We design this study to detect levels of Elabela (ELA) and Apelin (APLN) in women with and without gestational diabetes mellitus (GDM) in the second and third trimesters, and to identify whether there is any association between ELA, APLN, and metabolic parameters. Seventy-nine GDM and 80 control subjects in the second trimester and 87 GDM and 88 healthy subjects in the third trimester were included. In the second trimester, lower ELA levels [(14.1 versus 16.9) ng/ml, p = .025] and higher APLN levels [(1021.8 versus 923.5) pg/ml, p = .046] were observed in GDM patients compared to controls. ELA levels were positively correlated with fasting plasma glucose (FPG) (r = 0.423, p < .001) in the control group, and APLN levels were negatively correlated with triglycerides (TG) (r = −0.251, p = .025) in the control group and total cholesterol (TC) (r = −0.227, p = .044) in the GDM group. ELA appeared to be related to glucose metabolism and APLN is involved in lipid metabolism during pregnancy. The expression of ELA is significantly downregulated from the second trimester to the third trimester.

Objective: Poor sleep quality is common during pregnancy. Although a few studies have investigated the associations between maternal sleep quality and fetal birth weight (BW), no evidence has been clearly demonstrated. Our aim was to investigate the effects of sleep quality during pregnancy on the newborn BW z-scores. Participants: 1466 mother-infant pairs were included in the present study based on an ongoing prospective cohort. Methods: Questionnaires including the Pittsburgh Sleep Quality Index (PSQI) and scales for psychosocial status were administered at each trimester. BW z-scores were calculated based on the INTERGROWTH-21st standard. A generalized estimating equation model was applied to evaluate the associations between trimester-specific sleep quality and newborn BW after adjusting for potential confounders. Multivariable logistic regression models were applied to examine the impacts of maternal sleep quality on small-for-gestational-age (SGA) or low birth weight (LBW). Results: We found that maternal PSQI scores in the first and third trimesters were negatively associated with BW z-scores among female newborns (β = −0.032, 95% CI: −0.063, −0.001, P= .043; β = −0.031, 95% CI: −0.060, −0.003, P= .033, respectively). However, no relationship was observed between maternal sleep quality and BW in male neonates. Additionally, poor sleep quality in late pregnancy was a risk factor for LBW (OR = 1.501, 95% CI: 1.082–2.082). Conclusions: The BW z-scores of female newborns decreased as maternal sleep quality in the first and third trimesters worsened. This finding suggests that sleep during pregnancy may influence fetal weight in a trimester- and gender-specific manner.

Background: Women are particularly vulnerable to depression during pregnancy, which is one of the strongest risk factors for developing postpartum depression (PPD). Addressing antenatal depressive symptoms in these women is crucial for preventing PPD. However, little is known about the effectiveness of internet-based cognitive behavioral therapy (ICBT) in preventing PPD in this high-risk group. Objective: This study aims to evaluate the short- and long-term effects of ICBT in preventing PPD among women with antenatal depressive symptoms. Methods: Participants were screened for antenatal depressive symptoms using the Edinburgh Postnatal Depression Scale (EPDS) and randomly allocated (1:1) to either the ICBT group (receiving weekly online modules starting antenatally and continuing into early postpartum) or the control group (observed without treatment). Follow-up assessments were conducted up to 12 months postpartum, and data were analyzed using generalized estimating equations. The primary outcome was the prevalence of depressive symptoms at 6 weeks postpartum. A subgroup analysis based on the severity of antenatal depressive symptoms was also performed. The secondary outcomes included the long-term effects of ICBT on maternal depression, as well as its impact on anxiety, sleep quality, social support, parenting stress, co-parenting relationships, and infant development. Results: Between August 2020 and September 2021, 300 pregnant individuals were recruited from 5 centers across China. No significant differences were observed in depressive symptoms at 6 weeks postpartum (P=.18) or at any longer-term follow-up time points (P=.18). However, a post hoc subgroup analysis showed that participants with antenatal EPDS scores of 10-12 in the ICBT group had a lower risk of developing depression during the first year postpartum (odds ratio 0.534, 95% CI 0.313-0.912; P=.02), but this was not observed for participants with more severe depression. Additionally, this subgroup demonstrated higher levels of co-parenting relationships (P=.02). Conclusions: Among individuals with antenatal depression, ICBT did not prevent the development of PPD. However, ICBT may be a preferable option for those with mild to moderate antenatal depressive symptoms. Future research is needed to explore modifications to ICBT to address more severe depressive symptoms. Trial Registration: Chinese Clinical Trial Registry ChiCTR2000033433; https://www.chictr.org.cn/showproj.html?proj=54482 International Registered Report Identifier (IRRID): RR2-10.1186/s13063-022-06728-5

Backgrounds: Mayer‐Rokitansky‐Küster‐Hauser (MRKH) syndrome, a severe congenital malformation of the female genital tract, is a highly heterogeneous disease which has no clear etiology. Previous studies have suggested that copy number variations (CNVs) and single‐gene mutations might contribute to the development of MRKH syndrome. In particular, deletions in 16p11.2, which are suggested to be involved in several congenital diseases, have been reported in Chinese type II MRKH patients and European MRKH patients. However, few CNVs including 16p11.2 microdeletions were identified in Chinese type I MRKH cases although it accounted for the majority of MRKH patients in China. Thus, we conducted a retrospective study to identify whether CNVs at human chromosome 16p11.2 are risk factors of type I MRKH syndrome in the Chinese Han population.Methods: We recruited 143 patients diagnosed with type I MRKH between 2012 and 2014. Five hundred unrelated Chinese without congenital malformation were enrolled in control group, consisting of 197 from the 1000 Genomes Project and 303 from Fudan University. Quantitative PCR, array comparative genomic hybridization, and sanger sequencing were conducted to screen and verify candidate variant.Results: Our study identified recurrent 16p11.2 microdeletions of approximately 600 kb in two out of the 143 type I MRKH syndrome patients using high‐density array‐based comparative genomic hybridization (aCGH), while no 16p11.2 deletion was found in the control group. We did not find any mutations in TBX6 gene in our samples.Conclusions: The results of the study identify 16p11.2 deletion in Chinese MRKH I patients for the first time, as well as support the contention that 16p11.2 microdeletions are associated with MRKH syndrome in both types across populations. It is suggested that 16p11.2 microdeletions should be included in molecular diagnosis and genetic counseling of female reproductive tract disorders.

Objective: To comprehensively evaluate the interaction between diet quality and multivitamin intake during pregnancy on offspring neurodevelopment. Methods: This analysis was grounded in mother-child dyads from the 3D Cohort Study in Quebec, Canada. Among the 2366 participants initially enrolled in the 3D study, 1535 women successfully completed the 3-day food record during 20–24 weeks of gestation. A Canadian adaptation of the Healthy Eating Index (HEI-C) 2010 was used to quantify diet quality. The total HEI-C score was dichotomized into low and high diet quality by median split. Cognitive and motor development in childhood were assessed using the Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III). Language abilities were measured using the toddler short-form version of the MacArthur–Bates Communicative Development Inventories (MCDI) questionnaire, administered in either English or French. After excluding participants with missing covariate data, cognitive, motor, and language development scores at 2 years of age were available for 1066, 1040, and 981 children, respectively. Multiple linear regression models were employed to calculate adjusted effect estimates. The interaction on an additive scale was assessed by incorporating a product term into the linear regression model. Results: Statistically significant interactions were detected between diet quality and multivitamin intake in relation to the cognitive and language development outcomes of the offspring (interaction p-values were 0.018 and 0.023, respectively). The lowest cognitive and language scores were observed in the group of women who neither took multivitamins nor maintained a high-quality diet. Among women not taking multivitamins, a high-quality diet was associated with improved offspring cognitive and language scores (mean difference [95% CI] = 4.2 [0.1, 8.2], p = 0.04; and 11.3 [3.1, 19.5], p = 0.01, respectively). However, among women taking multivitamins, no such associations were identified. Conversely, in participants with a low-quality diet, multivitamin intake was associated with a 3.0-point increase in cognitive composite scores (95% CI: 0.3, 5.8, p = 0.03), but this was not the case for those with a high-quality diet. No statistically significant interactions were observed between maternal diet quality and multivitamin intake for motor development outcomes. Conclusions: Adequate nutritional supply during pregnancy, achieved either through a high-quality diet or multivitamin supplementation, is fundamental for the neurodevelopment of children.

BACKGROUND Women are particularly vulnerable to depression during pregnancy, which is one of the strongest risk factors for developing postpartum depression (PPD). Addressing antenatal depressive symptoms in these women is crucial for preventing PPD. However, little is known about the effectiveness of internet-based cognitive behavioral therapy (ICBT) in preventing PPD in this high-risk group. OBJECTIVE This study aims to evaluate the short- and long-term effects of ICBT in preventing PPD among women with antenatal depressive symptoms. METHODS Participants were screened for antenatal depressive symptoms using the Edinburgh Postnatal Depression Scale (EPDS) and randomly allocated (1:1) to either the ICBT group (receiving weekly online modules starting antenatally and continuing into early postpartum) or the control group (observed without treatment). Follow-up assessments were conducted up to 12 months postpartum, and data were analyzed using generalized estimating equations. The primary outcome was the prevalence of depressive symptoms at 6 weeks postpartum. A subgroup analysis based on the severity of antenatal depressive symptoms was also performed. The secondary outcomes included the long-term effects of ICBT on maternal depression, as well as its impact on anxiety, sleep quality, social support, parenting stress, co-parenting relationships, and infant development. RESULTS Between August 2020 and September 2021, 300 pregnant individuals were recruited from 5 centers across China. No significant differences were observed in depressive symptoms at 6 weeks postpartum (P=.18) or at any longer-term follow-up time points (P=.18). However, a post hoc subgroup analysis showed that participants with antenatal EPDS scores of 10-12 in the ICBT group had a lower risk of developing depression during the first year postpartum (odds ratio 0.534, 95% CI 0.313-0.912; P=.02), but this was not observed for participants with more severe depression. Additionally, this subgroup demonstrated higher levels of co-parenting relationships (P=.02). CONCLUSIONS Among individuals with antenatal depression, ICBT did not prevent the development of PPD. However, ICBT may be a preferable option for those with mild to moderate antenatal depressive symptoms. Future research is needed to explore modifications to ICBT to address more severe depressive symptoms. CLINICALTRIAL Chinese Clinical Trial Registry ChiCTR2000033433; https://www.chictr.org.cn/showproj.html?proj=54482 INTERNATIONAL REGISTERED REPORT RR2-10.1186/s13063-022-06728-5