Diabetic cardiomyopathy （DCM） is a common chronic complication of diabetes， categorized as consumptive thirst in traditional Chinese medicine （TCM）， and it subsequently gives rise to chest impediment. DCM is characterized by a complex pathogenesis and exhibits long-term progression with poor prognosis in clinical practice. Astragali Radix， as a medicinal material with edible value， possesses diverse active components including saponins， polysaccharides， and flavonoids. It has the effects of tonifying Qi， elevating Yang， promoting fluid production， nourishing blood， expressing toxin， and expelling pus. Modern pharmacological studies have confirmed that Astragali Radix and its active components exert therapeutic effects in various aspects such as inhibition of inflammation， alleviation of stress injury， regulation of programmed cell death， modulation of glucose and lipid metabolism， inhibition of myocardial fibrosis， and regulation of gut microbiota and metabolites， treating DCM in a multi-component， multi-target， and multi-pathway manner. The compatibility of Astragali Radix exerts both synergistic and antagonistic effects. The compound preparations and extracts of Astragali Radix are widely used in clinical practice， and the development of novel nano and gel materials and extracellular vesicles helps to improve the oral bioavailability， providing more possibilities for the clinical application of Astragali Radix in DCM， though its potential for clinical translation requires ongoing exploration. This review summarizes the TCM theoretical basis of Astragali Radix in the treatment of DCM， and integrates modern pharmacological research results to delve into the effects and mechanisms of the herb combinations， compound preparations， extracts， and new composite materials of Astragali Radix in the treatment of DCM， aiming to provide a reference for in-depth research and new drug development of Astragali Radix for DCM.

OBJECTIVES: Cardiovascular disease (CVD) poses a major threat to global health. Evaluating atherosclerosis in asymptomatic individuals can help identify those at high risk of CVD. This study aims to establish an individualized nomogram prediction model to estimate the risk of vascular plaque formation in asymptomatic individuals. METHODS: A total of 5 655 participants who underwent CVD screening at the Health Management Center of The Third Xiangya Hospital, Central South University, between January 2022 and June 2024 we retrospectively enrolled. Using simple random sampling, participants were divided into a training set (n=4 524) and a validation set (n=1 131) in an 8꞉2 ratio. Demographic and clinical data were collected and compared between groups. Multivariate logistic regression analysis was used to identify independent factors associated with vascular plaques and to construct a nomogram prediction model. The predictive performance and clinical utility of the model were evaluated using receiver operating characteristic (ROC) curves, the Hosmer-Lemeshow goodness-of-fit test, calibration plots, and decision curve analysis (DCA). RESULTS: The mean age of participants was 52 years old. There were 3 400 males (60.12%). The overall detection rate of vascular plaque in the screening population was 49.87% (2 820/5 655). No statistically significant differences were observed in clinical indicators between the training and validation sets (all P>0.05). Multivariate Logistic regression analysis identified age, systolic blood pressure, high-density lipoprotein (HDL), low-density lipoprotein (LDL), lipoprotein(a), male sex, smoking history, hypertension history, and diabetes history as independent risk factors for vascular plaque in asymptomatic individuals (all P<0.05). The area under the curve (AUC) of the nomogram model for predicting vascular plaque risk were 0.778 (95% CI 0.765 to 0.791, P<0.001) in the training set and 0.760 (95% CI 0.732 to 0.787, P<0.001) in the validation set. The Hosmer-Lemeshow goodness-of-fit test indicated good model calibration (training set: P=0.628; validation set: P=0.561). The calibration curve plotted using the Bootstrap method demonstrated good agreement between predicted probabilities and actual probabilities. DCA showed that the nomogram provided a clinical net benefit for predicting vascular plaque risk when the threshold probability ranged from 0.02 to 0.99. CONCLUSIONS The nomogram prediction model for vascular plaque risk, constructed using readily available and cost-effective physical examination indicators, exhibited good predictive performance. This model can assist in the early identification and intervention of asymptomatic individuals at high risk for cardiovascular disease.
Humans ; Male ; Middle Aged ; Female ; Nomograms ; Retrospective Studies ; Risk Factors ; Plaque, Atherosclerotic/diagnosis* ; Aged ; Adult ; Physical Examination ; Logistic Models ; Cardiovascular Diseases/epidemiology* ; ROC Curve

Objective:To explore the relationship between college students' exercise identity and physical exercise, as well as the chain mediating role of exercise intention and exercise plan.Methods:Using the exercise identity scale, exercise intention scale, exercise plan scale and physical exercise rating scale, a cross-sectional survey was conducted on 2 452 college students.After 324 sets of invalid questionnaires were excluded, a total of 2 128 sets of valid questionnaires were obtained.SPSS 27.0 and Mplus 8.3 software were used to statistically process the collected data and establish structural equation model.Results:The results of the partial correlation analysis showed that after controlling for the demographic variables of gender and grade, the four variables of college students' exercise identity (38.80±11.55), exercise intention (14.28±3.61), exercise plan (25.61±9.21), and physical exercise(23.25±21.33) were positively correlated with each other ( r=0.58-0.74, all P<0.05). Exercise intention and exercise plan acted as partial individual mediators between exercise identity and physical exercise in college students, respectively, with mediating effects of 0.39 (95% CI=0.32-0.46), 0.07 (95% CI=0.04-0.11), and chain mediating effect of exercise intention and exercise plan of 0.06 (95% CI=0.04-0.09). Conclusion:Exercise identity can not only directly influence college students' physical exercise, but also indirectly influence college students' physical exercise through the two mediating variables of exercise intention and exercise plan.

Objective:To explore the relationship between college students' exercise identity and physical exercise, as well as the chain mediating role of exercise intention and exercise plan.Methods:Using the exercise identity scale, exercise intention scale, exercise plan scale and physical exercise rating scale, a cross-sectional survey was conducted on 2 452 college students.After 324 sets of invalid questionnaires were excluded, a total of 2 128 sets of valid questionnaires were obtained.SPSS 27.0 and Mplus 8.3 software were used to statistically process the collected data and establish structural equation model.Results:The results of the partial correlation analysis showed that after controlling for the demographic variables of gender and grade, the four variables of college students' exercise identity (38.80±11.55), exercise intention (14.28±3.61), exercise plan (25.61±9.21), and physical exercise(23.25±21.33) were positively correlated with each other ( r=0.58-0.74, all P<0.05). Exercise intention and exercise plan acted as partial individual mediators between exercise identity and physical exercise in college students, respectively, with mediating effects of 0.39 (95% CI=0.32-0.46), 0.07 (95% CI=0.04-0.11), and chain mediating effect of exercise intention and exercise plan of 0.06 (95% CI=0.04-0.09). Conclusion:Exercise identity can not only directly influence college students' physical exercise, but also indirectly influence college students' physical exercise through the two mediating variables of exercise intention and exercise plan.

Background::Pancreatic adenocarcinoma (PAAD) is an extremely lethal malignancy. Identification of the functional genes and genetic variants related to PAAD prognosis is important and challenging. Previously identified prognostic genes from several expression profile analyses were inconsistent. The regulatory genetic variants that affect PAAD prognosis were largely unknown.Methods::Firstly, a meta-analysis was performed with seven published datasets to systematically explore the candidate prognostic genes for PAAD. Next, to identify the regulatory variants for those candidate genes, expression quantitative trait loci analysis was implemented with PAAD data resources from The Cancer Genome Atlas. Then, a two-stage association study in a total of 893 PAAD patients was conducted to interrogate the regulatory variants and find the prognostic locus. Finally, a series of biochemical experiments and phenotype assays were carried out to demonstrate the biological function of variation and genes in PAAD progression process.Results::A total of 128 genes were identified associated with the PAAD prognosis in the meta-analysis. Fourteen regulatory loci in 12 of the 128 genes were discovered, among which, only rs4887783, the functional variant in the promoter of Ring Finger and WD Repeat Domain 3 ( RFWD3), presented significant association with PAAD prognosis in both stages of the population study. Dual-luciferase reporter and electrophoretic mobility shift assays demonstrated that rs4887783-G allele, which predicts the worse prognosis, enhanced the binding of transcript factor REST, thus elevating RFWD3 expression. Further phenotypic assays revealed that excess expression of RFWD3 promoted tumor cell migration without affecting their proliferation rate. RFWD3 was highly expressed in PAAD and might orchestrate the genes in the DNA repair process. Conclusions::RFWD3 and its regulatory variant are novel genetic factors for PAAD prognosis.

Tumor metastasis is one of the important biological characteristics of malignant tumor,which is closely related with the prognosis of the cancer patients.High expression of ADAM8 in varieties of tumors was revealed in many recent studies,and such aberrant expression played a crucial role in regulating of tumor metastasis.Studies showed that overexpression of ADAM8 attenuated the intercellular adhesion effect,promoted tumor angiogenesis,and enhanced the degradation of ECM as well as the releasing of cytokines.Therefore,suppression of ADAM8 may lead to inhibition of tumor metastasis,which makes ADAM8 a particular attractive target as it can be used as a prognostic indicator and a potential therapeutic target of malignant tumor.A review about the relations between ADAM8 protein′s abnormal expression and tumor occurrence was discussed in this paper,also include discussion about the mechanisms of ADAM8 protein′s disorder-induced tumor formation,as well as therapeutic strategies based on ADAM8-targeted,which may provide references for follow-up research and clinical treatment.

Aim To discuss the impact of important ac-tive ingredient of garlic diallyl sulfide———DATS on platelet activating factor (PAF ) mediated melanoma metastasis and its mechanisms.Methods ①MTT was used to test the effect of different concentrations of DATS on B16F10 and A375 melanoma cell growth number;②Scratch test and transwell were employed to test the effect of different concentrations of DATS on B16F10 and A375 melanoma cell migration;③ West-ern blot was used to test the effect of DATS on expres-sion of MMP-2,ERK,p38 induced by PFA;④Intrave-nous injection of tumor metastasis model was used to check the inhibition of DATS in PAF-mediated melano-ma metastasis.Results B16F10 cells relative growth rate fell to 73.21% and 48.78%,respectively,when DATS concentration reached 50 and 100 μmol·L-1 . DATS inhibited the levels of PAF-induced migration of melanoma cells B16F10 and vertical migration signifi-cantly,and inhibited B16F10 cells migration induced by PAF through inhibiting the expression of MMP-2, paxillin protein,FAK and other proteins.Conclusion DATS can significantly inhibit PAF-induced tumor metastasis, which is related to the inactivation of MAPKs.

The study on tumor metabolism has been gradually be-come a hot spot in recent years .A lot of proteins involved in the regulation of tumor metabolism especially the glucose transporter protein 1(GLUT1).As a key regulatory factor mediating energy metabolism within tumor cells , GLUT1 can regulate the glucose intake and maintain the basic level of metabolism in tumor cells . More importantly, the abnormal expression of GLUT1 was asso-ciated with many kinds of tumors , of which GLUT1 was used to meet the energy requirement for the fast growth of tumor .Thus GLUT1 also played a crucial role in growth , differentiation and metastasis of tumor cells and prognosis of tumors .Meanwhile , as three-dimensional crystal structure of GLUT 1 was determined , it is possible to design the small molecular inhibitors of GLUT 1, which can realize “starve to death” tumor cells.GLUT1 can be a particularly attractive target for tumor treatment and interfer-ence.The relationship between abnormal expression of GLUT 1 protein and tumor metabolism was reviewed . Moreover , the mechanism of tumor metabolism regulated by GLUT 1 protein ex-pression and treatment of cancers were discussed , which may provide references for future research and clinical treatment .

Aim To observe the effects of the total fla-vonoids of scutellaria barbataon ( TFSB ) on high-fat
feeding ApoE gene deficiency mice in early atheroscle-rosis ( AS ) and its underlying mechanisms. Methods
40 ApoE-/ -male mice were divided into five groups:model group, SIM group and L-TFSB, M-TFSB, H-TFSB group, 5 C57BL/6J mice were selected as nor-mal control group. All mice in experimental group were fed with high-lipid diet for 4 weeks and all mice were killed after 8 weeks. H&E staining was used to observe morphology of aorta. Blood rheometer was used to ex-amine plasm viscosity and whole blood viscosity. Fully automatic biochemical analyser was used to detect the serum levels of TG, TC, LDL-C and HDL-C. The ex-pression levels of PLTP and VE in serum were meas-ured by ELISA. The expression levels of PLTP and FXR in liver were examined by Western blot. Results The model was established successfully. TFSB groups could improve the aorta AS morphology of model mice and significantly reduce the serum levels of TG, TC and LDL-C, while increase the level of HDL-C ( P<0. 05 or P<0. 01 ) . TFSB groups could decrease the
hematocrit value, plasma viscosity and whole blood vis-cosity of AS model mice significantly and had statistical significance when compared with model group ( P <0. 01 ) . The expression levels of PLTP of serum were reduced significantly when compared with model group ( P <0. 01 ) . We also found that the expression of PLTP was in negative correlation with VE ( r = -0. 675,P<0. 01). M-TFSB and H-TFSB group could decrease the expressions of PLTP and FXR of liver when compared with model group ( P <0. 01 ) . Con-clusion TFSB may exert its anti-AS effect partly through inhibiting the levels of FXR and PLTP of ApoE-/ -mice, increasing the level of VE, regulating blood lipids, improving blood rheology and reducing the damage of AS in mice.

Tumor metastasis is one of the most important biologi-cal characteristics of malignant tumor, and it is also the main factor resulting in poor prognosis and leading to failure of treat-ment. In recent years, studies have shown that the extracellular matrix ( ECM) of tumor microenvironment plays a critical role in tumor metastasis. Tumor ECM fibrogenesis could form the cross-linked network structure, which not only provides nutrition and support to tumor, also it is necessary to tumor growth and inva-sion. These research results indicate that blocking ECM fibro-genesis may exert an inhibitory effect on tumor metastasis. Therefore, targeting ECM fibrogenesis has become a particularly attractive strategy as it can be used in the treatment of metasta-sis-related diseases. The ECM fibrogenesis in tumor is reviewed in this paper as well as the treatment strategies on tumor metas-tasis by targeting ECM fibrogenesis, which may provide refer-ences for follow-up research and clinical treatment.