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.

Calcineurin inhibitor（CNI） is potent immunosuppressive agents and serve as cornerstone therapies in the treatment of organ transplantation and autoimmune diseases， with cyclosporine A and tacrolimus being the representative drugs. Long-term use of CNI can lead to drug-induced hyperglycemia， severely affecting patients’ prognosis. The pathogenesis involves multilevel pathological alterations： at the pancreatic β-cell level， CNI directly damage β-cell by inducing calcium overload， oxidative stress， and mitochondrial dysfunction， suppressing the expression of key insulin synthesis factors and promoting apoptosis； in peripheral tissues， CNI interfere with insulin receptor substrate phosphorylation and inhibit the phosphatidylinositol 3 kinase/protein kinase B signaling pathway， resulting in decreased glucose uptake and insulin resistance； additionally， CNI can also induce β-cell injury by suppressing the secretion and receptor signal transduction of glucagon-like peptide-1， as well as by activating the nuclear factor kappa B pathway to promote inflammatory responses. Clinical studies demonstrate that the incidence of CNI-associated hyperglycemia is closely related to drug type， dosage， and individual patient factors. For high-risk patients， dose adjustment of CNI， switching to agents with lower metabolic toxicity when necessary， and selection of appropriate glucose-lowering regimens based on glycemic levels are recommended. Future research should further elucidate the molecular mechanisms of CNI metabolic toxicity and optimize individualized pharmacotherapy strategies to improve long-term patient outcomes.

Objective To understand the status of body image disturbance and its influencing factors in patients with ankylosing spondylitis (AS), so as to provide a scientific basis for the clinical management of AS. Methods A total of 353 AS patients admitted from January 2022 to December 2024 were selected as research subjects. Chinese version of Body Image Disturbance Questionnaire (BIDQ) was used to investigate the body image disturbance in AS patients. Single factor analysis was performed by t test and analysis of variance, and multiple factors were analyzed by multivariate linear regression. Results The total score of BIDQ in 342 AS patients was (25.01±4.22). Multivariate linear regression analysis results showed that self-paid medical expense, nighttime VAS score and negative emotion PANAS score could positively predict body image disturbance in AS patients (standardized regression coefficient=0.413, 0.413, 0.460, P<0.05), and PSSS score, positive emotion PANAS score and exercise management CDSSM score could negatively predict body image disturbance (standardized regression coefficient=-0.245, -0.134, -0.247, P<0.05). Conclusion The body image disturbance in AS patients is worthy of clinical attention. Nighttime pain, negative emotion and self-paid medical treatment can increase the risk of body image disturbance. Positive emotion, social support and high self-management level of exercise behavior can reduce the formation of body image disturbance, which can provide new ideas for clinical management of AS patients.

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.

Background: High-mobility group box protein 1 (HMGB1) is a chromatin-binding protein involved in arthritis, ischemia, sepsis, atherosclerosis, neurodegenerative disorders, meningitis, and cancer. HMGB1 exhibits dual roles in cancer, acting as either a tumor suppressor or oncoprotein depending on context. Objective: This research aimed to elucidate HMGB1’s functional significance in cutaneous squamous cell carcinoma (cSCC). Methods: We overexpressed HMGB1 in cSCC cell lines using recombinant adenovirus and examined its effects on cell proliferation, colony formation, and cell migration. Results: Immunohistochemical analysis revealed elevated HMGB1 expression levels in cSCC tissue relative to normal epidermis. To assess the influence of HMGB1, we employed recombinant adenoviruses expressing HMGB1 to transduce SCC cell lines (SCC12 and SCC13). Enhanced HMGB1 expression significantly promoted cellular proliferation and colony formation capacity.Notably, HMGB1 overexpression elevated the levels of proliferation regulators, including P63, SOX2, CDK4 and CDK6. Furthermore, HMGB1 overexpression substantially enhanced tumor invasiveness, accompanied by upregulation of epithelial-mesenchymal transition (EMT) biomarkers. Mechanistically, overexpression of HMGB1 enhanced transforming growth factor-β signaling by increasing phosphorylation of SMAD2/3, the key mediators of EMT. Conclusion These data imply that HMGB1 acts as a tumor-promoting factor in cSCC.

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.

The nervous system is the dominant regulatory system in the human body. The traditional theory is that tumors lack innervation. However, an increasing number of studies have shown complex bidirectional interactions between tumors and the nervous system. Globally, colorectal cancer (CRC) is the third most common cancer. With the rise of tumor neuroscience, the role of nervous system imbalances in the occurrence and development of CRC has attracted increasing amounts of attention. However, there are still many gaps in the research on the interactions and mechanisms involved in the nervous system in CRC. This article systematically reviews emerging research on the bidirectional relationships between the nervous system and CRC, focusing on the following areas: (1) Effects of the nervous system on colon cancer. (2) Effects of CRC on the nervous system. (3) Treatment of CRC associated with the nervous system.
Humans ; Colorectal Neoplasms/therapy* ; Animals ; Nervous System/metabolism*

Enamel demineralization, the formation of white spot lesions, is a common issue in clinical orthodontic treatment. The appearance of white spot lesions not only affects the texture and health of dental hard tissues but also impacts the health and aesthetics of teeth after orthodontic treatment. The prevention, diagnosis, and treatment of white spot lesions that occur throughout the orthodontic treatment process involve multiple dental specialties. This expert consensus will focus on providing guiding opinions on the management and prevention of white spot lesions during orthodontic treatment, advocating for proactive prevention, early detection, timely treatment, scientific follow-up, and multidisciplinary management of white spot lesions throughout the orthodontic process, thereby maintaining the dental health of patients during orthodontic treatment.
Humans ; Consensus ; Dental Caries/etiology* ; Dental Enamel/pathology* ; Tooth Demineralization/etiology* ; Tooth Remineralization

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*