Impact of catch-up growth on brain structures involved in emotional regulation in preterm children at 2years of age.

Childhood growth restriction can lead to lasting developmental changes, increasing susceptibility to chronic diseases and neurodegenerative conditions in adulthood. High-intensity interval training (HIIT) elevates brain-derived neurotrophic factor (BDNF) levels more effectively than moderate-intensity continuous exercise, supporting neuroplasticity. Building on these findings, this study aimed to determine whether HIIT could enhance neuroplasticity-related protein expression in the brains of postnatally growth-restricted (PNGR) mice. Friend leukemia virus B mouse pups born to normal-protein and low-protein-fed dams were cross-fostered at postnatal day (PN) 1 to establish two groups: PNGR mice and control mice (CON). At PN 21, all pups were weaned onto a normal-protein diet and assigned to either a HIIT group (training group [TRD]) or a sedentary group (SED). At PN 45, a maximal exercise performance test was conducted to determine HIIT intensities. Based on these results, mice performed treadmill HIIT 5 d·wk -1 for 4 wk, with alternating intervals of 8 min at 85% and 2 min at 50% of maximal exercise capacity, totaling 60 min per session. At PN 73, all mice were euthanized, and cerebrum tissue was collected for Western blot analysis of BDNF, tropomyosin receptor kinase B, growth-associated protein 43, and synaptophysin protein expression. Despite significant body mass reductions observed in both CON and PNGR groups after HIIT, neuroplasticity-related protein expression did not increase in PNGR mice. The PNGR group exhibited consistently lower tropomyosin receptor kinase B and reduced BDNF and growth-associated protein 43 levels compared with CON mice, indicating a limited neuroplastic response to exercise. Contrary to expectations, HIIT did not elevate neuroplasticity markers in PNGR mice, highlighting the lasting impact of early-life growth restriction on brain plasticity and suggesting the need for alternative interventions.

Vitamin D deficiency during pregnancy is common, especially in low- and middle-income countries. The objective of the study was to determine the prevalence of vitamin D deficiency among pregnant women of Bangladesh and its association with adverse maternal and fetal outcomes. The cross-sectional study was conducted among 420 pregnant women admitted to the department of Obstetrics and Gynecology of Popular Medical College Hospital for delivery from July 2019 to June 2022. Data collection was done through face-to-face interview using a semi-structured case record form and laboratory tests. A logistic regression model was constructed to determine the association between maternal vitamin D status and pregnancy outcomes. Prevalence of vitamin D deficiency [serum 25(OH)D <30 nmol/L] among pregnant women was 11.7% and vitamin D insufficiency [serum 25(OH)D 30-75 nmol/L] was 77.6%. In logistic regression model, vitamin D deficiency was not significantly associated with gestational diabetes mellitus (aOR 2.32, 95% CI 0.54, 12.0), preeclampsia (aOR 2.94, 95% CI 0.75, 14.6), preterm labor (aOR 2.41, 95% CI 0.98, 6.25), low birth weight (aOR 2.04, 95% CI 0.81, 5.30), intrauterine growth retardation (aOR 2.55, 95% CI 0.51, 18.7) and low APGAR score (aOR 1.51, 95% CI 0.24, 12.0). A large proportion of the pregnant women had a suboptimal level of vitamin D. However, no significant association between vitamin D deficiency and pregnancy outcome was found in the study.

This study aimed to investigate the effect of fetal growth restriction (FGR) on cortical maturation and fissure development using detailed neurosonography. We compared cortical grades and fissure measurements between FGR and healthy fetuses to determine if growth restriction is linked to delayed cortical maturation in specific regions. This observational case-control study included singleton pregnancies at 31-35 weeks of gestation between January 2025 and September 2025. FGR was diagnosed according to the Delphi consensus criteria. All participants underwent obstetric ultrasonography, fetoplacental Doppler, and fetal neurosonography. The depths of the Sylvian, parieto-occipital, calcarine, and cingulate fissures, as well as the insula, were measured and normalized to biparietal diameter (BPD). Cortical maturation was assessed using the Pistorius grading system. A total of 148 fetuses were analyzed (74 FGR, 74 controls). The FGR group showed higher uterine artery pulsatility index (PI) (P = .015) and lower middle cerebral artery (MCA) PI (P < .001). Neurosonography revealed significantly shallower parieto-occipital (P < .001), calcarine (P < .001), and cingulate (P < .001) fissures in the FGR group, while Sylvian fissure depth showed a nonsignificant trend (P = .057). After normalization to BPD, parieto-occipital/BPD and calcarine/BPD ratios remained significantly lower. In addition to quantitative fissure measurements, cortical maturation was evaluated. Only the Sylvian fissure showed a significantly lower maturation grade (P = .003). Cerebellar, vermian, and corpus callosum measurements were comparable. FGR is associated with region-specific cortical developmental delay, predominantly involving the parieto-occipital, calcarine, and cingulate fissures, while infratentorial and commissural structures remain preserved. Neurosonography provides a practical, accessible, and reliable tool for detecting these subtle cortical alterations in high-risk pregnancies.

Interstitial deletions involving 3q27.1 define a distinct microdeletion syndrome characterized by prenatal-onset growth restriction, postnatal microcephaly, hypotonia, intellectual disability, and distinctive craniofacial features. While AP2M1 haploinsufficiency has been proposed as the primary driver of this phenotype, the full spectrum of dosage-sensitive genes within the locus remains unclear. Here, we report a patient with a de novo heterozygous 3q27.1 microdeletion and delineate a refined minimal smallest region of overlap (SRO) of approximately 189 kb, representing the narrowest critical interval associated with the 3q27.1 microdeletion phenotype to date. Chromosomal microarray and exome-based CNV analysis confirmed the deletion, which encompasses PSMD2, EIF4G1, and POLR2H but excludes AP2M1 and DVL3. The patient exhibited severe intrauterine growth restriction, microcephaly, global developmental delay, and mild dysmorphism, consistent with the established 3q27.1 phenotype. PSMD2 encodes a non-ATPase regulatory subunit of the 26S proteasome, and its loss may disrupt proteasome-mediated protein turnover and neuronal homeostasis. Comparison with previously published cases and an overlapping ClinVar variant (ID: 60129) with similar features supports the pathogenicity of this minimal deletion. Our findings refine the 3q27.1 critical region, propose PSMD2 haploinsufficiency as a likely molecular mechanism underlying growth and neurodevelopmental defects. Further cases and functional studies are needed to confirm PSMD2 causality and clarify the proteasome-related mechanisms underlying 3q27.1 microdeletion syndrome.

Synergistic effects of nanoplastics and BDE-47 on glutathione dysregulation in rice: Insights from integrated multi-omics and computational modeling.

This scoping review aimed to comprehensively map the available evidence on the migration of fixation hardware and skeletal growth aberrations caused by craniomaxillofacial (CMF) osteosynthesis in the paediatric population. A systematic search was made in PubMed, Embase, Cochrane Library, Scopus, and Web of Science based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR). Search terms were tailored to captures studies addressing growth restriction and hardware migration associated with CMF fixation in children. A total of 762 articles were identified. 10 clinical studies and 23 animal studies were eligible. Due to the nature of the studies found, only a descriptive analysis was performed. Out of 183 children, 76% of them (mean age 10.6 months) underwent CMF fixation for management of craniosynostosis. 24.6% of these patients experienced hardware migration, exclusively in the calvaria. The temporal, parietal & frontal regions were the most frequent sites for migration, with the majority of fixation being titanium plates and screws (54.1%). Most transcranial migrations were asymptomatic (77.8%) and surgical intervention was performed in 28.8% of these affected children. Amongst the animal studies, intracranial hardware migration was reported in only 2 studies. Growth restriction was observed when CMF fixation involved cranial sutures or midfacial sites (16 studies), whereas mandibular growth remained unaffected (5 studies). Overall, the evidence regarding the long-term impact of titanium-based fixation on paediatric CMF growth and transcranial migration of hardware remains limited. This is largely attributed to the retrospective nature of available clinical studies and heterogeneity of animal models. Well-designed longitudinal studies are needed to provide more robust evidence to inform clinical practice. Nevertheless, this review consolidates current findings, highlights existing knowledge gaps and underscores the need for the development of bioresorbable fixation systems in paediatric CMF surgery.

Preeclampsia (PE) is a complex hypertensive disorder resulting from placental insufficiency during pregnancy. PE contributes to maternal and fetal morbidity and mortality and often co-occurs with fetal growth restriction (FGR); these two are both considered placental insufficiency syndromes. Alterations in mitochondrial function levels due to placental insufficiency play an important role in the pathophysiology of PE and FGR. Changes in these processes can lead to maternal and fetal organ damage with subsequent risk to develop cardiovascular disease. This review therefore investigates the effects of placental insufficiency syndromes, including PE and FGR, on mitochondrial function and its underlying mechanisms, using a perinatal approach including maternal heart and kidney, placenta, and fetal heart and kidney. This review also explores the potential of mitochondrial-targeted therapies in mitigating these effects. We provide an overview of the literature at hand and demonstrate the critical role of mitochondrial function in different organ systems. Subsequently, we also discuss the need for mitochondrial-targeted therapies, in particular, focused on oxidative stress, metabolic pathways, mitochondrial quality control, and mitochondrial calcium handling. This knowledge provides guidance for future studies and potential therapies to improve PE and FGR and their consequences for maternal and fetal outcomes during pregnancy and cardiovascular health later in life.

Clinical indications and timing of antenatal corticosteroids: A single-centre retrospective study

The pro-inflammatory cytokines IFN-α and TNF-α inhibit organoid-derived extravillous trophoblast invasion.

Mechanistic insights into Salmonella growth kinetics under solute-induced water activity stresses via transcriptomics and NMR analysis.

Preeclampsia (PE) is a pregnancy disorder characterized by placental maladaptation and maternal hypertension, with oxidative stress and lipid peroxidation as central features. Here we identify 2,4-dienoyl-CoA reductase 1 (DECR1), the rate-limiting enzyme in the auxiliary β-oxidation of unsaturated fatty acids, as a key regulator of trophoblast lipid redox balance. DECR1 expression is reduced in placentas from patients with late-onset preeclampsia (LOPE) and an L-NAME-induced PE mouse models. Genetic or pharmacological inhibition of DECR1 increases PUFA-rich lipid accumulation, enhances lipid peroxidation, and induces mitochondrial dysfunction, leading to loss of membrane potential, reactive oxygen species buildup, ATP depletion, and impaired trophoblast migration and invasion. In vivo, DECR1 inhibition causes hypertension, renal injury, fetal growth restriction, and defective placental vascular remodeling. Mechanistically, DECR1 loss disrupts mitochondrial quality control by suppressing mitocytosis, effects that are reversed by radical-trapping agents or mitochondria-targeted antioxidants. Liproxstatin-1 treatment restores maternal, fetal, and placental homeostasis. These findings define a DECR1-lipid peroxidation-mitochondria axis that maintains trophoblast function and placental adaptation, highlighting DECR1 as a potential therapeutic target for PE.

TDCIPP induces placental dysfunction and fetal growth restriction via oxidative stress-mediated PINK1/Parkin mitophagy.

Environmental cadmium drives placental senescence and fetal growth restriction via activating CLPP-dependent mitochondrial stress.

Aripiprazole, a third-generation atypical antipsychotic drug, crosses the placental barrier, yet its developmental skeletal effects remain unexplored. This study aimed to evaluate impact of prenatal aripiprazole exposure, administered at three different doses, on the ossification of axial skeleton in 20-day old rat fetuses. Forty pregnant Sprague-Dawley rats were assigned to four groups: control and three aripiprazole treated-groups receiving 3 mg/kg (low dose aripiprazole), 6 mg/kg (high dose aripiprazole), and 12 mg/kg (double high dose aripiprazole [DHDA]) daily from gestational days 6-19. Fetuses were delivered on gestation day 20, weighed, and processed for skeletal evaluation using Alizarin Red staining. Ossification of craniofacial bones, hyoid bone, vertebral centra and arches, sternum, and ribs were assessed and categorized as complete, delayed, or absent. A total of 151 fetuses were analyzed. Aripiprazole exposure induced a dose dependent reduction in fetal weight and in the number of completely ossified skeletal centers. Craniofacial bones, particularly parietal, interparietal, supraoccipital, and presphenoid, were the most affected. Significant impairments were observed in vertebral centra and arches across cervical, thoracic, lumbar, sacral, and coccygeal regions, with the DHDA group exhibiting the greatest deficits. Sternebrae ossification showed marked reduction, whereas rib ossification remained unaffected. A strong positive correlation was found between fetal weight and total number of complete ossification centers across all groups. Prenatal exposure to aripiprazole leads to dose dependent fetal growth restriction and delayed ossification of axial skeleton in rat fetuses. Future investigations should focus on the molecular mechanisms and consequences related to prenatal impacts of aripiprazole.

This study aimed to analyze metabolic characteristics of the umbilical cord blood associated with brain injury in neonates with selective fetal growth restriction (sFGR). A prospective cohort of 30 sFGR twin pairs delivered at Peking University Third Hospital between September 2017 and December 2019 was enrolled. Maternal-fetal clinical data and information on neonatal complications, including brain injury, were collected for both the growth-restricted (sFGR-S) and larger (sFGR-L) fetuses. The mean maternal age at delivery was (30.7±3.9) years, and the mean gestational age at delivery was (32.7±2.2) weeks. Among the 30 sFGR cases, there were 12 cases of type Ⅰ, 11 type Ⅱ, and 7 type Ⅲ. The cohort comprised 30 male and 30 female neonates (50% each). Brain injury occurred in 12 (40%) of the sFGR-S group, including 7 cases of intracranial hemorrhage (IVH), 3 cases of periventricular leukomalacia (PVL), and 2 case with both. In the sFGR-L group, brain injury occurred in 9 (30%) neonates, including 6 cases of IVH, 2 cases of PVL, and 1 case with both. Receiver operating characteristic (ROC) curve analysis for the sFGR-S group yielded an area under the curve (AUC) of 0.853 (95%CI: 0.698-1.000) for tyrosine alone, and an AUC of 0.944 (95%CI: 0.859-1.000) for the combination of tyrosine and myristic acid. For the sFGR-L group, the AUC was 0.880 (95%CI: 0.708-1.000) for S-adenosyl methionine (SAM) alone, and 0.917 (95%CI: 0.749-1.000) for the combination of SAM and trans-vaccenic acid. In conclusion, neonates in the sFGR-S and sFGR-L groups exhibit distinct metabolic profiles, and differential metabolites with their related pathways hold potential predictive value for neonatal brain injury.

Emerging environmental contaminants increasingly accumulate in soil ecosystems, yet their chronic biological impacts on soil-dwelling organisms remain poorly understood. Here, we demonstrate that tris(2,4-ditert-butylphenyl) phosphate (AO168═O), a prevalent soil-borne contaminant formed through the oxidative transformation of the widely used plastic antioxidant (AO168), compromises nematode fitness at relatively low concentrations. Exposure of C. elegans to AO168═O induces pronounced developmental and physiological impairments, including suppressed somatic growth, delayed developmental progression, disrupted energy homeostasis, and reduced reproductive output at 400-10,000 ng/g. Transcriptomic profiling reveals a robust reprogramming of gene expression that molecularly corroborates growth and developmental restriction. Notably, longevity-regulating pathways centered on the conserved insulin/IGF-1 signaling (IIS) are consistently and significantly enriched. Integrated gene-set enrichment analyses further demonstrate that AO168═O-associated transcriptional signatures closely recapitulate established IIS- and DAF-16-regulated expression programs, which were functionally validated by pharmacological inhibition and genetic ablation. Furthermore, early-life exposure leads to persistent and long-lasting fitness deficits, such as impaired locomotor performance and a marked reduction in adult lifespan, detectable even at the lowest exposure concentration. Together, these findings identify AO168═O as a previously underrecognized factor compromising nematode fitness, providing essential laboratory-based evidence that highlights the potential vulnerability of soil biota to ubiquitous soil-borne contaminants.

We compare adverse pregnancy outcomes after the Solomon technique versus selective laser surgery for twin-twin transfusion syndrome (TTTS). Retrospective cohort study of monochorionic diamniotic (MCDA) twin pregnancies that underwent laser surgery for TTTS at two centers between 2006-2023. Pregnancy outcomes were compared between patients treated with the Solomon versus the selective laser technique. The primary outcomes were delivery <4 weeks after surgery and delivery <28 weeks. Secondary outcomes included placental abruption, and recurrent TTTS or twin anemia polycythemia sequence requiring additional surgery. Multivariable robust Poisson regression models were used to estimate relative risks (RR) for outcomes adjusted for TTTS stage, selective fetal growth restriction, and cervical length, among other covariables. Solomonization' s effect on surgery-to-delivery interval was evaluated via Cox regression. P<0.05 was used. Of 1,680 TTTS cases, 80 were excluded due to dual fetal death (n=47) or missing laser technique or delivery data (n=33). In the remaining 1,600 cases, 44.9% (n=719) underwent the Solomon technique. Multivariable robust Poisson regression showed that Solomonization was independently associated with delivery <4 weeks after surgery (RR: 2.46 95% CI: 1.31-4.60; p=0.005), delivery <28 weeks (RR: 1.67 95% CI: 1.15-2.51; p=0.008), and placental abruption (RR: 1.74; 95% CI: 1.02-2.97; p=0.04). Cox regression demonstrated a shorter surgery-to-delivery interval with the Solomon technique (hazard ratio: 1.66; 95% CI: 1.49-1.84; p<0.001). The Solomon group had higher laser time, energy consumption, and PPROM rates, earlier gestational age at delivery, and lower 30-day survival rate of at least one twin. Recurrent TTTS or post-laser TAPS requiring additional surgery were similar between groups. The Solomon technique is associated with increased risks, including extreme preterm delivery, shorter surgery-to-delivery interval, and placental abruption.

Insulin modulates mPFC gene expression and emotional behavior in a sex-specific manner following fetal growth restriction.

To investigate the ultrasonographic characteristics and perinatal outcomes of fetuses diagnosed with FIUVV and compare isolated FIUVV cases with low-risk pregnancies. This retrospective study was conducted among patients diagnosed with FIUVV at a tertiary referral center between 2020 and 2024, along with a control group of low-risk pregnancies. The gestational age at the diagnosis and birth, the presence of additional structural and/or chromosomal anomalies in the fetus, and neonatal outcomes were recorded. A total of 66 fetuses were included in the study, comprising 26 diagnosed with FIUVV and 40 in the control group. Additional structural abnormalities were identified in 23.1% of FIUVV cases, and chromosomal abnormalities were detected in three nonisolated cases. In the comparison of isolated FIUVV cases with the control group, fetal growth restriction (FGR) and preterm birth were significantly higher in FIUVV cases. FIUVV, even when identified as an isolated finding, may be associated with an increased risk of adverse perinatal outcomes. Careful prenatal surveillance for fetal growth, along with screening for additional structural abnormalities, may contribute to more effective clinical management of these cases.