OBJECTIVES: Exposure to rare earth elements (REEs) has been linked to various systemic diseases, but their impact on the offspring blood-brain barrier (BBB) via the gut-brain axis remains unclear. This study aims to investigate the effects of maternal exposure to neodymium oxide (Nd₂O₃) on the BBB integrity of offspring rats, and to evaluate the potential protective role of bifidobacterium tetrad viable tablets (BTVT) against Nd₂O₃-induced intestinal and BBB damage. METHODS: Healthy adult SD rats were mated at a 1:1 male-to-female ratio, with the day of vaginal plug detection marked as gestational day 0. A total of 60 pregnant rats were randomly assigned to the following groups: Control, 50 mg/(kg·d) Nd₂O₃, 100 mg/(kg·d) Nd₂O₃, 200 mg/(kg·d) Nd₂O₃, and 200 mg/(kg·d) Nd₂O₃ + BTVT group. Treatments were administered by daily oral gavage throughout pregnancy and lactation. On postnatal day 21 (weaning), offspring feces, brain, and colon tissues were collected. Hematoxylin and eosin (HE) staining was used to assess structural changes in brain and intestinal tissues. Short-chain fatty acids (SCFAs) in feces were quantified by gas chromatography-mass spectrometry (GC-MS). Evans Blue (EB) dye extravasation assessed BBB permeability. Gene and protein expression levels of tight junction proteins occludin and zonula occludens-1 (ZO-1) were measured by reverse transcription PCR (RT-PCR) and Western blotting (WB), respectively. Neodymium levels in brain tissue were determined via inductively coupled plasma mass spectrometry (ICP-MS). RESULTS: HE staining revealed that maternal Nd₂O₃ exposure caused mucosal edema, increased submucosal spacing, and lymphocyte infiltration in offspring colon, as well as neuronal degeneration and vacuolization in brain tissue. BTVT intervention alleviated these changes. GC-MS analysis showed that levels of acetic acid, propionic acid, butyric acid, and isobutyric acid significantly decreased, while valeric acid and isovaleric acid increased in offspring of Nd₂O₃-exposed mothers (P<0.05). BTVT significantly restored levels of acetic, propionic, and isobutyric acids and reduced valeric acid content (P<0.05). EB permeability was significantly elevated in Nd₂O₃-exposed offspring brains (P<0.05), but reduced with BTVT treatment (P<0.05). RT-PCR and WB showed downregulation of occludin and ZO-1 expression following Nd₂O₃ exposure (P<0.05), which was reversed by BTVT (P<0.05). ICP-MS results indicated significantly increased brain neodymium levels in offspring from all Nd₂O₃-exposed groups (P<0.05), while BTVT significantly reduced neodymium accumulation compared to the 200 mg/(kg·d) Nd₂O₃ group (P<0.05). CONCLUSIONS Maternal exposure to Nd₂O₃ during pregnancy and lactation disrupts intestinal health and BBB integrity in offspring, elevates brain neodymium accumulation, and induces neuronal degeneration. BTVT effectively mitigates Nd₂O₃-induced intestinal and BBB damage in offspring, potentially through modulation of the gut-brain axis.
Animals ; Female ; Blood-Brain Barrier/pathology* ; Pregnancy ; Rats, Sprague-Dawley ; Rats ; Male ; Neodymium/toxicity* ; Prenatal Exposure Delayed Effects/prevention & control* ; Lactation ; Maternal Exposure/adverse effects* ; Brain

BACKGROUND: Particulate matter (PM), a major component of ambient air pollution, accounts for a substantial burden of diseases and fatality worldwide. Maternal exposure to PM during pregnancy is particularly harmful to children's health since this is a phase of rapid human growth and development. METHOD: In this review, we synthesize the scientific evidence on adverse health outcomes in children following prenatal exposure to the smallest toxic components, fine (PM RESULTS: Maternal exposure to fine and ultrafine PM directly and indirectly yields numerous adverse birth outcomes and impacts on children's respiratory systems, immune status, brain development, and cardiometabolic health. The biological mechanisms underlying adverse effects include direct placental translocation of ultrafine particles, placental and systemic maternal oxidative stress and inflammation elicited by both fine and ultrafine PM, epigenetic changes, and potential endocrine effects that influence long-term health. CONCLUSION Policies to reduce maternal exposure and health consequences in children should be a high priority. PM
Adult ; Air Pollutants/adverse effects* ; Air Pollution/prevention & control* ; Animals ; Cardiovascular Diseases/chemically induced* ; Child Health ; Child, Preschool ; Disease Models, Animal ; Endocrine System Diseases/chemically induced* ; Epigenomics ; Female ; Humans ; Immune System Diseases/chemically induced* ; Infant ; Infant, Newborn ; Male ; Maternal Exposure/adverse effects* ; Nervous System Diseases/chemically induced* ; Oxidative Stress ; Particle Size ; Particulate Matter/adverse effects* ; Placenta ; Pregnancy ; Pregnancy Outcome/epidemiology* ; Prenatal Exposure Delayed Effects/epidemiology* ; Respiratory Tract Diseases/chemically induced* ; Young Adult

OBJECTIVETo explore prenatal related factors of high BMI status in children at 1 and 2 years of age.

METHODA total of 2 220 newborns from Shenyang, Wuhan and Guangzhou were recruited in this birth cohort, thereafter they were followed up to two years of age.Self-administered questionnaires were used to collect such variables as social-demographic characteristics and feeding practice, etc. The anthropometric measures of children were collected by trained health staff. The data were subjected to multiple logistic regression analysis to determine the related factors for high BMI among infants and toddlers.

RESULTThe number of children with high BMI status were 550 (32.80%) at one year of age and 309 (26.23%) at two, respectively. The number of boys with high BMI status were 178 and girls 309 at age two years. The prevalence of high BMI status among boys (29.1%) at age two was significantly higher than that of girls (23.1%) (χ² = 5.52, P = 0.02). Logistic regression analysis showed that after the adjustment for sex, parental educational level, family economic status and other confounding factors, maternal passive smoking during pregnancy [OR:aged one:1.38 (1.05-1.82);aged two:1.48 (1.05-2.09)], maternal pre-pregnancy overweight and obesity [aged one:1.29 (1.05-1.58); aged two:1.35 (1.04-1.76)], paternal overweight and obesity [aged one:1.50 (1.21-1.87); aged two:1.47 (1.11-1.95)] and birth weight [aged one:1.53 (1.05-1.82); aged two:1.87 (1.33-2.63)]were identified to be associated with high BMI status in children.

CONCLUSIONMaternal passive smoking during pregnancy, paternal and maternal (pre-pregnancy) overweight or obesity and high birth weight are found to be important related factors for high BMI status in young children. Childhood overweight/obesity prevention should be considered starting as early as before pregnancy.

Birth Weight ; Body Mass Index ; Child, Preschool ; China ; epidemiology ; Cohort Studies ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Multivariate Analysis ; Odds Ratio ; Overweight ; epidemiology ; etiology ; prevention & control ; Parents ; Pediatric Obesity ; epidemiology ; etiology ; prevention & control ; Pregnancy ; Prenatal Exposure Delayed Effects ; epidemiology ; Risk Factors ; Smoking ; adverse effects ; Surveys and Questionnaires