ObjectiveTo investigate the screen exposure situation and its determinants among children aged 0‒3 years, so as to offer insights for intervening in children’s screen exposure. MethodsA total of 1 797 children who received routine physical examinations in Shaoxing Maternal and Child Health Care Hospital from January 2024 to December 2024 were enrolled. A self-designed screen exposure questionnaire was used to collect demographic information for children, educational attainment of parents and main caregivers, contents of video screen exposure, and video devices. The screen exposure rate among children was analyzed, and a multivariable logistic regression model was used to analyze its influencing factors. ResultsAmong the 1 797 children aged 0‒3 years, 935 were boys (52.03%), and 862 were girls (47.97%). The mean age was (21.81±9.97) months old. A total of 335 infants and toddlers had an average daily cumulative screen exposure >1 hour over the past week, with a screen exposure rate of 18.64%. Multivariable logistic regression analyses showed that the risk of screen exposure was higher with each one-year increase in the child’s age (OR=1.90, 95%CI: 1.58‒2.28), with cartoons or nursery rhymes as the main video content (OR=2.09, 95%CI: 1.27‒3.44; OR=1.75, 95%CI: 1.02‒2.97, respectively), and with watching videos during the period for meals or for parents doing housework, or before bedtime (OR=3.51, 95%CI: 2.08‒5.92; OR=2.92, 95%CI: 1.75‒4.88; OR=2.01, 95%CI: 1.16‒3.49, respectively). In contrast, higher maternal educational levels (OR=0.67, 95%CI:0.49‒0.92) were associated with a reduced rate of screen exposure. ConclusionAmong children aged 0‒3 years, their screen exposure is associated with their age, maternal educational level, screen content, and time of video watching. The departments should strengthen the education on screen exposure for older children and the mothers with lower education, while advocating for parents to scientifically and normatively manage screen content and time.

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.

Objective To observe the value of intratumoral and peritumoral CT radiomics for evaluating KRAS gene status in patients with colorectal adenocarcinoma.Methods Totally 245 patients with colorectal adenocarcinoma were retrospectively enrolled and divided into mutant group(n=139)and wild group(n=106)according to KRAS gene status,also divided into training set(n=171)and test set(n=74)at a ratio of 7∶3.Clinical data were compared between groups,and clinical factors were screened with logistic regression analysis to establish a clinical model.Based on enhanced venous phase CT images,intratumoral volume of interest(VOI),peritumoral VOI,and intratumoral+peritumoral VOI were delineated,radiomics features were extracted,and radiomics models were constructed.The combination model was constructed based on the best radiomics model combined with clinical factors.The value of each model for evaluating KRAS gene status in patients with colorectal adenocarcinoma was analyzed.Results Significant differences of patients’gender and carcinoembryonic antigen(CEA)were found between mutant group and wild group(both P＜0.05),which were independent impact factors of KRAS gene status in patients with colorectal adenocarcinoma(both P＜0.05).The area under the curve(AUC)of clinical model for evaluating KRAS gene status in patients with colorectal adenocarcinoma in training set and test set was 0.633 and 0.658,respectively.Intratumoral+peritumoral 3 mm model was the best radiomics model,with AUC of 0.921 and 0.894 in training set and test set,respectively.AUC of the combination model in training set and test set was 0.949 and 0.956,respectively.In training set,significant differences of AUC were found between clinical model and intratumoral+peritumoral 3 mm model,also between clinical model and combination model(both P＜0.001),while in test set,significant differences of AUC were found between each two models(all P＜0.05).Conclusion Intratumoral+peritumoral 3 mm radiomics based on enhanced venous phase CT could help to evaluate KRAS gene status in patients with colorectal adenocarcinoma.Combining with patients’gender and CEA could further improve efficacy of this model.

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.