Objective: To explore the factors affecting language development delay among children aged <3 years, so as to provide a basis for the prevention and early intervention of children's language development problems. Methods: Eighty-one children aged <3 years with language development delay who visited the children's language development clinic of Shaoxing Maternal and Child Health Hospital from January to December 2024 as the case group. Meanwhile, 118 children who underwent routine physical examinations at the children's health clinic during the same period, had normal language development were randomly selected as the control group. Data on children's basic information, parenting environment, and screen exposure were collected through questionnaire surveys. Language development delay was assessed using the Early Language Milestone Scale and the Gesell Developmental Diagnosis Scale. The factors for language development delay were analyzed using a multivariable logistic regression model. Results: The case group comprised 81 children, including 56 boys (69.14%) and 25 girls (30.86%), with a mean age of (23.14±4.84) months. The control group consisted of 118 children, including 81 boys (68.64%) and 37 girls (31.36%), with a mean age of (23.81±4.60) months. Multivariable logistic regression analysis showed that daily parental companionship time of ≥2 hours (OR=0.121, 95%CI: 0.040-0.367), attending childcare institutions (OR=0.103, 95%CI: 0.030-0.352), the average daily screen exposure time <1 hour (OR=0.614, 95%CI: 0.400-0.942), interactive parental accompaniment during screen exposure (OR=0.350, 95%CI: 0.157-0.779), and restricting screen exposure time (OR=0.162, 95%CI: 0.056-0.470) were associated with a lower risk of language development delay among children aged <3 years. Conclusion Daily paternal companionship of 2 hours or more, attending childcare institutions, daily screen exposure time of less than 1 hour, interactive parental companionship during screen time, and limiting screen exposure time can reduce the risk of language developmental delay among children aged under 3 years.

Objective To explore the potential mechanism of Gegen qinlian decoction(GGQLD)containing serum in ameliorating nonalcoholic fatty liver disease(NAFLD)in human hepatocellular carcinoma HepG2 cells based on transcriptomics.Methods An in vitro model of NAFLD was constructed by free fatty acid(FFA)-induced fat accumulation in HepG2 cells,and cells were treated with different proportions of GGQLD and pioglitazone-containing serum.The lipid deposition in each group was detected by oil red O staining,and the lipid content in each group was evaluated by triglyceride level.Transcriptome technology was used to detect the differentially expressed genes between the intervention groups,and GO annotation analysis,KEGG enrichment analysis and protein interaction(PPI)network analysis were performed to verify the differentially expressed genes by RT-PCR.Results Compared with normal control group,the number of red lipid droplets in the model control group increased,and the triglyceride content increased significantly(P＜0.01).Compared with model control group,the content of red lipid droplets in the GGQLD medium dose group showed a decreasing trend,and the intracellular triglyceride content decreased significantly(P＜0.05).A total of 608 differentially expressed genes were identified by transcriptome analysis,of which 163 differentially expressed genes were up-regulated and 445 differentially expressed genes were down-regulated.GO enrichment analysis showed that the differentially expressed genes were mainly involved in the regulation of MAP kinase phosphatase activity.KEGG analysis showed that the differentially expressed genes were mainly involved in MAPK signaling pathway.RT-PCR results showed that GGQLD up-regulated the expression level of MAP2K6 mRNA and down-regulated the expression levels of FOSL1,CTSL,DUSP5,DUSP1,JUN,HSPA6,IL1A,IL11 and RELB mRNA,which may be mainly involved in MAPK signaling pathway.Conclusion GGQLD has the effect of improving NAFLD,which may be related to MAPK signaling pathway.

Objective To explore the potential mechanism of Gegen qinlian decoction(GGQLD)containing serum in ameliorating nonalcoholic fatty liver disease(NAFLD)in human hepatocellular carcinoma HepG2 cells based on transcriptomics.Methods An in vitro model of NAFLD was constructed by free fatty acid(FFA)-induced fat accumulation in HepG2 cells,and cells were treated with different proportions of GGQLD and pioglitazone-containing serum.The lipid deposition in each group was detected by oil red O staining,and the lipid content in each group was evaluated by triglyceride level.Transcriptome technology was used to detect the differentially expressed genes between the intervention groups,and GO annotation analysis,KEGG enrichment analysis and protein interaction(PPI)network analysis were performed to verify the differentially expressed genes by RT-PCR.Results Compared with normal control group,the number of red lipid droplets in the model control group increased,and the triglyceride content increased significantly(P＜0.01).Compared with model control group,the content of red lipid droplets in the GGQLD medium dose group showed a decreasing trend,and the intracellular triglyceride content decreased significantly(P＜0.05).A total of 608 differentially expressed genes were identified by transcriptome analysis,of which 163 differentially expressed genes were up-regulated and 445 differentially expressed genes were down-regulated.GO enrichment analysis showed that the differentially expressed genes were mainly involved in the regulation of MAP kinase phosphatase activity.KEGG analysis showed that the differentially expressed genes were mainly involved in MAPK signaling pathway.RT-PCR results showed that GGQLD up-regulated the expression level of MAP2K6 mRNA and down-regulated the expression levels of FOSL1,CTSL,DUSP5,DUSP1,JUN,HSPA6,IL1A,IL11 and RELB mRNA,which may be mainly involved in MAPK signaling pathway.Conclusion GGQLD has the effect of improving NAFLD,which may be related to MAPK signaling pathway.

Abstract: Objective　To investigate the pollution characteristics of major heavy metals in PM2.5 in urban areas of Haikou City, and to assess their potential health risks to humans. Methods　From 2021 to 2022, samples of atmospheric PM2.5 were monthly collected from the typical urban areas of Haikou, and the concentrations of nine heavy metal elements including arsenic (As), cadmium (Cd), chromium (Cr), lead (Pb), manganese (Mn), nickel (Ni), copper (Cu), vanadium (V), and zinc (Zn) were measured using the inductively coupled plasma mass spectrometry (ICP-MS). The health risk assessment of these heavy metals was conducted using a health risk model. Results　The average mass concentration of PM2.5 in Haikou was (20.506±13.054) µg/m³, with a range of 4.000 to 64.000 µg/m³ during the year 2021 and 2022. The PM2.5 concentrations showed significant seasonal variations: highest in winter, followed by autumn and spring, and lowest in summer. The total concentration of the nine heavy metal elements ranged from 0.030 to 138.000 ng/m³, with Zn, Mn, and Pb having the highest concentrations, particularly notable during the autumn and winter seasons. Enrichment factor (EF) analysis indicated moderate enrichment (10 Cd > Cr > As > Pb > V > Zn > Cu > Ni. The total non-carcinogenic hazard index (HI) ranged from 0.171 to 0.361. The inhalation incremental lifetime carcinogenic risk values (ILCR) for the four elements Cr, As, Cd, and Ni ranged from 2.911×10-7 to 1.558×10-5, with ILCR decreasing in that order. The total carcinogenic risk index (TR) varied between 1.502×10-5 and 3.169×10-5, with risk intensities for HI and TR in the order: children > adult males > adult females. Conclusions　The average PM2.5 concentration in the Haikou urban area is lower than the 24-hour average concentration limit of Grade I (35 µg/m3) in the "Environmental Air Quality Standard" (GB 3095-2012), but still higher than the control standard recommended by the WHO in 2021 (15 µg/m3). The non-carcinogenic health risks of the nine heavy metal elements detected in PM2.5 are not significant, but Cr and As have potential carcinogenic risks, with children being more vulnerable than other populations.

Circadian disruption is being increasingly recognized as a critical factor in the development and progression of Parkinson’s disease (PD). This review aims to provide an in-depth overview of the relationship between circadian disruption and PD by exploring the molecular, cellular, and behavioral aspects of this interaction. This review will include a comprehensive understanding of how the clock gene system and transcription–translation feedback loops function and how they are diminished in PD. The article also discusses the role of clock genes in the regulation of circadian rhythms, as well as the impact of clock gene dysregulation on mitochondrial function, oxidative stress, and neuroinflammation, including the microbiota-gut-brain axis, which have all been proposed as being crucial mechanisms in the pathophysiology of PD. Finally, this review highlights potential therapeutic strategies targeting the clock gene system and circadian rhythm for the treatment of PD.

Objective:To detect gene mutations in a pedigree with dominant dystrophic epidermolysis bullosa (DDEB) .Methods:A 20-year-old male proband presented with repeated blisters, ulceration, pigmentation, scars on the limbs, and deformation of the nails/toenails after birth. There were 5 patients in the 3-generation family, and they all presented with typical skin lesions. Peripheral blood samples were obtained from 14 members of the pedigree (including the 5 patients) and 100 unrelated healthy controls. Whole-exome sequencing was performed in the proband to identify relevant mutation sites, which were then confirmed in the family by Sanger sequencing.Results:Genetic testing indicated that the proband and the other 4 patients all carried a missense mutation (c.7885G>A) in exon 107 of the COL7A1 gene, resulting in the substitution of glycine by arginine at amino acid position 2629 (p.G2629R). The mutation was identified neither in the 9 healthy relatives nor in the 100 unrelated healthy controls. The mutation co-segregated with DDEB in the family, and was not included in databases such as Pubmed, HGMD or ClinVar, suggesting it was a novel missense mutation. The amino acid encoded by this mutation may alter the structure of type Ⅶ collagen, thereby affecting its function.Conclusion:A novel missense mutation was identified in exon 107 of the COL7A1 gene in the family with DDEB, expanding the spectrum of mutations in the COL7A1 gene.