Efficient ofloxacin degradation via peroxymonosulfate activation using an S-scheme MoS2/Co3O4 heterojunction composite under visible light: Performance and mechanistic insights.

Sulfate-radical-mediated photocatalysis technology peroxymonosulfate (PMS) activation via visible light irradiation shows great promise for water treatment applications. However, its effectiveness largely depends on the bifunctional performance of photocatalysis and PMS activation provided by the catalysts. In this study, we successfully synthesized a novel S-scheme MoS2/Co3O4 (MC) heterojunction composite by a hydrothermal method and employed it for the first time to activate PMS for ofloxacin (OFX) degradation under visible light irradiation. The MC-5/PMS/Vis system achieved an impressive 85.11% OFX degradation efficiency within 1 min and complete OFX removal within 15 min under optimal conditions, with an apparent first-order kinetics rate constant of 0.429 min-1. Reactive species trapping experiments and electron spin resonance analysis identified 1O2, h+, and •O2- as the primary active species responsible for OFX degradation. Photoelectrochemical analyses and density functional theory calculations indicated the formation of a built-in electric field between MoS2 and Co3O4, which enhanced the separation and migration of photoinduced carriers. Additionally, the Co-Mo interaction further increased the yield of dominant reactive species, thereby boosting photocatalytic activity. This work underscores the potential of visible-light-assisted PMS-mediated photocatalysis using Co3O4-based catalysts for effective pollutant control.

Scalable Generation and Detection of on-Demand W States in Nanophotonic Circuits.

Quantum physics phenomena, entanglement and coherence, are crucial for quantum information protocols, but understanding these in systems with more than two parts is challenging due to increasing complexity. The W state, a multipartite entangled state, is notable for its robustness and benefits in quantum communication. Here, we generate eight-mode on-demand single-photon W states, using nanowire quantum dots and a silicon nitride photonic chip. We demonstrate a reliable and scalable technique for reconstructing the W state in photonic circuits using Fourier and real-space imaging, supported by the Gerchberg-Saxton phase retrieval algorithm. Additionally, we utilize an entanglement witness to distinguish between mixed and entangled states, thereby affirming the entangled nature of our generated state. The study provides a new imaging approach of assessing multipartite entanglement in W states, paving the way for further progress in image processing and Fourier-space analysis techniques for complex quantum systems.

lncRNA Nuclear Factor of Activated T Cells Knockdown Alleviates Hypoxia/Reoxygenation-induced Cardiomyocyte Apoptosis by Upregulating HIF-1α Expression.

ABSTRACT: Acute myocardial infarction (AMI) has become the most common cause of death in the developed countries. However, its pathogenesis is poorly understood. Increasing studies have revealed that lncRNAs are important modulators of AMI development. This study aimed to explore the function of lncRNA noncoding repressor of nuclear factor of activated T cells (NRON) in hypoxia/reoxygenation (H/R)-stimulated H9c2 cells. NRON expression in peripheral blood of AMI patients and H/R-stimulated H9c2 cells was measured by quantitative real-time polymerase chain reaction. H9c2 cells were transfected with si-NRON or cotransfected with si-NRON and si-hypoxia-inducible factor-1 alpha (HIF-1α). The viability and apoptosis of these cells were evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) assay and flow cytometer, respectively. In addition, HIF-1α, AKT/mTOR signal pathways and ERK1/2 were detected by western blot. NRON knockdown in the myocardial infarction mouse model was conducted through adeno-associated virus injection, and cardiac function was evaluated by motion-mode echocardiography. The results showed that NRON was highly expressed in peripheral blood of AMI patients and H/R-stimulated H9c2 cells. NRON knockdown promoted cell viability and inhibited cell apoptosis of H/R-stimulated H9c2 cells. Meanwhile, NRON knockdown also significantly attenuated heart damage and improved cardiac function in an AMI mouse model. Furthermore, compared with si-normal control, NRON knockdown increased the levels of HIF-1α, p-AKT, p-mTOR, and p-ERK1/2. HIF-1α knockdown reversed the effects of NRON knockdown in H/R-stimulated-H9c2 cells damage. Overall, our study revealed that NRON knockdown alleviated H/R-induced cardiomyocyte apoptosis by upregulating HIF-1α expression, suggesting that NRON might be a novel therapeutic target for AMI.

Titanium-based metal-organic framework MIL-125(Ti) for the highly selective isolation and purification of immunoglobulin G from human serum.

Titanium-based metal-organic framework MIL-125(Ti) was synthesized by the hydrothermal method of terephthalic acid and tetra butyl titanate in N-N,dimethylformamide, and methanol. MIL-125(Ti) was characterized by Fourier-transform infrared spectroscopy, X-ray diffraction, thermogravimetric analysis, nitrogen adsorption-desorption, energy-dispersive X-ray spectroscopy, zeta potential, scanning electron microscope, and transmission electron microscopy. The results showed MIL-125(Ti) could be used as a potential adsorbent for protein separation and purification due to the high specific surface area, high stability, and strong hydrophobicity. As a result, MIL-125(Ti) had adsorption selectivity for immunoglobulin G, which was due to the hydrogen bond between MIL-125(Ti) and protein. At pH 8.0, the maximum adsorption efficiency of 0.25 mg MIL-125(Ti) for 300 µL 100 µg/mL immunoglobulin G was 98.3%, and its maximum adsorption capacity was 232.56 mg/g. The elution efficiency of immunoglobulin G was 92.4% by 0.1% sodium dodecyl sulfate. sodium dodecyl sulfate-polyacrylamide gel electrophoresis result demonstrated the successful isolation of highly purified immunoglobulin G from the human serum. Therefore, a new method of separation and purification of immunoglobulin G in human serum using titanium-based metal-organic framework MIL-125(Ti) as a solid-phase adsorbent was established, which broadened the application scope of metal-organic frameworks.

Serum VCAM-1 and ICAM-1 measurement assists for MACE risk estimation in ST-segment elevation myocardial infarction patients.

BACKGROUND: Vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) modulate atherosclerosis by promoting leukocyte infiltration, neutrophil recruitment, endothelial cell proliferation, etc., which may directly or indirectly facilitate the occurrence of major adverse cardiac events (MACE). This study intended to investigate the value of VCAM-1 and ICAM-1 for predicting MACE in ST-segment elevation myocardial infarction (STEMI) patients. METHODS: Totally, 373 STEMI patients receiving the percutaneous coronary intervention and 50 health controls (HCs) were included. Serum VCAM-1 and ICAM-1 were detected by ELISA. Meanwhile, MACE was recorded during a median follow-up of 18 (range: 1-46) months in STEMI patients. RESULTS: Vascular cell adhesion molecule-1 and ICAM-1 were raised in STEMI patients compared with HCs (both p < 0.001). VCAM-1 (p = 0.002) and ICAM-1 (p = 0.012) high were linked with raised accumulating MACE rate in STEMI patients. Notably, VCAM-1 high (hazard ratio [HR] = 2.339, p = 0.031), age ≥ 65 years (HR = 2.019, p = 0.039), history of diabetes mellitus (DM) (HR = 2.395, p = 0.011), C-reactive protein (CRP) ≥ 5 mg/L (HR = 2.550, p = 0.012), multivessel disease (HR = 2.561, p = 0.007) independently predicted MACE risk in STEMI patients. Furthermore, a nomogram-based prediction model combining these factors was established, exhibiting an acceptable value for estimating 1, 2, and 3-year MACE risk, with AUC of 0.764, 0.716, and 0.778, respectively, in STEMI patients. CONCLUSION: This study confirms the value of VCAM-1 and ICAM-1 measurement in predicting MACE risk in STEMI patients. Moreover, VCAM-1 plus other traditional prognostic factors (such as age, history of DM, CRP, and multivessel disease) cloud further improve the predictive accuracy of MACE risk in STEMI patients.

Association of tumor necrosis factor-α gene polymorphisms and coronary artery disease susceptibility: a systematic review and meta-analysis.

BACKGROUND: The goal of this study was to review relevant case-control studies to determine the association of tumor necrosis factor-α (TNF-α) gene polymorphisms and coronary artery disease (CAD) susceptibility. METHODS: Using appropriate keywords, we identified relevant studies using PubMed, Cochrane, Embase, CNKI, VANFUN, and VIP. Key pertinent sources in the literature were also reviewed, and all articles published through April 2019 were considered for inclusion. Based on eligible studies, we performed a meta-analysis of association between 308G/A, 238G/A, 857C/T, 863C/A and 1031 T/C polymorphisms in TNF-α and risk of CAD. RESULTS: We found 25 studies that were consistent with this meta-analysis, including 7697 patients in the CAD group and 9655 control patients. TNF-α 308G/A locus A showed no significant association with CAD susceptibility by the five models in the analysis of the overall population, European, African, South Asian, and North Asian patients. TNF-α 863C/A locus A and 1031 T/C locus C exhibited no significant association with CAD susceptibility. TNF-α 238G/A locus A had no significant association with CAD susceptibility in the overall population. However, TNF-α 238G/A locus A showed significant association with higher CAD susceptibility in the subgroup of Europeans and north Asians. TNF-α 857C/T locus T had no significant association with CAD susceptibility in the analysis of the overall population and Europeans. In the north Asian population, TNF-α 857C/T locus T was associated with lower CAD susceptibility by the heterozygote model. CONCLUSION: TNF-α 308G/A, 857C/T, 863C/A, and 1031 T/C has no significant association with CAD susceptibility. TNF-α 238G/A locus A has significant association with CAD susceptibility in Europeans and north Asians, but has no significant association in the overall population. Studies with a larger sample size are required to confirm the association between TNF-α 238G/A and CAD susceptibility.

MicroRNA-424-5p regulates aortic smooth muscle cell function in atherosclerosis by blocking APOC3-mediated nuclear factor-κB signalling pathway.

NEW FINDINGS: What is the central question of this study? What is the role of microRNA-424-5p (miR-424-5p) in aortic smooth muscle cells? How does miR-424-5p function as a suppressor of the inflammatory response? What is the main finding and its importance? Upregulation of miR-424-5p inhibits the inflammatory response in aortic smooth muscle cells. miR-424-5p inactivates the nuclear factor-κB signalling pathway through the downregulation of apolipoprotein C3. ABSTRACT: Dysregulated aortic smooth muscle cells in chronic inflammation result in plaque formation in atherosclerosis (AS), which is a systemic disease that affects the large arteries with the activation of inflammatory pathways as a key process in its pathogenesis. The aim of the study was to investigate the regulatory mechanism of microRNA-424-5p (miR-424-5p) in aortic smooth muscle cell activities and inflammation in AS via the regulation of apolipoprotein C3 (APOC3) and the nuclear factor-κB (NF-κB) signalling pathway. The results showed that miR-424-5p was poorly expressed and APOC3 highly expressed in the peripheral blood of AS patients and rat models of AS. Molecularly, our results confirmed that miR-424-5p targeted the APOC3 gene directly and inhibited APOC3 expression, which resulted in repressed activation of the NF-κB signalling pathway. The gain- and loss-of-function approaches were used to determine the effects of miR-424-5p and APOC3 on inflammation and on the proliferation, apoptosis and migration of aortic smooth muscle cells. Upregulation of miR-424-5p or silencing of APOC3 significantly suppressed proliferation, migration and inflammation and promoted apoptosis of aortic smooth muscle cells, which was achieved through inactivation of the NF-κB signalling pathway. Taken together, our results show that miR-424-5p upregulation impedes the progression of AS by blocking the APOC3-mediated NF-κB signalling pathway, which could be used as a novel target and a potential therapeutic pathway against AS.

Silencing CCL8 inhibited the proliferation and migration of PDGF-BB-stimulated human aortic smooth muscle cells.

C-C motif Chemokine ligand 8 (CCL8) has been found in diseases' pathogenesis. But its molecular mechanism in atherosclerosis (AS) remains to be elucidated. Human aortic smooth muscle cells (HASMCs) were stimulated by PDGF-BB to establish cell model. α-SMA in PDGF-BB-stimulated HASMCs was measured by immunofluorescence staining. Relative gene expressions in PDGF-BB-stimulated HASMCs were detected by quantitative real-time polymerase chain reaction and western blot. HASMCs proliferation, migration, and cell cycle were assessed by cell counting kit-8, wound-healing assay, and flow cytometry. HASMCs viability was increased after PDGF-BB stimulation, with α-SMA downregulation yet CCL8 upregulation. Silencing CCL8 inhibited PDGF-BB-stimulated HASMCs proliferation and migration, and increased cells percentage in G1 phases but decreased those in S phase. Also, silencing CCL8 decreased OPN and cyclinD1 expressions and AKT and ERK1/2 phosphorylation while increased those of α-SMA and Sm22α. However, upregulating CCL8 led to opposite effects, suggesting CCL8 could be an atherosclerosis therapeutic target.

Comparison between MassARRAY and pyrosequencing for CYP2C19 and ABCB1 gene variants of clopidogrel efficiency genotyping.

Clopidogrel is one of the most frequently used drugs in patients to reduce cardiovascular events. Since patients with different genetic variations respond quite differently to clopidogrel therapy, the related genetic testing plays a vital role in its dosage and genetic testing related to clopidogrel therapy is currently considered as routine test worldwide. In this study, we aim to use two different methods MALDI-TOF mass spectrometry and pyrosequencing to detect gene variant of CYP2C19 and ABCB1. Six single nucleotides polymorphisms (SNP) within CYP2C19 (*2, *3, *4, *5, *17) and ABCB1 C3435T in 458 Chinese Han patients were determined using both MassARRAY and Pyrosequencing. Sanger sequencing was used for verification. Results of both methods were analyzed and compared. Allele frequencies of each SNP and distribution of different genotypes were calculated based on the MassARRAY and Sanger sequencing results. Both methods provided 100% call rates for gene variants, while results of six samples were different with two methods. With Sanger sequencing as the reference results, MassARRAY generated all the same results. The minor allele frequencies of the above six SNPs were 27.1% (CYP2C19*), 5.9% (CYP2C19*3), 0% (CYP2C19*4), 0% (CYP2C19*5), 1.1% (CYP2C19*17), 40.9% (ABCB1), respectively. MassARRAY provides accurate clopidogrel related genotyping with relatively high cost-efficiency, throughput and short time when compared with pyrosequencing.

miR-129-5p ameliorates ischemia-reperfusion injury by targeting HMGB1 in myocardium.

Globally, acute myocardial infarction (AMI) is a serious condition affecting millions of individuals. While AMI therapy improves blood flow during surgery, reperfusion-induced injury may also occur, leading to secondary cardiac damage or even death. Here, we investigated miR-129-5p in myocardial ischemia-reperfusion (I/R) injury in rats, to explore reperfusion-related molecular mechanisms in myocardium. We used Sprague Dawley rats to establish a myocardial I/R model, with agomiR-129-5p injection, and used rat cardiomyocytes (H9c2) treated with anoxia-reoxygenation (A/R) to mimic myocardial I/R injury in vitro. A dual-luciferase reporter assay determined miR-129-5p binding to high mobility group box-1 (HMGB1) in H9c2 cells. We showed that exogenous miR-129-5p restored cardiac function indices, alleviated cardiac injury, relieved inflammatory effects and reduced infarct size and cell apoptosis in rat myocardium after I/R treatment. Elevated miR-129-5p induced a reduction in HMGB1 expression in rat I/R myocardium. miR-129-5p also targeted HMGB1, and negatively regulated its expression in H9c2 cells. Moreover, miR-129-5p overexpression in the cardiomyocytes reduced cell apoptosis and recovered cell viability after A/R injury, which was reversed by subsequent HMGB1 overexpression. These findings suggest miR-129-5p plays a cardioprotective role in ameliorating myocardial I/R injury in rats, by negatively targeting HMGB1. This mechanism provides new insights into the treatment of myocardium reperfusion-related damage.

A case presentation of patient from northern China with endomyocardial fibrosis.

BACKGROUND: Endomyocardial fibrosis (EMF) is a rare condition and a major cause of death in tropical countries. The etiology of EMF remains elusive, and no specific treatment has been developed yet, therefore it carries poor prognosis. CASE PRESENTATION: An 81-year-old male Chinese patient with a history of long-standing exertional breathlessness, presented with worsening symptoms rapidly evolving to orthopnea. A proper specific treatment was prescribed to the patient in the following days, including diuretics, angiotensin-converting-enzyme inhibitor and beta blockers. The patient died of progressive multiple organ failure. CONCLUSION: Echocardiography is technically limited due to the acoustic shadowing as a result of the calcification. Chest computed tomography is a more accurate diagnostic tool to examine the anatomic distribution and extent of endomyocardial calcification in this rare case.

Vitamin D Deficiency Harms Patients with Coronary Heart Disease by Enhancing Inflammation.

BACKGROUND Vitamin D (VD) deficiency and local inflammation of plaque are potential new risk factors and prevention goals for coronary heart disease (CHD). MATERIAL AND METHODS This study included 135 CHD patients and 45 chest tightness or chest pain patients (control group). Basic clinical data and serum 25-OH-VD, TNF-α, IL-6, IL-8, and IL-1ß of the 2 groups were compared by SPSS 25.0. A CHD rat model was used to explore the potential molecular mechanisms. RESULTS The serum 25-OH-VD level in the control group was significantly higher compared to the CHD group, and decreased with the worsening of the CHD condition. Logistic regression found that serum 25-OH-VD was a protective factor in the occurrence of CHD. In CHD patients, the level of serum 25-OH-VD had a negative correlation with serum TNF-α (r=-0.651, P<0.001), IL-6 (r=-0.457, P<0.001), IL-8 (r=-0.755, P<0.001), and IL-1ß (r=-0.628, P<0.001). In animal experiments, VD deficiency enhanced the level of serum TC, TG, and LDL-C. VD deficiency could increase the inflammatory response by upregulating the expression of p65 protein and reducing SIRT1 protein expression in heart tissue, thereby inducing or aggravating the state of CHD. CONCLUSIONS Serum 25-OH-VD was a protective factor in the occurrence of CHD, and VD deficiency could induce or aggravate the state of CHD by enhancing inflammation through the NF-κB pathway.

Sex difference among patients with unprotected left main coronary artery disease undergoing percutaneous coronary intervention in northern China.

BACKGROUND: Unprotected left main coronary artery (ULMCA) disease is associated with high mortality and morbidity. The aim of this study is to investigate the efficacy of percutaneous coronary intervention (PCI) on gender-specific patients with ULMCA in the Chinese population and provide a basis for further treatment of PCI in ULMCA disease. METHODS: 173 patients (female, N = 52; male, N = 121; mean age = 61.02 ± 7.95) with ULMCA disease, who underwent PCI between January 2010 and December 2014, were investigated in our study. The mean follow-up time was 23.8 ± 7.3 months. The baseline clinical characteristics, coronary angiography (CAG) and PCI procedures, and in-hospital and follow-up outcomes of gender-specific patients were evaluated. RESULTS: There were no statistically significant differences in baseline clinical characteristics with the exception of body weight, height, and smoking indexes between women and men. During PCI procedure, femoral artery puncture was more preferred in women than men (P < .05), whereas radial artery puncture was more preferred in men than women (P < .05). The characteristics of CAG and PCI procedures (except puncture path) were showed with no markedly difference between women and men. The incidences of MACCEs in male patients during the in-hospital and follow-up periods were slightly higher than those of the female patients although with no statistical differences. CONCLUSION: In northern China, the incidence of ULMCA disease in men is likely to be higher than in women, whereas PCI for ULMCA disease shows similarly favorable outcomes in women as well as in men. During the PCI procedure, femoral artery puncture in women and radial artery puncture in men are recommended.

Electrochemical Degradation of Rhodamine B over Ti/SnO2-Sb Electrode.

Electrochemical degradation of rhodamine B (C28H31ClN2O3) over Ti/SnO2-Sb anode was investigated in a rectangular cell. The degradation reaction follows pseudo-first-order kinetics. The degradation efficiency of rhodamine B attained >90.0% after 20 minutes of electrolysis at initial concentrations of 5 to 200 mg/L at a constant current density of 20 mA/cm2 with a 10 mmol/L Na2SO4 supporting electrolyte solution. Rhodamine B (50 mg/L) degradation and total organic carbon (TOC) removal ratio achieved 99.9 and 86.7%, respectively, at the optimal conditions after 30 minutes of electrolysis. The results showed that the energy efficiency of rhodamine B (50 mg/L) degradation at the optimal current densities from 2 to 30 mA/cm2 were 23.2 to 84.6 Wh/L, whereas the electrolysis time for 90% degradation of rhodamine B with Ti/SnO2-Sb anode was 36.6 and 7.3 minutes, respectively. The electrochemical method can be an advisable option for the treatment of dyes such as rhodamine B in wastewater.

Study of coronary artery perforation during percutaneous coronary intervention in the Cangzhou Chinese population.

OBJECTIVE: Coronary artery perforation (CAP) is a rare, serious complication of percutaneous coronary intervention (PCI). Many studies have addressed the incidence, risk factors, and management of CAP in different countries except China. The aim of this study is to determine the risk factors and types of treatment for coronary perforation occurring in patients undergoing PCI and living in the Cangzhou Chinese population. METHODS AND RESULTS: A retrospective cohort of 12,113 patients who underwent PCI was used: 64 patients with CAP and 192 case-control patients were evaluated. Clinical data and findings from coronary arteriography and PCI were analysed. Logistic regression was used to evaluate candidate risk factors for CAP. The treatments were also evaluated. The incidence of CAP in patients undergoing PCI was 0.53%, and the mortality was 7.8% (5/64). Risk factors included female gender, hypertension, non-ST-elevation acute coronary syndrome (NSTE-ACS), right coronary artery (RCA) lesion, calcified lesion, and chronic total occlusion (CTO) (all P < 0.05, all OR > 1). CTO had the highest risk (OR = 5.077, P < 0.001). Patients with class I CAP underwent conservative treatment. Patients with class II CAP underwent conservative treatment or low-pressure balloon dilatation (61.1% and 22.2%, respectively). Patients with class III CAP underwent low-pressure balloon dilatation, coated-stent implantation, and emergency surgery (40.9%, 27.3%, and 22.7%, respectively). CONCLUSIONS: CAP risk factors in Cangzhou Chinese patients undergoing PCI included CTO, NSTE-ACS, hypertension, calcified and RCA lesions, and female gender. Different treatment methods should be used according to the different classes of CAP.

Research Progress on the Preparation of Manganese Dioxide Nanomaterials and Their Electrochemical Applications.

Manganese dioxide (MnO2) nanomaterials have shown excellent performance in catalytic degradation and other fields because of their low density and great specific surface area, as well as their tunable chemical characteristics. However, the methods used to synthesize MnO2 nanomaterials greatly affect their structures and properties. Therefore, the present work systematically illustrates common synthetic routes and their advantages and disadvantages, as well as examining research progress relating to electrochemical applications. In contrast to previous reviews, this review summarizes approaches for preparing MnO2 nanoparticles and describes their respective merits, demerits, and limitations. The aim is to help readers better select appropriate preparation methods for MnO2 nanomaterials and translate research results into practical applications. Finally, we also point out that despite the significant progress that has been made in the development of MnO2 nanomaterials for electrochemical applications, the related research remains in the early stages, and the focus of future research should be placed on the development of green synthesis methods, as well as the composition and modification of MnO2 nanoparticles with other materials.

Correlation between triglyceride glucose index and coronary plaque: An observational study.

The association between the triglyceride-glucose (Tyg) index and coronary plaque in patients with coronary heart disease remains unclear. This study aimed to investigate the relationship between Tyg index and coronary plaque under different levels of blood glucose metabolism. This retrospective study included patients with coronary artery disease who underwent coronary angiography and OCT between January 1, 2023 and January 1, 2024, and ultimately collected 232 coronary plaques. All patients were grouped according to the median Tyg index (T1 group 7.71 ≤ TyG index ≤ 9.13; T2 group 9.14 ≤ TyG index ≤ 10.99). The thickness of plaque fiber cap was measured under OCT, and the plaques were divided into vulnerable plaque and non-vulnerable plaque. The status of glucose metabolism is divided into non-diabetic and diabetic. Baseline data analysis showed that there were significant differences in clinical and biological characteristics between the T1 and T2 groups (P < .05). Logistic regression analysis showed that T2 group was significantly associated with vulnerable plaques compared with T1 group (odds ratio [OR]: 2.638; 95% confidence interval [CI] 1.548-4.494; P < .001). The OR of Tyg index was 2.175 (95% CI 1.409-3.357; P < .001). Receiver operating characteristic showed that the area under ROC curve (AUC) was 0.727 (95% CI 0.663-0.792; P < .001), the best cutoff value was 9.23, the sensitivity was 60%, and the specificity was 81%. In diabetic patients, there was a statistically significant correlation between Tyg index and coronary vulnerable plaque (OR: 3.273; 95% CI 1.240-8.636, P < .05). Triglyceride glucose index is a good predictor of coronary vulnerable plaque.

Innovative wearable solutions: Semi-releasing ion-conductive lignin hydrogel sensors for enhanced practicability.

The severe negative effects of impurities adhering to the external surface of wearable devices can significantly influence the signal transmission, performance, and lifespan of hydrogel sensors. Herein, we developed an ion-conducting hydrogel sensor with a strong adhesive side and a non-adhesive side, similar to a "semi-releasing material." This hydrogel, formulated using deep eutectic solvents obtained from choline chloride and acrylic acid, contained lignin. This versatile material, exhibiting properties similar to semi-releasing materials, was treated with an AlCl3 solution on one side. Additionally, the hydrogel was successfully used as a highly adhesive strain sensor for real-time monitoring of various human activity signals. Moreover, the hydrogel demonstrated excellent environmental tolerance and conductivity. Lignin extracted from wood flour endowed the hydrogel sensor with excellent adhesion energy (up to 427.1 J/m2) and UV resistance. Treatment of hydrogels with AlCl3 completely eliminated their adhesiveness, thereby enhancing fracture elongation and tensile strength. This improvement can be attributed to the absence of carboxyl groups and the formation of a metal-phenolic network. The implementation of this convenient and efficient strategy provides a more feasible approach to address challenges related to impurity adhesion and signal transmission in flexible wearable devices.

An innovative method based on Gaussian cloud distribution and sample information richness for eutrophication assessment of Yangtze's lakes and reservoirs under uncertainty.

The precise assessment of a water body's eutrophication status is essential for making informed decisions in water environment management. However, conventional approaches frequently fail to consider the randomness, fuzziness, and inherent hidden information of water quality indicators. These would result in an unreliable assessment. An enhanced method was proposed for the eutrophication assessment under uncertainty in this study. The multi-dimension gaussian cloud distribution was introduced to capture the randomness and fuzziness. The Shannon entropy based on various sample size and trophic levels was proposed to maximize valuable information hidden in the datasets. Twenty-seven significant lakes and reservoirs located in the Yangtze River Basin were selected to demonstrate the proposed method. The sensitivity and consistency were used to evaluate the accuracy of the proposed method. Results indicate that the proposed method has the capability to effectively assess the eutrophication status of lakes and reservoirs under uncertainty and that it has a better sensitivity since it can identify more than 33-50% trophic levels compared to the traditional methods. Further scenario experiments analysis revealed that the sample information richness, i.e., sample size and the number of trophic levels is of great significance to the accuracy/robustness of the method. Moreover, a sample size of 60 can offer the most favorable balance between accuracy/robustness and the monitoring expenses. These findings are crucial to optimizing the eutrophication assessment.

Observation of reentrant metal-insulator transition in a random-dimer disordered SSH lattice.

The interrelationship between localization, quantum transport, and disorder has remained a fascinating focus in scientific research. Traditionally, it has been widely accepted in the physics community that in one-dimensional systems, as disorder increases, localization intensifies, triggering a metal-insulator transition. However, a recent theoretical investigation [Phys. Rev. Lett. 126, 106803] has revealed that the interplay between dimerization and disorder leads to a reentrant localization transition, constituting a remarkable theoretical advancement in the field. Here, we present the first experimental observation of reentrant localization using an experimentally friendly model, a photonic SSH lattice with random-dimer disorder, achieved by incrementally adjusting synthetic potentials. In the presence of correlated on-site potentials, certain eigenstates exhibit extended behavior following the localization transition as the disorder continues to increase. We directly probe the wave function in disordered lattices by exciting specific lattice sites and recording the light distribution. This reentrant phenomenon is further verified by observing an anomalous peak in the normalized participation ratio. Our study enriches the understanding of transport in disordered mediums and accentuates the substantial potential of integrated photonics for the simulation of intricate condensed matter physics phenomena.