Human chorionic gonadotropin improves endometriosis through downregulation of leptin expression in rats.

OBJECTIVE: To investigate whether and how human chorionic gonadotropin (HCG) treatment ameliorates endometriosis in an endometriotic rat model. METHODS: Twenty-four endometriosis rats were established and were randomly divided into four groups, and then the rats were treated with 19.4, 25.8, and 51.6 IU/100 g weight/day of HCG, respectively. The control group was treated with 0.9% NaCl. After 15 days (3 estrous cycles), the ectopic lesion volume and the expression of leptin protein in eutopic and ectopic endometrium were investigated. RESULTS: After HCG treatment, the volumes of endometriotic lesions were significantly smaller than those before treatment. During endometriosis development, the expression of leptin protein in eutopic and ectopic endometrium was remarkably increased. HCG administration reversed leptin upregulation in endometriotic tissues. CONCLUSION: HCG therapy appears to be an effective treatment for endometriosis in rats through down-regulation of leptin expression in eutopic and ectopic endometrium.

Placental methylation markers in normal and trisomy 21 tissues.

OBJECTIVE: The objective of this study is to combine multiplex ligation-dependent probe amplification (MLPA) and bisulfite sequencing to determine DNA methylation markers for noninvasive prenatal diagnosis of Down syndrome. METHODS: DNA methylation ratios (MR) of four fragments (CGI149, CGI045, HLCS-1, and HLCS-2) on chromosome 21 were evaluated in blood cells from 13 nonpregnant women, 15 euploidies, and 11 Down Syndrome (DS) placentae. Ratios were measured by bisulfite sequencing and methylation-specific (MS)-MLPA. RESULTS: The MS-MLPA and bisulfite sequencing results were concordant. CGI149, CGI045, and HLCS-2 were unmethylated in all nonpregnant blood cells. CGI149, CGI045, HLCS-1, and HLCS-2 were methylated in most of the euploid (13, 11, 15, and 15, respectively) and DS placentae (10, 11, 11, and 11, respectively). The median placental DNA MR in CGI149 was 0.4578 (interquartile range, 0.3568-0.5169) and 0.5918 (interquartile range, 0.5618-0.6659) in euploid and DS placentae, respectively (p = 0.001). Using placental MR at 0.5390 as a threshold, we detected DS at 90.9% sensitivity and 93.3% specificity. CONCLUSION: The MS-MLPA is an effective alternative to bisulfite sequencing in assessing placental MR. CGI149 is a potential marker for the noninvasive diagnosis of Down syndrome.

Development of strategies for screening, predicting, and diagnosing intrauterine HBV infection in infants born to HBsAg positive mothers.

This study aimed at developing strategies for screening, predicting, and diagnosing intrauterine HBV infection in infants born to HBsAg positive mothers. A total of 1,360 infants born to 1,355 HBsAg positive mothers were followed for 1 year. All newborn infants received active and passive immunization within 24 hr after birth. Maternal and infant blood samples were collected and tested for the status of serum HBsAg, HBeAg, and HBV DNA positivity. The accuracy of infant HBsAg positivity, HBV DNA positivity, HBsAg and HBV DNA double positivity, and HBsAg and/or HBV DNA positivity at birth in the diagnosis of intrauterine HBV infection was evaluated by receiver operating characteristic curve analysis. Of 1,360 infants, 145 tested positive for HBsAg and/or HBV DNA at birth. Twenty-one (1.5%) infants, who were diagnosed with intrauterine HBV infection, showed HBsAg positivity from birth to 7 and 12 months of age. Infant HBsAg positivity at birth had the highest sensitivity in predicting intrauterine HBV infection, while neonatal HBsAg and HBV DNA double positivity had the highest specificity. These findings suggest that infants, who were born to HBsAg positive mothers and were positive for both HBsAg and HBV DNA at birth, may be at a higher risk for intrauterine HBV infection. HBsAg positivity at birth may be a good marker for screening intrauterine HBV infection. Infant HBsAg positivity both at birth and 7 months of age may be used as a diagnostic criterion to simplify diagnostic procedures and improve diagnostic efficiency.

[Identification of risk factors related to the failure of immunization to interrupt hepatitis B virus perinatal transmission].

OBJECTIVE: To explore the factors influencing failure of an immunization to interrupt perinatal (mother-to-child) transmission of hepatitis B virus (HBV). METHODS: Between June 2006 and March 2010, a total of 1355 pregnant women testing positive for the hepatitis B surface antigen (HBsAg), at gestational weeks 20 to 42, and without use of antiviral or immunomodulatory drugs during the pregnancy were prospectively recruited to the study. The mothers were given a choice of receiving hepatitis B immunoglobulin (HBIG; three 200 IU intramuscular injections give at four-week intervals starting from gestation week 28) or not. All neonates (1360, including five sets of twins) received hepatitis B vaccine (10 mug) plus HBIG (200 IU) combined immunization within 24 h of birth, as early as possible. Peripheral venous blood samples were collected from the neonates within 24 h of birth and at 7 and 12 months of age for detection of HBV markers, including hepatitis B e antigen (HBeAg) and HBV DNA. The infants were classified according to HBV perinatal transmission status (infection group and non-infection group) and various factors (maternal-related: age, gravidity, parity; pregnancy/birth-related: threatened premature labor, complications; neonate-related: sex, birth weight, apgar score) were compared between the two groups by using non-conditional logistic regression analysis to determine their potential influence on failure of immunization to inhibit transmission. RESULTS: After 12 months of follow-up, 1.54% (21/1360) of the neonates had presented with HBV infection. Analysis of the HBV-infected neonates revealed differences in infection rates between neonates born to mothers with HBIG injection (2.22% vs. without HBIG injection: 1.11%, P less than 0.05) and caesarean section (1.35% vs. vaginal delivery: 1.73%) but neither reached statistical significance (P less than 0.05); only the practice of breastfeeding showed a significant difference for infection rate, with neonates fed artificial formula having higher infection rate (3.13%) than the breastfed neonates (0.27%, P less than 0.05). The neonate HBV infection rate was also significantly higher for neonates born to HBeAg-positive mothers (4.44% vs. HBeAg-negative mothers: 0%, P less than 0.05) and HBV DNA-positive mothers (3.13% vs. HBV DNA-negative mothers: 0%, P less than 0.05). When the mothers were stratified by serum level of HBV DNA, there was a significant difference in HBV-infected neonates born to mothers with more than or equal to 1*10(7) IU/ml(6.01% vs. 10(3)-10(6) IU/ml: 0.56% and less than 1*10(3) IU/ml: 0%, both P less than 0.05). Logistic regression analysis indicated that the independent risk factors for HBV perinatal transmission despite immunization were maternal serum HBeAg-positive status (relative risk (RR)=31.74, 95% confidence interval (CI): 3.88-259.38) and maternal HBV DNA of ≥ 107 copies/mL (RR=22.58, 95% CI: 4.75-107.40). CONCLUSION: Failure of vaccine plus HBIG to interrupt mother-to-child transmission of HBV is influenced by maternal serum HBeAg-positive status and maternal HBV DNA of ≥107 copies/mL.

[Intrauterine HBV infection: risk factors and impact of HBV DNA].

OBJECTIVE: To investigate the risk factors of intrauterine hepatitis B virus (HBV) infection and the impact of HBV DNA on the infection. METHODS: The serum levels of HBsAg, HbsAb, HBeAg, HBeAb, HBcAb and HBV DNA were determined in blood samples from 230 HBsAg-positive pregnant women and their newborns by enzyme-linked immunosorbent assay (ELISA) and fluorescence quantitative PCR (FQ-PCR), respectively. The newborns acquiring HBV infection via intrauterine transmission were selected as the case group and others as the control group. The risk factors for intrauterine HBV infection were analyzed by non-conditional logistic regression model. RESULTS: Six infants were found to be HBsAg-positive, and 18 HBV DNA-positive, and 3 of them were positive for both HBsAg and HBV DNA. The rate of intrauterine HBV infection was 9.6% (22/230). The grade of HBV DNA level was identified as the only risk factor of intrauterine HBV infection by non-conditional logistic regression model, with odds ratio (OR) of 1.57 (95% confidence interval 1.12-2.21). Of the 119 pregnant women positive for HBV DNA, 18 were diagnosed as having intrauterine HBV infection, and the likeliness of the infection significantly increased for a maternal serum HBV DNA level > or =10(7) copies/ml (chi(2)=7.92, P<0.05). CONCLUSION: The grade of serum HBV DNA level is the predominant risk factor for intrauterine HBV infection in pregnant women, and for those with serum HBV DNA lever > or =10(7) copies/ml, the chance for intrauterine HBV infection can be significantly increased.

[Relations of pre-pregnant weight and weight gain during pregnancy with pregnancy-induced hypertension and birth weight].

OBJECTIVE: To determine the influence of pre-pregnant body mass index (BMI) and weight gain during pregnancy on the occurrence of pregnancy-induced hypertension (PIH) and birth weight. METHODS: Pre-pregnant BMI and pregnancy weight gain of 769 mothers giving full-term birth to a single baby for the first time were measured and the pregnancy outcomes were followed up. RESULTS: (1) The incidence of PIH and fetal macrosomia was significantly higher in the overweight group than in the normal weight and underweight groups (P<0.01 and P<0.05, respectively), but differed little between the latter two groups (P>0.05). Underweight mothers were more likely to give birth to babies with low birth weight than the normal and overweight mothers (P<0.01), but the likelihood was similar between the latter two groups (P>0.05). (2) Irrespective of the pre-pregnant BMI, PIH and fetal macrosomia occurred at higher rates with the mothers with pregnancy weight gain no less than 18 kg (P<0.01), whereas low birth weight was significantly more likely with mothers with pregnancy weight gain less than 9 kg (P<0.01). (3) A weight gain during pregnancy over 18 kg gave rise to higher risk of PIH in normal and underweight mothers, but in overweight group, PIH occurred at a significantly higher rates when a weight gain more than 9 kg was recorded (P<0.05). The incidence of fetal macrosomia was significantly higher when the maternal weight gain exceeded 18 kg in the normal weight group (P<0.01), and low birth weight occurred more frequently in relation to a maternal weight gain less than 9 kg in the normal and underweight groups (P<0.01). CONCLUSION: Pre-pregnant BMI and weight gain during pregnancy can be important factors influencing the occurrence of PIH and the neonates' birth weight.