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Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is currently defined as the worst pandemic disease. SARS-CoV-2 infects human cells via the binding of its S protein to the receptor angiotensin-converting enzyme (ACE2). The use of ACEIs/ARBs (RAAS inhibitors) regulates the renin-angiotensin-aldosterone system (RAAS) and may increase ACE2 expression. Considering the large use of ACEIs/ARBs in hypertensive patients, some professional groups are concerned about whether the use of RAAS inhibitors affects the risk of SARS-CoV-2 infection or the risk of severe illness and mortality in COVID-19 patients. In this review, we summarize preclinical and clinical studies to investigate whether the use of ACEIs/ARBs increases ACE2 expression in animals or patients. We also analyzed whether the use of these drugs affects the risk of SARS-CoV-2 infection, severe illness or mortality based on recent studies. Finally, the review suggests that current evidence does not support the concerns. Unlabelled Image [ABSTRACT FROM AUTHOR]

• Underlying cardiovascular diseases increase the incidence and severity of coronavirus infection. • Cardiac injury is common in patients with COVID-19. It is a risk factor for mortality of COVID-19 patients. • Cardiovascular complications are mainly related to fever, inflammation, the direct effects of Covs and drug side effects. The outbreak of coronavirus disease 2019 (COVID-19) has once again aroused people's concern about coronavirus. Seven human coronaviruses (HCoVs) have been discovered so far, including HCoV-229E, HCoV-NL63, HCoV-OC43, HCoV-HKU115, severe acute respiratory syndrome coronavirus, Middle East respiratory syndrome coronavirus and severe acute respiratory syndrome coronavirus 2. Existing studies show that the cardiovascular disease increased the incidence and severity of coronavirus infection. At the same time, myocardial injury caused by coronavirus infection is one of the main factors contributing to poor prognosis. In this review, the recent clinical findings about the relationship between coronaviruses and cardiovascular diseases and the underlying pathophysiological mechanisms are discussed. This review aimed to provide assistance for the prevention and treatment of COVID-19. [ABSTRACT FROM AUTHOR]

Complex multi-chamber nanostructures are difficult to prepare in a facile and straightforward manner although they are very useful for designing novel functional nanomaterials. In this study, based on the application of electrospun monolithic composites, a new tri-chamber composite nano structure was fabricated using a special trifluid electrospinning. The composite structure had a common shell and two separate cores, and thus was termed as a sheath-separate-core structure. A homemade structural spinneret was developed to assemble an electrospinning system for fabrication. All the three core/sheath sections of the sheath-separate-core structure were monolithic composites consisting of pH-sensitive polymers (i.e. Eudragit® series) and an active ingredient (paracetamol). The sheath-separate-core composite nano structure was able to combine the performances of the three electrospun monolithic nanocomposites to provide a smart controlled release profile according to the physiological characteristics of the digestive tract. The reported protocol opens a new way for designing and producing novel functional nanomaterials based on a complex nanostructure and the related process-structure-performance relationship. Unlabelled Image • A complex nanostructure consists of a sheath and two separate cores. • A multifluid electrospinning is implemented to fabricate the complex structure. • A structural spinneret is developed for guiding and organizing the three fluids. • The sheath-separate-core structures can provide a smart drug controlled release. [ABSTRACT FROM AUTHOR]

Regulated cell death (RCD) is a complex process that involves several cell types and plays a crucial role in vascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant elements of the medial layer of blood vessels, and their regulated death contributes to the pathogenesis of vascular diseases. The types of regulated VSMC death include apoptosis, necroptosis, pyroptosis, ferroptosis, parthanatos, and autophagy‐dependent cell death (ADCD). In this review, we summarize the current evidence of regulated VSMC death pathways in major vascular diseases, such as atherosclerosis, vascular calcification, aortic aneurysm and dissection, hypertension, pulmonary arterial hypertension, neointimal hyperplasia, and inherited vascular diseases. All forms of RCD constitute a single, coordinated cell death system in which one pathway can compensate for another during disease progression. Pharmacologically targeting RCD pathways has potential for slowing and reversing disease progression, but challenges remain. A better understanding of the role of regulated VSMC death in vascular diseases and the underlying mechanisms may lead to novel pharmacological developments and help clinicians address the residual cardiovascular risk in patients with cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Thoracic aortic dissection (TAD) is a severe disease, characterized by numerous apoptotic vascular smooth muscle cells (VSMCs). EDIL3/Del-1 is a secreted protein involved in macrophage efferocytosis in acute inflammation. Here, we aimed to investigate whether EDIL3 promoted the internalization and degradation of apoptotic VSMCs during TAD. The levels of EDIL3 were decreased in the serum and aortic tissue from TAD mice. Global edil3 knockout (edil3−/−) mice and edil3−/− bone marrow chimeric mice exhibited a considerable exacerbation in β-aminopropionitrile monofumarate (BAPN)-induced TAD, accompanied with increased apoptotic VSMCs accumulating in the damaged aortic tissue. Two types of phagocytes, RAW264.7 cells and bone marrow-derived macrophages (BMDMs) were used for in vitro efferocytosis assay. edil3-deficient phagocytes exhibited inefficient internalization and degradation of apoptotic VSMCs. Instead, EDIL3 promoted the internalization phase through interacting with phosphatidylserine (PtdSer) on apoptotic VSMCs and binding to the macrophage ITGAV/αv-ITGB3/β3 integrin. In addition, EDIL3 accelerated the degradation phase through activating LC3-associated phagocytosis (LAP). Mechanically, following the engulfment, EDIL3 enhanced the activity of SMPD1/acid sphingomyelinase in the phagosome through blocking ITGAV-ITGB3 integrin, which facilitates phagosomal reactive oxygen species (ROS) production by NAPDH oxidase CYBB/NOX2. Furthermore, exogenous EDIL3 supplementation alleviated BAPN-induced TAD and promoted apoptotic cell clearance. EDIL3 may be a novel factor for the prevention and treatment of TAD.Abbreviations: BAPN: β-aminopropionitrile monofumarate; BMDM: bone marrow-derived macrophage; C12FDG: 5-dodecanoylaminofluorescein-di-β-D-galactopyranoside; CTRL: control; CYBB/NOX2: cytochrome b-245, beta polypeptide; DCFH-DA: 2’,7’-dichlorofluorescin diacetate; EDIL3/Del-1: EGF-like repeats and discoidin I-like domains 3; EdU: 5-ethynyl-2’-deoxyuridine; EVG: elastic van Gieson; H&E: hematoxylin and eosin; IL: interleukin; LAP: LC3-associated phagocytosis; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; NAC: N-acetylcysteine; PtdSer: phosphatidylserine; rEDIL3: recombinant EDIL3; ROS: reactive oxygen species; SMPD1: sphingomyelin phosphodiesterase 1; TAD: thoracic aortic dissection; TEM: transmission electron microscopy; VSMC: vascular smooth muscle cell; WT: wild-type [ABSTRACT FROM AUTHOR]

Background: The third-generation hybrid rice technology can be constructed by transforming a recessive nuclear male sterile (NMS) mutant with a transgenic cassette containing three functional modules: the wild type male fertility gene to restore the fertility of the mutant, the pollen killer gene that specifically kills the pollen grains carrying the transgene, and the red fluorescence protein (RFP) gene to mark the transgenic seed (maintainer). The transgenic plant produces 1:1 NMS seeds and maintainer seeds that can be distinguished by the RFP signal. However, the RFP signals in the partially filled or pathogen-infected maintainer seeds are often too weak to be detected by RFP-based seed sorting machine, resulting in intermingling of the maintainer seeds with NMS seeds. Results: Here we constructed a weight-based seed sorting system for the third-generation hybrid rice technology by silencing the genes encoding ADP-glucose pyrophosphorylase (AGP) essential for endosperm starch biosynthesis via endosperm-specific expression of artificial microRNAs (amiRNAs). In this system, the NMS seeds have normal endosperm and are heavy, but the maintainer seeds have shrunken endosperms and are light-weighted. The maintainer seeds can be easily and accurately sorted out from the NMS seeds by weight-sorting machines, so pure and fully filled NMS seeds are available. Conclusions: The weight-based seed sorting system shows obvious advantages over the RFP-based seed sorting system in accuracy, efficiency, and cost for propagation of pure male sterile seeds. These characteristics will significantly increase the value and transgenic safety of the third-generation hybrid rice technology. [ABSTRACT FROM AUTHOR]

High performance colossal permittivity ceramic materials are indispensable for the development of electronic devices. In this work, Mg and Nb co-doping BaTiO 3 ceramics were prepared by solid-state reaction under reducing atmosphere. The polarization mechanism, dielectric properties and insulation mechanism were investigated. The defect dipoles ( [ M g T i ″ − V O • • ] × and [ M g T i ″ − 2 N b T i • ] ×) could be formed inside co-doping BaTiO 3 ceramics with various content of MgO, which is the source of colossal permittivity. Appropriate MgO content doping is favorable to enhance short-range hopping, thus improve grain resistance, grain boundary resistance and grain boundary activation energy. The 1.0 at% MgO modified BaTiO 3 -0.01Nb 2 O 5 ceramics possess excellent performance at room temperature with colossal dielectric constant (ԑ r = 4.5 × 104), low dielectric loss (tanδ<0.018), and high insulation resistivity (ρ v = 6.52 × 1011 Ω cm). Meanwhile, good temperature stability is obtained in 1.0 at% MgO modified BaTiO 3 -0.01Nb 2 O 5 ceramics, which satisfies the Electronic Industries Association (EIA) X8R (−55–150 °C, △ε r /ε 25 ≤ ±15%) specification. This study suggests that the defect-dipoles related polarization mechanism can be used to design the colossal permittivity BaTiO 3 -based ceramics. [ABSTRACT FROM AUTHOR]

Rare earth with radius ranges from 0.868 Å to 1.36 Å are introduced in BaTiO 3 (BT) -based ceramics by solid-state reaction method, representing different charge compensation modes. Based on X-ray diffraction (XRD) and electron paramagnetic resonance (EPR) measurement, the behavior and solid solubility of La3+, Ho3+, Y3+, and Yb3+ in BT-based ceramics are systematically analyzed, then the charge compensation mechanism in this system is ascertained. Meanwhile, the function of dielectric properties with temperature at different concentrations is measured, which can be reasonably clarified by the Curie–Weiss and modified Curie–Weiss laws. Through the excellent dielectric performance, it is proved that rare earth ions play a role in improving the performance of BT-based ceramics, and the defect complexes formed therein are conductive to insulation resistivity in reducing atmosphere. Among all samples, the Yb3+ doped BT-based ceramic possesses a relatively good comprehensive performance with high dielectric contant (ε > 2600), low dielectric loss (tanδ = 1.83%) and high insulation resistivity (4.38 × 1011 Ω·cm). Consequently, the defect compensation mechanism provides an effective regulatory method for BT-based ceramics, establishing a theoretical basis for multi-layer ceramic capacitor (MLCC). [ABSTRACT FROM AUTHOR]

Immune response plays a crucial role in post-myocardial infarction (MI) myocardial remodeling. Neogenin (Neo1), a multifunctional transmembrane receptor, plays a critical role in the immune response; however, whether Neo1 participates in pathological myocardial remodeling after MI is unclear. Our study found that Neo1 expression changed significantly after MI in vivo and after LPS + IFN-γ stimulation in bone marrow-derived macrophages (BMDMs) in vitro. Neo1 functional deficiency (using a neutralizing antibody) and macrophage-specific Neo1 deficiency (induced by Neo1flox/flox;Cx3cr1cre mice) increased infarction size, enhanced cardiac fibrosis and cardiomyocyte apoptosis, and exacerbated left ventricular dysfunction post-MI in mice. Mechanistically, Neo1 deficiency promoted macrophage infiltration into the ischemic myocardium and transformation to a proinflammatory phenotype, subsequently exacerbating the inflammatory response and impairing inflammation resolution post-MI. Neo1 deficiency regulated macrophage phenotype and function, possibly through the JAK1-STAT1 pathway, as confirmed in BMDMs in vitro. Blocking the JAK1-STAT1 pathway with fludarabine phosphate abolished the impact of Neo1 on macrophage phenotype and function, inflammatory response, inflammation resolution, cardiomyocyte apoptosis, cardiac fibrosis, infarction size and cardiac function. In conclusion, Neo1 deficiency aggravates inflammation and left ventricular remodeling post-MI by modulating macrophage phenotypes and functions via the JAK1-STAT1 signaling pathway. These findings highlight the anti-inflammatory potential of Neo1, offering new perspectives for therapeutic targets in MI treatment. Neo1 deficiency aggravated inflammation and left ventricular remodeling after MI by modulating macrophage phenotypes and functions via the JAK1-STAT1 signaling pathway. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that bone morphogenetic proteins (BMPs) play important roles in cardiovascular diseases, including atherosclerosis, artery calcification, myocardial remodeling, pulmonary arterial hypertension, and diabetic cardiomyopathy. Kielin/chordin-like protein (KCP) is a secreted protein that regulates the expression and function of BMPs. However, the role of KCP in cardiac aging remains unknown. In this study, we aimed to investigate the role of KCP in cardiac aging and its possible mechanisms. Echocardiogram showed that heart function was impaired in aged mice (24 months). In addition, analysis of heart structure showed that KCP knockout (KO) aggravated cardiac remodeling in aged mice. Moreover, KCP KO increased p-smad2/3 and TGF-β expression, while decreased BMP-2 expression in aged mice. Furthermore, KCP KO increased the expression of cardiac senescence-related proteins in aged mice. KCP KO aggravated the imbalance of oxidants and antioxidants and increased the expression of proinflammatory cytokines and cardiomyocyte apoptosis in aged mice. Our study demonstrated that KCP KO aggravated cardiac aging in mice by increasing the levels of oxidative stress, inflammation, and cardiomyocyte apoptosis. Key message: KCP KO aggravated aging-related cardiac dysfunction and remodeling in male mice. KCP KO aggravated cardiac aging by increasing the levels of oxidative stress, inflammation, and cardiomyocyte apoptosis. [ABSTRACT FROM AUTHOR]

Accurate and timely precipitation forecasts can help people and organizations make informed decisions, plan for potential weather-related disruptions, and protect lives and property. Instead of using physics-based numerical forecasts, which can be computationally prohibitive, there has been a growing interest in using deep learning techniques for precipitation prediction in recent years due to the success of these approaches in various other fields. These deep learning approaches generally use historical composite reflectivity (CR) at the surface level to predict future time steps. However, other relevant factors related to the potential motion and vertical structure of the storm have not been considered. To address this issue, this research proposes a multisource ConvLSTM (MS-ConvLSTM) model to improve the accuracy of precipitation forecasting by incorporating multiple data sources into the prediction process. The model was trained on a dataset of radar echo features, which includes not only composite reflectivity (CR), but also echo top (ET), vertically integrated liquid (VIL) water, and radar-retrieved wind field data at different elevations. Experiment results showed that the proposed model outperformed traditional methods in terms of various evaluation metrics, such as mean absolute error (MAE), mean squared error (MSE), probability of detection (POD), false alarm rate (FAR), and critical success index (CSI). [ABSTRACT FROM AUTHOR]

Efferocytosis is defined as the clearance of apoptotic cells (ACs) in physiological and pathological states and is performed by efferocytes, such as macrophages. Efferocytosis can lead to the resolution of inflammation and restore tissue homoeostasis; however, the mechanisms of efferocytosis in determining inflammation resolution are still not completely understood, and the effects of efferocytosis on other proresolving properties need to be explored and explained. In this review, the process of efferocytosis will be summarized briefly, and then these mechanisms and effects will be thoroughly discussed. In addition, the association between mechanisms of efferocytosis in determining resolution of inflammation and cardiovascular diseases will also be reviewed, as an understanding of this association may provide information on novel treatment targets. [ABSTRACT FROM AUTHOR]

The resolution of inflammation, the other side of the inflammatory response, is defined as an active and highly coordinated process that promotes the restoration of immune microenvironment balance and tissue repair. Inflammation resolution involves several key processes, including dampening proinflammatory signaling, specialized proresolving lipid mediator (SPM) production, nonlipid proresolving mediator production, efferocytosis and regulatory T-cell (Treg) induction. In recent years, increasing attention has been given to the effects of inflammation resolution on hypertension. Furthermore, our previous studies reported the antihypertensive effects of SPMs. Therefore, in this review, we aim to summarize and discuss the detailed association between arterial hypertension and inflammation resolution. Additional, the association between gut microbe-mediated immune and hypertension is discussed. This findings suggested that accelerating the resolution of inflammation can have beneficial effects on hypertension and its related organ damage. Exploring novel drug targets by focusing on various pathways involved in accelerating inflammation resolution will contribute to the treatment and control of hypertensive diseases in the future. [Display omitted] • Resolution of inflammation is an active process to restore the balance of immune microenvironment. • Accelerating the resolution of inflammation provides beneficial effects on hypertension and its related organ damage. • Focusing on the various pathways of accelerating inflammation resolution will benefit the treatment of hypertension. [ABSTRACT FROM AUTHOR]

Semaphorins (Semas), which belongs to the axonal guidance molecules, include 8 classes and could affect axon growth in the nervous system. Recently, semaphorins were found to regulate other pathophysiological processes, such as immune response, oncogenesis, tumor angiogenesis, and bone homeostasis, through binding with their plexin and neuropilin receptors. In this review, we summarized the detailed role of semaphorins and their receptors in the pathological progression of various cardiovascular diseases (CVDs), highlighting that semaphorins may be potential therapeutic targets and novel biomarkers for CVDs. [ABSTRACT FROM AUTHOR]

The (1-x) BaTiO 3 -x (0.5Bi 2 O 3 -0.67MgO-0.33ZrO 2) ceramics (x = 5, 10, 15 and 20 mol%) are fabricated by a conventional solid-state method in a reducing atmosphere. All ceramics display a pure perovskite phase without any trace of secondary phase, and a phase transition from tetragonal phase to pseudo-cubic phase occurs between x = 0.1 and x = 0.15. The dielectric analysis manifests that both the dielectric constant and insulation resistivity at room temperature decrease with increasing dopants, which is mainly related to the reduction of grain boundaries. Meanwhile, high dielectric constant (∼2020) and excellent insulation resistivity (∼4.81 × 1013 ΩΩ ·cm) are obtained when x = 0.05. Besides, the temperature stability of ceramics in the high temperature region is improved with little BMZ-doping, and BMZ05 ceramic satisfies the EIA X8R standard. The complex impedance demonstrates that obvious heterogeneous interfaces and strong interface polarization are existed in ceramics. The fitted activation energy of grain boundary reflects that the long-range hopping polarization of oxygen vacancies dominates in the dielectric constant of ceramics when x < 0.1, while the short-range hopping polarization of defect dipoles dominates when x > 0.15. • (Bi, Mg, Zr)‐doped BT ceramics are synthesized via a conventional solid‐state reaction method in a reducing atmosphere. • Good dielectric properties with Ԑ r ∼2020, tanδ <1.59%, ρ v ∼4.81 × 1013 ΩΩ ·cm and temperature stability ∼ EIA X8R are obtained. • The hopping polarization of oxygen vacancies and defect dipoles are responsible for the dielectric performance. [ABSTRACT FROM AUTHOR]

• The gas-sensing system with EC-coated QCM sensors was developed. • The developed sensor has better selectivity and sensitivity for d -limonene aromas. • The early infestation citrus can be nondestructively and rapidly detected by the sensor. D-limonene is one of the main olefin gas compounds released from citrus and its relative content changes most obviously with the infection time of Bactrocera dorsalis (Hendel). Thus, it is necessary to detect d -limonene content released from citrus, which may lead to detect the presence of early infestation by B. dorsalis in citrus. In this study, a gas-sensing system based on quartz crystal microbalance (QCM) sensors coated with ethyl cellulose (EC) was developed to detect d -limonene aromas emanating from Australian citrus. There was a linear relationship between the frequency shift and d -limonene concentrations ranging from 60 mg m−3 to 6000 mg m−3 with a determination coefficient (R2) of 0.9899, and the limit of detection for d -limonene in pure gas was 300 mg m−3. It has also been observed that the QCM sensor has better selectivity towards d -limonene aroma. Additionally, the sensor was found to be repeatable with an average R value of 96.31 %, and the lifetime of the sensor can be extended at least to one month with an acceptable drift (3.40 %) in their sensing characteristics. Furthermore, it was confirmed that there was high consistency between the QCM sensor's response and the GC–MS for d -limonene aroma. The six VOCs contributing the most to differentiating citrus infested with B. dorsalis were identified. The gas-sensing system based on QCM sensors has potential feasibility for the rapid detection of the presence of B. dorsalis infestations in postharvest citrus. [ABSTRACT FROM AUTHOR]

• IL-20 and its receptors were increased in arterial wall dissection from AAD patients. • The plasma IL-20 were significantly higher in the AAD patients. • IL-20 may contribute to the inflammatory pathogenesis of AAD. Acute aortic dissection (AAD) is the most devasting cardiovascular disease associated with high mortality. The occurrence and progression of AAD can be regulated by inflammatory processes, and further understanding of this inflammatory pathogenesis may improve the treatment of AAD. Interleukin 20 (IL-20), as an inflammatory mediator, has been demonstrated to be associated with several inflammatory diseases. However, the association between IL and 20 and AAD is still unknown. Five aortic dissection tissue samples and five control aortic tissue samples were evaluated in our study. The expression of IL-20 and its receptor subunits (IL-20Rα and IL-20Rβ) was detected by immunofluorescence staining. From January 2018 to March 2018, 70 consecutive AAD patients and 25 non-AAD (NAD) patients were enrolled in this study. Diagnosis was based on computed tomography angiography (CTA) results. Blood samples were obtained from the patients on the first day of hospitalization. Plasma IL-20, TNF-α and IL-6 concentrations were evaluated with enzyme-linked immunosorbent assay (ELISA) kits. The expression levels of IL-20 and its receptor subunits (IL-20Rα and IL-20Rβ) were increased in the sites of arterial wall dissection in the AAD patients. In a separate group, the plasma IL-20, TNF-α and IL-6 concentrations were significantly higher in the AAD patients than in the non-AAD patients. Spearman's correlation analysis showed that plasma IL-20 was positively correlated with plasma TNF-α and IL-6, D-dimer, C-reaction protein (CRP), creatinine, fasting blood glucose, systolic blood pressure (SBP), and diastolic blood pressure (DBP). Multiple linear regression revealed that IL-20, in addition to IL-6, glucose, CRP and D-dimer, was independently associated with the presence of AAD. IL-20 was closely associated with the presence of AAD. IL-20 may contribute to the inflammatory pathogenesis of AAD. [ABSTRACT FROM AUTHOR]

Complex nanostructures are increasingly becoming important in the development of novel functional nanomaterials. Nano drug depots, characterized by core-shell structures with core drug reservoirs, are drawing increasing attention because of its potential applications in furnishing drug-sustained release profiles. In the present study, two kinds of nano drug depots, one containing a crystal drug reservoir and the other having a medicated composite drug reservoir, were prepared through modified triaxial electrospinning. Their drug-sustained release performances were compared in terms of initial burst release, middle linear release, and the late tailing off release. Although both depots had a linear morphology, clear core-shell nanostructures and the same cellulose acetate shell layer, they provided considerably different tailing off release performances, and thus different sustained release profiles. The composite-based drug depots showed a smaller tailing off drug amount of 2.2%, a shorter time period of 12 h, and a better zero-order controlled release kinetics in general than the crystal-based drug depots, whose tailing off amount was 9.3% over a time period of 36 h. The mechanism was proposed, which had a close relationship with the state of drug in the core reservoir. The present protocols open a new way for producing medicated structural nanomaterials. Unlabelled Image • A polymer composite-based drug depot is conceived based on core-shell structure • A modified triaxial electrospinning for producing the hybrid nano depots • The composite-based drug depot can significantly reduce the tailing-off release • New mechanism is proposed for the process-structure-performance relationship [ABSTRACT FROM AUTHOR]

• Simultaneous hydrogen and oxygen production from pure water over CN is achieved. • The quantum confinement ensures the sufficient driving force for water oxidation. • Doping P atoms in corner-carbon sites provides efficient charge transfer channels. • Apparent quantum efficiencies reach 6.8% at 400 nm and 2.4% at 500 nm. Photocatalytic overall water splitting is a challenging topic in the research field of solar energy conversion. Herein, we proposed an effective strategy of adopting quantum confinement effect and site-selective doping to realize simultaneous hydrogen and oxygen production from pure water over polymeric carbon nitride (CN) photocatalysts. Selectively doping P atoms in the corner-carbon sites provided efficient charge transfer channels between different structural units. Meanwhile, the site-selective P doping could generate mid-gap states below the conduction band of CN, which extended the utilization of visible light up to 600 nm, and served as trapping centres to inhibit the charge recombination. In addition, the quantum confinement effect could ensure the sufficient driving force for the rate-determining water oxidation. As a consequence, the hydrogen production rate from overall water splitting reached 619.5 μmol·h−1 g−1 under simulated sunlight irradiation, with notable apparent quantum yields of 6.8% at 400 nm and 2.4% at 500 nm. [ABSTRACT FROM AUTHOR]

[Display omitted] Recent studies have shown that neutrophils play an important role in the development and progression of heart failure. Developmental endothelial locus-1 (DEL-1) is an anti-inflammatory glycoprotein that has been found to have protective effects in various cardiovascular diseases. However, the role of DEL-1 in chronic heart failure is not well understood. In a mouse model of pressure overload-induced non-ischemic cardiac failure, we found that neutrophil infiltration in the heart increased and DEL-1 levels decreased in the early stages of heart failure. DEL-1 deficiency worsened pressure overload-induced cardiac dysfunction and remodeling in mice. Mechanistically, DEL-1 deficiency promotes neutrophil infiltration and the formation of neutrophil extracellular traps (NETs) through the regulation of P38 signaling. In vitro experiments showed that DEL-1 can inhibit P38 signaling and NETs formation in mouse neutrophils in a MAC-1-dependent manner. Depleting neutrophils, inhibiting NETs formation, and inhibiting P38 signaling all reduced the exacerbation of heart failure caused by DEL-1 deletion. Overall, our findings suggest that DEL-1 deficiency worsens pressure overload-induced heart failure by promoting neutrophil infiltration and NETs formation. [ABSTRACT FROM AUTHOR]

• Clinical evidence has revealed a close relationship between acute liver injury (AKI) and remote organ dysfunction, especially liver injury. • VNS protects against liver injury induced by AKI via anti-inflammation, anti-apoptosis, and enhancing antioxidative capability. • VNS may become a promising adjuvant therapeutic strategy for treating liver injury from AKI in the future. Renal ischemia reperfusion (I/R) is not an isolated event; however, it results in remote organ dysfunction. Vagus nerve stimulation (VNS) has shown protective effects against renal I/R injury via an anti-inflammatory mechanism. This study aimed to investigate whether VNS could attenuate liver injury induced by renal I/R and identify the underlying mechanisms. Eighteen healthy male Sprague-Dawley rats (200–250 g) were equally divided into three groups: sham group (sham surgery without I/R or VNS), I/R group (renal I/R) and VNS group (renal I/R plus VNS). The I/R model was established by excising the right kidney and then clamping the left renal pedicle with an occlusive nontraumatic microaneurysm clamp for 45 min followed by a 6-h reperfusion. The rats in the VNS group received spontaneous left cervical VNS with renal ischemia and reperfusion. At the end of the experiment, blood and liver tissues were collected to detect liver function, oxidative stress and inflammatory parameters. Additionally, TUNEL staining, real-time PCR, western blotting and hematoxylin and eosin staining of liver tissues were performed to assess liver injury and the underlying mechanisms. Kidney and liver function was severely damaged in the I/R group compared to the sham group. However, VNS significantly protected kidney and liver function. Rats treated with VNS revealed decreases in oxidative enzymes, apoptosis and levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) in serum and liver compared with rats in the I/R group. Rats in the VNS group also showed increased antioxidant stress responses compared to rats in the I/R group. VNS exerts protective effects against liver injury from renal I/R via inhibiting oxidative stress and apoptosis, downregulating inflammatory cytokines and enhancing antioxidative capability in the liver, and may become a promising adjuvant therapeutic strategy for treating liver injury induced by acute renal injury. [ABSTRACT FROM AUTHOR]

Accumulating evidence suggests that inflammation plays an important role in the pathophysiology of the initiation and progression of cardiovascular and metabolic diseases (CVMDs). Anti-inflammation strategies and those that promote inflammation resolution have gradually become potential therapeutic approaches for CVMDs. Resolvin D2 (RvD2), a specialized pro-resolving mediator, exerts anti-inflammatory and pro-resolution effects through its receptor GPR18, a G protein–coupled receptor. Recently, the RvD2/GPR18 axis has received more attention due to its protective role in CVMDs, including atherosclerosis, hypertension, ischaemia reperfusion, and diabetes. Here, we introduce basic information about RvD2 and GPR18, summarize their roles in different immune cells, and review the therapeutic potential of the RvD2/GPR18 axis in CVMDs. In summary, RvD2 and its receptor GPR18 play an important role in the occurrence and development of CVMDs and are potential biomarkers and therapeutic targets. [Display omitted] [ABSTRACT FROM AUTHOR]

[Display omitted] Several interleukins (ILs) have been demonstrated to participate in cardiac injury. This study aimed to investigate whether IL-27p28 plays a regulatory role in doxorubicin (DOX)-induced cardiac injury by regulating inflammation and oxidative stress. Dox was used to establish a mouse cardiac injury model, and IL-27p28 was knocked out to observe its role in cardiac injury. In addition, monocytes were adoptively transferred to clarify whether monocyte-macrophages mediate the regulatory role of IL-27p28 in DOX-induced cardiac injury. IL-27p28 knockout significantly aggravated DOX-induced cardiac injury and cardiac dysfunction. IL-27p28 knockout also upregulated the phosphorylation levels of p65 and STAT1 and promoted M1 macrophage polarization in DOX-treated mice, which increased cardiac inflammation and oxidative stress. Moreover, IL-27p28-knockout mice that were adoptively transferred WT monocytes exhibited worse cardiac injury and cardiac dysfunction and higher cardiac inflammation and oxidative stress. IL-27p28 knockdown aggravates DOX-induced cardiac injury by worsening the M1 macrophage/M2 macrophage imbalance and its associated inflammatory response and oxidative stress. [ABSTRACT FROM AUTHOR]

Photocatalytic hydrogen generation from water is an appealing strategy for solar energy conversion, and fabricating heterostructured photocatalysts is demonstrated to be an effective way to improve the photocatalytic performance. Herein, we applied a facile one-step hydrothermal method to construct Zn x Cd 1− x S/ZnO heterostructures for photocatalytic hydrogen production. By varying the initial S 2− /Cd 2+ molar ratio, the composition, structure, and morphology of Zn x Cd 1− x S/ZnO heterostructures could be gradually tuned. It was demonstrated that the photocatalytic activity of Zn x Cd 1− x S/ZnO first increased and then underwent a decrease with the increased S 2− /Cd 2+ molar ratio. Zn x Cd 1− x S/ZnO sample showed a highest photocatalytic hydrogen production rate of 1.89 mmol/h with an apparent quantum yield of 26.0% at 420 nm. To our knowledge, this value was the highest for the reported Zn x Cd 1− x S/ZnO composite photocatalysts. The excellent performance could be attributed to the balance of the light absorption and conduction band offset of Zn x Cd 1− x S/ZnO heterostructures, as well as the intimate contact of two components at the interface. This work not only provided a facile one-step route to fabricate efficient composite photocatalysts, but also demonstrated the importance of balancing the band-gap and band offset of heterostructured photocatalysts for the improved hydrogen production. [ABSTRACT FROM AUTHOR]

• Recent years, inflammation resolution gradually captures the eyes of researches. • Inflammation has been proved to be closely related with the development of cardiovascular diseases and many cytokines actively involved in this process. • In this review, we will focus on the role of IL-10 family in inflammation and cardiovascular diseases and its future clinical value. Interleukin (IL)-10 cytokine family members, including IL-10, IL-19, IL-20, IL-22, IL-24, IL-26 and the distantly related IL-28A, IL-28B, and IL-29, play critical roles in the regulation of inflammation. The occurrence and progression of cardiovascular diseases closely correlate with the regulation of inflammation, which may provide novel strategies for the treatment of cardiovascular diseases. In recent years, studies have focused on the association between the IL-10 cytokine family and the physiological and pathological progression of cardiovascular diseases. The aim of this review is to summarize relevant studies and clarify whether the IL-10 cytokine family contributes to the regulation of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

In order to enhance the tracking performance of a two-axis airborne optoelectronic stabilized platform with external disturbances, a novel composite control strategy is proposed based on a modified variable gains super-twisting sliding mode control and an adaptive fuzzy-based disturbance observer (MVGSTSMC-FDO), which highlights advantages of both two strategies. The adaptive FDO is designed to observe and compensate time-varying lump external disturbances of the closed stabilizing loop, which strengthens the robustness of the system. Under the counteraction of the external disturbances, the modified super-twisting sliding mode control law is designed with variable gains to achieve the excellent control performance including strong robustness, weak chattering, low steady-state errors, fast convergence, and high adaptability. Moreover, the uniform stability of the adaptive control system is rigorously proved by the Lyapunov theory analysis method. Simulations on the stabilization loop system of a two-axis stabilized platform with cross-coupling disturbances and are carried out to show the effectiveness of the proposed control strategy. Compared with other different control methods, the results illustrate that the proposed control strategy not only obtains high tracking precision with fast convergence, but also provides a stronger robustness against external disturbances. [ABSTRACT FROM AUTHOR]

Interleukin (IL) 9 is a pleiotropic cytokine, and recent studies have demonstrated that IL-9 is associated with several cardiovascular diseases, via regulation of the inflammatory response. Doxorubicin (DOX) is known to induce severe cardiac injury and dysfunction by enhancing inflammation. This study aimed to investigate the role of IL-9 in DOX-induced cardiotoxicity. DOX was used to induce cardiac dysfunction and the expression of IL-9 in the murine cardiac tissues was measured. The mice were intraperitoneally injected with recombinant mouse IL-9 (rmIL-9) or anti-IL-9 neutralizing antibody (IL-9nAb) for investigating the effect of IL-9 on DOX-induced cardiac injury and dysfunction. The messenger ribonucleic acid (mRNA) expression levels of the pro-inflammatory cytokines were determined in each group by quantitative real-time polymerase chain reaction (RT-qPCR). The effect of rmIL-9 or IL-9nAb on DOX-induced apoptosis was determined both in vivo and vitro. IL-9 levels significantly increased in the heart following DOX injection. Cardiac injury and dysfunction were induced by DOX, and treatment with IL-9nAb significantly alleviated DOX-induced injury, whereas rmIL-9 administration aggravated the cardiac damage. IL-9nAb decreased the expression of pro-inflammatory cytokines in the DOX-treated mice, while rmIL-9 administration increased the levels of pro-inflammatory cytokines. IL-9nAb reduced DOX-induced myocardial apoptosis, whereas rmIL-9 administration produced the opposite results. Additionally, IL-9nAb mitigated the DOX-induced apoptosis in H9C2 cells, while administration of rmIL-9 produced the opposite effect. Our results demonstrated that IL-9 aggravated DOX-induced cardiac injury and dysfunction by promoting the inflammatory response and cardiomyocyte apoptosis. [ABSTRACT FROM AUTHOR]

• Two distinct generations (three types) of garnets were identified in the Hongyuntan deposit. • The temperature, salinity, oxygen fugacity (f O 2), and pH of the Hongyuntan ore-forming fluid fluctuated. • Multiple episodic supplies of hydrothermal fluids occurred in the Hongyuntan deposit. • The Hongyuntan ore-forming fluid was likely formed through a magmatic–hydrothermal process. The Hongyuntan deposit, which is one of the typical volcanic-hosted Fe deposits in the Aqishan–Yamansu metallogenic belt of the Eastern Tianshan Orogenic Belt, primarily consists of Fe and skarn minerals (especially garnet). Two generations (three types) of garnets were identified in the Hongyuntan deposit based on field and optical characteristics. Hongyuntan garnets are Fe-rich and belong to the grossular–andradite solid solution series (And = 50.99%–100.00%, average: 79.06%). Garnets of the first generation (Grt1) are massive aggregates and are fine-grained with well-developed oscillatory zonings. They have Type I (two-phase liquid and vapor) and Type II (multi-phase daughter mineral-bearing) fluid inclusions and experienced high temperature (540–560 °C) and salinity (9.2–63.2 wt% NaCl eqv) conditions. The Grt1 have high ΣREE, LfREE/HREE, δEu, U, Y, and high field strength element (HFSE: sum of Nb, Ta, Zr, and Hf) contents. Garnets of the second generation (Grt2) are vefin types and are characterized by irregular shapes with irregular zonings. Type A garnets of the second generation (Grt2-A) usually coexist with mafgnetite and have Type I and Type II fluid inclusions with relatively high temperature (480–500 °C) and salinity (9.5–36.6 wt% NaCl eqv) values. Compared to Grt1, Grt2-A have low And, U, and LREE/HREE together with medium ΣREE, δEu, HFSE, and Y contents. Type B garnets of the second generation (Grt2-B) usually coexist with epidote and quartz. They merely have Type I fluid inclusions with medium–low temperature (260–280 °C) and salinity (6.6–12.7 wt% NaCl eqv) values. Grt2-B have high And, δEu, and LREE/HREE contents but very low ΣREE, HFSE, and Y contents. The fluid inclusions and geochemical properties of the garnets indicate that the temperature, salinity, oxygen fugacity (f O 2), and pH of the ore-forming fluid fluctuated, indicating Hongyuntan deposit likely experienced superimposed mineralization. Grt1 originated in a magmatic–hydrothermal fluid and formed through diffusive metasomatism under relatively high f O 2 , neutral pH, and low water/rock (W/R) ratio conditions. The reduced Fe and other siderophile elements in the ore-forming fluid, which formed Grt1, are believed to be the material basis for iron ores in the later main metallogenic stage. Grt2-A demonstrate the characteristics associated with transitional fluid, which most likely originated from the episodic hydrothermal supplies. However, the ore-forming fluid system gradually opened up during the crystallization of Grt2-B, and the decreasing temperatures and depletion of ore-forming materials were ultimately unfavorable for the deposition of magnetite. [ABSTRACT FROM AUTHOR]

• CoP with superhigh cocatalytic effect was prepared by deriving from Co 3 O 4 quantum dots. • The H 2 evolution rate of CoP/CN was 5 times higher than that of Pt/CN. • Interactions between Co and N atoms create new routes for e− migration. In this work, we prepared a series of novel quasi 0D/2D nanohybrids of CoP/g-C 3 N 4 derived from the composites of Co 3 O 4 quantum dots with g-C 3 N 4 nanosheets. Particularly, 0.45 wt% CoP modified g-C 3 N 4 had the highest H 2 generation rate as 1.074 mmol·h−1 g−1 (AQY: 6.1% at 420 nm) under visible light irradiation, which was 283 and 5 times of that for pure g-C 3 N 4 (0.0038 mmol·h−1 g−1) and 0.5 wt% Pt/g-C 3 N 4 (0.216 mmol·h−1 g−1), respectively. The excellent performance was attributed to the formation of a new electron transfer route owing to the interaction of Co atoms with N atoms, the reaction sites of metal-like Co-P bonds due to the lower energy barrier than Pt toward H 2 evolution, and finally the well dispersed CoP nanoparticles offering much more reaction sites than bulk counterpart. Our work provides a new methodology to construct highly dispersed noble metal free cocatalyst in the matrix of host photocatalyst with excellent performance. [ABSTRACT FROM AUTHOR]

Aims: The majority of people with diabetes are susceptible to cardiac dysfunction and heart failure, and conventional drug therapy cannot correct the progression of diabetic cardiomyopathy. We assessed the potential role and therapeutic value of LGR6 (G protein-coupled receptor containing leucine-rich repeats 6) in diabetic cardiomyopathy., Methods and Results: Type 2 diabetes models were established using high-fat diet/streptozotocin-induced diabetes in mice. LGR6 knockout mice were generated. Recombinant adeno-associated virus serotype 9 carrying LGR6 under the cardiac troponin T promoter was injected into diabetic mice. Cardiomyocytes incubated with high glucose (HG) were used to imitate diabetic cardiomyopathy in vitro. The molecular mechanism was explored through RNA sequencing and a chromatin immunoprecipitation assay. We found that LGR6 expression was upregulated in diabetic hearts and HL1 cardiomyocytes treated with HG. The LGR6 knockout aggravated, but cardiomyocyte-specific LGR6 overexpression ameliorated, cardiac dysfunction and remodeling in diabetic mice. Mechanistically, in vivo and in vitro experiments revealed that LGR6 deletion aggravated, whereas LGR6 overexpression alleviated, ferroptosis and disrupted mitochondrial biogenesis by regulating STAT3/Pgc1a signaling. STAT3 inhibition and Pgc1a activation abrogated LGR6 knockout-induced mitochondrial dysfunction and ferroptosis in diabetic mice. In addition, LGR6 activation by recombinant RSPO3 treatment ameliorated cardiac dysfunction, ferroptosis and mitochondrial dysfunction in diabetic mice., Conclusions: We identified a previously undescribed signaling pathway of the LGR6-STAT3-Pgc1a axis that plays a critical role in ferroptosis and mitochondrial disorders during diabetic cardiomyopathy and provides an option for treatment of diabetic hearts., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Aims: Interleukin (IL)-12p40 is a common subunit of the bioactive cytokines IL-12 and IL-23, and it also has its own intrinsic functional activity. However, its role in doxorubicin-induced chronic cardiomyopathy (DICCM) as well as the underlying mechanisms are still unknown., Methods and Results: In this study, we used IL-12p40-knockout mice, IL-23p19-knockout mice, Rag1-knockout mice, a ferroptosis inhibitor, recombinant IL-12 (rIL-12), rIL-23, rIL-12p40, rIL-12p80, and anti-IL17A to investigate the effects of IL-12p40 on DICCM and elucidate the underlying mechanisms. We found that myocardial ferroptosis were increased in DICCM and that the inhibition of ferroptosis protected against DICCM. The expression of IL-12p40 was upregulated, and IL-12p40 was predominantly expressed by CD4+ T cells in the hearts of mice with DICCM. IL-12p40 knockout attenuated cardiac dysfunction, fibrosis and ferroptosis in DICCM, and similar results were observed in the context of CD4+ T cell IL-12p40 deficiency in Rag1-/- mice. Treatment with rIL-23, but not rIL-12, rIL-12p40 monomer or rIL-12p80, abolished the protective effects of IL-12p40 knockout. Moreover, rIL-23 treatment and IL-23p19 knockout exacerbated and ameliorated DICCM, respectively. IL-12p40 knockout might protect against DICCM by inhibiting Th17 differentiation and IL-17A production but not Th1, Th2 and Treg differentiation. Neutralizing IL-17A with an antibody also attenuated cardiac dysfunction, fibrosis and ferroptosis. The IL-12p40/Th17/IL-17A axis might promote cardiomyocyte ferroptosis by activating TNF receptor-associated factor 6 (TRAF6)/mitogen-activated protein kinase (MAPK)/P53 signaling in DICCM., Conclusions: Interleukin-12p40 deficiency protects against DICCM by inhibiting Th17 differentiation and the production of IL-17A, which plays critical roles in cardiomyocyte ferroptosis in DICCM via activating TRAF6/MAPK/P53 signaling. Our study may provide novel insights for the identification of therapeutic targets for treating DICCM in the clinic., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Background: Heart failure with preserved ejection fraction (HFpEF) is an emerging major unmet need and one of the most significant clinic challenges in cardiology. The pathogenesis of HFpEF is associated with multiple risk factors. Hypertension and metabolic disorders associated with obesity are the 2 most prominent comorbidities observed in patients with HFpEF. Although hypertension-induced mechanical overload has long been recognized as a potent contributor to heart failure with reduced ejection fraction, the synergistic interaction between mechanical overload and metabolic disorders in the pathogenesis of HFpEF remains poorly characterized., Method: We investigated the functional outcome and the underlying mechanisms from concurrent mechanic and metabolic stresses in the heart by applying transverse aortic constriction in lean C57Bl/6J or obese/diabetic B6.Cg-Lep ob /J (ob/ob) mice, followed by single-nuclei RNA-seq and targeted manipulation of a top-ranked signaling pathway differentially affected in the 2 experimental cohorts., Results: In contrast to the post-transverse aortic constriction C57Bl/6J lean mice, which developed pathological features of heart failure with reduced ejection fraction over time, the post-transverse aortic constriction ob/ob mice showed no significant changes in ejection fraction but developed characteristic pathological features of HFpEF, including diastolic dysfunction, worsened cardiac hypertrophy, and pathological remodeling, along with further deterioration of exercise intolerance. Single-nuclei RNA-seq analysis revealed significant transcriptome reprogramming in the cardiomyocytes stressed by both pressure overload and obesity/diabetes, markedly distinct from the cardiomyocytes singularly stressed by pressure overload or obesity/diabetes. Furthermore, glucagon signaling was identified as the top-ranked signaling pathway affected in the cardiomyocytes associated with HFpEF. Treatment with a glucagon receptor antagonist significantly ameliorated the progression of HFpEF-related pathological features in 2 independent preclinical models. Importantly, cardiomyocyte-specific genetic deletion of the glucagon receptor also significantly improved cardiac function in response to pressure overload and metabolic stress., Conclusions: These findings identify glucagon receptor signaling in cardiomyocytes as a critical determinant of HFpEF progression and provide proof-of-concept support for glucagon receptor antagonism as a potential therapy for the disease., Competing Interests: D.J. Drucker has served as a consultant or speaker within the past 12 months to Altimmune, Amgen, Boehringer Ingelheim, Kallyope, Merck Research Laboratories, Novo Nordisk Inc, and Pfizer Inc. Neither D.J. Drucker or his family members hold issued stock directly or indirectly in any of these companies. He holds nonexercised options in Kallyope. The other authors report no conflicts.

Hybrid seed production technology (SPT) is achieved through the utilization of a recessive nuclear male-sterile mutant transformed with a transgenic cassette comprising three essential components: the wild-type gene to restore the fertility of the male-sterile mutant, an α-amylase gene to disrupt transgenic pollen grains, and red fluorescence protein gene DsRed to distinguish the transgenic seeds from the nontransgenic male sterile seeds. In rice, we establish the pollen disruption system by introducing an amyloplast targeting signal peptide (ASP) at the N-terminus of maize α-amylase protein ZM-AA1 ΔSP (ZM-AA1 with the N-terminal signal peptide removed). The ASP facilitates the transport of ZM-AA1 ΔSP protein into amyloplast where it degrades starch, resulting in disruption of the pollen fertility. To obtain such signal peptides for rice, we searched the rice proteins homologous to the defined wheat amyloplast proteins followed by protein-protein interaction network predictions and targeting signal peptides prediction. These analyses enabled the identification of four candidate ASPs in rice, which were designated as ASP1, ASP2, ASP3, and ASP4, respectively. ASP1 and ASP2, when linked with ZM-AA1 ΔSP , exhibited the capability to disrupt transgenic pollen grains, whereas ASP3 and ASP4 did not produce this effect. Interestingly, the localization experiments showed that ASP3 and ASP4 were able to target the proteins into chloroplast. The ASP1 and ASP2 sequences provide valuable tools for genetic engineering of the rice male-sterile system, which will contribute to the hybrid rice breeding and production., Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-024-01471-y., Competing Interests: Competing interestsThe authors declare no competing interests., (© The Author(s), under exclusive licence to Springer Nature B.V. 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Dressings with multiple functional performances (such as hemostasis, promoting regeneration, analgesia, and anti-inflammatory effects) are highly desired in orthopedic surgery. Herein, several new kinds of medicated nanofibers loaded with several active ingredients for providing multiple functions were prepared using the modified coaxial electrospinning processes. With an electrospinnable solution composed of polycaprolactone and fenoprofen as the core working fluid, several different types of unspinnable fluids (including pure solvent, nanosuspension containing tranexamic acid and hydroxyapatite, and dilute polymeric solution comprising tranexamic acid, hydroxyapatite, and polyvinylpyrrolidone) were explored to implement the modified coaxial processes for creating the multifunctional nanofibers. Their morphologies and inner structures were assessed through scanning and transmission electron microscopes, which all showed a linear format without the discerned beads or spindles and a diameter smaller than 1.0 μm, and some of them had incomplete core-shell nanostructures, represented by the symbol @. Additionally, strange details about the sheaths' topographies were observed, which included cracks, adhesions, and embedded nanoparticles. XRD and FTIR verified that the drugs tranexamic acid and fenoprofen presented in the nanofibers in an amorphous state, which resulted from the fine compatibility among the involved components. All the prepared samples were demonstrated to have a fine hydrophilic property and exhibited a lower water contact angle smaller than 40° in 300 ms. In vitro dissolution tests indicated that fenoprofen was released in a sustained manner over 6 h through a typical Fickian diffusion mechanism. Hemostatic tests verified that the intentional distribution of tranexamic acid on the shell sections was able to endow a rapid hemostatic effect within 60 s.

Background: Dilated cardiomyopathy (DCM) is the leading cause of heart failure with a poor prognosis. Recent studies suggest that endothelial to mesenchymal transition (EndMT) may be involved in the pathogenesis and cardiac remodeling during DCM development. EDIL3 (epidermal growth factor-like repeats and discoidin I-like domains 3) is an extracellular matrix glycoprotein that has been reported to promote EndMT in various diseases. However, the roles of EDIL3 in DCM still remain unclear., Methods and Results: A mouse model of DCM and human umbilical vein endothelial cells were used to explore the roles and mechanisms of EDIL3 in DCM. The results indicated that EndMT and EDIL3 were activated in DCM mice. EDIL3 deficiency attenuated cardiac dysfunction and remodeling in DCM mice. EDIL3 knockdown alleviated EndMT by inhibiting USP10 (ubiquitin specific peptidase 10) dependent Smad4 deubiquitination in vivo and in vitro. Recombinant human EDIL3 promoted EndMT via reinforcing deubiquitination of Smad4 in human umbilical vein endothelial cells treated with IL-1β (interleukin 1β) and TGF-β (transforming growth factor beta). Inhibiting USP10 abolished EndMT exacerbated by EDIL3. In addition, recombinant EDIL3 also aggravates doxorubicin-induced EndMT by promoting Smad4 deubiquitination in HUVECs., Conclusions: Taken together, these results indicate that EDIL3 deficiency attenuated EndMT by inhibiting USP10 dependent Smad4 deubiquitination in DCM mice.

Targeting cardiac remodeling is regarded as a key therapeutic strategy for heart failure. Kielin/chordin-like protein (KCP) is a secretory protein with 18 cysteine-rich domains and associated with kidney and liver fibrosis. However, the relationship between KCP and cardiac remodeling remains unclear. Here, we aimed to investigate the role of KCP in cardiac remodeling induced by pressure overload and explore its potential mechanisms. Left ventricular (LV) KCP expression was measured with real-time quantitative PCR, western blotting, and immunofluorescence staining in pressure overload-induced cardiac remodeling in mice. Cardiac function and remodeling were evaluated in wide-type (WT) mice and KCP knockout (KO) mice by echocardiography, which were further confirmed by histological analysis with hematoxylin and eosin and Masson staining. RNA sequence was performed with LV tissue from WT and KO mice to identify differentially expressed genes and related signaling pathways. Primary cardiac fibroblasts (CFs) were used to validate the regulatory role and potential mechanisms of KCP during fibrosis. KCP was down-regulated in the progression of cardiac remodeling induced by pressure overload, and was mainly expressed in fibroblasts. KCP deficiency significantly aggravated pressure overload-induced cardiac dysfunction and remodeling. RNA sequence revealed that the role of KCP deficiency in cardiac remodeling was associated with cell division, cell cycle, and P53 signaling pathway, while cyclin B1 (CCNB1) was the most significantly up-regulated gene. Further investigation in vivo and in vitro suggested that KCP deficiency promoted the proliferation of CFs via P53/P21/CCNB1 pathway. Taken together, these results suggested that KCP deficiency aggravates cardiac dysfunction and remodeling induced by pressure overload via P53/P21/CCNB1 signaling in mice., (© 2024 Federation of American Societies for Experimental Biology.)

Hypertensive vascular remodeling is defined as the changes in vascular function and structure induced by persistent hypertension. Maresin-1 (MaR1), one of metabolites from Omega-3 fatty acids, has been reported to promote inflammation resolution in several inflammatory diseases. This study aims to investigate the effect of MaR1 on hypertensive vascular remodeling. Here, we found serum MaR1 levels were reduced in hypertensive patients and was negatively correlated with systolic blood pressure (SBP). The treatment of MaR1 reduced the elevation of blood pressure and alleviated vascular remodeling in the angiotensin II (AngII)-infused mouse model. In addition, MaR1-treated vascular smooth muscle cells (VSMCs) exhibited reduced excessive proliferation, migration, and phenotype switching, as well as impaired pyroptosis. However, the knockout of the receptor of MaR1, leucine-rich repeat-containing G protein-coupled receptor 6 (LGR6), was seen to aggravate pathological vascular remodeling, which could not be reversed by additional MaR1 treatment. The mechanisms by which MaR1 regulates vascular remodeling through LGR6 involves the Ca 2+ /calmodulin-dependent protein kinase II/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling pathway. Overall, supplementing MaR1 may be a novel therapeutic strategy for the prevention and treatment of hypertension., Competing Interests: The authors declare that they have no conflict of interest., (© 2024 The Authors. MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.)

The proliferation, migration and phenotypic transformation of vascular smooth muscle cells contribute to vascular remodeling and hypertension. Resolvin D1 (RvD1) is a specialized pro-resolving lipid mediator that has been shown to have anti-inflammatory effects and can protect against different cardiovascular diseases. However, the role and mechanism of RvD1 in hypertension are not clear. The current study investigated the role of RvD1 in Ang II-induced hypertensive mice and Ang II-stimulated rat vascular smooth muscle cells. The results showed that RvD1 treatment significantly attenuated hypertension and vascular remodeling, as indicated by decreases in blood pressure, aortic media thickness and collagen deposition. In addition, RvD1 inhibited the proliferation, migration and phenotypic transformation of vascular smooth muscle cells (VSMCs) in vivo and in vitro . Notably, the protective effects of RvD1 were mediated by the Ras homolog gene family member A (RhoA)/mitogen-activated protein kinase (MAPK) signaling pathway. In conclusion, our findings demonstrated the potential benefits of RvD1 as a promising therapeutic agent in the treatment of vascular remodeling and hypertension., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Inflammation plays a critical role in the development of hypertension and vascular remodeling. Resolvin E1 (RvE1), as one of the specialized proresolving lipid mediators, promotes inflammation resolution by binding with a G protein-coupled receptor, ChemR23 (chemerin receptor 23). However, whether RvE1/ChemR23 regulates hypertension and vascular remodeling is unknown., Methods: Hypertension in mice was induced by Ang II (angiotensin II) infusion (750 ng/kg per minute), and RvE1 (2 µg/kg per day) was administered through intraperitoneal injection. Loss of ChemR23 was achieved by mice receiving intravenous injection of adeno-associated virus 9-encoding shRNA against ChemR23., Results: Aortic ChemR23 expression was increased in Ang II-induced hypertensive mice and that ChemR23 was mainly expressed on vascular smooth muscle cells (VSMCs). RvE1 lowered blood pressure, reduced aortic media thickness, attenuated aortic fibrosis, and mitigated VSMC phenotypic transformation and proliferation in hypertensive mice, which were all reversed by the knockdown of ChemR23. Moreover, RvE1 reduced the aortic infiltration of macrophages and T cells, which was also reversed by ChemR23 knockdown. RvE1 inhibited Ccl5 expression in VSMCs via the AMPKα (AMP-activated protein kinase α)/Nrf2 (nuclear factor E2-related factor 2)/canonical NF-κB (nuclear factor κB) pathway, thereby reducing the infiltration of macrophages and T cells. The AMPKα/Nrf2 pathway also mediated the effects of RvE1 on VSMC phenotypic transformation and proliferation. In patients with hypertension, the serum levels of RvE1 and other eicosapentaenoic acid-derived metabolites were significantly decreased., Conclusions: RvE1/ChemR23 ameliorated hypertension and vascular remodeling by activating AMPKα/Nrf2 signaling, which mediated immune cell infiltration by inhibiting the canonical NF-κB/Ccl5 pathway, and regulated VSMC proliferation and phenotypic transformation. RvE1/ChemR23 may be a potential therapeutic target for hypertension., Competing Interests: Disclosures None.

Background: Increased inflammation contributes to pressure overload-induced myocardial remodeling. 17(R)-Resolvin D1 (17(R)-RvD1), a potent lipid mediator derived from docosahexaenoic acid, possesses anti-inflammatory and pro-resolving properties. However, the association between 17(R)-RvD1 and pressure overload-induced cardiac hypertrophy remains unclear., Methods: Transverse aortic constriction (TAC) surgery was performed to establish a cardiac hypertrophy model. C57BL/6J mice were randomly assigned to the Sham, TAC and TAC+17(R)-RvD1 groups. 17(R)-RvD1 was injected (2 μg/kg, i.p.) before TAC surgery and once every other day after surgery for 4 weeks. The same volume of saline was injected into the mice in both Sham group and TAC group. Then, cardiac function was evaluated and heart tissues were collected for biological analysis., Results: 17(R)-RvD1 treatment attenuated TAC-induced increase in left ventricular diameter and decrease in left ventricular contractility, mitigated increased cardiomyocyte cross-sectional area, and downregulated the expression of hypertrophic genes. Besides, 17(R)-RvD1 attenuated myocardial fibrosis, as indicated by the decreased LV collagen volume and expression of fibrotic genes. In addition, 17(R)-RvD1 ameliorated the inflammatory response in cardiac tissue, as illustrated by the decreased infiltration of CD68 + macrophages and reduced production of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6. 17(R)-RvD1 treatment significantly suppressed the activation of NLRP3 inflammasome after TAC surgery, which might be responsible for the attenuation of inflammation in cardiac tissue., Conclusion: 17(R)-RvD1 attenuated pressure overload-induced cardiac hypertrophy and fibrosis, and the possible mechanism may be associated with the inhibition of NLRP3 inflammasome. 17(R)-RvD1 may serve as a potential drug for the treatment of cardiac hypertrophy., Competing Interests: The authors declare no conflict of interest in relation to this paper. Each author takes responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation., (© 2023 Wang et al.)

Background: Previous animal studies have suggested that air pollution (AP) exposure may be a potential risk factor for obesity; however, there is limited epidemiological evidence available to describe the association of obesity with AP exposure., Methods: A retrospective cross-sectional study was conducted on 11,766 participants across mainland China in 2015. Obesity was assessed using body mass index (BMI), waist circumference (WC), and visceral adiposity index (VAI). The space-time extremely randomized tree (STET) model was used to estimate the concentration of air pollutants, including SO 2 , NO 2 , O 3 , PM 1 , PM 2.5 , and PM 10 , matched to participants' residential addresses. Logistic regression models were employed to estimate the associations of obesity with outdoor AP exposure. Further stratified analysis was conducted to evaluate whether sociodemographics or lifestyles modified the effects., Results: Increased AP exposure was statistically associated with increased odds of obesity. The odds ratio (ORs) and 95% confidence interval (CI) of BMI-defined obesity were 1.21 (1.17, 1.26) for SO 2 , 1.33 (1.26, 1.40) for NO 2 , 1.15 (1.10, 1.21) for O 3 , 1.38 (1.29, 1.48) for PM 1 , 1.19 (1.15, 1.22) for PM 2.5 , and 1.11 (1.09, 1.13) for PM 10 per 10 μg/m 3 increase in concentration. Similar results were found for central obesity. Stratified analyses suggested that elderly participants experienced more adverse effects from all 6 air pollutants than middle-aged participants. Furthermore, notable multiplicative interactions were found between O 3 exposure and females as well as second-hand smokers in BMI-defined obesity., Conclusions: This study suggested that outdoor AP exposure had a significant association with the risk of obesity in the middle-aged and elderly Chinese population. Elderly individuals and women may be more vulnerable to AP exposure., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Pan, Wang, Hu, Lian, Cheng, Qin and Wan.)

Various doping concentrations of boron (B)-doped germanium nanocrystal (Ge NC) films were prepared using the plasma-enhanced chemical vapor deposition (PECVD) technique followed by thermal annealing treatment. The electronic properties of B-doped Ge NCs films combined with the microstructural characterization were investigated. It is worthwhile mentioning that the Hall mobilities [Formula: see text] of Ge NCs films were enhanced after B doping and reached to the maximum of 200 cm 2  V -1 , which could be ascribed to the reduction in surface defects states in the B-doped films. It is also important to highlight that the temperature-dependent mobilities [Formula: see text] exhibited different temperature dependence trends in the Ge NCs films before and after B doping. A comprehensive investigation was conducted to examine the distinct carrier transport properties in B-doped Ge NC films, and a detailed discussion was presented, focusing on the scattering mechanisms involved in the transport process., (© 2023. Springer Science+Business Media, LLC, part of Springer Nature.)

Cardiac dysfunction is a well-recognized complication of sepsis and seriously affects the prognosis of sepsis patients. IL-30 has been reported to exert anti-inflammatory effects in various diseases. However, the role of IL-30 in sepsis-induced myocardial dysfunction (SIMD) remains unclear. Here, we explored the protective role of IL-30 in cecum ligation and puncture (CLP)-induced SIMD mice. IL-30 expression increased in the cardiac tissues of septic mice and was mainly derived from macrophages. IL-30 deletion or neutralization aggravated sepsis-induced cardiac dysfunction and injury, whereas recombinant IL-30 treatment significantly ameliorated it. Mechanistically, IL-30 deficiency exerts pro-inflammatory effects by promoting Ly6C high macrophage polarization and pyroptosis. Inhibiting NLRP3 with MCC950 significantly reversed cardiac dysfunction, macrophage polarization and pyroptosis aggravated by IL-30 deficiency. Recombinant IL-30 inhibited pro-inflammatory macrophage polarization and pyroptosis in vivo and vitro. Taken together, these results suggest that IL-30 protects against SIMD by inhibiting pro-inflammatory macrophage polarization and pyroptosis., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

New engineering methods and advanced strategies are highly desired for creating novel drug sustained release nanomaterials. In this study, a trilayer concentric spinneret was explored to implement several multifluid electrospinning processes. A trilayer core-shell nanofiber was successfully fabricated, which comprise a drug-free polymeric coating and an inner drug gradient distribution, and then compared with bilayer core-shell and monolithic medicated nanofibers. All the electrospun nanofibers similarly consisted of two components (guest drug acetaminophen and host polymer cellulose acetate) and presented a linear morphology. Due to the secondary interactions within nanofibers, loaded drug with amorphous state was detected, as demonstrated by SEM, DSC, XRD, and FTIR determinations. In vitro and in vivo gavage treatments to rats tests were carried out, the trilayer nanofiber with an elaborate structure design were demonstrated to provide better drug sustained release profile than the bilayer core-shell nanofibers in term of initial burst release, later tail-off release and long sustained release time period. The synergistic mechanism for improving the drug sustained release behaviors is disclosed. By breaking the traditional concepts about the implementation of multifluid electrospinning and the strategy of combining surface properties and inner structural characteristics, the present protocols open a new way for developing material processing methods and generating novel functional nanomaterials., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background Sympathetic hyperactivity contributes to pathological remodeling after myocardial infarction (MI). However, the mechanisms underlying the increase in sympathetic activity remain unknown. Microglia are the predominant immune cells in the central nervous system and can regulate sympathetic neuron activity through neuroimmune response in the hypothalamic paraventricular nucleus. The present study aimed to investigate whether microglia-mediated neuroimmune response can regulate sympathetic activity and cardiac remodeling after MI. Methods and Results PLX3397 (pexidartinib) was used to deplete central microglia via intragastric injection or intracerebroventricular injection. After that, MI was induced by ligation of the left anterior descending coronary artery. Our study showed that MI resulted in the activation of microglia in the paraventricular nucleus. Microglia depletion, which was induced by PLX3397 treatment via intragastric injection or intracerebroventricular injection, improved cardiac function, reduced infarction size, and attenuated cardiomyocyte apoptosis, fibrosis, pathological electrical remodeling, and myocardial inflammation after MI. Mechanistically, these protective effects were associated with an attenuated neuroimmune response in the paraventricular nucleus, which contributed to the decrease of sympathetic activity and attenuation of sympathetic remodeling in the heart. However, intragastric injection with PLX3397 obviously depleted macrophages and induced neutrophil and T-lymphocyte disorders in the heart, blood, and spleen. Conclusions Microglia depletion in the central nervous system attenuates pathological cardiac remodeling after MI by inhibiting neuroimmune response and sympathetic activity. Intragastric administration of PLX3397 leads to serious deleterious effects in peripheral immune cells, especially macrophages, which should be a cause for concern in animal experiments and clinical practice.

Transient receptor potential ankyrin 1 (TRPA1) plays an important role in different cardiovascular diseases. However, the role of TRPA1 in dilated cardiomyopathy (DCM) remains unclear. Here, we aimed to investigate the role of TRPA1 in DCM induced by doxorubicin (DOX) and explore its possible mechanisms. GEO data were used to explore the expression of TRPA1 in DCM patients. DOX (2.5 mg/kg/week, 6 weeks, i.p.) was used to induce DCM. Bone marrow-derived macrophages (BMDMs) and neonatal rat cardiomyocytes (NRCMs) were isolated to explore the role of TRPA1 in macrophage polarization, cardiomyocyte apoptosis, and pyroptosis. In addition, DCM rats were treated with the TRPA1 activator, cinnamaldehyde to explore the possibility of clinical translation. TRPA1 expression was increased in left ventricular (LV) tissue in DCM patients and rats. TRPA1 deficiency aggravated the cardiac dysfunction, cardiac injury, and LV remodeling in DCM rats. In addition, TRPA1 deficiency promoted the M1 macrophage polarization, oxidative stress, cardiac apoptosis, and pyroptosis induced by DOX. RNA-seq results showed that TRPA1 knockout promoted the expression of S100A8, an inflammatory molecule that belongs to the family of Ca 2+ -binding S100 proteins, in DCM rats. Furthermore, S100A8 inhibition attenuated M1 macrophage polarization in BMDMs isolated from TRPA1 deficiency rats. Recombinant S100A8 promoted the apoptosis, pyroptosis, and oxidative stress in primary cardiomyocytes stimulated with DOX. Finally, TRPA1 activation via cinnamaldehyde alleviated the cardiac dysfunction and reduced S100A8 expression in DCM rats. Taken together, these results suggested that TRPA1 deficiency aggravates DCM by promoting S100A8 expression to induce M1 macrophage polarization and cardiac apoptosis., (© 2023 Federation of American Societies for Experimental Biology.)

Spinel cobalt oxide displays excellent photocatalytic performance, especially in solar driven water oxidation. However, the process of water reduction to hydrogen is considered as the Achilles' heel of solar water splitting over Co 3 O 4 owing to its low conduction band. Enhancement of the water splitting efficiency using Co 3 O 4 requires deeper insights of the carrier dynamics during water splitting process. Herein, the carrier dynamic kinetics of colloidal Co 3 O 4 quantum dots-Pt hetero-junctions is studied, which mimics the hydrogen reduction process during water splitting. It is showed that the quantum confinement effect induced by the small QD size raised the conduction band edge position of Co 3 O 4 QDs, so that the ligand-to-metal charge transfer from 2p state of oxygen to 3d state of Co 2+ occurs, which is necessary for overall water splitting and cannot be achieved in Co 3 O 4 bulk crystals. The findings in this work provide insights of the photocatalytic mechanism of Co 3 O 4 catalysts and benefit rational design of Co 3 O 4 -based photocatalytic systems., (© 2023 Wiley-VCH GmbH.)