Objective: To investigate the prevalence of overweight and obesity among children and adolescents in Yangzhou City, and its association with screen behaviors, so as to provide scientific evidence for weight management among students. Methods: In May 2025, an electronic questionnaire survey was conducted among children and adolescents in Yangzhou City. A total of 3 722 participants were selected from grades 4 to 12 in 18 primary and secondary schools (108 classes) by using stratified cluster random sampling. The Chi square test was used to compare the differences in the detection rates of overweight and obesity among children and adolescents with 5 types of screen behaviors (watching TV, playing electronic games, scrolling short videos, screen based learning, electronic socializing) in different time groups each day (never, >0~<2 h, ≥2 h). Multivariate Logistic regression analysis was performed to examine the associations of five types of screen behaviors, presence of electronic devices in the bedroom, and screen use during meals on the weight status of children and adolescents. Results: The prevalence of overweight and obesity among children and adolescents was 37.3%. For all five types of screen behaviors, the differences in the distribution of overweight and obesity detection rates among children and adolescents across the three time spent categories were statistically significant ( χ 2=30.76- 70.78 , all P <0.01). After adjusting for confounding factors, multivariate Logistic regression analysis revealed that frequent or always using screens during meals( OR =1.63, 95％ CI =1.14~2.31), playing video games ( OR =1.28, 95% CI =1.11-1.48), browsing short videos ( OR =1.29, 95％ CI=1.09-1.54), and screen based learning ( OR =1.26, 95％ CI =1.10-1.44) were significantly associated with overweight and obesity among children and adolescents (all P <0.05). Conclusions Excessive screen use is positively correlated with the incidence of overweight and obesity in children and adolescents. Targeted interventions on screen behaviors among children and adolescents are therefore warranted.

BACKGROUND: Valvular heart disease (VHD) has become increasingly common with the aging in China. This study aimed to evaluate regional differences in the clinical features, management strategies, and outcomes of patients with VHD across different regions in China. METHODS: Data were collected from the China-VHD Study. From April 2018 to June 2018, 12,347 patients who presented with moderate or severe native VHD with a median of 2 years of follow-up from 46 centers at certified tertiary hospitals across 31 provinces, autonomous regions, and municipalities in Chinese mainland were included in this study. According to the locations of the research centers, patients were divided into five regional groups: eastern, southern, western, northern, and central China. The clinical features of VHD patients were compared among the five geographical regions. The primary outcome was all-cause mortality or rehospitalization for heart failure. Kaplan-Meier survival analysis was used to compare the cumulative incidence rate. RESULTS: Among the enrolled patients (mean age, 61.96 years; 6877 [55.70%] male), multiple VHD was the most frequent type (4042, 32.74%), which was mainly found in eastern China, followed by isolated mitral regurgitation (3044, 24.65%), which was mainly found in northern China. The etiology of VHD varied significantly across different regions of China. The overall rate of valve interventions was 32.67% (4008/12,268), with the highest rate in southern China at 48.46% (205/423). In terms of procedure, the proportion of transcatheter valve intervention was relatively low compared to that of surgical treatment. Patients with VHD in western China had the highest incidence of all-cause mortality or rehospitalization for heart failure. Valve intervention significantly improved the outcome of patients with VHD in all five regions (all P  <0.05). CONCLUSIONS: This study revealed that patients with VHD in China are characterized by significant geographic disparities in clinical features, treatment, and clinical outcomes. Targeted efforts are needed to improve the management and prognosis of patients with VHD in China according to differences in geographical characteristics. REGISTRATION ClinicalTrials.gov , NCT03484806.
Aged ; Female ; Humans ; Male ; Middle Aged ; China/epidemiology* ; Heart Valve Diseases/therapy* ; Kaplan-Meier Estimate ; Tertiary Care Centers ; Treatment Outcome

Objective:To explore the expression of lamin (LMN) gene in Colorectal cancer (CRC) , as well as the effects of knockdown LMNA expression in colorectal cancer cells on its migration ability and related molecular mechanisms.Methods:Paraffin-embedded specimens of tumor tissues and corresponding peritumoral tissues were collected from 37 colorectal cancer patients for the detection of LMNA protein expression. Colorectal cancer cell line SW480 was cultured in vitro and divided into Mock group (transfected MOCk-siRNA) and LMNA group (transfected LMNA-siRNA) . Real-time quantitative PCR was used to detect the LMNA mRNA content in SW480 cells of experimental group and control group. The expression levels of LMNA, Wnt and β-catenin in SW480 cells of experimental group and control group were detected by Western blotting. The migration ability of cells in each group was detected by cell scratch test. The migration ability of cells in each group were detected by transwell assay.Results:Immunohistochemical test showed that the positive rate of LMNA protein in colorectal cancer tissues was 89.19% (33/37 cases) , and the expression rate in corresponding paracancer tissues was 48.65% (18/37 cases) . The expression level of LMNA in colorectal cancer tissues was significantly higher than that in paracancer tissues ( P<0.001) . siRNA decreased the expression of LMNA protein in colorectal cancer cells SW480. The scratch healing rate was (53.71±5.34) % in the experimental group and (83.84±6.98) % in the control group. The results of Transwell experiment showed that the number of successfully migrated cells in the experimental group was 34.92±5.11, and that in the control group was 93.87±12.57. The results showed that the migration ability of SW480 cells was significantly decreased after low expression of LMNA ( P<0.01) . Western blot results showed that the relative expression level of Wnt and β-catenin in LMNA group was 0.42±0.12 and 0.22±0.11 respectively. The relative expression levels of Wnt and β-catenin in MOCK group were 1.28±0.26 and 1.14±0.21 respectively. The expression levels of P16 and Wnt and β-catenin in PC3 cells with low LMNA expression were increased ( P<0.05) , while the expressions of WNT and β-catenin were decreased (both P<0.05) . Conclusion:The expression of LMNA was significantly increased in colorectal cancer, which may be related to the malignant degree of colorectal cancer. LMNA proteins may affect the migration ability of colorectal cancer cells by regulating the Wnt/β-catenin signaling pathway.

Objective To explore the association between phase angle(PhA)and sarcopenia in middle-aged and elderly patients with type 2 diabetes mellitus(T2DM),and to evaluate its predictive value for the risk of sarcopenia in these patients.Methods We collected data from 356 middle-aged and elderly T2DM patients hospitalized in the Department of Endocrinology,Nanjing Drum Tower Hospital Group Suqian Hospital from March 2022 to June 2024,including 274 patients with diabetes only and 82 patients with T2DM combined with sarcopenia.A Logistic regression analysis was conducted to assess the relationship between phase angle and sarcopenia.The predictive value of PhA for sarcopenia in T2DM patients was analyzed using the receiver operating characteristic(ROC)curve,and the trend of PhA with the severity of sarcopenia in T2DM patients was tested by the Jonckheere-Terpstra method.Results Univariate analysis showed that the PhA value in the T2DM with sarcopenia group was significantly lower than that in the diabetes alone group,with a statistically significant difference(P<0.05).Additionally,height,body mass,body mass index(BMI),waist circumference,arm circumference,calf circumference,fasting insulin,postprandial 2 h insulin,fasting C-peptide,postprandial 2 h C-peptide,triglycerides,albumin,blood urea nitrogen,body composition indicators,6 m walking speed,muscle mass,and muscle strength-related indicators were significantly lower in the T2DM with sarcopenia group compared to the diabetes alone group.Age,duration of diabetes,glycated hemoglobin,25-hydroxyvitamin D[25-(OH)D]were significantly higher in the T2DM with sarcopenia group,with statistically significant differences(P<0.05).Multivariate Logistic regression analysis indicated that,after adjusting for other factors,PhA remained associated with sarcopenia in T2DM patients(P<0.05),with a decreased PhA increasing the risk of sarcopenia.ROC curve analysis showed that the area under the curve(AUC)for PhA predicting sarcopenia in T2DM patients was 0.769(95% CI:0.710-0.829),indicating the predictive efficacy of PhA.Trend analysis demonstrated a significant negative correlation between PhA and the severity of sarcopenia in T2DM patients(P<0.05).Conclusion The PhA is significantly associated with sarcopenia in patients with T2DM.It can serve as an early predictive and diagnostic tool for sarcopenia in individuals with T2DM.

Objective:To compare the changes in fracture displacement under different vertical loadings between the 2 different internal fixation modalities for vertically unstable femoral neck fractures of Pauwels type Ⅲ by a mechanical study and a finite element analysis.Methods:Twelve biomimic bones were transversely dissected from 10 cm below the lesser trochanter of the femur to create femoral neck fracture models with a Pauwels angle of 70° using a swing saw. The models were equally divided into 2 groups ( n=6): group A was fixed with 3 cannulated screws after fracture reduction (scheme A), and group B with 3 cannulated screws plus a self-designed anteromedial support plate after fracture reduction (scheme B). Continuous vertical force was applied using a mechanical testing machine. Changes in displacement were recorded and load-displacement curves were plotted. One volunteer (female, 28 years old, 168 cm in height and 65 kg in weight) was selected for finite element analysis of her CT images of both lower limbs to examine the maximum displacement and the maximum Mises stress in scheme A and scheme B respectively. Results:In groups A and B respectively: All the 6 biomimic mimetic bones had similar load and displacement curves, and similar fracture displacements (Dx) at different loading points (N X); the curves of 6 biomimic bones were highly fitted with S-shaped curve equation (the r-square value was close to 1). At the initial loading stage (0 N0.05). When the load was 100 N

Objective:To explore the expression of lamin (LMN) gene in Colorectal cancer (CRC) , as well as the effects of knockdown LMNA expression in colorectal cancer cells on its migration ability and related molecular mechanisms.Methods:Paraffin-embedded specimens of tumor tissues and corresponding peritumoral tissues were collected from 37 colorectal cancer patients for the detection of LMNA protein expression. Colorectal cancer cell line SW480 was cultured in vitro and divided into Mock group (transfected MOCk-siRNA) and LMNA group (transfected LMNA-siRNA) . Real-time quantitative PCR was used to detect the LMNA mRNA content in SW480 cells of experimental group and control group. The expression levels of LMNA, Wnt and β-catenin in SW480 cells of experimental group and control group were detected by Western blotting. The migration ability of cells in each group was detected by cell scratch test. The migration ability of cells in each group were detected by transwell assay.Results:Immunohistochemical test showed that the positive rate of LMNA protein in colorectal cancer tissues was 89.19% (33/37 cases) , and the expression rate in corresponding paracancer tissues was 48.65% (18/37 cases) . The expression level of LMNA in colorectal cancer tissues was significantly higher than that in paracancer tissues ( P<0.001) . siRNA decreased the expression of LMNA protein in colorectal cancer cells SW480. The scratch healing rate was (53.71±5.34) % in the experimental group and (83.84±6.98) % in the control group. The results of Transwell experiment showed that the number of successfully migrated cells in the experimental group was 34.92±5.11, and that in the control group was 93.87±12.57. The results showed that the migration ability of SW480 cells was significantly decreased after low expression of LMNA ( P<0.01) . Western blot results showed that the relative expression level of Wnt and β-catenin in LMNA group was 0.42±0.12 and 0.22±0.11 respectively. The relative expression levels of Wnt and β-catenin in MOCK group were 1.28±0.26 and 1.14±0.21 respectively. The expression levels of P16 and Wnt and β-catenin in PC3 cells with low LMNA expression were increased ( P<0.05) , while the expressions of WNT and β-catenin were decreased (both P<0.05) . Conclusion:The expression of LMNA was significantly increased in colorectal cancer, which may be related to the malignant degree of colorectal cancer. LMNA proteins may affect the migration ability of colorectal cancer cells by regulating the Wnt/β-catenin signaling pathway.

Iron overload is strongly associated with heart disease. Ferroptosis is a new form of regulated cell death indicated in cardiac ischemia-reperfusion (I/R) injury. However, the specific molecular mechanism of myocardial injury caused by iron overload in the heart is still unclear, and the involvement of ferroptosis in iron overload-induced myocardial injury is not fully understood. In this study, we observed that ferroptosis participated in developing of iron overload and I/R-induced cardiomyopathy. Mechanistically, we discovered that Parkin inhibited iron overload-induced ferroptosis in cardiomyocytes by promoting the ubiquitination of long-chain acyl-CoA synthetase 4 (ACSL4), a crucial protein involved in ferroptosis-related lipid metabolism pathways. Additionally, we identified p53 as a transcription factor that transcriptionally suppressed Parkin expression in iron-overloaded cardiomyocytes, thereby regulating iron overload-induced ferroptosis. In animal studies, cardiac-specific Parkin knockout mice (Myh6-CreER ^T2 /Parkin ^fl/fl ) fed a high-iron diet presented more severe myocardial damage, and the high iron levels exacerbated myocardial I/R injury. However, the ferroptosis inhibitor Fer-1 significantly suppressed iron overload-induced ferroptosis and myocardial I/R injury. Moreover, Parkin effectively protected against impaired mitochondrial function and prevented iron overload-induced mitochondrial lipid peroxidation. These findings unveil a novel regulatory pathway involving p53-Parkin-ACSL4 in heart disease by inhibiting of ferroptosis.

Alzheimer's disease (AD), characterized by β-amyloid (Aβ) aggregation and neuroinflammation, remains a formidable clinical challenge. Herein, we present an innovative nose-to-brain delivery platform utilizing lactoferrin (Lf)-functionalized lipid nanoparticles (LNPs) co-encapsulating α-mangostin (α-M) and β-site APP cleaving enzyme 1 (BACE1) siRNA (siB). This dual-modal therapeutic system synergistically combines the neuroprotective and microglia-reprogramming capabilities of α-M with the transcriptional silencing of BACE1 via siB, thereby simultaneously inhibiting Aβ production and enhancing its clearance. Fabricated via a microfluidic approach, the LNPs exhibited uniform particle size distribution, great encapsulation efficiency, and robust colloidal stability. Upon intranasal administration, Lf-functionalization enabled superior brain-targeting efficacy through receptor-mediated transcytosis. In vitro studies demonstrated that α-M reversed Aβ-induced low-density lipoprotein receptor downregulation, promoting microglial phagocytosis and autophagic degradation of Aβ, while siB effectively suppressed BACE1 expression, abrogating Aβ synthesis. In vivo investigations in APP/PS1 transgenic mice revealed remarkable cognitive recovery, substantial Aβ plaque reduction, and alleviation of neuroinflammation and oxidative stress. This intricately designed LNP system, exploiting a non-invasive and efficient nose-to-brain delivery route, provides a biocompatible, synergistic, and transformative therapeutic strategy for the multifaceted management of AD.

Objective : To investigate the effect of long non-coding RNA LUCAT1 (lncRNA LUCAT1) on the biological behavior of MIA PaCa-2 in human pancreatic cancer cells , and to explore the potential role of LUCAT1 in the malignant progression of pancreatic cancer. Methods : The mutation and expression of LUCAT1 in pancreatic cancer were analyzed by GEPIA , the expression levels of LUCAT1 in human pancreatic ductal cells HPNE and hu- man pancreatic cancer cells were detected by q-PCR , and the expression and distribution of LUCAT1 in human pancreatic cancer tissues were detected by FISH . CCK-8 assay and Transwell assay were used to detect the effects of LUCAT1 on the proliferation , apoptosis , drug resistance , and migration of MIA PaCa-2 cells . Gene ensemble enrichment analysis was performed to compare the related signaling pathways involved in LUCAT1 , and Western blot assay was used to verify the protein expression level . Results : The results of GEPIA analysis showed that the expression level of LUCAT1 in human pancreatic cancer tissues was up-regulated , and the expression of LUCAT1 in human pancreatic cancer cells was significantly higher ( P < 0. 05 ) . Knockdown and overexpression of LUCAT1 could affect the proliferation , apoptosis , gemcitabine resistance , migration and invasion of pancreatic cancer cells , and the differences were statistically significant (P < 0. 05) . In addition , LUCAT1 affected p-Akt expression levels in pancreatic cancer and was inhibited after treatment with Akt inhibitor MK-2206 . Conclusion LUCAT1 regulates the malignant progression of MIA PaCa-2 in pancreatic cancer cells through the PI3K-Akt signaling pathway.

Fetal growth restriction(FGR)refers to the failure of a fetus to reach the level of growth potential determined by its genetic potential.It is a common obstetric complication,occurring in 5%to 10%of pregnancies.As a major risk factor for perinatal death and adverse neonatal outcomes,early prediction of FGR is crucial for optimizing pregnancy management.Existing evidence suggests that FGR is significantly associated with a variety of adverse pregnancy outcomes,including intrauterine hypoxia,preterm birth,neonatal asphyxia,and even neonatal mortality.It may also affect long-term neurological development and increase the risk of metabolic diseases in adulthood.Its pathogenesis is complex,which may involve placental blood flow perfusion insufficiency and genetic factors.Ultrasound parameters are the main basis for the diagnosis of FGR,among which fetal biological and hemodynamic parameters are of great value.Elevated umbilical artery blood flow resistance index,absent or reversed end-diastolic blood flow,and placental insufficiency are associated with the severity of FGR.However,approximately 10%of fetuses diagnosed by ultrasound as having FGR are later confirmed to be healthy small-for-gestational-age(SGA)infants after birth,and this false positive result may lead to unnecessary clinical interventions.Currently,there is no recognized accurate prediction model for FGR in clinical practice.Future research should focus on establishing unified diagnostic criteria and developing multi-index joint prediction tools based on artificial intelligence(AI).Early prediction and intervention for FGR are of great significance to improve perinatal outcomes.This paper reviewed the predictive value of ultrasound parameters,blood indicators,and their integration with AI for FGR,in order to provide a basis for clinical decision-making.