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Background: Current research separately analyzed the connection between postpartum depression, fatigue, sleep and infant development. However, depression, fatigue and sleep quality often coexisted as adverse symptoms in postpartum women and influenced infant development together. This study explored the maternal postpartum symptoms on infant growth. Methods: Our study included 224 pairs of singleton full‐term mothers and their infants who underwent routine pediatric outpatient clinics. Latent profile analysis was applied to identify the latent classes based on mothers' postpartum depression, fatigue and sleep profile characteristics. We evaluated the maternal adverse symptoms and infant development using multivariable logistic regressions. Results: Totally, 224 pairs of eligible mothers (28.85 ± 4.43 years) and infants (30.93 ± 3.26 days) participated in this study. Latent profile analysis identified 3 latent groups: mild (58.04%), moderate (34.37%), and severe (7.59%) postpartum adverse symptoms. Postpartum adverse symptoms were associated with delayed development in the baby's motor level (χ2 = 6.572, p =.037) and weight‐for‐length (χ2 = 9.652, p =.008). After controlling for mother and infant related factors, postpartum adverse symptoms remained a risk factor for infant motor level (odds ratio [OR]: 4.35; 95% confidence interval [CI]: 1.25–15.08) and weight‐for‐length (OR: 5.53; 95% CI: 1.55–19.74). Conclusions: Maternal postpartum depression, fatigue and sleep quality are associated with infant development. Clinically, mothers with these symptoms should be intervened timely to avoid the aggravation of maternal symptoms, which affect baby's development. [ABSTRACT FROM AUTHOR]

Background: To explore the value of umbilical artery cord blood glucose (UACBG) in predicting hypoglycemia in gestational diabetes mellitus (GDM) and other at-risk newborns, and to provide a cut-off UACBG value for predicting hypoglycemia occurrence. Methods: In this prospective study, we enrolled at-risk infants delivered vaginally, including neonates born to mothers with GDM, premature, macrosomic, and low birth weight. We separated the infants into GDM group and other at-risk group. All subjects underwent UACBG measurement during delivery. Neonatal peripheral blood glucose measurement was performed at 0.5 and 2 h after birth. The predictive performance of UACBG for neonatal hypoglycemia was assessed using receiver operating characteristic curve (ROC), area under curve (AUC), sensitivity, specificity, negative predictive value (NPV) and positive predictive value (PPV). Results: 916 newborns were included, with 538 in GDM group and 378 in other at-risk group. 85 neonates were diagnosed hypoglycemia within 2 h after birth, including 36 belonging to GDM group and 49 to other at-risk group. For hypoglycemia prediction within 2 h, the best cut-off of UACBG was 4.150 mmol/L, yielding an AUC of 0.688 (95% CI 0.625–0.751) and a NPV of 0.933. In detail, the AUC was 0.680 in GDM group (95% CI 0.589–0.771), with the optimal cut-off of 4.150 mmol/L and a NPV of 0.950. In other at-risk group, the AUC was 0.678(95% CI 0.586–0.771), the best threshold was 3.950 mmol/L and the NPV was 0.908. No significant differences were observed between GDM group and other at-risk group in AUC at 0.5 h, 2 h and within 2 h. Conclusions: UACBG has a high NPV for predicting neonatal hypoglycemia within 2 h after birth. It was implied that individuals with cord blood glucose levels above the threshold were at lower risk for hypoglycemia. UACBG monitoring provides evidence for subsequent classified management of hypoglycemia. [ABSTRACT FROM AUTHOR]

Aim: The review is to explore the connection between gestational hypertension diseases (GHD) and small for gestational age (SGA) in twin pregnancies. Methods: According to the recommendations of PRISMA, relevant studies were systematically searched through PubMed, Web of Science, Cochrane Library, Embase from inception until January 16, 2022. Subgroup analysis was performed according to chorionicity and diagnostic criteria of SGA. Odds ratios (OR) were assessed to judge the link between GHD and SGA in twin pregnant women. A random‐effect model was used to estimate the pooled hazard ratio when there was significant heterogeneity (I2 > 50%); otherwise, a fixed‐effect model was conducted. Results: Seven articles containing 470 589 twin pregnant women were included. The increased risk of SGA was connected to the twin pregnancies complicated with GHD (OR = 1.57, 95% confidence interval [CI] = 1.10–2.24, p = 0.01). After subgroup analysis, the connection between SGA and GHD had no statistical significance (OR = 1.17, 95% CI = 0.95–1.44, p = 0.14) when the enrolled studies using the SGA diagnosis referred to singleton birth weight, but significant (OR = 2.14, 95% CI = 1.77–2.60, p<0.001) in the group using the SGA diagnosis referred to twin birth weight. Stratified by chorionicity, SGA was relevant to GHD in the dichorionic (DC) group (OR = 1.68, 95% CI = 1.17–2.42, p = 0.005), while not in the monochorionic (MC) group (OR = 1.68, 95% CI = 0.93–3.03, p = 0.09). More future articles are warranted to confirm these outcomes. Conclusions: Our review demonstrated that GHD in DC twin pregnancies was related to an enlarged risk of SGA. Two SGA diagnosis references led to different results. Twin pregnancies complicated with GHD were at significantly higher risk of SGA when twin birth weight reference was used. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of miR-515-5p on proliferation, migration and invasion of esophageal cancer (EC) cells and the molecular mechanism. Methods: Cancer tissue specimens from 60 patients with esophageal cancer that surgically resected at the Fourth Hospital of Hebei Medical University from June 2020 to December 2020, esophageal epithelial tissue specimens from 20 healthy adults, as well as esophageal cancer cell lines (TE1, Eca109, KYSE30 and KYSE170) were selected for this study. Quantitative reverse transcription polymerase chain reaction (qPCR) was performed to detect miR-515-5p expression in above mentioned EC tissues and cells. Eca109 cells were transfected with miR-515-5p mimics or its negative controls, and TE1 cells were transfected with miR-515-5p inhibitors or its negative controls. The transfection efficiency was detected by qPCR, and the proliferation, migration and invasion of transfected cells were detected by CCK-8 assay and transwell assay respectively. Bioinformatics tools were used to predict the downstream target genes of miR-515-5p, and HDAC2 (histone deacetylase 2) was verified to be a target gene of miR-515-5p by dual luciferase reporter gene assay. GEPIA and TCGA databases were used to analyze the expression of HDAC2 in EC tissues and its correlation with clinical characteristics of EC patients. Results: miR-515-5p was downregulated in EC tissues and cells (all P<0.01). Over-expression of miR-515-5p inhibited the proliferation, migration and invasion ability of Eca109 cells (P<0.05 or P<0.01), while down-regulation of miR-515-5p enhanced the proliferation, migration and invasion ability of TE1 cells (both P<0.05). Furthermore, HDAC2 was demonstrated to be a target gene of miR-515-5p by dual luciferase reporter gene assay. qPCR and Western blotting results showed that miR-515-5p negatively regulated the mRNA and protein expression of HDAC2. Rescue experiments confirmed that miR-515-5p inhibited the proliferation, migration and invasion ability of esophageal cancer Eca109 cells by targeting HDAC2 (P<0.05 orP<0.01). Conclusion: miR-515-5p affects proliferation, migration and invasion of EC cells by targeting HDAC2. [ABSTRACT FROM AUTHOR]