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136 result(s) for "Xuyang Meng"
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Association between the triglyceride–glucose index and severity of coronary artery disease
Background The triglyceride–glucose (TyG) index, which is a reliable surrogate marker of insulin resistance (IR), has been associated with cardiovascular diseases. However, evidence of the impact of the TyG index on the severity of coronary artery disease (CAD) is limited. This study investigated the relationship between the TyG index and CAD severity of individuals with different glucose metabolic statuses. Methods This study enrolled 2792 participants with CAD in China between January 1, 2018 and December 31, 2021. All participants were divided into groups according to the tertiles of the TyG index as follows: T1 group, TyG index < 6.87; T2 group, TyG index ≥ 6.87 to < 7.38; and T3 group, TyG index ≥ 7.38. The glucose metabolic status was classified as normal glucose regulation, pre-diabetes mellitus (pre-DM), and diabetes mellitus according to the standards of the American Diabetes Association. CAD severity was determined by the number of stenotic vessels (single-vessel CAD versus multi-vessel CAD). Results We observed a significant relationship between the TyG index and incidence of multi-vessel CAD. After adjusting for sex, age, body mass index, smoking habits, alcohol consumption, hypertension, estimated glomerular filtration rate, antiplatelet drug use, antilipidemic drug use, and antihypertensive drug use in the logistic regression model, the TyG index was still an independent risk factor for multi-vessel CAD. Additionally, the highest tertile of the TyG group (T3 group) was correlated with a 1.496-fold risk of multi-vessel CAD compared with the lowest tertile of the TyG group (T1 group) (odds ratio [OR], 1.496; 95% confidence interval [CI], 1.183–1.893; P < 0.001) in the multivariable logistic regression model. Furthermore, a dose–response relationship was observed between the TyG index and CAD severity (non-linear P = 0.314). In the subgroup analysis of different glucose metabolic statuses, the T3 group (OR, 1.541; 95% CI 1.013–2.344; P = 0.043) were associated with a significantly higher risk of multi-vessel CAD in individuals with pre-DM. Conclusions An increased TyG index was associated with a higher risk of multi-vessel CAD. Our study indicated that TyG as an estimation index for evaluating IR could be a valuable predictor of CAD severity, especially for individuals with pre-DM.
Oxidized sulfur-rich arc magmas formed porphyry Cu deposits by 1.88 Ga
Most known porphyry Cu deposits formed in the Phanerozoic and are exclusively associated with moderately oxidized, sulfur-rich, hydrous arc-related magmas derived from partial melting of the asthenospheric mantle metasomatized by slab-derived fluids. Yet, whether similar metallogenic processes also operated in the Precambrian remains obscure. Here we address the issue by investigating the origin, f O 2 , and S contents of calc-alkaline plutonic rocks associated with the Haib porphyry Cu deposit in the Paleoproterozoic Richtersveld Magmatic Arc (southern Namibia), an interpreted mature island-arc setting. We show that the ca. 1886–1881 Ma ore-forming magmas, originated from a mantle-dominated source with minor crustal contributions, were relatively oxidized (1‒2 log units above the fayalite-magnetite-quartz redox buffer) and sulfur-rich. These results indicate that moderately oxidized, sulfur-rich arc magma associated with porphyry Cu mineralization already existed in the late Paleoproterozoic, probably as a result of recycling of sulfate-rich seawater or sediments from the subducted oceanic lithosphere at that time. Tectonomagmatic conditions in the Precambrian were hypothesized to be unfavorable for porphyry Cu deposit formation. Here, the authors show that metallogenic processes typify Phanerozoic porphyry Cu deposits operated by ~1.88 Ga, reflecting modification of mantle lithosphere by oxidized slab-derived fluids at that time.
Multi-Global Navigation Satellite System for Earth Observation: Recent Developments and New Progress
The Global Navigation Satellite System (GNSS) has made important progress in Earth observation and applications. With the successful design of the BeiDou Navigation Satellite System (BDS), four global navigation satellite systems are available worldwide, together with Galileo, GLONASS, and GPS. These systems have been widely employed in positioning, navigation, and timing (PNT). Furthermore, GNSS refraction, reflection, and scattering signals can remotely sense the Earth’s surface and atmosphere with powerful implications for environmental remote sensing. In this paper, the recent developments and new application progress of multi-GNSS in Earth observation are presented and reviewed, including the methods of BDS/GNSS for Earth observations, GNSS navigation and positioning performance (e.g., GNSS-PPP and GNSS-NRTK), GNSS ionospheric modelling and space weather monitoring, GNSS meteorology, and GNSS-reflectometry and its applications. For instance, the static Precise Point Positioning (PPP) precision of most MGEX stations was improved by 35.1%, 18.7%, and 8.7% in the east, north, and upward directions, respectively, with PPP ambiguity resolution (AR) based on factor graph optimization. A two-layer ionospheric model was constructed using IGS station data through three-dimensional ionospheric model constraints and TEC accuracy was increased by about 20–27% with the GIM model. Ten-minute water level change with centimeter-level accuracy was estimated with ground-based multiple GNSS-R data based on a weighted iterative least-squares method. Furthermore, a cyclone and its positions were detected by utilizing the GNSS-reflectometry from the space-borne Cyclone GNSS (CYGNSS) mission. Over the years, GNSS has become a dominant technology among Earth observation with powerful applications, not only for conventional positioning, navigation and timing techniques, but also for integrated remote sensing solutions, such as monitoring typhoons, river water level changes, geological geohazard warnings, low-altitude UAV navigation, etc., due to its high performance, low cost, all time and all weather.
Association of stress hyperglycemia ratio and in-hospital mortality in patients with coronary artery disease: insights from a large cohort study
Background Stress hyperglycemia is strongly associated with poor clinical outcomes in patients with acute coronary syndrome (ACS). Recently, the stress hyperglycemia ratio (SHR) has been proposed to represent relative hyperglycemia. Studies regarding the relationship between SHR and mortality in coronary artery disease (CAD) are limited. This study aimed to clarify the association between SHR and in-hospital mortality in patients with CAD. Methods A total of 19,929 patients with CAD who were hospitalized in Beijing Hospital were enrolled in this study. Patients with an estimated glomerular filtration rate < 30 ml/min, cancer, or missing blood glucose/HbA1c data were excluded; therefore, 8,196 patients were included in the final analysis. The patients were divided into three groups based on tertiles of SHR: T1 group (SHR < 0.725, n = 2,732), T2 group (0.725 ≤ SHR < 0.832, n = 2,730), and T3 group (SHR ≥ 0.832, n = 2,734). The primary endpoint was in-hospital mortality. Results The overall in-hospital mortality rate was 0.91% (n = 74). After adjusting for covariates, SHR was significantly associated with in-hospital mortality in patients with CAD [odds ratio (OR) = 17.038; 95% confidence interval (CI) = 9.668–30.027; P <  0.001], and the T3 group had a higher risk of in-hospital mortality (OR = 4.901; 95% CI = 2.583–9.297; P <  0.001) compared with T1 group. In the subgroup analysis, the T3 group had an increased risk of mortality among patients with pre-diabetes mellitus (pre-DM) (OR = 9.670; 95% CI = 1.886–49.571; P  = 0.007) and diabetes mellitus (DM) (OR = 5.023; 95% CI = 2.371–10.640; P < 0.001) after adjustments for covariates. The relationship between SHR and in-hospital mortality among patients with ACS and chronic coronary syndrome was consistent with the main finding. SHR and in-hospital mortality exhibited a dose-response relationship, and the risk of in-hospital mortality increased when the SHR index was above 1.20. Moreover, the area under the curve of SHR for predicting in-hospital mortality in patients with CAD was 0.741. Conclusion SHR is significantly associated with in-hospital mortality in patients with CAD. SHR may be an effective predictor of in-hospital mortality in patients with CAD, especially for those with pre-DM and DM.
Cardiomyocyte pyroptosis inhibited by dental pulp-derived mesenchymal stem cells via the miR-19a-3p/IRF-8/MAPK pathway in ischemia–reperfusion
Abstract Background: The protective effect of mesenchymal stem cells (MSCs) on cardiac ischemia–reperfusion (I/R) injury has been widely reported. Dental pulp-derived mesenchymal stem cells (DP-MSCs) have therapeutic effects on various diseases, including diabetes and cirrhosis. This study aimed to determine the therapeutic effects of DP-MSCs on I/R injury and elucidate the underlying mechanism. Methods: Myocardial I/R injury model mice were treated with DP-MSCs or a miR-19a-3p mimic. The infarct volume, fibrotic area, pyroptosis, inflammation level, and cardiac function were measured. Cardiomyocytes exposed to hypoxia–reoxygenation were transfected with the miR-19a-3p mimic, miR-19a-3p inhibitor, or negative control. Pyroptosis and protein expression in the interferon regulatory factor 8/mitogen-activated protein kinase (IRF-8/MAPK) pathway were measured. Results: DP-MSCs protected cardiac function in cardiac I/R-injured mice and inhibited cardiomyocyte pyroptosis. The upregulation of miR-19a-3p protected cardiac function, inhibited cardiomyocyte pyroptosis, and inhibited IRF-8/MAPK signaling in cardiac I/R-injured mice. DP-MSCs inhibited cardiomyocyte pyroptosis and the IRF-8/MAPK signaling by upregulating the miR-19a-3p levels in cardiomyocytes injured by I/R. Conclusion: DP-MSCs protected cardiac function by inhibiting cardiomyocyte pyroptosis through miR-19a-3p under I/R conditions.
Aerobic exercise inhibits GSDME-dependent myocardial cell pyroptosis to protect ischemia-reperfusion injury
Background Acute myocardial infarction (AMI) remains a significant cause of global mortality, exacerbated by ischemia-reperfusion (IR) injury. Myocardial cell pyroptosis has emerged as a critical pathway influencing IR injury severity. Methods We aimed to investigate the cardioprotective effects of aerobic exercise on IR injury by examining the modulation of IGFBP2 and its impact on GSDME-dependent myocardial cell pyroptosis. Mechanistic pathways were explored using western blot analysis, ELISA, immunofluorescence, and echocardiography. Results Our findings demonstrate that aerobic exercise leads to increased circulating levels of IGFBP2, which effectively suppresses GSDME-dependent myocardial cell pyroptosis. This regulation occurs via the AKT-GSK3β signaling pathway, involving VDAC1 phosphorylation, thereby enhancing mitochondrial function and reducing oxidative stress. Conclusion In conclusion, our study highlights the role of IGFBP2 in mitigating GSDME-dependent pyroptosis as a mechanism through which aerobic exercise exerts cardioprotective effects against IR injury. These insights suggest potential therapeutic targets for managing acute myocardial infarction.
Joint efficacy of the three biomarkers SNCA, GYPB and HBG1 for atrial fibrillation and stroke: Analysis via the support vector machine neural network
Atrial fibrillation (AF) is the most common type of persistent arrhythmia. Although its incidence has been increasing, the pathogenesis of AF in stroke remains unclear. In this study, a total of 30 participants were recruited, including 10 controls, 10 patients with AF and 10 patients with AF and stroke (AF + STROKE). Differentially expressed genes (DEGs) were identified, and functional annotation of DEGs, comparative toxicogenomic database analysis associated with cardiovascular diseases, and predictions of miRNAs of hub genes were performed. Using RT‐qPCR, biological process and support vector machine neural networks, numerous DEGs were found to be related to AF. HBG1, SNCA and GYPB were found to be upregulated in the AF group. Higher expression of hub genes in AF and AF + STROKE groups was detected via RT‐PCR. Upon training the biological process neural network of SNCA and GYPB for HBG1, only small differences were detected. Based on the support vector machine, the predicted value of SNCA and GYPB for HBG1 was 0.9893. Expression of the hub genes of HBG1, SNCA and GYPB might therefore be significantly correlated to AF. These genes are involved in the incidence of AF complicated by stroke, and may serve as targets for early diagnosis and treatment.
IGFBP2 plays a key role in aerobic exercise-mediated inhibition of ferroptosis in cardiac ischemia/reperfusion (I/R) injury
Background Ferroptosis is an important mechanism underlying cardiac ischemia/reperfusion (I/R) injury. However, the specific molecular mechanisms by which aerobic exercise alleviates cardiac I/R injury and inhibits ferroptosis remain unclear. Methods In this study, we investigated the effects of IGFBP2 on aerobic exercise-mediated protection of cardiac function following I/R and its influence on ferroptosis in cardiomyocytes and SIRT1 activation. Wild-type (WT) or IGFBP2 knockout (IGFBP2_KO) C57BL/6J mice with I/R injury were subjected to aerobic exercise intervention, and cardiomyocytes exposed to hypoxia/reoxygenation (H/R) were treated with IGFBP2. We explored the role of IGF-1R in IGFBP2-mediated cardiac protection using IGF-1R conditional knockout (IGF-1R_CKO) mice subjected to aerobic exercise intervention and cardiomyocytes exposed to H/R and incubated with IGFBP2 and IGF-1R silenced via adenoviral vector (ADV) transfection. The effects of SIRT1 and TXNIP/TRX on ferroptosis in cardiomyocytes exposed to H/R were also examined using SIRT1 inhibitors, SIRT1 agonists, and adenovirus transfection to modulate TXNIP expression levels. Results Aerobic exercise increased circulating IGFBP2 levels in mice, inhibited ferroptosis in cardiomyocytes, and protected cardiac function following I/R ( p < 0.001). IGFBP2 suppressed ferroptosis in cardiomyocytes subjected to H/R and enhanced SIRT1 activation ( p < 0.001). IGF-1R_CKO abrogated the inhibitory effects of IGFBP2 and aerobic exercise on cardiomyocyte ferroptosis ( p < 0.001). SIRT1 activation inhibited ferroptosis in cardiomyocytes exposed to H/R by downregulating TXNIP expression, upregulating TRX expression, and increasing TXNIP/TRX binding ( p < 0.001). Inhibition of TXNIP suppressed ferroptosis following H/R ( p < 0.001). Conclusion Aerobic exercise-induced circulating IGFBP2 directly interacts with IGF-1R, leading to increased activation of SIRT1 and reduced levels of free TXNIP, thus inhibiting cardiomyocyte ferroptosis in cardiac I/R injury. Graphical abstract
Recurrent strokes after transcatheter aortic valve replacement in an elderly patient with severe bicuspid aortic valve stenosis: a case report
Background Transcatheter aortic valve replacement (TAVR) has evolved from a novel technology to an established therapy for high-risk patients with symptomatic severe aortic valve stenosis (AS). Recently, its use has also been extended to low-risk patients, resulting in its increasing utilization in patients with bicuspid aortic valve (BAV). But as a serious post-TAVR complication, ischemic stroke was associated with a nearly 6‐fold increased 30‐day mortality. BAV presents unique challenges for post-TAVR antithrombotic therapy due to its distinct valvular anatomy. Case presentation We present a case of a 72-year-old female who presented with angina pectoris symptoms and was found to have severe BAV stenosis (Type 0). According to the patient’s age, obvious symptom and willingness herself, TAVR was successful performed with deployment of a 23 mm Venus-A Plus valve (Venus Medtech, Hangzhou, China). A post-procedure echocardiogram confirmed the appropriate placement of the bioprosthetic valve with minor paravalvular regurgitation. Six months after TAVR, this patient experienced multiple strokes, presenting a significant challenge for clinicians. Conclusions This case underscores the serious complications that can occur post-TAVR and highlights the need for improved strategies to prevent early strokes.
Association between triglyceride-glucose index and in-hospital all-cause mortality under different glucose metabolism status among patients with coronary artery disease
Background This current study aimed to investigate the relationship between the triglyceride-glucose (TyG) index and in-hospital all-cause mortality of coronary artery disease (CAD) in patients with different glucose metabolic statuses. Methods Participants were divided into three groups according to tertiles of the TyG index. Glucose metabolic status was classified as normal glucose regulation, pre-diabetes mellitus, and diabetes mellitus (DM). The primary outcome was in hospital all-cause mortality. Results We observed a significant relationship between the TyG index and in-hospital deaths of patients with CAD in this study. After adjusting for multiple factors in the logistic regression model, the TyG index was still an independent risk factor, and the T3 group (OR, 2.311; 95% CI = 1.237–4.317; P  = 0.009) was correlated with a 2.311-fold risk compared with the T1 group. In the subgroup analysis of different glucose metabolic status, the T3 group (OR, 1.541; 95% CI: 1.013–2.344; P  = 0.043) were associated with a significantly higher risk of in-hospital deaths in CAD patients with DM. Conclusions An increased TyG index was correlated with a higher risk of in-hospital all-cause mortality. Our study indicated that TyG index could be a valuable predictor of in-hospital death of CAD patients, especially for individuals with DM.