Yang Gu

Clinical biomarkers and ejection fraction (EF) lack sufficient specificity for heart failure (HF) diagnosis. Metabolomics can report disease‐associated metabolic remodeling, but clinical translation is constrained by the lack of rapid, sensitive, and reproducible metabolite profiling. Here, we develop plasmonic silver‐based alloy nanotubes (AgMANTs, M = Au, Pt, Pd) as novel matrices for laser desorption/ionization mass spectrometry (LDI‐MS). Their engineered hollow‐porous architecture and tunable composition synergistically enhance ionization efficiency via near‐field effects and photothermal conversion. The optimized AgAuANTs achieve low detection limits (e.g., 0.22 pmol per spot for glucose), high reproducibility (CV < 3%), and 30‐day stability (CV < 10%). In a clinical cohort, machine‐learning models based on AgAuANTs‐enhanced serum metabolic fingerprints (SMFs) discriminate healthy controls from coronary heart disease (CHD) (AUC = 0.941) and HF (AUC = 0.951), and distinguish CHD from HF (AUC = 0.929). SMFs are acquired within seconds with minimal sample consumption and without complex pretreatment. Multimodal integration of metabolic biomarkers with routine clinical parameters further improves diagnostic performance (AUC > 0.98). Our platform provides a rapid and efficient method to acquire metabolic fingerprints as a potential diagnostic approach for HF and other diseases.

Cardiovascular diseases (CVD), such as coronary artery disease (CAD), arrhythmia, or congestive heart failure, are characterised by structural or functional abnormalities in the cardiovascular system that disrupt its functioning. They have contributed significantly to the global disease burden during the last several decades, with 523 million cases reported in 2019 [1]. The number of […]

The predictive value of the triglyceride-glucose (TyG) index in patients with obstructive sleep apnea (OSA) remains unclear. Therefore, we aimed to investigate the associations between the TyG index and all-cause and non-cardiovascular (non-CV) mortality in an OSA cohort, focusing on age differences. This study enrolled 10,274 patients with OSA from the National Health and Nutrition Examination Survey (2005–2008 and 2015–2018). Mortality outcomes were ascertained by linking to National Death Index records through December 31, 2019. Multivariate Cox proportional hazards regression models with restricted cubic splines and interaction tests with age were employed to evaluate the association between the TyG index and all-cause and non-CV mortality. Kaplan-Meier analysis was used to evaluate mortality differences. During a mean follow-up of 88 months, 1027 all-cause deaths occurred, of which non-CV deaths accounted for 77.8% of the total mortality burden. After fully adjusting for potential confounders, our study explored a U-shaped association between the TyG index and all-cause/non-CV mortality (both non-linear p < 0.001), with inflection points at 9.27 and 9.2. Age yielded a statistically significant interaction between the TyG index and mortality. The TyG index was linearly associated with higher risks of all-cause [Hazard Ratio (HR) 1.30, 95% Confidence Interval (CI): 1.09–1.55, p = 0.004] and non-CV mortality (HR 1.33, 95% CI: 1.08–1.62, p = 0.006) in participants aged < 65, but not in participants age ≥ 65. Kaplan–Meier curves indicated that the patients with the higher TyG index had a significantly lower survival probability (All-cause mortality: p for log-rank test < 0.001; non-CV mortality: p for log-rank test = 0.001). This study identified a U-shaped association between the TyG index and all-cause and non-CV mortality in an OSA population, with a statistically significant interaction with age. A linear relationship was detected between the TyG index and mortality in those aged < 65, while a non-linear association was established in those aged ≥ 65.

The relationship between the total cholesterol/high-density lipoprotein cholesterol (TC/HDL) and TC/HDL with the combination of obesity indicators and obstructive sleep apnea (OSA) remains unclear. Therefore, we aimed to explore the associations between TC/HDL-related indices and OSA as well as clinical outcomes. This study enrolled 20,076 patients from the National Health and Nutrition Examination Survey (2005–2008 and 2015–2018). Three indicators were constructed including TC/HDL index, TC/HDL combining with relative fat mass (TC/HDL-RFM), and TC/HDL combining with body mass index (TC/HDL-BMI). We performed multivariable logistic regression and generalized additive models to evaluate the association between TC/HDL-related indices and OSA. Multivariable Cox proportional hazards regression models with restricted cubic splines were performed to assess the relationships between TC/HDL-related indices and mortality. Stratified analyses were conducted to further investigate population-specific differences. The multivariable logistic regression analyses showed that high levels of TC/HDL-related indices were significantly associated with increased prevalences of OSA (TC/HDL: odds ratio [OR] per 1 standard deviation [SD] increase: 1.1, 95% confidence interval [CI]: 1.07–1.14, P < .001; TC/HDL-RFM: OR per 1SD increase: 1.22, 95% CI: 1.18–1.27, P < .001; TC/HDL-BMI: OR per 1SD increase: 1.28, 95% CI: 1.23–1.33, P < .001). Inverted U-shaped curves were depicted between TC/HDL-related indices and OSA. During a mean follow-up of 91 months, 1917 (9.5%) all-cause deaths occurred, and 567 (2.8%) were contributed to cardiovascular deaths. Meanwhile, the TC/HDL-related indices were associated with cardiovascular mortality, but not with all-cause mortality. Subgroup analyses showed that the strength of this relationship was found to be more pronounced in participants with OSA. The TC/HDL-related indices were independent predictors of OSA and cardiovascular mortality. Our study indicated that TC/HDL-related indices can assist clinicians in making more informed clinical decisions for patients with OSA and help reduce the risk of cardiovascular mortality.

Background: The association between obstructive sleep apnea (OSA) and plasma lipid concentrations is not consistent. This study aimed to investigate the association of plasma lipid concentrations with the prevalence of OSA among US adults, with an additional examination of the mediating effect of body mass index (BMI).Methods: This cross-sectional study included 8,086 individuals who participated in the National Health and Nutrition Examination Survey (NHANES), conducted from 2005 to 2008 and 2015–2018. Multivariable logistic regression analysis was conducted to compute the odds ratios (ORs) and 95% confidence intervals (CIs) for the association between plasma lipid concentrations and the prevalence of OSA. Additionally, subgroup analysis was used to explore the potential interactions. Generalized additive models (GAM) were constructed to evaluate the nonlinear relationships between lipid concentrations and OSA. Furthermore, mediation analysis was performed to assess the potential mediating role of BMI.Results: In the fully adjusted model, when comparing the lowest quartile, the ORs for the prevalence of OSA among participants in the highest quartile were 1.367 (95% CI, 1.107–1.688) for triglyceride and 1.212 (95% CI, 1.004–1.462) for low-density lipoprotein cholesterol (LDL-C). However, total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) were not associated with OSA. Notably, the relationship between triglyceride and OSA differed in the subgroups of gender, race, and body mass index (BMI) (P for interaction <0.05). Furthermore, we discovered an inverted U-shaped association between triglyceride and OSA (inflection point: 0.813 mmol/L). Causal mediation analysis revealed that BMI significantly mediated the relationship between triglyceride and the prevalence of OSA.Conclusions: This study revealed that an elevated level of triglyceride increased the prevalence of OSA, and this effect was potentially mediated through BMI. Lowering triglyceride concentration may help to reduce the prevalence of OSA.

Background: Iron metabolism may play a role in cardiovascular disease (CVD) pathogenesis. The association between iron metabolism and CVD has yet to be fully investigated. This study evaluated whether iron metabolism was associated with CVD risk and whether the body mass index (BMI) of US adults varied the association. Methods: A cross-sectional study was performed using the National Health and Nutrition Examination Survey (NHANES), conducted from 2017 to 2018. Generalized additive models (GAMs) and multivariable logistic regression were adopted to analyze the association between iron metabolism (serum iron (SI), serum ferritin (SF), transferrin saturation (TSAT), and soluble transferrin receptor (sTfR)) and CVD risk. Further, stratified analysis was conducted to identify patients with high CVD risk. Results: Participants with CVD tended to have significantly increased levels of sTfR (p < 0.001) and decreased levels of TSAT (p < 0.001) and SI (p < 0.001). After adjusting for confounding factors, sTfR levels had a significant positive association with CVD risk (Q1 as reference, Q4 odds ratio (OR) 2.1, 95% CI 1.54–2.87, p < 0.001). Notably, the association between sTfR and CVD risk differed in the BMI subgroup (p for interaction < 0.05). We identified an inverted U-shaped relationship between sTfR and the CVD risk in the group of overweight individuals (non-linear p < 0.001). When the sTfR level was below the turning point (sTfR = 5.35 mg/L), a per unit increase in the sTfR level was correlated with a 78% greater adjusted OR of CVD risk (OR, 1.78 [1.44, 2.19]). Conclusions: Increased sTfR levels were non-linearly related to the CVD risk in the overweight population.

Purpose To investigate the effect of azilsartan on myocardial remodeling after acute myocardial infarction (AMI). Methods A total of 200 AMI patients under percutaneous coronary intervention (PCI) were selected from the Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University from Jan 2021 to Dec 2021. The subjects were randomly divided to take either azilsartan or benazepril. Serum C1q tumor necrosis factor-associated protein 1 (CTRP1) levels were detected in all subjects after admission, and the indices of left ventricular end-diastolic volume (LVEDV), left ventricular end-diastolic diameter (LVEDD), and left ventricular ejection fraction (LVEF) were measured by using echocardiography. At the follow-up of 6 months and 1 year after PCI, the differences in CTRP1 and echocardiogram indices between the two groups were compared, and the influencing factors of myocardial remodeling after acute myocardial infarction were analyzed. Results The levels of LVEDV and CTRP1 in all subjects at 6 months and 1 year after PCI were lower than those before discharge, and the LVEDV in the azilsartan group at 6 months and 1 year after PCI was lower than that in the benazepril group. An improvement in myocardial remodeling was obviously observed within 6 months after PCI, but the effect declined over time. Conclusions Azilsartan can improve myocardial remodeling after acute myocardial infarction. CTRP1 may become an effective target for the prevention and treatment of myocardial remodeling after acute myocardial infarction.

Sanggenon C is isolated from Morus alba, a plant that has been used for anti‑inflammatory purposes in Oriental medicine. Little is known about the effect of Sanggenon C on cardiomyocyte hypoxia injury. This study, using H9c2 rat cardiomyoblasts, was designed to determine the effects of Sanggenon C on cardiomyocyte hypoxia injury. Inflammatory cytokine levels were measured by reverse transcription‑polymerase chain reaction, reactive oxygen species were measured by 2',7'‑dichlorofluorescin diacetate fluorescent probe, autophagy was detected using the LC3II/I ratio and cell apoptosis was detected by TUNEL staining. The molecular mechanisms underlying Sanggenon C‑induced cyto‑protection were also determined by western blotting, especially the possible involvement of autophagy and AMP‑activated protein kinase (AMPK). Results indicated that samples pretreated with different concentrations of Sanggenon C (1, 10 and 100 µM) reduced the expression levels of pro‑inflammatory cytokines, including tumor necrosis factor α, interleukin (IL)‑1 and IL‑6, under hypoxia. The beneficial effects of Sanggenon C were also associated with reduced levels of reactive oxygen species generation and increased levels of antioxidant nitric oxide and superoxide dismutase. Sanggenon C enhanced hypoxia‑induced autophagy as evidenced by the increased expression levels of autophagy‑associated proteins Beclin and autophagy related 5 as well as the decreased the accumulation of p62, and increased the LC3II/I ratio. Sanggenon C also reduced hypoxia‑induced apoptosis as detected by TUNEL staining and the expression of Bcl‑2 proteins. The beneficial effects of Sanggenon C were associated with enhanced activation level of AMPKα and suppressed hypoxia‑induced mechanistic target of rapamycin (mTOR) and forkhead box O3a (FOXO3a) phosphorylation. The AMPK inhibitor Compound C (CpC) was used, and the anti‑apoptotic and pro‑autophagy effects of Sanggenon C in response to hypoxia were abolished by CpC. In conclusion, the current study demonstrated that Sanggenon C possessed direct cytoprotective effects against hypoxia injury in cardiac cells via signaling mechanisms involving the activation of AMPK and concomitant inhibition of mTOR and FOXO3a.

To examine the change of epidermal growth factor (EGF) concentration in saliva of recurrent aphthous ulcer (RAU) patients during the ulcerous and interval period and epidermal growth factor receptor (EGFR) in ulcer biopsy samples. ECF data of the samples, which were 27 saliva samples from RAU gained not only in the ulcerous period but also in interval period and 33 ones from normal persons, were acquired through enzyme linked immunosorhent assay (ELISA) and EGF standard curve. ECFR-RNA date of RAU biopsies, which were 31 biopsy samples from RAU got during the ulcerous period and 35 ones from normal persons, were surveyed by QF-RT-PCR. All RAU samples were obtained under the same level, which were the whole patients were minor aphthous ulcers and their ulcers occurred not over the first four days. All patients and normal persons were selected seriously under the rule of physical situations without any other diseases and histories of using medicines. The EGF concentration of saliva in RAU group at ulcer occurrence was higher than that in the interval period and the normal control with a significant test (F = 3.24, P < 0.05). The EGF concentration of saliva in RAU group during the interval period was lower than that in the control, which was significant on statistics (t = 2.73, P < 0.05). The EGFR-RNA in RAU group at ulcer occurrence was higher than the normal control with a significant test (t = 3.15, P < 0.05). It was suggested that the ulcer occasion of RAU patients could be related with the decreasing of EGF in saliva during interval period, and that the ulcer sell-cure of RAU patients would be contributed to