Objective: To investigate the association between sleep duration and depressive symptoms in children and adolescents, so as to provide scientific evidence for promoting mental health and preventing depression among relevant populations. Methods: A total of 2 192 children and adolescents aged 10-17 years with complete data from the 2018 China Family Panel Studies Database were included. Eight item Center for Epidemiologic Studies Depressive Scale(CES-D8) was used to assess participants depressive levels, and sleep duration was assessed via questionnaire. Multivariate Logistic regression model was used to analyze the association between different sleep duration categories and depressive symptom occurrence among children and adolescents. A restricted cubic spline(RCS) model analyzed the dose response relationship between sleep duration and the risk of depressive symptoms occurrence and segmented Logistic regression models to identify dose response effects. Results: Among the surveyed children and adolescents, 524(23.91%) exhibited depressive symptoms. Compared to those with sufficient sleep, children aged 10-12 years had a higher risk of depressive symptoms on average per day( OR =1.66, 95% CI =1.19-2.33) and during weekdays( OR =1.76, 95% CI =1.26-2.46), as well as in adolescents aged 13-17 years on a daily basis( OR =1.40，95% CI =1.06-1.85) and during weekdays( OR = 1.48，95% CI =1.12-1.95), and excessive sleep in adolescents on rest days was also significantly associated with higher risk of depressive symptoms( OR =1.65，95% CI =1.11-2.43)(all P <0.05). RCS analysis results indicate that children s sleep duration exhibits a linear negative correlation with the risk of depressive symptoms(all P nonlinear >0.05), while adolescents sleep duration showed a U shaped association with depressive symptoms(all P nonlinear <0.05) on a daily basis, during weekdays and weekends, with potential threshold effects at 10.00, 9.88, and 9.60 hours, respectively. Conclusions Sleep duration among children and adolescents is associated with depressive symptoms, with notable age related differeneces. It is recommended to develop targeted age specific interventions to reduce the risk of depressive symptoms in children and adolescents.

Objective: To investigate the association of the joint effect of body fat levels and dyslipidemia with cardiovascular structural abnormalities in children, so as to provide a scientific reference for the early prevention of cardiovascular damage. Methods: Based on the data from the second follow up (October 2021 to January 2022) of the Huantai Children Cardiovascular Health Follow up Cohort, 1 308 children with complete data were included. The fat mass percentage (FMP), fat mass index (FMI), subcutaneous fat mass (SFM) and visceral fat mass (VFM), left ventricular mass index (LVMI), relative wall thickness (RWT), thickening of carotid intima-media thickening (cIMT) , left ventricular hypertrophy (LVH) and left ventricular geometric remodeling (LVG), triglyceride (TG), total cholesterol (TC) ,high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) were obtained. Multivariable Logistic regression model was used to analyze the associations of FMP, FMI, SFM and VFM with thickening of cIMT, LVH and LVG. The joint effects of these body fat indicators and dyslipidemia on the aforementioned cardiovascular outcomes were further explored. Restricted cubic spline model was used to examine the dose response relationships between body fat levels and cardiovascular structural abnormalities. Results: Elevated body fat levels were significantly associated with an increased risk of cardiovascular structural abnormalities, exhibiting J shaped dose response relationships (all P <0.05). Compared with the group with normal body fat and normolipidemia, the risks of thickening of cIMT, LVH, and LVG in the group with elevated FMP combined with dyslipidemia were higher[ OR (95% CI )=11.70 (6.49-21.27), 5.53 (2.97-10.17), 2.33 (1.30-4.05)]; in the group with elevated FMI combined with dyslipidemia, the corresponding risks were higher[ OR (95% CI )= 11.68 (6.43-21.38), 6.98 (3.73-12.92), 2.65 (1.50-4.61)]; in the group with elevated SFM combined with dyslipidemia, the corresponding risks were higher[ OR (95% CI )=10.55 (5.83-19.24), 5.11 (2.71-9.45), 1.99 (1.11- 3.46 )]; and in the group with elevated VFM combined with dyslipidemia, the corresponding risks were higher[ OR (95% CI )=12.44 (6.76-23.14), 6.17 ( 3.31 -11.38), 2.30 (1.30-3.99)] (all P <0.05). Sex stratified analyses showed that the risk of thickening of cIMT in the combined exposure group of all four body fat indicators and dyslipidemia was significantly higher in girls than in boys (all P <0.01). Conclusions Elevated body fat levels and dyslipidemia have a combined effect in children, collectively increasing the risk of cardiovascular structural abnormalities. Prevention of cardiovascular damage in children should focus on both adiposity management and blood lipid regulation.

Objective: To explore the association between the joint association of screen time on weekdays and weekends with self rated sleep quality among adolescents, providing scientific basis for improving adolescent sleep health. Methods: Using data from "Huantai Children s Cardiovascular Health Follow up Cohort" survey conducted during November to December 2023, a total of 1 197 adolescents aged 12-17 years with complete demographic characteristics, physical measurements, and questionnaire data were included. The dose response relationship between screen time and sleep quality was evaluated by restrictive cubic splines (RCS). Based on screen time on weekdays and weekends (normal: < 2 h/d; excessive: ≥ 2 h/d), adolescents were categorized into 4 groups. Multivariate Logistic regression models were used to analyze the association between the combined effect of screen time on weekdays and weekends and sleep quality. Results: The RCS analysis results showed that there was a linear dose response relationship between average daily screen time and poor sleep quality in adolescents (non linear P >0.05). The results of multiple Logistic regression analysis showed that adjusting for potential covariates,compared with adolescents having normal screen time on both weekdays and weekends, those with excessive screen time on both weekdays and weekends had increased risk of poor sleep quality ( OR=2.51, 95%CI=1.33-4.62, P <0.01). Sex stratified analysis revealed that girls with excessive screen time on both weekdays and weekends had increased odds of poor sleep quality ( OR=3.03, 95%CI=1.23-7.14, P =0.01), compared to girls who had normal screen time on both weekdays and weekends. Conclusions A linear dose response relationship exists between daily screen time and poor sleep quality in adolescents. Excessive screen time on both weekdays and weekends is positively associated with poor sleep quality, particularly more pronounced among female adolescents.

Objective To investigate the relationship between geriatric nutritional risk index (GNRI) and osteoporosis (OP) in elderly hypertensive population. Methods Elderly physical examination population who received dual-energy bone mineral density examination and bone metabolic marker test in the hospital were selected from January 2021 to December 2024. According to whether they had hypertension and dual-energy bone mineral density results, the enrolled patients were divided into hypertension OP group (142 cases ), hypertension non-OP group (173 cases), non-hypertension OP group (102 cases) and non-hypertension non-OP group (100 cases). GNRI of all study subjects was measured. The correlation of GNRI and the occurrence of OP was explored by logistic regression analysis. The predictive efficiency of GNRI on the occurrence of OP was evaluated by receiver operating characteristic (ROC) curve. Results The BMD and GNRI in the hypertension group, and the non-hypertension OP group were significantly lower than those in the non-hypertension non-OP group (P<0.05). Compared with the hypertension non-OP group, the BMI, GNRI, BMD, and 25-OH Vit D in the hypertension OP group were significantly reduced (P<0.05) while the PTH level was significantly enhanced (P<0.05).logistic regression analysis showed that GNRI, 25-OH Vit D and PTH were closely related to OP in the elderly hypertensive population (P < 0.05). ROC curve analysis manifested that the AUC value of GNRI alone in predicting OP in elderly hypertensive population was 0.802, which was higher than that of 25-OH Vit D (AUC=0.723) and PTH (AUC=0.643). The AUC, sensitivity and specificity of combination of GNRI, 25-OH Vit D and PTH in predicting OP in elderly hypertensive population were 0.837, 66.20% and 86.13% (P<0.05). Conclusion GNRI is closely related to the occurrence of OP in elderly hypertensive population, and GNRI can be used as a potential indicator to assess the risk of OP.

Objective: To explore the association between blood pressure levels and brachial-ankle pulse wave velocity (baPWV) in adolescents, so as to provide a scientific basis for early prevention and control of cardiovascular disease. Methods: The study utilized data from the October to December 2023 survey conducted by of the Huantai Child Cardiovascular Health Cohort, which included 1 197 adolescents aged 12-17 years. According to the Reference of Screening for Elevated Blood Pressure among Children and Adolescents aged 7-18 years, participants were classified into normal, high normal, and elevated blood pressure groups. The baPWV elevation was defined as a baPWV value greater than or equal to the 90th percentile of the sex and age specific baPWV values in the study population. The association between elevated blood pressure and increased baPWV was assessed by binary Logistic regression models. Restricted cubic spline model was applied to evaluate the dose response curve of the relationship between blood pressure Z scores and increased baPWV. Results: Among adolescents, the prevalence of high normal and elevated blood pressure were 22.6% and 14.1%, respectively. The mean baPWV values were 918, 978 and 1 030 cm/s in the normal, high normal, and elevated blood pressure groups, respectively. The prevalence rates of elevated baPWV were 7.3%, 9.6% and 27.2% in these three groups correspondingly. Logistic regression analysis showed that, after adjusting for covariates, both high normal and elevated blood pressure were significantly associated with higher odds of increased baPWV[ OR(95%CI )=1.87(1.08-3.20) and 8.24(4.73-14.50), both P < 0.05]. Linear dose response associations were identified between systolic and diastolic blood pressure Z scores and increased baPWV ( P non linearity>0.05). Conclusions Elevated blood pressure in adolescents is positively associated with high baPWV. Greater emphasis should therefore be placed on blood pressure monitoring and health management during adolescence.

This study explores the mechanism of Guben Jiannao Liquid on Alzheimer's disease(AD) by regulating autophagy based on the liver kinase B1(LKB1)/adenosine monophosphate-activated protein kinase(AMPK)/mammalian target of rapamycin(mTOR) pathway. Male SD rats were randomly divided into the blank group, model group, low-dose and high-dose groups of Guben Jiannao Liquid, and rapamycin group, with 10 rats in each group. Except for the blank group, all other groups of rats were injected bilaterally in the hippocampus with β-amyloid(Aβ)_(1-42) to establish the AD model. The low-dose(6.21 g·kg~(-1)) and high-dose(12.42 g·kg~(-1)) groups of Guben Jiannao Liquid and rapamycin group(1 mg·kg~(-1)) were given the corresponding drugs by gavage, and the blank and model groups were given an equal volume of saline by gavage for four weeks. Morris water maze was used to test the learning and memory ability of rats in each group; hematoxylin-eosin(HE) and Nissl staining were used to observe the morphological and quantitative changes of neurons and Nissl bodies in the CA1 region of rat hippocampus; immunohistochemistry was utilized to detect Aβ-positive cell expression in the CA1 region of rat hippocampus; transmission electron microscopy was employed to observe ultrastructural changes in rat hippocampal tissue, and Western blot was used to examine the protein expression levels of LKB1, p-AMPK/AMPK, p-mTOR/mTOR, Beclin1, p62, and LC3-Ⅱ in the hippocampal tissue of the rats. The results showed that compared with those in the blank group, rats in the model group had elevated evasion latency and decreased number of platform transversal and residence time in the platform quadrant. The number of neurons in the hippocampal area was reduced, and the morphology was impaired. The average integral optical density value of Aβ-positive cells was elevated; the expression levels of LKB1, p-AMPK/AMPK, Beclin1, and LC3-Ⅱ were decreased, and the expression levels of p-mTOR/mTOR and p62 were increased. Compared with those in the model group, rats in the low-dose and high-dose groups of Guben Jiannao Liquid had shorter evasion latency, higher number of platform transversal, longer residence time in the platform quadrant, increased number of neurons, decreased expression of Aβ-positive cells and average integral optical density values, and increased number of autophagic lysosomes in hippocampal tissue. The expression levels of LKB1, Beclin1, and LC3-Ⅱ were elevated in the hippocampus of rats in the low-dose group of Guben Jiannao Liquid. The expression levels of LKB1, p-AMPK/AMPK, Beclin1, and LC3-Ⅱ were elevated in the hippocampal tissue of rats in the high-dose group of Guben Jiannao Liquid, and the expression levels of p-mTOR/mTOR and p62 were decreased. The findings suggest that Guben Jiannao Liquid can improve cognitive impairment in AD rats, and its mechanism of action may be related to the activation of the LKB1/AMPK/mTOR signaling pathway and the up-regulation of autophagy level.
Animals ; Alzheimer Disease/physiopathology* ; Male ; TOR Serine-Threonine Kinases/genetics* ; Autophagy/drug effects* ; Rats, Sprague-Dawley ; Protein Serine-Threonine Kinases/genetics* ; AMP-Activated Protein Kinases/genetics* ; Rats ; Drugs, Chinese Herbal/administration & dosage* ; Signal Transduction/drug effects* ; AMP-Activated Protein Kinase Kinases ; Humans ; Hippocampus/metabolism*

This study aims to investigate the optimal ratio of Astragali Radix-Curcumae Rhizoma(AC) for inhibiting the proliferation of 143B osteosarcoma cells, and to investigate the mechanism by which AC inhibits osteosarcoma growth and metastasis through angiogenesis and cell adhesion mediated by the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/hypoxia inducible factor-1α(HIF-1α) pathway. A subcutaneous 143B tumor-bearing nude mouse model was successfully established and randomly divided into the model group, and the AC 1∶1, 2∶1, and 4∶1 groups. Body weight, tumor volume, and tumor weight were recorded. Real-time quantitative polymerase chain reaction(RT-qPCR) and Western blot were used to detect the mRNA and protein expression levels of PI3K, Akt, phosphorylated Akt(p-Akt), HIF-1α, vascular endothelial growth factor A(VEGFA), transforming growth factor-β1(TGF-β1), epithelial cadherin(E-cadherin), neural cadherin(N-cadherin), vimentin, matrix metalloproteinase 2(MMP2), matrix metalloproteinase 9(MMP9), B-cell lymphoma-2(Bcl-2), Bcl-2-associated X protein(Bax), and caspase-3 in the hypoxic core region of the tumor tissue. A cell hypoxia model was established, and the effects of AC-medicated serum(model group, AC 1∶1, 2∶1, and 4∶1 groups) on angiogenesis, proliferation, adhesion, invasion, and migration of 143B osteosarcoma cells were examined through CCK-8, flow cytometry, Transwell assay, cell adhesion assay, and HUVEC tube formation assay. The results showed that compared with the model group, the tumor weight and volume were smallest in the 2∶1 group. The expression levels of PI3K, Akt, p-Akt, HIF-1α, VEGFA, and TGF-β1 were significantly decreased, and the protein expression of E-cadherin was significantly increased, while the protein expression of N-cadherin, vimentin, MMP2, and MMP9 was significantly decreased. Additionally, the protein expression of Bax and caspase-3 was significantly increased, and Bcl-2 protein expression was significantly decreased. In vitro experiments showed that after intervention with AC-medicated serum at a 2∶1 ratio, the cell activity, adhesion, invasion, and migration of 143B cells were significantly reduced, apoptosis was significantly increased, and HUVEC tube formation was significantly decreased. In conclusion, the 2∶1 ratio of AC showed the most effective inhibition of 143B cell growth. AC can inhibit the growth and metastasis of osteosarcoma 143B cells by regulating the PI3K/Akt/HIF-1α signaling pathway, inhibiting angiogenesis and reducing cell adhesion, invasion, and migration.
Osteosarcoma/pathology* ; Animals ; Proto-Oncogene Proteins c-akt/genetics* ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics* ; Humans ; Mice ; Cell Adhesion/drug effects* ; Cell Proliferation/drug effects* ; Neovascularization, Pathologic/metabolism* ; Drugs, Chinese Herbal/administration & dosage* ; Phosphatidylinositol 3-Kinases/genetics* ; Cell Line, Tumor ; Mice, Nude ; Signal Transduction/drug effects* ; Astragalus Plant/chemistry* ; Bone Neoplasms/physiopathology* ; Male ; Rhizome/chemistry* ; Mice, Inbred BALB C ; Angiogenesis

OBJECTIVE: To explore the protective effects and underlying mechanisms of H ₂S against lipid peroxidation-mediated carbonyl stress in the uranium-treated NRK-52E cells. METHODS: Cell viability was evaluated using CCK-8 assay. Apoptosis was measured using flow cytometry. Reagent kits were used to detect carbonyl stress markers malondialdehyde, 4-hydroxynonenal, thiobarbituric acid reactive substances, and protein carbonylation. Aldehyde-protein adduct formation and alcohol dehydrogenase, aldehyde dehydrogenase 2, aldo-keto reductase, nuclear factor E2-related factor 2 (Nrf2), and cystathionine β-synthase (CBS) expression were determined using western blotting or real-time PCR. Sulforaphane (SFP) was used to activate Nrf2. RNA interference was used to inhibit CBS expression. RESULTS: GYY4137 (an H ₂S donor) pretreatment significantly reversed the uranium-induced increase in carbonyl stress markers and aldehyde-protein adducts. GYY4137 effectively restored the uranium-decreased Nrf2 expression, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2, accompanied by a reversal of the uranium-decreased expression of CBS and aldehyde-metabolizing enzymes. The application of CBS siRNA efficiently abrogated the SFP-enhanced effects on the expression of CBS, Nrf2 activation, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2 and concomitantly reversed the SFP-enhanced effects of the uranium-induced mRNA expression of aldehyde-metabolizing enzymes. Simultaneously, CBS siRNA reversed the SFP-mediated alleviation of the uranium-induced increase in reactive aldehyde levels, apoptosis rates, and uranium-induced cell viability. CONCLUSION H ₂S induces Nrf2 activation and nuclear translocation, which modulates the expression of aldehyde-metabolizing enzymes and the CBS/H ₂S axis. Simultaneously, the Nrf2-controlled CBS/H ₂S axis may at least partially promote Nrf2 activation and nuclear translocation. These events form a cycle-regulating mode through which H ₂S attenuates the carbonyl stress-mediated NRK-52E cytotoxicity triggered by uranium.
NF-E2-Related Factor 2/genetics* ; Animals ; Hydrogen Sulfide/pharmacology* ; Rats ; Signal Transduction/drug effects* ; Lipid Peroxidation/drug effects* ; Cell Line ; Uranium/toxicity* ; Antioxidant Response Elements ; Kidney/metabolism* ; Oxidative Stress/drug effects* ; Cell Survival/drug effects* ; Apoptosis/drug effects*

Acute kidney injury (AKI) has high morbidity and mortality, but effective clinical drugs and management are lacking. Previous studies have suggested that macrophages play a crucial role in the inflammatory response to AKI and may serve as potential therapeutic targets. Emerging evidence has highlighted the importance of forkhead box protein O1 (FoxO1) in mediating macrophage activation and polarization in various diseases, but the specific mechanisms by which FoxO1 regulates macrophages during AKI remain unclear. The present study aimed to investigate the role of FoxO1 in macrophages in the pathogenesis of AKI. We observed a significant upregulation of FoxO1 in kidney macrophages following ischemia-reperfusion (I/R) injury. Additionally, our findings demonstrated that the administration of FoxO1 inhibitor AS1842856-encapsulated liposome (AS-Lipo), mainly acting on macrophages, effectively mitigated renal injury induced by I/R injury in mice. By generating myeloid-specific FoxO1-knockout mice, we further observed that the deficiency of FoxO1 in myeloid cells protected against I/R injury-induced AKI. Furthermore, our study provided evidence of FoxO1's pivotal role in macrophage chemotaxis, inflammation, and migration. Moreover, the impact of FoxO1 on the regulation of macrophage migration was mediated through RhoA guanine nucleotide exchange factor 1 (ARHGEF1), indicating that ARHGEF1 may serve as a potential intermediary between FoxO1 and the activity of the RhoA pathway. Consequently, our findings propose that FoxO1 plays a crucial role as a mediator and biomarker in the context of AKI. Targeting macrophage FoxO1 pharmacologically could potentially offer a promising therapeutic approach for AKI.