BACKGROUND:LncRNA-TNFRSF13C,an important factor in B cell development and function,is expressed in periodontal tissues of patients with periodontitis,but the specific mechanism is still unclear. OBJECTIVE:To investigate the mechanism of lncRNA-TNFRSF13C regulating miR-1246 on hypoxia-inducible factor 1α in periodontal cells. METHODS:Human periodontal ligament cells(hPDLCs)were treated with lipopolysaccharide and divided into group A(hPDLCs cell lines without transfection),group B(hPDLCs cell lines transfected with TNFRSF13C NC-siRNA),group C(hPDLCs cell lines transfected with TNFRSF13C-siRNA),group D(hPDLCs cell line transfected with miR-1246 mimics),group E(hPDLCs cell line transfected with miR-1246 siRNA),group F(hPDLCs cell line transfected with TNFRSF13C-siRNA+miR-1246 mimics),and group G(hPDLCs cell line transfected with TNFRSF13C-siRNA+miR-1246 siRNA).The relative expression of lncRNA-TNFRSF13C and miR-1246 in each group was detected by qRT-PCR.Cell counting kit-8 assay was used to detect cell viability.Apoptosis was detected by flow cytometry.Expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins was detected by western blot.The correlation between lncRNA-TNFRSF13C and miR-1246 was analyzed by Pearson,and the targeting relationship was analyzed by dual-luciferase reporter assay. RESULTS AND CONCLUSION:There was no significant difference in human periodontal ligament cell activity,apoptosis rate and protein indexes between groups A and B(P>0.05).Compared with group B,hPDLCS cell activity in group C was increased,and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were decreased(P<0.05).Compared with group C,hPDLCS cell activity in group D was decreased,and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were increased(P<0.05).Compared with group D,the cell activity of group E was increased(P<0.05).The cell activity in group F was lower than that in group E,and the apoptosis rate was reduced in both groups E and F(P<0.05).Compared with group F,the cell activity of group G was increased,and the apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor were decreased(P<0.05).LncRNA-TNFRSF13C was positively correlated with miR-1246(P<0.05).Compared with the TNFRSF13C-siRNA group,the fluorescence activity of miR-1246-wt in the TNFRSF13C-NC group was reduced(P>0.05);compared with the miR-1246-NC group,the fluorescence activities of hypoxia-inducible factor 1α-wt and vascular endothelial growth factor-wt in the miR-1246 mimics group were increased(P<0.05).To conclude,down-regulation of lncRNA-TNFRSF13C can promote the activity of periodontal cells treated with lipopolysaccharide,reduce apoptosis,and inhibit hypoxia-inducible factor 1α and vascular endothelial growth factor.The mechanism is related to the regulation of miR-1246 activity.

Vascular cognitive impairment (VCI), caused by cerebrovascular dysfunction, severely impacts the quality of life in the elderly population, yet effective therapeutic approaches remain limited. Mitophagy, a selective mitochondrial quality-control mechanism, has emerged as a critical focus in neurological disease research. Accumulating evidence indicates that mitophagy modulates oxidative stress, neuroinflammation, and neuronal apoptosis. Key signaling pathways associated with mitophagy—including PINK1/Parkin, BNIP3/Nix, FUNDC1, PI3K/Akt/mTOR, and AMPK—have been identified as potential therapeutic targets for VCI. This review summarizes the mechanistic roles of mitophagy in VCI pathogenesis and explores emerging therapeutic strategies targeting these pathways, aiming to provide novel insights for clinical intervention and advance the development of effective treatments for VCI.

ObjectiveTo investigate the independent risk factors for poor prognosis in patients with acute pancreatitis （AP） by analyzing inflammatory factors， lung ultrasound （LUS） scores， and CT scores， to establish a nomogram prediction model， and to provide a basis for early clinical intervention. MethodsA total of 409 patients with AP who were admitted to Changshu Hospital Affiliated to Soochow University from January 2021 to October 2023 were enrolled as subjects， and they were divided into modeling group with 288 patients and validation group with 121 patients using the simple random sampling method at a ratio of 7∶3. According to the prognosis， each group was further divided into poor prognosis group and good prognosis group. The levels of C-reactive protein （CRP）， procalcitonin （PCT）， interleukin-6 （IL-6）， interleukin-10 （IL-10）， and tumor necrosis factor-α （TNF-α） were measured for both groups within 72 hours after admission， and LUS scores， modified CT severity index （MCTSI）， and extrapancreatic inflammation on computed tomography （EPIC） scores were assessed within 48‍ ‍—‍ ‍72 hours after admission. The independent-samples t test was used for comparison of normally distributed continuous data between groups， and the Mann-Whitney U rank sum test was used for comparison of non-normally distributed continuous data between groups； the chi-square test was used for comparison of categorical data between groups. A LASSO regression analysis was used to screen for the variables that were included in the multivariate logistic regression model to identify the independent risk factors for the poor prognosis of AP， and then a nomogram prediction model was established. The receiver operating characteristic （ROC） curve and the calibration curve were used to assess the discriminatory ability and goodness of fit of the nomogram model， and a decision curve analysis was used to assess the clinical applicability of the model. ResultsAmong the 288 patients with AP in the modeling group， there were 33 （11.46%） in the poor prognosis group and 255 （88.54%） in the good prognosis group； among the 121 patients with AP in the validation group， there were 13 （10.74%） in the poor prognosis group and 108 （89.26%） in the good prognosis group. Compared with the good prognosis group， the poor prognosis group had significantly higher levels of CRP （Z=3.607， P<0.05）， IL-6 （Z=4.189， P<0.05）， and TNF-α （t=2.584， P<0.05）， and significantly higher scores of LUS （t=8.075， P<0.05）， MCTSI （t=5.929， P<0.05）， and EPIC （t=8.626， P<0.05）. The multivariate logistic regression analysis showed that CRP （odds ratio ［OR］=3.592， 95% confidence interval ［CI］： 1.272‍ ‍—‍ ‍10.138， P<0.05）， IL-6 （OR=4.225， 95%CI： 1.468‍ ‍—‍ ‍12.156， P<0.05）， TNF-α （OR=3.540， 95%CI： 1.205‍ ‍—‍ ‍10.401， P<0.05）， LUS （OR=7.094， 95%CI： 2.398‍ ‍—‍ ‍20.986， P<0.05）， MCTSI （OR=7.612， 95%CI： 2.832‍ ‍—‍ ‍20.462， P<0.05）， and EPIC （OR=11.915， 95%CI： 4.007‍ ‍—‍ ‍35.432， P<0.05） were independent risk factor for poor prognosis in patients with AP. A nomogram prediction model was established based on the above 6 indicators， which had an area under the ROC curve of 0.924 （95%CI： 0.883‍ ‍—‍ ‍0.964）， and the Youden index for the optimal cut-off value was 0.670， with a sensitivity of 0.909 and a specificity of 0.761. The calibration curve showed good consistency between the predicted and observed results in both the modeling group and the validation group. The decision curve analysis showed that the predictive model had certain clinical effectiveness. ConclusionThe nomogram model for predicting the risk of poor prognosis in AP patients based on CRP， IL-6， TNF-α， LUS score， MCTSI score， and EPIC score has relatively good predictive performance and can provide important strategic guidance for developing early intensified treatment regimens for AP patients in clinical practice.

Objective: To explore the comorbidity and associated factors of dental caries and overweight/obesity among primary and secondary school students in Guangxi, so as to provide a scientific basis for the development of targeted prevention strategies. Methods: A stratified cluster random sampling method was used to survey 178 700 students from the fourth grade of primary school to the third year of high school in Guangxi Zhuang Autonomous Region from September to November 2023, including physical examination, oral screening, and questionnaire survey. Chisquare tests and binary Logistic regression analysis were employed to investigate the related factors of the cooccurrence of dental caries and overweight/obesity among students. Results: The comorbidity rate of dental caries and overweight/obesity was 9.55%, with urban areas (9.95%) higher than rural counties (9.24%), boys (10.54%) higher than girls (8.54%), primary school students (11.49%) higher than senior high school students (8.92%) and junior high school students (8.05%), and nonboarding students (11.44%) higher than boarding students (7.94%), and all differences were statistically significant (χ2=26.07, 207.91, 471.54, 629.14,P<0.01). Multivariate Logistic regression analysis showed that consuming cereal for breakfast (OR=0.91, 95%CI=0.88-0.94), drinking milk in the past week (OR=0.89, 95%CI=0.83-0.95), meeting sleep standards (OR=0.95, 95%CI=0.91-0.99), and brushing teeth at least once a day (OR=0.82, 95%CI=0.73-0.93) had a lower risk of the comorbidity of dental caries and overweight/obesity. In contrast, drinking beverages in the past week (OR=1.14, 95%CI=1.09-1.20), consuming fried foods in the past week (OR=1.11, 95%CI=1.06-1.17), eating fruit ≥1 time every day (OR=1.06, 95%CI=1.02-1.11), consuming fruit ≥1 type every day (OR=1.07, 95%CI=1.01-1.12), and having fish, poultry, meat, or eggbased breakfasts (OR=1.03, 95%CI=1.05-1.13) had a higher risk of the comorbidity of dental caries and overweight/obesity (P<0.05). Conclusions Dietary habits and lifestyle behaviors are associated with the comorbidity of dental caries and overweight/obesity among primary and secondary school students in Guangxi. Guiding students to form healthy living habits is helpful to preven dental caries and overweight/obesity.

Fibrosis, the pathological scarring of vital organs, is a severe and often irreversible condition that leads to progressive organ dysfunction. It is particularly pronounced in organs like the liver, kidneys, lungs, and heart. Despite its clinical significance, the full understanding of its etiology and complex pathogenesis remains incomplete, posing substantial challenges to diagnosing, treating, and preventing the progression of fibrosis. Among the various molecular players involved, platelet-derived growth factor-C (PDGF-C) has emerged as a crucial factor in fibrotic diseases, contributing to the pathological transformation of tissues in several key organs. PDGF-C is a member of the PDGFs family of growth factors and is synthesized and secreted by various cell types, including fibroblasts, smooth muscle cells, and endothelial cells. It acts through both autocrine and paracrine mechanisms, exerting its biological effects by binding to and activating the PDGF receptors (PDGFRs), specifically PDGFRα and PDGFRβ. This binding triggers multiple intracellular signaling pathways, such as JAK/STAT, PI3K/AKT and Ras-MAPK pathways. which are integral to the regulation of cell proliferation, survival, migration, and fibrosis. Notably, PDGF-C has been shown to promote the proliferation and migration of fibroblasts, key effector cells in the fibrotic process, thus accelerating the accumulation of extracellular matrix components and the formation of fibrotic tissue. Numerous studies have documented an upregulation of PDGF-C expression in various fibrotic diseases, suggesting its significant role in the initiation and progression of fibrosis. For instance, in liver fibrosis, PDGF-C stimulates hepatic stellate cell activation, contributing to the excessive deposition of collagen and other extracellular matrix proteins. Similarly, in pulmonary fibrosis, PDGF-C enhances the migration of fibroblasts into the damaged areas of lungs, thereby worsening the pathological process. Such findings highlight the pivotal role of PDGF-C in fibrotic diseases and underscore its potential as a therapeutic target for these conditions. Given its central role in the pathogenesis of fibrosis, PDGF-C has become an attractive target for therapeutic intervention. Several studies have focused on developing inhibitors that block the PDGF-C/PDGFR signaling pathway. These inhibitors aim to reduce fibroblast activation, prevent the excessive accumulation of extracellular matrix components, and halt the progression of fibrosis. Preclinical studies have demonstrated the efficacy of such inhibitors in animal models of liver, kidney, and lung fibrosis, with promising results in reducing fibrotic lesions and improving organ function. Furthermore, several clinical inhibitors, such as Olaratumab and Seralutinib, are ongoing to assess the safety and efficacy of these inhibitors in human patients, offering hope for novel therapeutic options in the treatment of fibrotic diseases. In conclusion, PDGF-C plays a critical role in the development and progression of fibrosis in vital organs. Its ability to regulate fibroblast activity and influence key signaling pathways makes it a promising target for therapeutic strategies aiming at combating fibrosis. Ongoing research into the regulation of PDGF-C expression and the development of PDGF-C/PDGFR inhibitors holds the potential to offer new insights and approaches for the diagnosis, treatment, and prevention of fibrotic diseases. Ultimately, these efforts may lead to the development of more effective and targeted therapies that can mitigate the impact of fibrosis and improve patient outcomes.

Objective: To investigate the prevalence and associated factors of spinal curvature abnormalities among primary and secondary school students in the Guangxi Zhuang Autonomous Region, so as to provide a scientific basis for the prevention and control of such abnormalities. Methods: From September to November 2023, adopting a stratified cluster random sampling method, spinal curvature screenings and questionnaire surveys were conducted among 168 931 students from grade 4 of primary school to grade 12 of high school in 111 districts and counties across 14 cities in Guangxi. Chi square tests and binary Logistic regression analysis were used to analyze influencing factors of spinal curvature abnormalities. Results: In 2023, the detection rate of poor posture among students above grade 4 in Guangxi was 4.24% , and the detection rate of spinal curvature abnormalities was 2.13%. The detection rate was higher among urban students (2.84%) than rural students (1.66%), boarding students (2.61%) than non-boarding students (1.60%), and high school students (3.16%) than junior high (2.45%) and primary school students (1.15%), and the differences were statistically significant ( χ 2=269.85, 221.44, 565.10, P <0.01). A trend of increasing detection rates with higher grade levels was observed ( χ 2 trend =617.63, P <0.01). Binary Logistic regression analysis indicated that students without boarding at school ( OR =0.82, 95% CI =0.75-0.90), engaging in high-intensity physical activity for over 60 min per day ≥5 days per week ( OR =0.90, 95% CI =0.82-0.98), and adequate sleep ( OR =0.87, 95% CI =0.81-0.94) had lower risks of detecting spinal curvature abnormalities ( P <0.05). Conclusions The prevalence of spinal curvature abnormalities increases with grade level among primary and secondary school students in Guangxi. Regular moderate-to-vigorous physical activity demonstrates protective effects against spinal abnormalities.

As new evidence emerges, treatment strategies toward the functional cure of chronic hepatitis B are evolving. In 2019, a panel of national hepatologists published a Consensus Statement on the functional cure of chronic hepatitis B. Currently, an international group of hepatologists has been assembled to evaluate research since the publication of the original consensus, and to collaboratively develop the updated statements. The 2.0 Consensus was aimed to update the original consensus with the latest available studies, and provide a comprehensive overview of the current relevant scientific literatures regarding functional cure of hepatitis B, with a particular focus on issues that are not yet fully clarified. These cover the definition of functional cure of hepatitis B, its mechanisms and barriers, the effective strategies and treatment roadmap to achieve this endpoint, in particular new surrogate biomarkers used to measure efficacy or to predict response, and the appropriate approach to pursuing a functional cure in special populations, the development of emerging antivirals and immunomodulators with potential for curing hepatitis B. The statements are primarily intended to offer international guidance for clinicians in their practice to enhance the functional cure rate of chronic hepatitis B.

As new evidence emerges, treatment strategies toward the functional cure of chronic hepatitis B are evolving. In 2019, a panel of national hepatologists published a Consensus Statement on the functional cure of chronic hepatitis B. Currently, an international group of hepatologists has been assembled to evaluate research since the publication of the original consensus, and to collaboratively develop the updated statements. The 2.0 Consensus was aimed to update the original consensus with the latest available studies, and provide a comprehensive overview of the current relevant scientific literatures regarding functional cure of hepatitis B, with a particular focus on issues that are not yet fully clarified. These cover the definition of functional cure of hepatitis B, its mechanisms and barriers, the effective strategies and treatment roadmap to achieve this endpoint, in particular new surrogate biomarkers used to measure efficacy or to predict response, and the appropriate approach to pursuing a functional cure in special populations, the development of emerging antivirals and immunomodulators with potential for curing hepatitis B. The statements are primarily intended to offer international guidance for clinicians in their practice to enhance the functional cure rate of chronic hepatitis B.

Objective To analyze the disease burden of chronic kidney diseases (CKD) attributed to high body mass index (BMI) in China from 1992 to 2021 and predict the disease burden for the next decade, and to provide evidence for the prevention and treatment of CKD. Methods Using the Global Burden of Disease (GBD) database and the Joinpoint model, the average annual percentage rate change (AAPC) of the mortality rate and disability-adjusted life year (DALY) rate was calculated to describe and analyze the CKD disease burden attributed to high BMI in China from 1992 to 2021. The ARIMA model was employed to predict and analyze the change trend of the CKD disease burden. Results From 1992 to 2021, the mortality rate and DALY rate attributed to high BMI-induced chronic kidney disease showed an upward trend. Compared to 1992, the attributed number of deaths increased by 324.38%, and DALYs increased by 268.56%; the mortality rate increased by 64.00%, and the DALY rate grew by 51.62%. From 1992 to 2021, the mortality rate and DALY rate for males were lower than those for females, but the growth rate for males exceeded that of females. From 1992 to 2021, the mortality rate and DALY rate of chronic kidney disease attributed to high BMI in China increased with age. The average annual change rate of chronic kidney disease attributed to high BMI in China from 1992 to 2021 (mortality rate: 1.40 per 100,000 (95% CI: 1.04–1.76), DALY rate: 1.43 per 100 000 (95% CI: 1.17–1.70)) was higher than thHuaiyin Normal University, Huai'anher social demographic index (SDI) regions. The ARIMA model predicted that the age-standardized mortality rate increased from 2.91 per 100 000 in 2022 to 3.05 per 100 000 in 2026, and the age-standardized DALY rate increased from 69.65 per 100 000 in 2022 to 73.58 per 100 000 in 2026. Conclusion Chronic kidney disease attributed to high BMI in China is on the rise, and it will continue to grow in the future. The focus of CKD prevention and control should be on males and the elderly, while active measures should be taken to reduce the occurrence and progression of chronic kidney disease.

Objective To explore enteral nutrition support and analyze its influencing factors in elderly patients with ischemic stroke. Methods A total of 328 patients with ischemic stroke in General Hospital of Western Theater Command were enrolled for nutritional screening between July 2020 and February 2024. Corresponding nutritional support plans were selected to investigate the compliance of patients with enteral nutrition support. Patients were divided into a standard group (n=140) and a non-standard group (n=97) based on whether their calorie intake met the standard. The effects of different clinical characteristics on enteral nutrition support were explored, and logistic analysis was used to analyze the influencing factors of non-standard enteral nutrition support. Results In the 328 patients with ischemic stroke, proportions of total parenteral nutrition support, total enteral nutrition support, and parenteral/enteral nutrition support were 25.30%, 27.74% and 46.95%, respectively. The proportions of vomiting or regurgitation, gastric residual volume >100 mL, mechanical ventilation and use of antibiotics >2 in the non-standard group were higher than those in the standard group (P<0.05). Logistic analysis showed that the above clinical characteristics were risk factors influencing patients with enteral nutrition support and parenteral/enteral nutrition support. Conclusion Vomiting or regurgitation , gastric residual volume, mechanical ventilation, and amount of antibiotics used are important influencing factors of enteral nutrition support in patients. Clinicians should pay attention to the above clinical characteristics.