Serum fetuin-a and risk of thoracic aortic aneurysms: a two-sample mendelian randomization study.

Background: Recent studies have revealed a significant decrease in serum fetuin-A levels in atherosclerotic aneurysms, indicating that fetuin-A may play a protective role in the progression of arterial calcification. However, the specific mechanism behind this phenomenon remains unclear. We aimed to examine the association between fetuin-A levels in thoracic aortic aneurysms (TAAs) and risk of TAAs and to evaluate whether this association was causal. Methods: A total of 26 SNPs were selected as instrumental variables for fetuin-A in 9,055 participants of European ancestry from the CHARGE consortium, and their effects on thoracic aortic aneurysm and decreased descending thoracic aortic diameter were separately estimated in 353,049 and 39,688 individuals from FinnGen consortium. We used two-sample Mendelian randomization (MR) analysis to examine the causal association. At the same time, we employed various methods, including random-effects inverse variance weighting, weighted median, MR Egger regression, and MR PRESSO, to ensure the robustness of causal effects. We assessed heterogeneity using Cochran's Q value and examined horizontal pleiotropy through MR Egger regression and retention analysis. Results: Fetuin-A level was associated with a significantly decreasing risk of thoracic aortic aneurysm (odds ratio (OR) 0.64, 95% CI 0.47 - 0.87, P = 0.0044). Genetically predicted fetuin-A was also correlated with the decreased descending thoracic aortic diameter (ß = -0.086, standard error (SE) 0.036, P = 0.017). Conclusions: Serum fetuin-A level was negatively associated with risk of TTAs and correlated with the decreased descending thoracic aortic diameter. Mendelian randomization provides support for the potential causal relationship between fetuin-A and thoracic aortic aneurysm.

The effects of psychiatric disorders on the risk of chronic heart failure: a univariable and multivariable Mendelian randomization study.

Background: Substantial evidence suggests an association between psychiatric disorders and chronic heart failure. However, further investigation is needed to confirm the causal relationship between these psychiatric disorders and chronic heart failure. To address this, we evaluated the potential effects of five psychiatric disorders on chronic heart failure using two-sample Mendelian Randomization (MR). Methods: We selected single nucleotide polymorphisms (SNPs) associated with chronic heart failure and five psychiatric disorders (Attention-Deficit Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD), Major Depression, Bipolar Disorder and Schizophrenia (SCZ)). Univariable (UVMR) and multivariable two-sample Mendelian Randomization (MVMR) were employed to assess causality between these conditions. Ever smoked and alcohol consumption were controlled for mediating effects in the multivariable MR. The inverse variance weighting (IVW) and Wald ratio estimator methods served as the primary analytical methods for estimating potential causal effects. MR-Egger and weighted median analyses were also conducted to validate the results. Sensitivity analyses included the funnel plot, leave-one-out, and MR-Egger intercept tests. Additionally, potential mediators were investigated through risk factor analyses. Results: Genetically predicted heart failure was significantly associated with ADHD (odds ratio (OR), 1.12; 95% CI, 1.04-1.20; p = 0.001), ASD (OR, 1.29; 95% CI, 1.07-1.56; p = 0.008), bipolar disorder (OR, 0.89; 95% CI, 0.83-0.96; p = 0.001), major depression (OR, 1.15; 95% CI, 1.03-1.29; p = 0.015), SCZ (OR, 1.04; 95% CI, 1.00-1.07; p = 0.024). Several risk factors for heart failure are implicated in the above cause-and-effect relationship, including ever smoked and alcohol consumption. Conclusion: Our study demonstrated ADHD, ASD, SCZ and major depression may have a causal relationship with an increased risk of heart failure. In contrast, bipolar disorder was associated with a reduced risk of heart failure, which could potentially be mediated by ever smoked and alcohol consumption. Therefore, prevention strategies for heart failure should also incorporate mental health considerations, and vice versa.

Crystalline architectures of C84 with tunable morphology and linearly polarized red emission.

Fullerene-based micro/nano-architectures (FMNAs) with remarkable photoluminescence (PL) emissions have attracted considerable interest as potential building blocks for optical and biolabeling applications, by virtue of their low toxicity and environmentally friendly nature. Nevertheless, the PL polarization properties of FMNAs have rarely been explored. Herein, we demonstrate the preparation of highly crystalline architectures of C84, which exhibit polymorphism depending on the preparation conditions but possess similar hexagonal close-packed (hcp) structures. The PL data demonstrate that the as-prepared carambola-like hexagonal microprisms (c-HPs) show enhanced red emission compared to regular hexagonal microprisms (r-HPs). More importantly, the linear polarization of the PL emission is verified and estimated through single-prism spectroscopy, which changes from 0.42 (r-HP) to 0.58 (c-HP), comparable to those of traditional rod-like semiconductors. Thus, we demonstrate a significant correlation between the morphology and emission characteristics of C84-based microprisms, highlighting the possibility of controlling the photophysical properties of FMNAs by finely tailoring their external morphologies. This study expands the range of carbon materials with linearly polarized emissions and offers potential for use in polarization-based micro-scale sensors or detectors.

[Effectiveness of arthroscopic binding fixation using suture through single bone tunnel for posterior cruciate ligament tibial insertion fracture in adults].

Objective: To explore the effectiveness of arthroscopic binding fixation using suture through single bone tunnel for posterior cruciate ligament (PCL) tibial insertion fractures in adults. Methods: Between October 2019 and October 2021, 16 patients with PCL tibial insertion fractures were treated with arthroscopic binding fixation using suture through single bone tunnel. There were 11 males and 5 females with an average age of 41.1 years (range, 26-58 years). The fractures were caused by traffic accident in 12 cases and sports in 4 cases. The time from injury to operation ranged from 2 to 10 days with an average of 6.0 days. The fractures were classified as Meyers-McKeever type Ⅱ in 4 cases and type Ⅲ in 9 cases, and Zaricznyi type Ⅳ in 3 cases. There were 2 cases of grade Ⅰ, 7 cases of grade Ⅱ, and 7 cases of grade Ⅲ in the posterior drawer test. There were 3 cases combined with lateral collateral ligament injury and 2 cases with meniscus injury. The visual analogue scale (VAS) score, Lysholm score, International Knee Documentation Committee (IKDC) score, and knee range of motion were used to evaluate knee joint function. The posterior drawer test and knee stability tester (Kneelax 3) were used to evaluate knee joint stability. The X-ray films were used to evaluate fracture reduction and healing. Results: All incisions healed by first intention after operation. There was no incision infection, popliteal neurovascular injury, or deep venous thrombosis of lower limbs. All patients were followed up 6-12 months, with an average of 10 months. X-ray films at 6 months after operation showed the fractures obtained bone union. There were 11 cases of grade 0, 4 cases of gradeⅠ, and 1 case of grade Ⅱin posterior drawer test, showing significant difference when compared with preoperative results ( Z=23.167, P<0.001). The VAS score, Lysholm score, IKDC score, knee range of motion, and the results of Kneelax3 examination all significantly improved when compared with preoperative results ( P<0.05). Conclusion: For adult patients with PCL tibial insertion fractures, the arthroscopic binding fixation using suture through single bone tunnel has the advantages of minimal trauma, good fracture reduction, reliable fixation, and fewer complications. The patient's knee joint function recovers well.

Neutrophil to high-density lipoprotein cholesterol ratio as the risk mark in patients with type 2 diabetes combined with acute coronary syndrome: a cross-sectional study.

Chronic inflammation and dyslipidemia are important risk factors in developing atherosclerotic cardiovascular disease, such as coronary heart disease. Acute coronary syndrome (ACS) is one of the most dangerous syndromes in coronary heart disease. Type 2 diabetes mellitus (T2DM) is considered equal to coronary heart disease owing to the high cardiac risk induced by chronic inflammation and dyslipidemia. The neutrophil to high-density lipoprotein cholesterol ratio (NHR) is a novel and straightforward marker that reflects inflammation and lipid metabolic disorder. However, few studies have been on the role of NHR in assessing the risk of ACS in T2DM patients. Here we analyzed NHR level in ACS patients with T2DM, exploring its predictive and diagnostic values. 211 hospitalized ACS patients with T2DM were recruited as the case group, and 168 hospitalized T2DM patients as the control group (all patients collected from 6/2020 to 12/2021 in Xiangya Hospital). Biochemical test results and echocardiograms, as well as demographic information such as age, BMI, diabetes mellitus, smoking, drinking, and history of hypertension, were recorded. Frequencies, percentages, means, and standard deviations were used to describe the data. The shapiro-Wilk test was used to assess the normality of the data. Normally distributed data were compared using the independent sample T-test, and non-normally distributed data were compared using Mann-Whitney U test. Correlation analysis was performed using the Spearman rank correlation test, and receiver operating characteristic (ROC) curve analysis and multivariable logistic regression analysis were performed by SPSS version 24.0 (SPSS Inc) and GraphPad Prism 9.0 (GraphPad Software Inc). p < 0.05 was considered significant. In the study population, NHR was higher in patients with T2DM combined with ACS than in T2DM patients without ACS (p < 0.001). After adjusting for BMI, alcohol consumption, and history of hypertension, multifactorial logistic regression analysis revealed that NHR is a risk factor for T2DM patients combined with ACS (OR 1.221, p = 0.0126). Correlation analysis on all ACS patients with T2DM showed that NHR level was positively correlated with cTnI (r = 0.437, p < 0.001), CK (r = 0.258, p = 0.001), CK-Mb (r = 0.447, p < 0.001), LDH (r = 384, p < 0.001), Mb (r = 0.320, p < 0.001), LA (r = 0.168, p = 0.042) and LV levels (r = 0.283, p = 0.001). And meanwhile, NHR level was negatively correlated with EF (r = - 0.327, p < 0.001) and FS levels (r = - 0.347, p < 0.001). ROC curve analysis showed that NHR ≧ 4.32 had a sensitivity of 65.45% and a specificity of 66.19% for predicting ACS in T2DM patients [area under the curve (AUC) = 0.722, p < 0.001]. Furthermore, in all ACS patients with T2DM, the diagnostic power of NHR was stronger in ST-segment elevated ACS patients (STE-ACS) than that in non-ST-segment elevated ACS patients (NSTE-ACS) (p < 0.001). With its convenience and effective character, NHR could be a potential and new marker for predicting the presence, progression, and severity of ACS in T2DM population.

Unraveling a bifunctional mechanism for methanol-to-formate electro-oxidation on nickel-based hydroxides.

For nickel-based catalysts, in-situ formed nickel oxyhydroxide has been generally believed as the origin for anodic biomass electro-oxidations. However, rationally understanding the catalytic mechanism still remains challenging. In this work, we demonstrate that NiMn hydroxide as the anodic catalyst can enable methanol-to-formate electro-oxidation reaction (MOR) with a low cell-potential of 1.33/1.41 V at 10/100 mA cm-2, a Faradaic efficiency of nearly 100% and good durability in alkaline media, remarkably outperforming NiFe hydroxide. Based on a combined experimental and computational study, we propose a cyclic pathway that consists of reversible redox transitions of NiII-(OH)2/NiIII-OOH and a concomitant MOR. More importantly, it is proved that the NiIII-OOH provides combined active sites including NiIII and nearby electrophilic oxygen species, which work in a cooperative manner to promote either spontaneous or non-spontaneous MOR process. Such a bifunctional mechanism can well account for not only the highly selective formate formation but also the transient presence of NiIII-OOH. The different catalytic activities of NiMn and NiFe hydroxides can be attributed to their different oxidation behaviors. Thus, our work provides a clear and rational understanding of the overall MOR mechanism on nickel-based hydroxides, which is beneficial for advanced catalyst design.

Hierarchical Nanospheres with Polycrystalline Ir&Cu and Amorphous Cu2 O toward Energy-Efficient Nitrate Electrolysis to Ammonia.

Electrochemical reduction reaction of nitrate (NITRR) provides a sustainable route toward the green synthesis of ammonia. Nevertheless, it remains challenging to achieve high-performance electrocatalysts for NITRR especially at low overpotentials. In this work, hierarchical nanospheres consisting of polycrystalline Iridium&copper (Ir&Cu) and amorphous Cu2 O (Cux Iry Oz NS) have been fabricated. The optimal species Cu0.86 Ir0.14 Oz delivers excellent catalytic performance with a desirable NH3 yield rate (YR) up to 0.423 mmol h-1  cm-2 (or 4.8 mg h-1  mgcat -1 ) and a high NH3 Faradaic efficiency (FE) over 90% at a low overpotential of 0.69 V (or 0 VRHE ), where hydrogen evolution reaction (HER) is almost negligible. The electrolyzer toward NITRR and hydrazine oxidation (HzOR) is constructed for the first time with an electrode pair of Cu0.86 Ir0.14 Oz //Cu0.86 Ir0.14 Oz , yielding a high energy efficiency (EE) up to 87%. Density functional theory (DFT) calculations demonstrate that the dispersed Ir atom provides active site that not only promotes the NO3 - adsorption but also modulates the H adsorption/desorption to facilitate the proton supply for the hydrogenation of *N, hence boosting the NITRR. This work thus points to the importance of both morphological/structural and compositional engineering for achieving the highly efficient catalysts toward NITRR.

Immune communication between the intestinal microbiota and the cardiovascular system.

The intestine hosts a large number of microbial communities. Recent studies have shown that gut microbiota-mediated immune responses play a vital role in developing cardiovascular diseases (CVD). Immune cells are extensively infiltrated in the gut and heart tissues, such as T cells, B cells, and macrophages. They play a crucial role in the crosstalk between the heart and gut microbiota. And the microbiota influences the bidirectional function of immune cells in CVD such as myocardial infarction and atherosclerosis, including through metabolites. The mapping of immune cell-mediated immune networks in the heart and gut provides us with new targets for treating CVD. This review discusses the role of immune cells in gut microbiota and cardiac communication during health and CVD.

Trimethylamine N-Oxide Generated by the Gut Microbiota: Potential Atherosclerosis Treatment Strategies.

Cardiovascular diseases (CVD) have become a disease burden that plagues the world, and a large proportion of the world's mortality currently stems from atherosclerotic CVD. In addition to traditional therapies, we need to find more therapeutic targets and strategies in scientific research to address this challenge. In recent years, as research on gut microbiota has continued, there has been a clearer understanding of the role that metabolites from gut microbes play during atherosclerosis (AS). A growing body of research suggests that trimethylamine oxide (TMAO) is an independent risk factor for CVD and that gut microbe-dependent TMAO plays a critical role in AS. Therefore, interventions targeting TMAO have the potential to become a new therapeutic strategy for AS. This review provides a brief overview of the relationship between TMAO and atherosclerosis. More importantly, several potential atherosclerosis treatment strategies targeting TMAO and its metabolic pathways have been revealed by recent studies and will be the focus of this review. This review summarizes possible therapeutic strategies in terms of change of diet, adjustment of gut microbiota, suppression of liver enzyme activity, and improvement of renal function, in the hope of providing new insights for developing efficient and cost-effective treatment and prevention for AS.

miR-653-5p suppresses the viability and migration of fibroblast-like synoviocytes by targeting FGF2 and inactivation of the Wnt/beta-catenin pathway.

BACKGROUND: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease. Several studies reported that fibroblast-like synoviocytes (FLSs) and miRNAs are associated with RA pathogenesis. This study explored the function of miR-653-5p in the regulation of human fibroblast-like synoviocytes-rheumatoid arthritis (HFLS-RA) cells. METHODS: The mRNA and protein levels of genes were measured by RT-qPCR and western blot, respectively. MTT, wound healing, and invasion assays were used to evaluate the viability and metastasis of FLSs. Luciferase reporter and RNA pull-down assays were employed to determine the interaction between miR-653-5p and FGF2. RESULTS: RT-qPCR results demonstrated that miR-653-5p expression was decreased and FGF2 level was increased in synovial tissues and FLSs of RA. Moreover, the viability and metastasis of FLSs were accelerated by miR-653-5p addition, which was restrained by miR-653-5p suppression. Furthermore, we demonstrated that levels of Rac1, Cdc42, and RhoA were decreased after miR-653-5p addition. Besides, luciferase reporter and RNA pull-down assays implied that miR-653-5p targeted the 3'-UTR of FGF2. Functional assays showed that FGF2 overexpression neutralized the suppressive effects of miR-653-5p addition on HFLS-RA cell viability, metastasis, and the levels of Rho family proteins. Meanwhile, the levels of ß-catenin, cyclin D1, and c-myc were declined by miR-653-5p supplementation, but enhanced by FGF2 addition. CONCLUSION: In sum, we manifested that miR-653-5p restrained HFLS-RA cell viability and metastasis via targeting FGF2 and repressing the Wnt/beta-Catenin pathway.

Dielectrophoresis-Based Method for Measuring the Multiangle Mechanical Properties of Biological Cells.

The mechanical properties of cells are closely related to their physiological functions and states. Analyzing and measuring these properties are beneficial to understanding cell mechanisms. However, most measurement methods only involve the unidirectional analysis of cellular mechanical properties and thus result in the incomplete measurement of these properties. In this study, a microfluidic platform was established, and an innovative microfluidic chip was designed to measure the multiangle cellular mechanical properties by using dielectrophoresis (DEP) force. Three unsymmetrical indium tin oxide (ITO) microelectrodes were designed and combined with the microfluidic chip, which were utilized to generate DEP force and stretch cell from different angles. A series of experiments was performed to measure and analyze the multiangle mechanical properties of red blood cells of mice. This work provided a new tool for the comprehensive and accurate measurement of multiangle cellular mechanical properties. The results may contribute to the exploration of the internal physiological structures of cells and the building of accurate cell models.