BackgroundDementia seriously affects the quality of life and lifespan of elderly people， with Alzheimer's disease （AD） being the most common type of dementia. Previous studies have suggested that gout may reduce the risk of developing AD， but the causal relationship between the two still requires further research. ObjectiveTo investigate the potential causal relationship between gout and AD through a two-sample Mendelian randomization （MR） analysis， so as to provide references for the prevention and treatment of AD. MethodsData from Genome-Wide Association Studies （GWAS） extracted in 2024 were analyzed， using pooled data on gout （6 810 cases in the case group and 477 788 cases in the control group） published by UK Biobank in 2021 as the exposure variable， and data on AD （3 899 cases in the case group and 214 893 cases in the control group） published by FinnGen in the same year as the outcome variable. The inverse-variance weighted， MR-Egger regression， weighted median estimation， simple model and weighted model were used to analyze the potential causal relationship between gout and AD. Pleiotropic effects were assessed using MR-Egger regression. Heterogeneity assessment was conducted using Cochran's Q test. The leave-one-out analysis was carried out for sensitivity analysis. And a funnel plot was drawn to detect potential publication bias. ResultsThe inverse-variance weighted analysis demonstrated a negative causal relationship between gout and AD （OR=0.004， 95% CI： 0~0.700， P<0.05）. The plot resembled a symmetrical inversed funnel， indicating the absence of publication bias. No heterogeneity was detected by Cochran's Q test. The MR-Egger regression indicated no significant horizontal pleiotropy. Concerning the reverse directions， no significant associations between AD and gout were noted. ConclusionThere is a negative causal relationship between gout and AD， with gout potentially reducing the risk of developing AD. ［Funded by The Third Batch of Social Welfare and Basic Research Projects （Medical and Health） of Zhongshan City in 2022 （number， 2022B3017）］

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Objective: To understand the prevalence of myopia among primary and secondary school students in minority areas of Yunnan Province, and to explore the influence of outdoor activities and short-distance use of eyes, so as to provide a basis for early myopia intervention. Methods: In October 2020, the survey was conducted among 1 782 primary and secondary school students in three cities of Yunnan through a multi stage random cluster sampling method. All subjects underwent a questionnaire survey and the visual acuity examination at baseline. The first follow-up was conducted in October 2021 to obtain 1 691 valid samples, and the second follow-up was conducted in May 2023 to obtain 1 367 valid samples. Factors associated with myopia among primary and secondary school students were explored by using generalized estimating equations. Results: The prevalence rates of myopia in 2020, 2021 and 2023 were 52.64%, 61.62% and 69.35%, respectively, showing an increasing trend ( χ 2 trend =91.77, P <0.05). The results of multivariate regression analysis on the generalized estimation equations showed that age at baseline ( OR =1.31), girls ( OR =1.76), Hani ethnicity ( OR =0.75), Bai ethnicity ( OR =0.69), parental myopia ( OR =1.97-2.29), parents often reducing children s exercise time for homework or tutoring ( OR =1.35), less than 1 time or 2-3 times of ball sports per week ( OR =1.27, 1.20 ), reading and writing in the classroom during the break ( OR =1.27), reading in direct sunlight occasionally ( OR =1.20), using only desk lamp for writing at home ( OR =0.71), more than 1 hours of short-distance eye use for a break once ( OR =1.23) were associated with myopia among primary and secondary school students ( P <0.05). Conclusions Outdoor activities and short-distance use of eye among primary and middle school students in minority areas in Yunnan province are suboptimal. Enhancing the related environmental and behavioral factors can effectively mitigate the occurrence and progression of myopia.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Endothelial to mesenchymal transition(EndMT)is a process in which endothelial cells lose their endothelial pheno-type and function and gain mesenchymal phenotype and func-tion.During the embryonic period,EndMT is an essential mech-anism for the development of heart valves,pulmonary arteries and aorta.In recent years,numerous studies have shown that EndMT is also involved in the occurrence and development of cardiovascular diseases such as atherosclerosis,cardiac fibrosis,pulmonary hypertension,and cerebrovascular malformation.In addition,EndMT is also an important mechanism of other organ fibrosis and tumors.Non-coding RNAs(ncRNAs)refer to RNAs that are transcribed from the genome but do not translate into proteins.Studies have shown that the abnormal expression of ncRNAs can participate in various diseases by regulating End-MT.Such ncRNAs with regulatory functions mainly include mi-croRNA(miRNA),long non-coding RNA(lncRNA)and cir-cular RNA(circRNA).This review summarizes the molecular mechanisms by which ncRNAs regulate EndMT in various disea-ses,looking forward to the application prospects of ncRNAs in the treatment of EndMT-related diseases.

AIM:To explore the mechanism of ac-tion of the microtubular inhibitor of CA-4 deriva-tive LGD5 on human cervical cancer HeLa cells.METHODS:HeLa cells were selected and divided in-to blank group,CA-4 positive control group,and dif-ferent concentrations of LGD5 were formed into the experimental group.MTT was used to investi-gate the growth inhibition of LGD5 on HeLa cells and to determine the assay concentration.Cell morphology and apoptosis were observed before and after drug administration by inverted micro-scope and acridine orange staining.Immunofluo-rescence staining was used to examine the effect of LGD5 on microtubules using DAPI.The effect of LGD5 on cell cycle by PI flow cytometry.Protein im-munoblotting was used to examine the effect of LGD5 on cyclins and apoptosis-related proteins.RE-SULTS:MTT experiments showed that LGD5 inhibit-ed HeLa cells in a time-and dose-dependent man-ner.Timed photography and acridine orange stain-ing observed that LGD5 induced apoptosis in HeLa cells and produced significant chromatin agglutina-tion and apoptotic bodies.Inhibition of microtu-bule polymerization in HeLa cells by LGD5 was ob-served by DAPI staining.The PI flow cytometry re-sults showed that LGD5 induced G2/M cycle arrest in HeLa cells,was time-dependent and dose-depen-dent within 12 h,and had a significant difference(P＜0.01),apoptosis was induced after 24 h and it was time-dependent.The results of Western blot show that,LGD5 downregulates Cdc 2 and Cdc25C,up-regulation of p-Cdc 2,and Cyclin B1 and p-histone H3,further verified that LGD5 induced G2/M cycle arrest in HeLa cells,besides,LGD5 caused in-creased Caspase 3 expression in HeLa cells,upregu-lated Caspase 9 and Bax,down-regulation of Pro-caspase 9 and Bcl-2,this result indicates that HeLa cell apoptosis induced by LGD5 is related to the mi-tochondrial pathway.CONCLUSION:The CA-4 deriv-ative LGD5 inhibited microtubule polymerization in HeLa cells,induced their G2/M cycle arrest,and subsequently induced cell apoptosis through the mitochondrial pathway.

Objective:To explore the gene mutations of Langerhans cell histiocytosis in children,and to analyze the correlation of BRAF V600E mutation with clinical features and prognosis of LCH,so as to provide reference for clinical diagnosis and treatment. Methods:Fluorescence PCR was used to detect gene mutations in paraffin-embedded tissue samples from 78 children with LCH,and the correlation of BRAF V600E mutation with clinical characteristics and prognosis of LCH in children was analyzed. Results:Among the 78 children,41 cases (52.6％) had BRAF V600E mutation,8 cases (10.3％) had MAP2K1 mutation,1 case (1.3％) had BRAF Exon 12 mutation,1 case (1.3％) had ARAF mutation,and 1 case (1.3％) had PIK3CA mutation. BRAF V600E mutation was not significantly correlated with sex,age,multisystem involvement,risk-organ involvement,CNS-risk lesions,and early treatment response in children with LCH (P>0.05),and it was also not significantly correlated with the recurrence and event-free survival (EFS) of children with LCH (P>0.05). Conclusion:LCH is an inflammatory myeloid tumor. BRAF V600E mutation is not correlated with clinical features,early treatment response,recurrence and prognosis of LCH.