Development of Plasmonic Attapulgite/Co(Ti)Ox Nanocomposite Using Spent Batteries toward Photothermal Reduction of CO2.

The rapid development of the battery industry has brought about a large amount of waste battery pollution. How to realize the high-value utilization of waste batteries is an urgent problem to be solved. Herein, cobalt and titanium compounds (LTCO) were firstly recovered from spent lithium-ion batteries (LIBs) using the carbon thermal reduction approach, and plasmonic attapulgite/Co(Ti)Ox (H-ATP/Co(Ti)Ox) nanocomposites were prepared by the microwave hydrothermal technique. H-ATP had a large specific surface area and enough active sites to capture CO2 molecules. The biochar not only reduced the spinel phase of waste LIBs into metal oxides including Co3O4 and TiO2 but also increased the separation and transmission of the carriers, thereby accelerating the adsorption and reduction of CO2. In addition, H-ATP/Co(Ti)Ox exhibited a localized surface plasmon resonance effect (LSPR) in the visible to near-infrared region and released high-energy hot electrons, enhancing the surface temperature of the catalyst and further improving the catalytic reduction of CO2 with a high CO yield of 14.7 µmol·g-1·h-1. The current work demonstrates the potential for CO2 reduction by taking advantage of natural mineral and spent batteries.

Aldolase promotes the development of cardiac hypertrophy by targeting AMPK signaling.

Metabolic dysfunction is a hallmark of cardiac hypertrophy and heart failure. During cardiac failure, the metabolism of cardiomyocyte switches from fatty acid oxidation to glycolysis. However, the roles of key metabolic enzymes in cardiac hypertrophy are not understood fully. Here in the present work, we identified Aldolase A (AldoA) as a core regulator of cardiac hypertrophy. The mRNA and protein levels of AldoA were significantly up-regulated in transverse aortic constriction (TAC)- and isoproterenol (ISO)-induced hypertrophic mouse hearts. Overexpression of AldoA in cardiomyocytes promoted ISO-induced cardiomyocyte hypertrophy, whereas AldoA knockdown repressed cardiomyocyte hypertrophy. In addition, adeno-associated virus 9 (AAV9)-mediated in vivo knockdown of AldoA in the hearts rescued ISO-induced decrease in cardiac ejection fraction and fractional shortening and repressed cardiac hypertrophy. Mechanism study revealed that AldoA repressed the activation of AMP-dependent protein kinase (AMPK) signaling in a liver kinase B1 (LKB1)-dependent and AMP-independent manner. Inactivation of AMPK is a core mechanism underlying AldoA-mediated promotion of ISO-induced cardiomyocyte hypertrophy. By contrast, activation of AMPK with metformin and AICAR blocked AldoA function during cardiomyocyte hypertrophy. In summary, our data support the notion that AldoA-AMPK axis is a core regulatory signaling sensing energetic status and participates in cardiac hypertrophy.

Melanoma differentiation-associated protein 5 prevents cardiac hypertrophy via apoptosis signal-regulating kinase 1-c-Jun N-terminal kinase/p38 signaling.

Pathological cardiac hypertrophy (CH) is driven by maladaptive changes in myocardial cells in response to pressure overload or other stimuli. CH has been identified as a significant risk factor for the development of various cardiovascular diseases, ultimately resulting in heart failure. Melanoma differentiation-associated protein 5 (MDA5), encoded by interferon-induced with helicase C domain 1 (IFIH1), is a cytoplasmic sensor that primarily functions as a detector of double-stranded ribonucleic acid (dsRNA) viruses in innate immune responses; however, its role in CH pathogenesis remains unclear. Thus, the aim of this study was to examine the relationship between MDA5 and CH using cellular and animal models generated by stimulating neonatal rat cardiomyocytes with phenylephrine and by performing transverse aortic constriction on mice, respectively. MDA5 expression was upregulated in all models. MDA5 deficiency exacerbated myocardial pachynsis, fibrosis, and inflammation in vivo, whereas its overexpression hindered CH development in vitro. In terms of the underlying molecular mechanism, MDA5 inhibited CH development by promoting apoptosis signal-regulating kinase 1 (ASK1) phosphorylation, thereby suppressing c-Jun N-terminal kinase/p38 signaling pathway activation. Rescue experiments using an ASK1 activation inhibitor confirmed that ASK1 phosphorylation was essential for MDA5-mediated cell death. Thus, MDA5 protects against CH and is a potential therapeutic target.

Effects and mechanism on cadmium adsorption removal by CaCl2-modified biochar from selenium-rich straw.

As every-one knows, cadmium contamination poses a significant and permanent threat to people and aquatic life. Therefore, research on how to remove cadmium from wastewater is essential to protect the natural environment. In this study, agricultural and forestry waste straw sprayed with selenium-enriched foliar fertilizer was prepared as biochar, which was altered by calcium chloride (CaCl2) to remove Cd2+ from water. The outcomes demonstrated that biochar generated by pyrolysis at 700 °C (BC700) had the best adsorption effect. Secondly, pseudo-second-order kinetics and Langmuir adsorption models were used to predict the Cd2+ adsorption. Finally, electrostatic adsorption, ion exchange, and complexation of oxygen functional groups (OFGs) were demonstratedto be the main adsorption mechanisms. These conclusions indicate that selenium-rich straw biochar is a novel adsorbent for agroforestry waste recovery. Meanwhile, this work will offer a promising strategy for the overall utilization of rice straw.

Boosting catalytic activity of SrCoO2.52 perovskite by Mn atom implantation for advanced peroxymonosulfate activation.

Material-enhanced heterogeneous peroxymonosulfate (PMS) activation for degradation of antibiotic in water has attracted intensive attention. However, one challenge is the electron transfer efficiency from the material to PMS for reactive oxygen species (ROS) production. Considering that the B-sites of perovskite oxides are closely associated with the catalytic performance, partial substitution of the B-sites of perovskite oxides can enhance the redox cycle of metals. Consequently, adjusting the ratio of each element at the B site can introduce oxygen vacancies on the surface of perovskite. Herein, a method was developed in which manganese (Mn) partially substitutes B-sites to modify surface properties of SrCoO2.52 perovskite oxides, resulting in the enhancement of catalytic activity. In degradation kinetics studies using SrCoMnO3-δ-0.5/PMS (SrCoMnO3-δ-0.5 denotes that the molar substitution of Mn at the B site of SrCoO2.52 perovskite oxide is 0.5) reaction system and sulfamethoxazole (SMX) as the target pollutant, it was found that the reaction rate constant (kobs) is 0.287 min-1 which is 2.4 times that of SrCoO2.52/PMS system. Experimental and theoretical analyses revealed that Mn-O covalent bonding governs the intrinsic catalytic activity of SrCoMnO3-δ-0.5 perovskite oxides. The Mn sites exhibits stronger adsorption energy with PMS than the Co sites, facilitating the breaking of O-O bond. Simultaneously, oxygen vacancies and surface adsorbed oxygen species have a synergistic effect for PMS adsorption. This work can provide a potential route in developing advanced catalysts based on manipulation of the B-sites of perovskite oxides for PMS activation.

Ovarian Tumor Domain-Containing 7B Attenuates Pathological Cardiac Hypertrophy by Inhibiting Ubiquitination and Degradation of Krüppel-Like Factor 4.

BACKGROUND: Cardiac hypertrophy (CH) is a well-established risk factor for many cardiovascular diseases and a primary cause of mortality and morbidity among older adults. Currently, no pharmacological interventions have been specifically tailored to treat CH. OTUD7B (ovarian tumor domain-containing 7B) is a member of the ovarian tumor-related protease (OTU) family that regulates many important cell signaling pathways. However, the role of OTUD7B in the development of CH is unclear. Therefore, we investigated the role of OTUD7B in CH. METHODS AND RESULTS: OTUD7B knockout mice were used to assay the role of OTUD7B in CH after transverse aortic coarctation surgery. We further assayed the specific functions of OTUD7B in isolated neonatal rat cardiomyocytes. We found that OTUD7B expression decreased in hypertrophic mice hearts and phenylephrine-stimulated neonatal rat cardiomyocytes. Furthermore, OTUD7B deficiency exacerbated transverse aortic coarctation surgery-induced myocardial hypertrophy, abnormal cardiac function, and fibrosis. In cardiac myocytes, OTUD7B knockdown promoted phenylephrine stimulation-induced myocardial hypertrophy, whereas OTUD7B overexpression had the opposite effect. An immunoprecipitation-mass spectrometry analysis showed that OTUD7B directly binds to KLF4 (Krüppel-like factor 4). Additional molecular experiments showed that OTUD7B impedes KLF4 degradation by inhibiting lysine residue at 48 site-linked ubiquitination and suppressing myocardial hypertrophy by activating the serine/threonine kinase pathway. CONCLUSIONS: These results demonstrate that the OTUD7B-KLF4 axis is a novel molecular target for CH treatment.

Detection of Tri-allelic Single Nucleotide Polymorphisms of ABCB1 and CRP Genes by Penta-Primer Amplification Refractory Mutation System-Polymerase Chain Reaction.

Objective: The standard methods for tri-allelic single nucleotide polymorphism (SNP) genotyping require special equipment and are costly to perform. The aim of this study was to establish a fast, simple, and low-cost method to differentiate among tri-allelic SNPs in general laboratories. Methods: Based on the tetra-primer amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) typing of bi-allelic SNPs, we developed a penta-primer amplification refractory mutation system-polymerase chain reaction (P-ARMS-PCR) method characterize tri-allelic SNPs. The two most studied tri-allelic SNPs, rs2032582 and rs3091244, were genotyped using P-ARMS-PCR in 110 volunteers, and the results were verified by direct DNA sequencing. Results: For rs2032582, there were 20 samples (18.18%) with the GG genotype, 3 (2.73%) with the AA genotype, 24 (21.82%) with the TT genotype, 43 (39.09%) with the GT genotype, 11 (10.00%) with the AG genotype, and 9 (8.18%) with the AT genotype. For rs3091244, there were 67 samples (60.91%) with the CC genotype, 1 (0.91%) with the AA genotype, 8 (7.27%) with the CT genotype, 31 (28.18%) with the CA genotype, and 3 (2.73%) with the AT genotype. The genotypic distributions of rs2032582 (p = 0.482) and rs3091244 (p = 0.492) were in Hardy-Weinberg equilibrium. The DNA sequencing results were entirely consistent with the results of P-ARMS-PCR. Conclusion: P-ARMS-PCR is an accurate, rapid, simple, and low-cost characterization method for tri-allelic SNP genotyping of rs2032582 and rs3091244.

Development and Validation of a Novel Nomogram to Predict Improved Left Ventricular Ejection Fraction in Patients With Heart Failure After Successful Percutaneous Coronary Intervention for Chronic Total Occlusion.

Background: Heart failure with improved left ventricular ejection fraction (HFiEF) is linked to a good clinical outcome. The purpose of this study was to create an easy-to-use model to predict the occurrence of HFiEF in patients with heart failure (HF), 1 year after successful percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) (CTO PCI). Methods: Patients diagnosed with HF who successfully underwent CTO PCI between January 2016 and August 2019 were included. To mitigate the effect of residual stenosis on left ventricular (LV) function, we excluded patients with severe residual stenosis, as quantitatively measured by a residual synergy between PCI with Taxus and Cardiac Surgery score (rSS) of >8. We gathered demographic data, medical history, angiographic and procedural characteristics, echocardiographic parameters, laboratory results, and medication information. The least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression models were used to identify predictors of HFiEF 1 year after CTO revascularization. A nomogram was established and validated according to the area under the receiver operating characteristic curve (AUC) and calibration curves. Internal validation was performed using bootstrap resampling. Results: A total of 465 patients were finally included in this study, and 165 (35.5%) patients experienced HFiEF 1 year after successful CTO PCI. According to the LASSO regression and multivariate logistic regression analyses, four variables were selected for the final prediction model: age [odds ratio (OR): 0.969; 95% confidence interval (CI): 0.952-0.988; p = 0.001], previous myocardial infarction (OR: 0.533; 95% CI: 0.357-0.796; p = 0.002), left ventricular end-diastolic dimension (OR: 0.940; 95% CI: 0.910-0.972; p < 0.001), and sodium glucose cotransporter two inhibitors (OR: 5.634; 95% CI: 1.756-18.080; p = 0.004). A nomogram was constructed to present the results. The C-index of the model was 0.666 (95% CI, 0.613-0.719) and 0.656 after validation. The calibration curve demonstrated that the nomogram agreed with the actual observations. Conclusions: We developed an simple and effective nomogram for predicting the occurrence of HFiEF in patients with HF, 1 year after successful CTO PCI without severe residual stenosis.

Dual-specificity phosphatase 12 attenuates oxidative stress injury and apoptosis in diabetic cardiomyopathy via the ASK1-JNK/p38 signaling pathway.

Diabetic cardiomyopathy (DCM) is ventricular dysfunction that occurs in patients with diabetes mellitus (DM), independent of recognized risk factors, such as coronary artery disease, hypertension, and valvular heart disease. Dual-specificity phosphatase 12 (DUSP12) is a dual-specificity phosphatase expressed in all tissues. Genome-wide linkage studies have found an association between DUSP12 and type 2 diabetes (T2D). However, the role of DUSP12 in DCM remains largely unknown. Ubiquitously expressed DUSP12 is involved in nonalcoholic fatty liver disease, bacterial infection, and myocardial hypertrophy and plays a critical role in tumorigenesis. Herein, we observed an increased expression of DUSP12 in a hyperglycemia cell model and a high-fat diet (HFD) mouse model. Heart-specific DUSP12-deficient mice showed severe cardiac dysfunction and remodeling induced by an HFD. DUSP12 deficiency exacerbated oxidative stress injury and apoptosis, whereas DUSP12 overexpression had the opposite effect. At the molecular level, DUSP12 physically bound to apoptotic signal-regulated kinase 1 (ASK1), promoted its dephosphorylation, and inhibited its action on c-Jun N-terminal kinase and p38 mitogen-activated protein kinase. Rescue experiments have shown that oxidative stress injury and apoptosis, exacerbated by DUSP12 deficiency, are alleviated by ASK1 inhibition. Therefore, we consider DUSP12 an important signaling pathway in DCM.

Preparation of modified pomelo peel's pulp adsorbent and its adsorption to uranyl ions.

Using pomelo peel's pulp (PPP) as raw material, a new chemically modified PPP was prepared by the process of fermentation, cooking, freeze-drying, and so on. The adsorbent has been characterized by EDS, IR, BET and SEM. The factors of different adsorption conditions such as pH value, adsorption temperature, mass of adsorbent, adsorption time and initial concentration of UO2 2+ were investigated. The adsorption mechanism was explored by adsorption thermodynamics and kinetics experiments. The results indicate that the pH value is 6.0, the dosage of adsorbent is 500 mg l-1, the temperature is 50°C and the adsorption time is 90 min, which is the best adsorption condition. When the initial concentration of UO2 2+ is 35 mg l-1, the adsorbed amount of uranyl ions by the modified PPP adsorbent can reach 42.733 mg g-1, 26.8% higher than the adsorption amount of unmodified adsorbent (31.276 mg g-1), which is obviously enhanced. The kinetic and thermodynamic experiments show that the adsorption process is in good agreement with the pseudo second-order kinetics model, that it is an endothermic reaction, and the reaction is spontaneous. The adsorption process is entropy-dominated. The Freundlich adsorption isotherm can describe the adsorption process more accurately.

MXene-Ti3C2/CuS nanocomposites: Enhanced peroxidase-like activity and sensitive colorimetric cholesterol detection.

Nanomaterials with enzyme-like activity have attracted much attention recently. Herein, we report the synthesis of a new type of 2D MXene-Ti3C2/CuS nanocomposites with peroxidase-like activity using a simple hydrothermal approach. Significantly, compared with the individual MXene-Ti3C2 nanosheets or CuS nanoparticles, the MXene-Ti3C2/CuS nanocomposites show a synergistically enhanced peroxidase-like activity and can be used as an efficient mimetic peroxidase to catalyze the reaction of 3,3,5,5-tetramethylbenzidine (TMB) in the presence of hydrogen peroxide (H2O2), causing a blue color change. Kinetic studies reveal that the MXene-Ti3C2/CuS nanocomposites have a higher catalytic activity to TMB than their single components, and the catalytic reaction follows the ping-pong mechanism. The MXene-Ti3C2/CuS nanocomposites are used for the colorimetric determination of cholesterol with a linear range of 10-100 µM and a limit of detection (LOD) of 1.9 µM. Our results show that the MXene-Ti3C2/CuS nanocomposites based colorimetric cholesterol biosensor is cost-effective, sensitive, and selective, which has potential application in H2O2 and cholesterol detection and clinic medicine diagnostics.

MiR-93 regulates vascular smooth muscle cell proliferation, and neointimal formation through targeting Mfn2.

Background/Aims: Vascular smooth muscle cell (VSMC) hyperplasia plays important roles in the pathogenesis of many vascular diseases, such as atherosclerosis and restenosis. Many microRNAs (miRs) have recently been reported to regulate the proliferation and migration of VSMC. In the current study, we aimed to explore the function of miR-93 in VSMCs and its molecular mechanism. Methods: First, qRT-PCR and immunofluorescence assays were performed to determine miR-93 expression in rat VSMCs following carotid artery injury in vivo and platelet-derived growth factor-BB (PDGF-BB) stimulation in vitro. Next, the biological role of miR-93 in rat VSMC proliferation and migration was examined in vivo and vitro. EdU incorporation assay and MTT assay for measuring cell proliferation, Transwell cell invasion assay and Cell scratch wound assay for measuring cell migration. Then, the targets of miR-93 were identified. Finally, the expression levels of proteins in the Raf-ERK1/2 pathway were measured by western blot. Results: MiR-93 was upregulated in rat VSMCs following carotid artery injury in vivo. Similar results were observed in ex vivo cultured VSMCs after PDGF-BB treatment. MiR-93 inhibition suppressed neointimal formation after carotid artery injury. Moreover, our results demonstrated that a miR-93 inhibitor suppressed the PDGF-BB induced proliferation and migration of in VSMC. This inhibitor also decreased the expression levels of MMP2 and cyclin D1. Mechanistically, we discovered that mitofusin 2(Mfn2) is a direct target of miR-93. Furthermore, an analysis of the signaling events revealed that miR-93-mediated VSMC proliferation and migration occurred via the Raf-ERK1/2 pathway. Conclusions: Our findings suggest that miR-93 promotes VSMCs proliferation and migration by targeting Mfn2. MiR-93 may be a new target for treating in-stent restenosis.

Bakuchiol protects against pathological cardiac hypertrophy by blocking NF-κB signaling pathway.

Bakuchiol (Bak), a monoterpene phenol isolated from the seeds of Psoralea corylifolia, has been widely used to treat a large variety of diseases in both Indian and Chinese folkloric medicine. However, the effects of Bak on cardiac hypertrophy remain unclear. Therefore, the present study was designed to determine whether Bak could alleviate cardiac hypertrophy. Mice were subjected to aortic banding (AB) to induce cardiac hypertrophy model. Bak of 1 ml/100 g body weight was given by oral gavage once a day from 1 to 8 weeks after surgery. Our data demonstrated for the first time that Bak could attenuate pressure overload-induced cardiac hypertrophy and could attenuate fibrosis and the inflammatory response induced by AB. The results further revealed that the effect of Bak on cardiac hypertrophy was mediated by blocking the activation of the NF-κB signaling pathway. In vitro studies performed in neonatal rat cardiomyocytes further proved that the protective effect of Bak on cardiac hypertrophy is largely dependent on the NF-κB pathway. Based on our results, Bak shows profound potential for its application in the treatment of pathological cardiac hypertrophy, and we believe that Bak may be a promising therapeutic candidate to treat cardiac hypertrophy and heart failure.