Macrophage-mediated heart repair and remodeling: A promising therapeutic target for post-myocardial infarction heart failure.

Heart failure (HF) remains prevalent in patients who survived myocardial infarction (MI). Despite the accessibility of the primary percutaneous coronary intervention and medications that alleviate ventricular remodeling with functional improvement, there is an urgent need for clinicians and basic scientists to further reveal the mechanisms behind post-MI HF as well as investigate earlier and more efficient treatment after MI. Growing numbers of studies have highlighted the crucial role of macrophages in cardiac repair and remodeling following MI, and timely intervention targeting the immune response via macrophages may represent a promising therapeutic avenue. Recently, technology such as single-cell sequencing has provided us with an updated and in-depth understanding of the role of macrophages in MI. Meanwhile, the development of biomaterials has made it possible for macrophage-targeted therapy. Thus, an overall and thorough understanding of the role of macrophages in post-MI HF and the current development status of macrophage-based therapy will assist in the further study and development of macrophage-targeted treatment for post-infarction cardiac remodeling. This review synthesizes the spatiotemporal dynamics, function, mechanism and signaling of macrophages in the process of HF after MI, as well as discusses the emerging bio-materials and possible therapeutic agents targeting macrophages for post-MI HF.

Induced Ferroptosis Pathway by Regulating Cellular Lipid Peroxidation With Peroxynitrite Generator for Reversing "Cold" Tumors.

Overcoming the resistance of tumor cells to apoptosis and immunosuppression is an important challenge to improve tumor immunotherapy. Non-apoptotic death mode of ferroptosis has been regarded as a new strategy to enhance tumor immunotherapy against drug-resistant cancers. The lethal accumulation of lipid peroxides (LPO) determines the progress of ferroptosis. The high susceptibleness of ferroptosis provides an opportunity for combating triple-negative breast cancer. Reactive nitrogen species (RNS) produced by nitric oxide (NO) and reactive oxygen species (ROS) is more lethal than ROS for tumor cells. Herein, an RNS-mediated immunotherapy strategy for inducing ferroptosis pathway is proposed by improving LPO accumulation, and constructed a multifunctional liposome (Lipo-MT-SNAP) comprised of peroxynitrite (ONOO-) generator, tumor targeted group, inhibiting glutathione peroxidase 4 (GPX4), and basic units (dipalmitoyl phosphatidylcholine and cholesterol). The significant enhancement of LPO resulted from the intense oxidative damage of ONOO- impaired synthesis of GPX4 by depleting glutathione, which further amplified ferroptosis and triggered immunogenic cell death. In vivo, RNS-mediated photoimmunotherapy can promote polarization of M2 to M1 macrophages and dendritic cells maturation, further infiltrate T cells, regulate the secretion of inflammatory factors, and reprogram the tumor microenvironment. The powerful RNS-mediated ferroptosis induces strong immunogenicity and effectively inhibit tumor proliferation.

Serum alpha 1 antitrypsin potent act as an early diagnostic biomarker for cardiac amyloidosis.

Cardiac amyloidosis is a refractory cardiomyopathy with a poor prognosis and lacks effective treatments. N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin T are poor prognostic factors for myocardial amyloidosis. However, NT-proBNP and troponin also serve as markers of heart failure and myocardial infarction, lacking specificity. Whether abnormal elevation of alpha-1 antitrypsin in myocardial amyloidosis also predicts the poor prognosis of patients remains unknown. We conducted a retrospective single-center case-control study to analyze the serological and physical examination data of 83 cardiac amyloidosis patients and 68 healthy controls matched by gender and age. We aimed to explore the onset and prognostic factors of cardiac amyloidosis. The serum alpha-1 antitrypsin level (169.78 ± 39.59 mg/dl) in patients with cardiac amyloidosis was significantly higher than that in the normal control (125.92 ± 18.26 mg/dl). Logistic regression results showed that alpha-1 antitrypsin, free sialic acid, high-density lipoprotein cholesterol, apolipoprotein A/B ratio, and homocysteine were predictors of cardiac amyloidosis. Multivariable logistic regression showed that only alpha 1 antitrypsin was an independent risk factor for cardiac amyloidosis. Receiver operating characteristic curve analysis based on the Mayo stage and troponin level showed the cut-off value of 140.55 mg/dl for alpha-1 antitrypsin in predicting cardiac amyloidosis with 81.7% sensitivity and 83.9% specificity. Elevated alpha-1 antitrypsin levels may be an early diagnostic biomarker for cardiac amyloidosis.

An overview of the application and potential mechanism on the triglyceride glucose index with multi-vessel coronary disease.

Multi-vessel coronary disease (MVCD) is a severe form of coronary artery disease (CAD) that significantly increases the risk of acute coronary syndrome (ACS) and heart attacks. The triglyceride glucose (TyG) index is a reliable and convenient marker for insulin resistance (IR). Recent studies have demonstrated its predictive value for CAD in patients with MVCD. This review aims to explore the application of the TyG index in managing MVCD and its underlying pathogenesis to enhance risk stratification and improve therapeutic decision-making.

Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-ß1/Smad3 Signaling Pathway.

Tendon injury is a prevalent orthopedic disease that currently lacks effective treatment. Galangin (GLN) is a vital flavonoid found abundantly in galangal and is known for its natural activity. This study aimed to investigate the GLN-mediated molecular mechanism of tendon-derived stem cells (TDSCs) in tendon repair. The TDSCs were characterized using alkaline phosphatase staining, alizarin red S staining, oil red O staining, and flow cytometry. The effect of GLN treatment on collagen deposition was evaluated using Sirius red staining and quantitative (q)PCR, while a Western bot was used to assess protein levels and analyze pathways. Results showed that GLN treatment not only increased the collagen deposition but also elevated the mRNA expression and protein levels of multiple tendon markers like collagen type I alpha 1 (COL1A1), decorin (DCN) and tenomodulin (TNMD) in TDSCs. Moreover, GLN was also found to upregulate the protein levels of transforming growth factor ß1 (TGF-ß1) and p-Smad3 to activate the TGF-ß1/Smad3 signaling pathway, while GLN mediated collagen deposition in TDSCs was reversed by LY3200882, a TGF-ß receptor inhibitor. The study concluded that GLN-mediated TDSCs enhanced tendon repair by activating the TGF-ß1/Smad3 signaling pathway, suggesting a novel therapeutic option in treating tendon repair.

Association of periodontitis with cardiovascular and all-cause mortality in hypertensive individuals: insights from a NHANES cohort study.

BACKGROUND: The objective of this research is to clarify the impact of periodontitis on overall and cardiovascular-related death rates among hypertensive individuals. METHOD: A total of 5665 individuals with hypertension were included from the National Health and Nutrition Examination Survey (NHANES) data spanning 2001-2004 and 2009-2014. These individuals were divided into two groups based on the presence or absence of periodontitis and further stratified by the severity of periodontitis. We employed weighted multivariate Cox proportional hazards regression and Kaplan-Meier curves (log-rank test) to evaluate the impact of periodontitis on all-cause and cardiovascular mortality. Additional analyses, including adjustments for various covariates, subgroups, and sensitivity analyses, were conducted to ensure the robustness and reliability of our results. RESULT: Over an average follow-up duration of 10.22 years, there were 1,122 all-cause and 297 cardiovascular deaths. Individuals with periodontitis exhibited an elevated risk of all-cause mortality (HR = 1.33, 95% CI 1.18-1.51; p < 0.0001) and cardiovascular mortality (HR = 1.48, 95% CI 1.15-1.89; p = 0.002). Moreover, we observed a progressive increase in both all-cause mortality and cardiovascular mortality (p for trend are both lower than 0.001) and correlating with the severity of periodontitis. These associations remained consistent across various subgroup and sensitivity analyses. CONCLUSION: Our findings suggest a significant association between periodontitis and increased risks of all-cause and cardiovascular mortality among hypertensive individuals. Notably, the severity of periodontitis appears to be a critical factor, with moderate to severe cases exerting a more pronounced impact on all-cause mortality. Additionally, cardiovascular disease mortality significantlly increases in individuals with varying degrees of periodontitis.

Engineered Extracellular Vesicles for Delivery of an IL-1 Receptor Antagonist Promote Targeted Repair of Retinal Degeneration.

Retinal degeneration (RD) is an irreversible blinding disease that seriously affects patients' daily activities and mental health. Targeting hyperactivated microglia and regulating polarization are promising strategies for treating the disease. Mesenchymal stem cell (MSC) transplantation is proven to be an effective treatment due to its immunomodulatory and regenerative properties. However, the low efficiency of cell migration and integration of MSCs remains a major obstacle to clinical use. The goal of this study is to develop a nanodelivery system that targets hyperactivated microglia and inhibits their release of proinflammatory factors, to achieve durable neuroprotection. This approach is to engineer extracellular vesicles (EVs) isolated from MSC, modify them with a cyclic RGD (cRGD) peptide on their surface, and load them with an antagonist of the IL-1 receptor, anakinra. Comparing with non-engineered EVs, it is observed that engineered cRGD-EVs exhibit an increased targeting efficiency against hyperactivated microglia and strongly protected photoreceptors in experimental RD cells and animal models. This study provides a strategy to improve drug delivery to degenerated retinas and offers a promising approach to improve the treatment of RD through targeted modulation of the immune microenvironment via engineered cRGD-EVs.

Long-term outcomes of single-incision plus one-port laparoscopic surgery versus conventional laparoscopic surgery for rectosigmoid cancer: a randomized controlled trial.

BACKGROUND: Though our previous study has demonstrated that the single-incision plus one-port laparoscopic surgery (SILS + 1) is safe and feasible for sigmoid colon and upper rectal cancer and has better short-term outcomes compared with conventional laparoscopic surgery (CLS), the long-term outcomes of SILS + 1 remains uncertain and are needed to evaluated by an RCT. METHODS: Patients with clinical stage T1-4aN0-2M0 rectosigmoid cancer were enrolled. The participants were randomly assigned to either SILS + 1 (n = 99) or CLS (n = 99). The 3-year DFS, 5-year OS, and recurrence patterns were analyzed. RESULTS: Between April 2014 and July 2016, 198 patients were randomly assigned to either the SILS + 1 group (n = 99) or CLS group (n = 99). The median follow-up in the SILS + 1 group was 64.0 months and in CLS group was 65.0 months. The 3-year DFS was 87.8% (95% CI, 81.6-94.8%) in SILS + 1 group and 86.9% (95% CI, 81.3-94.5%) in CLS group (hazard ratio: 1.09 (95% CI, 0.48-2.47; P = 0.84)). The 5-year OS was 86.7% (95% CI,79.6-93.8%) in the SILS + 1 group and 80.5% (95% CI,72.5-88.5%) in the CLS group (hazard ratio: 1.53 (95% CI, 0.74-3.18; P = 0.25)). There were no significant differences in the recurrence patterns between the two groups. CONCLUSIONS: We found no significant difference in 3-year DFS and 5-year OS of patients with sigmoid colon and upper rectal cancer treated with SILS + 1 vs. CLS. SILS + 1 is noninferior to CLS when performed by expert surgeons. TRIAL REGISTRATION: ClinicalTrials.gov: NCT02117557 (registered on 21/04/2014).

Supra-Normal Left Ventricular Ejection Fraction as a Prognostic Marker for Long-Term Outcomes in Patients with Acute Coronary Syndrome.

Recently, the supra-normal left ventricular ejection fraction (snLVEF) has been proposed, based on extensive datasets indicating increased all-cause mortality in individuals with an LVEF exceeding 65%. However, the implications of an LVEF > 65% in the context of acute coronary syndrome (ACS) remain underexplored.The aim of the present study was to investigate the correlation between supra-normal left ventricular ejection fraction (snLVEF) and major adverse cardiovascular events (MACE) in patients with ACS.Methods: A total of 874 ACS patients (560 men, mean age 59.5 ± 10.0; 314 women, mean age 61.5 ± 8.9) who underwent their first coronary angiography during the period from March 2013 to October 2015 were divided into 2 groups: normal LVEF (nLVEF) (55% ≤ EF ≤ 65%) and snLVEF (EF > 65%), according to their echocardiography results. The patients were evaluated for MACE after surgery by collecting clinical data and long-term follow-up data. This correlation was further analyzed by Kaplan-Meier analysis and Cox regression analysis.The follow-up data revealed a significantly higher incidence of MACE among snLVEF patients compared to the nLVEF group (15.6% versus 7.4%; P = 0.020). This heightened risk persisted even after adjustment for multiple variables, indicating a strong association between snLVEF and increased MACE risk (HR: 2.346; 95% CI: 1.196-4.602; P = 0.013).SnLVEF was independently associated with poor prognosis after ACS. Enhanced management strategies for snLVEF patients could potentially reduce the incidence of MACE in ACS patients.

Photothermal Nanozymatic Nanoparticles Induce Ferroptosis and Apoptosis through Tumor Microenvironment Manipulation for Cancer Therapy.

It is highly desirable to design a single modality that can simultaneously trigger apoptosis and ferroptosis to efficiently eliminate tumor progression. Herein, a nanosystem based on the intrinsic properties of tumor microenvironment (TME) is designed to achieve tumor control through the simultaneous induction of ferroptosis and apoptosis. CuCP molecules are encapsulated in a liposome-based nanosystem to assemble into biocompatible and stable CuCP nanoparticles (CuCP Lipo NPs). This nanosystem intrinsically possesses nanozymatic activity and photothermal characteristics due to the property of Cu atoms and the structure of CuCP Lipo NPs. It is demonstrated that the synergistic strategy increases the intracellular lipid-reactive oxides species, induces the occurrence of ferroptosis and apoptosis, and completely eradicates the tumors in vivo. Proteomics analysis further discloses the key involved proteins (including Tp53, HMOX1, Ptgs2, Tfrc, Slc11a2, Mgst2, Sod1, and several GST family members) and pathways (including apoptosis, ferroptosis, and ROS synthesis). Conclusively, this work develops a strategy based on one nanosystem to synergistically induce ferroptosis and apoptosis in vivo for tumor suppression, which holds great potential in the clinical translation for tumor therapy.

ARB might be superior to ACEI for treatment of hypertensive COVID-19 patients.

The administration of ACEI/ARB (angiotensin-converting enzyme inhibitors/Angiotension II receptor blockers) in COVID-19 (coronavirus disease 2019) patients with hypertension exhibits a lower risk of mortality compared with ACEI/ARB non-users. In this context, an important question arises: is ACEI or ARB more suitable for the treatment of hypertensive COVID-19 patients? Taken into consideration the following four rationales, ARB may offer a more significant benefit than ACEI for the short-term treatment of hypertensive COVID-19 patients: 1. ACEI has no inhibition on non-ACE-mediated Ang II production under infection conditions, whereas ARB can function properly regardless of how Ang II is produced; 2. ACEI-induced bradykinin accumulation may instigate severe ARDS while ARB has no effects on kinin metabolism; 3. ARB alleviates viscous sputa production and inflammatory reaction significantly in contrast to ACEI; 4. ARB may attenuate the lung fibrosis induced by mechanical ventilation in severe patients and improve their prognosis significantly compared with ACEI. To examine the advantages of ARB over ACEI on hypertensive COVID-19 patients, retrospective case-control studies comparing the clinical outcomes for COVID-19 patients receiving ARB or ACEI treatment is strikingly needed in order to provide guidance for the clinical application.

Circulating exosomal microRNAs as emerging non-invasive clinical biomarkers in heart failure: Mega bio-roles of a nano bio-particle.

Exosomes are nano-sized extracellular vesicles containing a cell-specific biologically active cargo of proteins and genetic materials. Exosomes are constitutively released from almost all cell-types and affect neighboring or distant cells through a complex intercellular exchange of the genetic information and/or regulation of certain gene expressions that change the function and behavior of recipient cells. Those released into body fluids are the major mediators of intercellular communications. The success of the biological functions of exosomes is highly mediated by the effective transfer of microRNAs (miRs). Exosomes secreted by a damaged or diseased heart can exhibit alterations in the miRs' profile that may reflect the cellular origin and (patho)physiological state, as a "signature" or "fingerprint" of the donor cell. It has been shown that the transportation of cardiac-specific miRs in exosomes can be rapidly detected and measured, holding great potential as biomarkers in heart diseases. Currently, the search for new biomarkers of heart diseases remains a large and increasing enterprise. Notably, circulating exosomal miRs (Exo-miRs) have successfully gained huge interests for their diagnostic and prognostic potentials. The present review highlights circulating Exo-miRs explored for diagnosis/prognosis and outcome prediction in patients with heart failure (HF). To this end, we explain the feasibility of exosomes as clinical biomarkers, discuss the priority of circulating Exo-miRs over non-exosomal ones as a biomarker, and then outline reported circulating Exo-miRs having the biomarker function in HF patients, together with their mechanism of action. In conclusion, circulating Exo-miRs represent emerging diagnostic (Exo-miR-92b-5p, Exo-miR-146a, Exo-miR-181c, and Exo-miR-495) and prognostic (Exo-miR-192, Exo-miR-194, Exo-miR-34a, Exo-miR-425, Exo-miR-744) biomarkers for HF.

Patients with COVID-19 in 19 ICUs in Wuhan, China: a cross-sectional study.

BACKGROUND: A COVID-19 outbreak started in Wuhan, China, last December and now has become a global pandemic. The clinical information in caring of critically ill patients with COVID-19 needs to be shared timely, especially under the situations that there is still a largely ongoing spread of COVID-19 in many countries. METHODS: A multicenter prospective observational study investigated all the COVID-19 patients received in 19 ICUs of 16 hospitals in Wuhan, China, over 24 h between 8 AM February 2h and 8 AM February 27, 2020. The demographic information, clinical characteristics, vital signs, complications, laboratory values, and clinical managements of the patients were studied. RESULTS: A total of 226 patients were included. Their median (interquartile range, IQR) age was 64 (57-70) years, and 139 (61.5%) patients were male. The duration from the date of ICU admission to the study date was 11 (5-17) days, and the duration from onset of symptoms to the study date was 31 (24-36) days. Among all the patients, 155 (68.6%) had at least one coexisting disease, and their sequential organ failure assessment score was 4 (2-8). Organ function damages were found in most of the patients: ARDS in 161 (71.2%) patients, septic shock in 34 (15.0%) patients, acute kidney injury occurred in 57 (25.2%) patients, cardiac injury in 61 (27.0%) patients, and lymphocytopenia in 160 (70.8%) patients. Of all the studied patients, 85 (37.6%) received invasive mechanical ventilation, including 14 (6.2%) treated with extracorporeal membrane oxygenation (ECMO) at the same time, 20 (8.8%) received noninvasive mechanical ventilation, and 24 (10.6%) received continuous renal replacement therapy. By April 9, 2020, 87 (38.5%) patients were deceased and 15 (6.7%) were still in the hospital. CONCLUSIONS: Critically ill patients with COVID-19 are associated with a higher risk of severe complications and need to receive an intensive level of treatments. COVID-19 poses a great strain on critical care resources in hospitals. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR2000030164. Registered on February 24, 2020, http://www.chictr.org.cn/edit.aspx?pid=49983&htm=4.

Downregulation of miR-483-5p decreases hypoxia-induced injury in human cardiomyocytes by targeting MAPK3.

BACKGROUND: MiR-483-5p was recently identified as a risk factor in the early stages of acute myocardial infarction (AMI) patients. Here, we further investigated how miR-483-5p affects cardiomyocyte apoptosis and oxidative stress under hypoxic conditions. METHODS: Plasma samples were collected from AMI patients and healthy volunteers. The expression of miR-483-5p was determined using quantitative real-time PCR. An in vitro hypoxic model was constructed to mimic AMI in AC16 cells. Cell viability, apoptosis and oxidative stress biomarker levels (MDA, SOD and CAT) were respectively determined using CCK-8, flow cytometry and commercial assay kits. RESULTS: The expression levels of miR-483-5p were significantly higher in AMI patients than in control subjects. Circulating levels of miR-483-5p positively correlated with creatine kinase MB isoform (CK-MB) and cardiac troponin I (cTnI) levels. The in vitro experiments showed that the expression levels of miR-483-5p were also upregulated in hypoxia-induced AC16 cell injury. MiR-483-5p overexpression significantly increased hypoxia-induced cardiomyocyte apoptosis and oxidative stress, while knockdown attenuated these effects. Mechanistically, miR-483-5p directly targets MAPK3 in AC16 cells. Furthermore, the protective effects of miR-483-5p knockdown against hypoxia-induced cardiomyocyte injury are partially dependent on MAPK3. CONCLUSIONS: MiR-483-5p, which targets MAPK3, might be a potential therapeutic target for the diagnosis and prevention of hypoxia-induced myocardial injury.

Atorvastatin attenuates vascular remodelling in spontaneously hypertensive rats via the protein kinase D/extracellular signal-regulated kinase 5 pathway.

The present study was conducted to determine whether atorvastatin reduces hypertension-induced vascular remodelling and whether its effects involve protein kinase D (PKD) and extracellular signal-regulated kinase 5 (ERK5). We used 16-week-old spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto (WKY) rats. The blood pressure and serum lipid concentration were measured. Changes in the vascular morphology and histology were examined using H&E, Masson' s trichrome, and Sirius Red staining. The media thickness (MT), ratio of MT to lumen diameter (LD) (MT/LD), collagen volume fraction (CVF) and hydroxyproline content were measured to evaluate vascular remodelling. Atorvastatin (50 mg/kg/day) was administered for 8 weeks. Increased blood pressure and vascular remodelling were more prominent in SHRs than in WKY rats. SHRs also had elevated PKD and ERK5 activation. The systolic blood pressure, MT/LD ratio, and hydroxyproline content were positively correlated with the activation level of PKD and ERK5 in SHRs. Atorvastatin significantly attenuated the activation of PKD and ERK5. Overall, this study demonstrated that atorvastatin could reverse vascular remodelling in SHRs. The PKD/ERK5 signalling pathway might be important for elucidating the beneficial pleiotropic effects of atorvastatin on vascular remodelling.

Effect of 2 Different Dosages of Rosuvastatin on Prognosis of Acute Myocardial Infarction Patients with New-Onset Atrial Fibrillation in Jinan, China.

BACKGROUND Atrial fibrillation (AF) often occurs in patients with acute myocardial infarction (AMI). This study aimed to observe the influence of different dosages of rosuvastatin on the prognosis of AMI patients with AF. MATERIAL AND METHODS We performed an observational, retrospective cohort study in Jinan, China, in which 323 AMI patients were recruited. All patients were randomized to receive optimal medication treatment and 10 mg or 20 mg of rosuvastatin. Holter monitor results, serum lipid levels, and heart function were recorded. We used multivariate Cox and Kaplan-Meier analyses to assess the independent factors and differences in AF and ischemia events and safety of rosuvastatin administered at different dosages. RESULTS TC, LDL-C, and TG at 1 and 12 months were significantly lower compared with those observed prior to treatment in both groups. The heart function of both groups was significantly improved after 12 months of treatment, especially in the 20 mg group. Multivariate Cox analysis showed that different dosages of rosuvastatin, age, smoking, drinking alcohol, and diabetes are independent factors related to the occurrence of AF and ischemic events. In addition, according to Kaplan-Meier analysis, no significant difference in adverse clinical events existed at different dosages of rosuvastatin. CONCLUSIONS Treatment with rosuvastatin can reduce the serum lipid level and improve cardiac function. Different dosages of rosuvastatin, age, smoking, drinking alcohol, and diabetes are independent risk factors for AF and ischemia events. The results suggested it is safe to use 20 mg rosuvastatin in the 12 months after hospital admission.

Dynamic Modeling of Weld Bead Geometry Features in Thick Plate GMAW Based on Machine Vision and Learning.

Weld bead geometry features (WBGFs) such as the bead width, height, area, and center of gravity are the common factors for weighing welding quality control. The effective modeling of these WBGFs contributes to implementing timely decision making of welding process parameters to improve welding quality and enhance automatic levels. In this work, a dynamic modeling method of WBGFs is presented based on machine vision and learning in multipass gas metal arc welding (GMAW) with typical joints. A laser vision sensing system is used to detect weld seam profiles (WSPs) during the GMAW process. A novel WSP extraction method is proposed using scale-invariant feature transform and machine learning. The feature points of the extracted WSP, namely the boundary points of the weld beads, are identified with slope mutation detection and number supervision. In order to stabilize the modeling process, a fault detection and diagnosis method is implemented with cubic exponential smoothing, and the diagnostic accuracy is within 1.50 pixels. A linear interpolation method is presented to implement sub pixel discrimination of the weld bead before modeling WBGFs. With the effective feature points and the extracted WSP, a scheme of modeling the area, center of gravity, and all-position width and height of the weld bead is presented. Experimental results show that the proposed method in this work adapts to the variable features of the weld beads in thick plate GMAW with T-joints and butt/lap joints. This work can provide more evidence to control the weld formation in a thick plate GMAW in real time.

Hollow Bimetallic Zinc Cobalt Phosphosulfides for Efficient Overall Water Splitting.

Bimetallic sulfides with earth-abundant transition-metal elements are proposed to enhance the electrocatalytic activities. Further replacement of S atom by less electronegative P atom improves the electrocatalytic performance of OER and HER. Herein, hollow bimetallic zinc cobalt phosphosulfides (Zn0.3 Co2.7 S3 P) are synthesized by a two-step process. The optimal catalyst of Zn0.3 Co2.7 S3 P with particle size of 50 nm displays an excellent electroactivity and long-term durability toward efficient overall water splitting process in alkaline medium. The excellent bifunctional electrocatalytic performance may be ascribed to the synergistic effect of hollow structure, anion substitution tuning and unique size control.

2D Metal-Organic Framework Derived CuCo Alloy Nanoparticles Encapsulated by Nitrogen-Doped Carbonaceous Nanoleaves for Efficient Bifunctional Oxygen Electrocatalyst and Zinc-Air Batteries.

The development of efficient bifunctional electrocatalysts for the oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) still remains a challenge in a wide range of renewable energy technologies. Herein, CuCo alloy nanoparticles encapsulated by nitrogen-doped carbonaceous nanoleaves (CuCo-NC) have been synthesized from a Cu(OH)2 /2D leaf-like zeolitic imidazolate framework (ZIF-L)-pyrolysis approach. Leaf-like Cu(OH)2 is first prepared by the ultrasound-induced self-assembly of Cu(OH)2 nanowires. The efficient encapsulation of Cu(OH)2 in ZIF-L is obtained owing to the morphology fitting between the leaf-like Cu(OH)2 and ZIF-L. CuCo-NC catalysts present superior electrocatalytic activity and stability toward ORR and OER over the commercial Pt/C and IrO2 , respectively, which are further used as bifunctional oxygen electrocatalysts in Zn-air batteries and exhibit impressive performance, with a high peak power density of 303.7 mW cm-2 , large specific capacity of up to 751.4 mAh g-1 at 20 mA cm-2 , and a superior recharge stability.

Ultra-thin Co-Fe Layered Double Hydroxide Hollow Nanocubes for Efficient Electrocatalytic Water Oxidation.

Hierarchical hollow nanocubes based on ultra-thin CoFe-layered double hydroxide (CoFe-LDH) nanosheets have been prepared. The obtained CoFe-LDH hollow nanocubes could effectively catalyze water oxidation at a low overpotential of 270 mV @ 10 mA cm-2 , low Tafel slope of 58.3 mV dec-1 and show a long-term stability in alkali.