Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is difficult to diagnose. Inflammatory bowel disease (IBD) is a common chronic digestive disease. Previous studies have shown a potential correlation between ASD and IBD, but the pathophysiological mechanism remains unclear. The purpose of this research was to examine the biological mechanisms underlying the differentially expressed genes (DEGs) of ASD and IBD using bioinformatics tools. Methods: Limma software was used to evaluate the DEGs between ASD and IBD. The GSE3365, GSE18123, and GSE150115 microarray data sets were acquired from the Gene Expression Omnibus (GEO) database. We then performed 6 analyses, namely, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional annotation; weighted gene coexpression network analysis; correlation analysis of hub genes with autophagy, ferroptosis and immunity; transcriptional regulation analysis of hub genes; single-cell sequencing analysis; and potential therapeutic drug prediction. Results: A total of 505 DEGs associated with ASD and 616 DEGs associated with IBD were identified, and 7 genes overlapped between these sets. GO and KEGG analyses revealed several pathways enriched in both diseases. A total of 98 common genes related to ASD and IBD were identified by weighted gene coexpression network analysis (WGCNA), and 4 hub genes were obtained by intersection with the 7 intersecting DEGs, which were PDGFC, CA2, GUCY1B3 and SDPR. We also found that 4 hub genes in the two diseases were related to autophagy, ferroptosis or immune factors. In addition, motif–TF annotation analysis showed that cisbp__M0080 was the most relevant motif. We also used the Connectivity Map (CMap) database to identify 4 potential therapeutic agents. Conclusion: This research reveals the shared pathogenesis of ASD and IBD. In the future, these common hub genes may provide new targets for further mechanistic research as well as new therapies for patients with ASD and IBD.

Cadmium (Cd) is a heavy metal and environmental toxin. Exposure to Cd has been associated with a variety of human cancers. In this study, we performed in vitro assays to examine the effects of cadmium chloride (CdCl₂) on A549 cells, a human lung adenocarcinoma cell line. Cd does not affect proliferation, migration, or apoptosis of A549 cells at concentrations of 0.1–10 μM. At 0.5 and 1 μM, Cd increases the expression of vascular endothelial growth factor (VEGF) (p < 0.05, p < 0.01, respectively), but not basic fibroblast growth factor (b-FGF) in A549 cells. The conditioned media were collected from the A549 cells treated with 1 μM Cd and were co-cultured with human umbilical vein endothelial cells (HUVECs). Upon treatment with the conditioned media, the proliferation and migration of HUVECs significantly increased (p < 0.01, p < 0.05, respectively), while apoptosis remained unchanged. In addition, 1 μM Cd increases the level of hypoxia inducible factor 1-α (HIF1-α), which is a positive regulator of VEGF expression. Although low-dose Cd does not directly affect the growth of lung adenocarcinoma cells, it might facilitate the development of tumors through its pro-angiogenic effects.

The gut microbiota, as a critical guardian of human health, maintains physiological homeostasis, modulating immunity, and facilitates nutrient metabolism. Parabacteroides goldsteinii, a probiotic gut commensal, has garnered increasing scientific attention. This review systematically examines its biological characteristics, then analyzes mechanisms promoting health (immunomodulation, metabolic regulation, and intestinal barrier reinforcement), and finally evaluates disease associations (metabolic disorders, neurological diseases, inflammatory conditions, and malignancies). Current evidence shows that therapeutic efficacy against obesity, non-alcoholic fatty liver disease, inflammatory bowel disease, autism spectrum disorder, and colorectal cancer via short-chain fatty acids secretion, bile acid transformation, and host immunity modulation. Dietary factors (e.g., inulin), pharmacological agents (e.g., metformin, aspirin), and lifestyle interventions (e.g., exercise synbiotics) dynamically regulate its abundance, underscoring therapeutic potential. Despite translational challenges–like optimizing cultivation, dose-response characterization, and genetic tool development–emerging applications (engineered probiotics, fecal microbiota transplantation, and synthetic biology) highlight broad prospects. Future research should prioritize context-dependent mechanisms across diseases and refined translation strategies for microbiome-based precision medicine.

There remains controversy regarding whether the growth charts constructed from data of term infants, such as those produced by the World Health Organization (WHO) standards, can appropriately evaluate the postnatal growth of preterm infants. This retrospective cohort study, conducted in the First Affiliated Hospital of Shandong First Medical University in Jinan China, aimed to compare the postnatal growth charts of singleton preterm and term infants using WHO standards at 40–160 weeks postmenstrual age (PMA). A total of 5,459 and 15,185 sets of longitudinal measurements [length/height, weight, head circumference (HC), and body mass index (BMI)] from birth to 160 weeks PMA were used to construct growth charts for 559 singleton preterm (mean PMA at birth, 33.84 weeks) and 1,596 singleton term infants (born at 40 weeks PMA), respectively, using the Generalized Additive Models for Location, Scale, and Shape (GAMLSS) method. Z-scores (prematurity corrected) were calculated using WHO Anthro software. Compared to WHO standards, all parameters of preterm infants were increased, especially in terms of length/height and weight; the gap between the two almost spanned two adjacent centile curves. Compared to term controls, the length/height, weight, and BMI of preterm infants were higher at 40 weeks PMA, surpassed by term infants at 52–64 weeks PMA, and quite consistent thereafter. The HC of preterm infants at 40–160 weeks PMA was quite consistent with both term controls and the WHO standards. The Z-scores for length/height, weight, and BMI of preterm infants relative to the WHO standards gradually decreased from 1.20, 1.13, and 0.74 at 40–44 weeks PMA to 0.67, 0.42, and 0.03 at 132–160 weeks PMA, respectively; Z-scores for HC of preterm infants rapidly decreased from 0.73 to 0.29 at 40–50 weeks PMA, and then fluctuated in the range of 0.08–0.23 at 50–160 weeks PMA. Preterm infants had higher growth trajectories than the WHO standards and similar but not identical trajectories to term infants during the first 2 years of life. These findings reemphasize the necessity of constructing local growth charts for Chinese singleton preterm infants.

Background: It is important to choose a suitable birthweight reference to assess newborns, especially those that are small for gestational age (SGA). Currently, there is no regional standard reference for the north of China or for Shandong province. Methods: A total of 130,911 data records of singleton, live neonates born at 24–42 weeks of gestation were collected from 2016 to 2018 in Shandong province. A new birthweight-for-gestational age percentile reference was constructed based on the Generalized Additive Model for Location, Scale and Shape (GAMLSS) package in R version 3.5. The established gestational age weight curve was compared separately with the Fenton curve, INTERGROWTH−21st curve, and the Chinese Neonatal Network Standard curve of 2015. Results: We established the reference values of birthweight by gestational age at the 3rd, 10th, 25th, 50th, 75th, 90th, and 97th percentiles. Newborns had much heavier birthweights than those in the INTERGROWTH-21st and Fenton curves at most gestational ages. Although the newborns' birthweight references were closer to the Chinese Neonatal Network Standard except a few for gestational age, this study and INTERGROWTH-21st had similar birthweight curve shapes. Conclusions: There are obvious differences among the criteria for newborn birthweights. Therefore, it is more accurate to assess newborns using the local birthweight reference.

Benign familial infantile seizure (BFIS) is an autosomal dominant infantile‐onset epilepsy syndrome with a typically benign prognosis. It is commonly associated with heterozygous mutations of the PRRT2 gene located on chromosome 16p11.2. The frameshift heterozygous mutation (c.649dupC, p.Arg217Profs^∗8) in PRRT2 is responsible for the majority of BFIS cases. In this report, we present a rare case of a girl with a confirmed clinical and genetic diagnosis of BFIS due to a frameshift heterozygous mutation in PRRT2 (c.649dupC). She exhibited typical neurodevelopment until 15 months of age, followed by an unexpected severe autistic regression. In addition to BFIS, PRRT2 mutations are also associated with paroxysmal kinesigenic dyskinesia (PKD) and infantile convulsions and paroxysmal choreoathetosis (ICCA), indicating a complex genotype‐phenotype heterogeneity in PRRT2 mutations. This clinical observation highlights the possibility that BFIS patients with PRRT2 mutations may not always have a benign neurodevelopmental prognosis, emphasizing the need for long‐term clinical follow‐up.