ObjectiveTo investigate the protective effect of α-ketoglutarate （α-KG） on hepatic lipid deposition in offspring caused by arsenic exposure during pregnancy. Methods8-week-old institute of cancer research （ICR） mice were mated in a ratio of 2∶1 between females and males， and the detection of vaginal plugs confirmed pregnant. A total of 32 pregnant mice were randomly divided into four groups： control group， arsenic group， α-KG group， arsenic+α-KG group. On gestational day 0-16 （GD0-GD16）， the arsenic and arsenic+α-KG groups were exposed to sodium arsenite （NaAsO₂ ，15 mg/L） in drinking water everyday， and the α-KG and arsenic+α-KG groups were gavaged with α-KG （2 g/kg） everyday. On GD16， pregnant mice were euthanized to collect fetal liver， and fetal body weight and crown-rump length were measured. Gene expression differences between the control group and the arsenic group were analyzed by transcriptome. The total triglycerides （TGs） and subtypes in fetal liver were detected by liquid chromatography tandem mass spectrometry （LC-MS/MS）. Oil red O staining was used to observe the histopathological changes in the liver. Quantitative polymerase chain reaction （qPCR） was used to detect the expression level of genes related to lipid synthesis， transport， and degradation， and phosphatidylinositol 3' -kinase/ protein kinase B （PI3K/AKT） in the liver of fetus. ResultsTranscriptomics analysis showed that 2 144 genes were downregulated and 1 675 genes were upregulated in the arsenic exposed fetal liver； body weight and crown-rump length were reduced （P_TuKey<0.05）； the level of hepatic TGs was elevated in arsenic group （P_TuKey<0.05）； oil-red O staining showed a significant increase in lipid droplets in arsenic group （P_TuKey<0.01）； the expression of lipid synthesis-related genes were significantly upregulated （P_TuKey<0.05）； the expression of β-oxidation-related genes and lipid degradation-related genes were downregulated （P_TuKey<0.05）； the expression of PI3K， AKT decreased（P_TuKey<0.05）. Compared with the arsenic group， the body weight and crown-rump length of fetus increased in the arsenic+α-KG group （P_TuKey<0.05）； the level of hepatic TGs decreased in the arsenic+α-KG group （P_TuKey<0.05）； oil red O staining showed lipid droplets significantly decreased （P_TuKey<0.01）； the expression of lipid synthesis-related genes were downregulated （P_TuKey<0.05）， the expression of β-oxidation-related genes and lipid degradation-related genes were upregulated （P_TuKey<0.05）； the expression levels of PI3K and AKT increased （P_TuKey<0.05）. Conclusionα-KG alleviated hepatic lipid deposition in offspring exposed to arsenic during pregnancy through activating PI3K/AKT signaling pathway.

Objective: To explore the barriers to physical activity behavior among overweight and obese children and adolescents, so as to provide evidence for developing physical activity intervention programs. Methods: From March to April 2025, 13 overweight or obese children and adolescents from one primary school and one secondary school in Nanjing were selected by purposive sampling for semi structured interviews. Guided by the capability, opportunity and motivation-behavior model, data were coded, categorized and analyzed using content analysis. Results: A total of 13 interviews were completed, with a cumulative duration of 358 minutes. Three themes and eight subthemes were identified:capability factors, including physical discomfort and limited physical fitness, weak exercise skills and insufficient behavioral regulation ability, and insufficient psychological capability; opportunity factors, including insufficient family support and negative influence, pressure from school and peer environments, and limited time resources and exercise conditions; and motivation factors, including low self efficacy and situations prone to giving up, and insufficient positive feedback and lack of attractiveness of exercise forms. Conclusions Barriers to physical activity among overweight and obese children and adolescents result from the combined effects of capability, opportunity and motivation. It is necessary to lower the threshold for initiating exercise, strengthen positive experiences and feedback, and build integrate family-school support environments to promote the initiation and maintenance of physical activity behaviors in children and adolescents.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

Background and Objectives: Heart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism. Methods: New hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area.The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12). Results: YAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9–11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B, NPPB, and myosin heavy chain 7, MYH7) and cardiomyocyte size in vitro but not in vivo. YAK577 ameliorated cardiac fibrosis and fibrosis-related genes in vivo and in vitro. Additionally, YAK577 reduced elevated HDAC8 and MMP12 mRNA and protein expressions in ISO-infused mice, H9c2 cells, and rat neonatal cardiomyocytes.HDAC8 overexpression stimulated MMP12 and NPPB mRNA levels, while HDAC8 knockdown downregulated these genes. Conclusions YAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.

Objective To analyze the diagnostic value of serum biomarkers in patients with pulmonary tuberculosis complicated by invasive pulmonary aspergillosis.Methods A retrospective collection of laboratory test results,including blood analysis,liver function,lymphocyte counts,and cytokine levels,from 54 patients diagnosed with pulmonary tuberculosis and invasive pulmonary aspergillosis admitted to the Third People's Hospital of Kunming between January 2021 and May 2024.Additionally,70 patients with simple pulmonary tuberculosis and 50 healthy individuals were collected as control groups to compare serum biomarker levels across the three groups and analyze relevant factors and diagnostic value for pulmonary tuberculosis patients with invasive pulmonary aspergillosis.Results Among different age groups,the incidence of pulmonary tuberculosis with invasive pulmonary aspergillosis was 29 cases(53.7％)in youth,15 cases(27.8％)in middle age,and 10 cases(18.5％)in the elderly.In terms of gender distribution,there were 41 males(75.9％)and 13 females(24.1％).The serum levels of CRP(6.85[2.10,27.0])ng/L,PCT(0.05[0.05,0.15])ng/mL,RBC(4.55±0.65)× 1012/L,Hb(129.13±19.10)g/L,TP(66.23±6.82)g/L,ALB(37.03±4.77)g/L,and CHOL(4.30[3.71,4.91])mmol/L in the invasive pulmonary aspergillosis group showed no significant difference compared to the simple tuberculosis group and healthy control group(P＞0.05).The levels of CD3+T,CD4+T,and CD8+T in the invasive pulmonary aspergillosis group were significantly lower than those in the simple tuberculosis group and healthy control group(P＜0.05).The levels of IL-2,IL-4,IL-5,IL-8,IL-10,IL-12p70,IFN-α,and TNF-α in the invasive pulmonary aspergillosis group were significantly higher than those in the healthy control group(P＜0.05);IL-8,IL-12p70,and IFN-α were also higher compared to the simple tuberculosis group,with statistical significance(P＜0.05).Conclusion The population with pulmonary tuberculosis complicated by invasive pulmonary aspergillosis is predominantly male and younger.The serum indicators of infection severity and nutritional status in these patients are similar to those with simple tuberculosis and lack specificity;however,their immune function is significantly lower than that of simple tuberculosis patients.Multiple cytokines are elevated,particularly IL-8,IL-12p70,and IFN-α,which can aid in the differential diagnosis of pulmonary tuberculosis infection.

Objective To analyze the risk factors of ultrasound-guided percutaneous transluminal angioplasty(PTA)for treating thrombotic occlusion of autogenous arteriovenous fistula(AVF).Methods A total of 144 patients with thrombotic occlusion of autologous AVF were retrospectively enrolled and divided into success group(n=114)and failure group(n=30)according to the success of treatment or not.Clinical data and ultrasonic parameters of AVF were compared between groups.A multivariate logistic regression model was constructed to analyze the risk factors of PTA for treating thrombotic occlusion of autologous AVF,and the results were visualized by nomogram.Then receiver operating characteristic curve was drawn,and the area under the curve(AUC)was calculated to evaluate the predictive efficacy of this model.Results Patients'age,use years of AVF,degree of vascular calcification,the mean Young modulus(Emean),the maximum Young modulus(Emax)and the minimum Young modulus(Emin)were all higher,while the number of venous outflow tracts of AVF was less in failure group than those in success group(all P＜0.05).Moderate to severe calcification of vascular,high Emean of thrombus and 1 venous outflow tract of in AVF were all independent risk factors of ultrasound-guided PTA for treating thrombotic occlusion of autologous AVF(all P＜0.05),and AUC of the obtained model for predicting failure of treatment was 0.969.Conclusion Moderate to severe calcification of vascular,high Emean of thrombus and 1 venous outflow tract of AVF were all independent risk factors of ultrasound-guided PTA for treating thrombotic occlusion of autologous AVF.

Gut microbiota is the microbial community that is specifically planted in the human gut and interacts with the human body.It plays an important role in the human body by regulating the basal metabolism and immunity of the host to maintain the homeostasis of the human body.Once the intestinal flora is dysregulated,it can lead to multi-system diseases.Hashimoto's thyroiditis is an organ-specific autoimmune disease.The pathogenesis of Hashimoto's thyroiditis is complex and its incidence is increasing year by year,which is gradually becoming a serious public health disease affecting the world.In recent years,the relationship between gut microbiota and bridge onychitis has received extensive attention.A large number of studies have shown that the richness and diversity of intestinal flora in Hashimoto's thyroiditis patients are changed compared with healthy people.Studies have shown that traditional Chinese medicine therapy can play a role in treating this disease by regulating intestinal flora.This article systematically summarizes the relationship between the two and the effect of traditional Chinese medicine on the treatment of bridge onychitis by regulating intestinal flora,so as to provide some reference for research in this field.

Gut microbiota is the microbial community that is specifically planted in the human gut and interacts with the human body.It plays an important role in the human body by regulating the basal metabolism and immunity of the host to maintain the homeostasis of the human body.Once the intestinal flora is dysregulated,it can lead to multi-system diseases.Hashimoto's thyroiditis is an organ-specific autoimmune disease.The pathogenesis of Hashimoto's thyroiditis is complex and its incidence is increasing year by year,which is gradually becoming a serious public health disease affecting the world.In recent years,the relationship between gut microbiota and bridge onychitis has received extensive attention.A large number of studies have shown that the richness and diversity of intestinal flora in Hashimoto's thyroiditis patients are changed compared with healthy people.Studies have shown that traditional Chinese medicine therapy can play a role in treating this disease by regulating intestinal flora.This article systematically summarizes the relationship between the two and the effect of traditional Chinese medicine on the treatment of bridge onychitis by regulating intestinal flora,so as to provide some reference for research in this field.