammalian target of rapamycin (mTOR). The antiproliferative effect and the possible mechanism of combining with mTOR of cardamonin were investigated on A549 cells.Cell proliferation, cell cycle and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) and flow cytometry, respectively. mTOR and 12 kDa FK506 binding protein (FKBP12) were transfected into A549 cells by Lipofectamine. Western blots were used to examine the mTOR expressions and its activities, and the expressions of 70 kDa ribosomal S6 kinase (p70S6K), FKBP12 and Interleukin-2 (IL-2), respectively.Treated with cardamonin, the proliferation of A549 cells was inhibited. Meanwhile, cell cycle was blocked and DNA synthesis was decreased whereas cell apoptosis was promoted, and the activation of mTOR and p70S6K was decreased by cardamonin. Transfected with mTOR or FKBP12, proliferation of A549 cells was increased. Rapamycin had a similar degree of effect on antiproliferation of both transfected cells. However, the antiproliferative effect of cardamonin on mTOR transfected cells was stronger than that on FKBP12 transfected cells. Both rapamycin and cardamonin decreased the phosphorylation of mTOR and p70S6K in two kinds of transfected cells. Cardamonin had no effect on the expression of FKBP12 and IL-2, whereas the expressions were decreased by rapamycin.Cardamonin inhibited proliferation and induced apoptosis of A549 cells via mTOR. It might directly interact with mTOR independently of binding with FKBP12.

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