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In the field of ultrafast magnetism, i.e., subpicosecond or femtosecond time scales, the dynamics of magnetization can be described by the inertial Landau-Lifhitz-Gilbert equation. In terms of this equation, the intrinsic characteristics is investigated in detail for the theoretical limit of the magnetization reversal field. We can find that there is a critical value for the inertia parameter τc , which is affected by the damping and anisotropy parameter of the system. When the inertial parameter factor τ < τc , the limit value of the magnetization reversal field under the ultrafast magnetic mechanism is less than that of the fast magnetic mechanism. When τ > τc , the limit value of the magnetization reversal field will be greater than the limit value under the fast magnetic mechanism. Moreover, it is important to point out that the limit value of the magnetization reversal field under the ultrafast magnetic mechanism decreases with the increasing inertial factor, as τ < τc /2, while increases with inertial factor τ as τ > τc /2. Finally, with the joint action of damping and anisotropy, compared with fast magnetism, we find that the limit value of the magnetization reversal field has rich variation characteristics, i.e., there is not only a linear and proportional relationship, but also an inverse relationship, which is very significant for the study of ultrafast magnetism.

Electron beam physical vapour deposition (EB-PVD) technology is a standard industrial method for the preparation of a thermal barrier coating (TBC) deposition on aeroengines. The internal stress of EB-PVD TBCs, including stress inside the top coating (TC) and thermal oxidation stress during long-term service is one of the key reasons for thermal barrier failures. However, research on the synergistic characterization of the internal stress of EB-PVD TBCs is still lacking. In this work, the stress inside the TC layer and the thermal oxidation stress of EB-PVD TBC during long-term thermal cycles were synergistically detected, combining Cr3+-PLPS and THz-TDS technologies. Based on a self-built THz-TDS system, stress-THz coefficients c1 and c2 of the EB-PVD TBC, which are the core parameters for stress characterization, were calibrated for the first time. According to experimental results, the evolution law of the internal stress of the TC layer was similar to that of the TGO stress, which were interrelated and influenced by each other. In addition, the internal stress of the TC layer was less than that of the TGO stress due to the columnar crystal microstructure of EB-PVD TBCs.

Spectrally uncorrelated bi-photon is an essential resource for achieving various quantum information processing protocols. We theoretically investigate the generation of spectrally uncorrelated bi-photon emitted by spontaneous four-wave mixing from a fiber nonlinear interferometer which consists of N stages nonlinear gain fiber and N-1 stages dispersion modulation fiber. The output bi-photon of nonlinear interference is the coherent superposition of various bi-photon born in each nonlinear fiber, and thus the interference fringe will reshape the bi-photon joint spectrum. As a result, resorting to Taylor expansion to first-order for phase mismatching, we theoretically verify that the orientation of phase matching contours will rotate in a specific way with only varying the length of dispersion modulation fiber. The rotation in orientation of phase matching contours may result in spectrally uncorrelated bi-photon and even arbitrary correlation bi-photon. Further, we choose micro/nanofiber as the nonlinear gain fiber and single-mode communication fiber as dispersion modulation fiber to numerically simulate the generation of spectrally uncorrelated bi-photon from spontaneous fourwave mixing. Here, due to significant frequency detuning (hundreds of THz), Raman background noise can be considerably suppressed, even at room temperature, and a largely tunable emitted photon wavelength can be achieved, indicating a practicability in many quantum fields. A photon mode purity of 97.2% will be theoretically attained without weakening the heralding nature of bi-photon source. We think the fiber nonlinear interference with the flexibly engineered quantum state can be an excellent practical source for quantum information processing.

Atherosclerosis (AS) is one of the principal causes of cardiovascular disorder. Reportedly, vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs) play key roles in AS development, and microRNAs (miRNAs) regulate their functions. The function of miR-216b-5p in AS remains unknown. Human VSMCs and human HUVECs were treated with ox-LDL to establish the in vitro model of AS. MiR-216b-5p and IGF2 expressions in VSMCs and HUVECs were probed by qRT-PCR and western blot. The viability, cell cycle progression, and apoptosis of VSMCs and HUVECs were evaluated by Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine, and flow cytometry assays, respectively. The binding sites between IGF2 3'UTR and miR-216b-5p were validated by dual-luciferase reporter assay. miR-216b-5p expression was declined in ox-LDL-induced VSMCs and HUVECs. In VSMCs, miR-216b-5p overexpression inhibited excessive proliferation and induced apoptosis. MiR-216b-5p could markedly restrain the viabiblity of VSMCs induced by ox-LDL and enhanced the viability of HUVECs. Additionally, IGF2 was confirmed as the direct target of miR-216b-5p and transfection of IGF2 overexpression plasmids rescued the effects of miR-216b-5p on VSMCs and HUVECs. miR-216b-5p alleviates the dysfunction of VSMCs and HUVECs caused by ox-LDL via repressing IGF2, and exerts protective functions to block the development of AS.

Cuboidal permanent magnets (PMs) are commonly used as elementary magnets for most magnetic systems that work by superposition of magnetic forces. This paper proposed a new method that combines the analytical model with the numerical calculation method to calculate the magnetic forces between two cuboidal PMs with parallel and perpendicular magnetization directions. The assumption was that the magnets were ideal with constant and homogeneous magnetizations. The method was also valid for other magnetization directions and any reference points in space, only needed to rotate the coordinate system and give corresponding distance expressions. An important result was that this method had the advantages of high accuracy and low computational cost, enabling rapid studies of the magnetic force characteristics related to magnet positions, geometric dimensions, and magnetic properties, which were easy to calculate by mathematical software, requiring very little running time. Meanwhile, the calculation results have been validated by comparison with the finite element simulation and experimental measurement. The effects of relative positions, dimensions, and magnetic properties on magnetic force characteristics between the two cuboidal PMs have been studied and discussed. Moreover, the improved magnetization distribution on the PM’s surface was made taking the PM’s relative permeability into account, and corresponding results have been given. These results indicated that the proposed method could help for a fast design and optimization of many PM devices that rely on magnetic forces, such as magnetic bearings, magnetic suspensions, magnetic actuators, etc.

Magnetic-based driving applications are receiving increasing attention. This study proposed a novel reciprocating permanent magnetic actuator (PMA) to manipulate magnetic micro robots to impact and clear blockages inside fluid pipes in a linear path. The PMA consisted of a cylindrical permanent magnet and a crank slider structure. A straight pipe with a circular cross-sectional area was located in front of the actuator to study the driving performance of PMA. A micro permanent magnet with a cylinder shape was employed as a working robot for manipulation inside the pipe. Firstly, analytical formulas were derived to obtain the magnetic driving force acting on the micro robot and determine the most suitable magnet configuration. The finite element simulation verified the analytical calculation. The developed reciprocating PMA prototype was then introduced, and the PMA and micro robot’s motion performance was analysed. Lastly, preliminary experiments were carried out for evaluating the micro robot’s motion characteristics. Performance tests for different excitation frequencies, flow rates, viscosities, and axial distances, indicating that PMA could manipulate the magnetic micro robot inside the pipe. The results confirmed that the developed PMA could effectively drive the micro robot with the advantage of consecutive magnetic driving. Especially, the micro robot featured good flexibility, rapid response, and a simple structure, suggesting that this micro robot may play an important role in industrial and medical applications, such as blockage elimination and thrombus clearance.

Pure-state single photons and large-bandwidth-correlation biphotons are fundamental resources for quantum information processing. The dispersion properties of micro/nanofiber (MNF) can be tailored by carefully choosing its diameter, resulting in a flexibly tailored biphoton spectrum. We theoretically investigate pure-state single photons and large-bandwidth-correlation biphotons produced by degenerate spontaneous four-wave mixing in MNF. In our simulation, a single-photon state with a purity of 99% will be theoretically attained by choosing the appropriate pump bandwidth and center wavelength with respect to the diameter and length of the MNF. Further, when an appropriate diameter with a negligible curvature at the zero dispersion wavelength is chosen, even a narrow pump bandwidth is capable of motivating remarkably broadband correlation biphotons, e.g., for a MNF diameter of 0.7 μm, the theoretical full width at half maximum is 473 nm. In practice, the application of a MNF-based quantum light source is dependent on the technologies that precisely control and measure the diameter. Our theoretical investigation will guide the experimental realization of high-quality quantum light sources based on MNF.

Sigma 1 receptor (S1R) has shown a preferable protective effect on left ventricular function, but whether it protects right ventricular (RV) function is still elusive.This study aimed to determine the effects of S1R on RV dysfunction secondary to pulmonary arterial hypertension.Sixty wild-type male Sprague-Dawley rats were randomly divided into the control group, the fluvoxamine group, the pulmonary arterial hypertension group and the pulmonary arterial hypertension combined with fluvoxamine group. Monocrotaline (60 mg/kg) was administered to induce pulmonary arterial hypertension, and fluvoxamine was given for 21 consecutive days to activate S1R after one week of monocrotaline administration. Echocardiographic, serologic, and histologic parameters, qRT-PCR, and western blotting were conducted after 4 weeks of monocrotaline administration.The expression of S1R was decreased in the right ventricle in pulmonary arterial hypertension. TAPSE, and the FAC of the right ventricle were significantly decreased, and RV EDP and the plasma concentration of N-terminal pro-B-type natriuretic peptide was increased in the pulmonary arterial hypertension group, but fluvoxamine partly restored those abnormalities (all P 0.05). Moreover, pulmonary arteriole remodeling, and fibrosis and hypertrophy in the RV were shown in the pulmonary arterial hypertension group; interestingly, fluvoxamine recovered RV structural remodeling (all P 0.05) but neither alleviated pulmonary arteriole remodeling nor reduced pulmonary artery pressure. Furthermore, S1R activation protects RV function by upgrading the NRF 2/HO 1-mediated antioxidant stress pathway. In conclusion, chronic S1R activation ameliorates structural remodeling and RV dysfunction secondary to pulmonary arterial hypertension without altering pulmonary artery pressure.

Due to environmental interference and defects in measured objects, measurement signals are frequently affected by unpredictable noise and periodic defects. Moreover, there is a lack of effective methods for accurately distinguishing defect components from measurement signals. In this study, a distribution-based selective optimisation method (SOM) is proposed to mitigate the effects of noise and defect components. The SOM can be seen as a binary- or multiple-class signal classifier based on an error distribution, which can simultaneously eliminate periodic defect components of measurement signals and proceed with signal-fitting regression. The effectiveness, accuracy, and feasibility of the SOM are verified in theoretical and realworld measurement settings. Based on theoretical simulations under various parameter conditions, some criteria for selecting operation variables among a selection of parameter conditions are explained in detail. The proposed method is capable of separating defect components from measurement signals while also achieving a satisfactory fitting curve for the measurement signals. The proposed SOM has broad application prospects in signal processing and defect detection for mechanical measurements, electronic filtering, instrumentation, part maintenance, and other fields.

The magnetic spring is a practical element to isolate external vibration to instruments in ultra-precision manufacturing and ultra-precision testing. Accurate magnetic force and stiffness models are necessary to analyze and optimize the design of magnetic spring isolators. Thus, this study proposes an accurate magnetic force and stiffness model to design and analyze a variable stiffness nonlinear magnetic spring (VSNMS) considering the permanent magnet’s (PM’s) relative permeability, positions, sizes, and magnetic properties. Firstly, the VSNMS’s structure is designed and introduced, and its magnetic force and stiffness models are derived. Secondly, the established model is validated by comparison with the numerical simulation. Thirdly, the VSNMS prototype is fabricated, and then tested through an electronic universal testing machine. The model has the advantage of high accuracy, high efficiency, and ease of use compared with numerical simulations and experimental tests. Furthermore, parametric studies are conducted to learn the effect of PMs’ sizes, positions, and magnetic properties on VSNMS’s magnetic force and stiffness characteristics. Finally, the optimized structural size parameters of VSNMS are obtained using the derived model and the interior-point algorithm. As a result, the established model contributes to the analysis and optimal design of VSNMS, supporting the design of magnetic spring isolators in ultra-precision applications.

Fatigue can cause cracks to propagate from the micro- to the macroscale, which results in a decrease of Young's modulus of the bone. Non-destructive measurements of bone fatigue damage are of great importance for bone quality assessment and fracture prevention. Unfortunately, there is still a lack of effective nondestructive methods sensitive to the initial deterioration during damage accumulation, particularly in the field of orthopedics and biomechanics. In this study, terahertz spectroscopy was adopted to evaluate microscale bone damage. Specifically, the refractive index and Young's modulus of bone samples subjected to different degrees of fatigue damage were tested at a fixed area. Both parameters are found to decrease in two stages under cycled fatigue loading, which is attributed to the initial onset and subsequent development of microdamage during fatigue loading. The change in refractive index reflects the accumulation of fatigue damage as well as the decrease in Young's modulus.

ObjectivesTo investigate the characteristics of new-onset atrial fibrillation (AF) and its impact on prognosis in acute pulmonary embolism (aPE).DesignA retrospective cohort studySettingThe study cohort included patients diagnosed with aPE who were admitted to the Renmin Hospital of Wuhan University from January 2017 to January 2019.ParticipantsPatients were ≥18 years of age and hospitalised for aPE.Outcome measuresAF was diagnosed based on an ECG recording or a Holter monitor during hospitalisation. aPE was diagnosed by CT pulmonary angiography. The prescription was determined from the discharge medication list. All-cause mortality was observed after 6-month follow-up. The logistic regression model and Cox proportional hazards model were used to study the risk factor of the new-onset AF and the predictor of all-cause mortality, respectively.ResultsA total of 590 patients with aPE were enrolled, 23 (3.9%) in the new-onset paroxysmal AF group, 31 (5.3%) in the new-onset persistent AF group and 536 (90.8%) in the sinus rhythm (SR) group. The incidence of the new-onset AF was 9.2% (54/590). A significant difference in age, heart rate, cardiac troponin I ultra, amino-terminal pro-brain natriuretic peptide, D-dimer, left atrial diameter, left ventricular ejection fraction, pulmonary infection, venous thromboembolism, congestive heart failure, chronic cor pulmonale and ischaemic heart disease was found among the three groups (pConclusionsMassive PE, ischaemic heart disease and congestive heart failure are high-risk factors which were related to new-onset AF in aPE. New-onset persistent AF was an independent predictor for 6-month all-cause mortality in PE patients.

Alterations to the bone structure from cycle loadings can undermine its damage resistance at multiple scales. The accumulation of fatigue damage in a bone is commonly characterized by the reduction in the elastic modulus. In this study, nano-indentation was used for investigating microscopic damage evolution of bovine tibia samples subjected to fatigue loading. Indentation tests were conducted in the same 60 μm × 120 μm area with different degrees of damage, including fracture, and the evolution of reduced modulus was observed. The results showed that bone’s reduced modulus decreased significantly during the initial 40% of the life fraction, whereas it proceeded slowly during the remaining period. As the size of the residual indentations was about 4 μm in length, the degradation of bone’s reduced modulus reflected the accumulation of fatigue damage at smaller scales.

Background Oxidative stress is an important factor involved in the progress of heart failure. The current study was performed to investigate whether pinocembrin was able to ameliorate post-infarct heart failure (PIHF) and the underlying mechanisms. Methods Rats were carried out left anterior descending artery ligation to induce myocardial infarction and subsequently raised for 6 weeks to produce chronic heart failure. Then pinocembrin was administrated every other day for 2 weeks. The effects were evaluated by echocardiography, western blot, Masson’s staining, biochemical examinations, immunohistochemistry, and fluorescence. In vitro we also cultured H9c2 cardiomyocytes and cardiac myofibroblasts to further testify the mechanisms. Results We found that PIHF-induced deteriorations of cardiac functions were significantly ameliorated by administrating pinocembrin. In addition, the pinocembrin treatment also attenuated collagen deposition and augmented vascular endothelial growth factor receptor 2 in infarct border zone along with an attenuated apoptosis, which were related to an amelioration of oxidative stress evidenced by reduction of reactive oxygen species (ROS) in heart tissue and malondialdehyde (MDA) in serum, and increase of superoxide dismutase (SOD). This were accompanied by upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) pathway. In vitro experiments we found that specific Nrf2 inhibitor significantly reversed the effects resulted from pinocembrin including antioxidant, anti-apoptosis, anti-fibrosis and neovascularization, which further indicated the amelioration of PIHF by pinocembrin was in a Nrf2/HO-1 pathway-dependent manner. Conclusion Pinocembrin ameliorated cardiac functions and remodeling resulted from PIHF by ROS scavenging and Nrf2/HO-1 pathway activation which further attenuated collagen fibers deposition and apoptosis, and facilitated angiogenesis.

It has been reported that patients with major depressive disorder (MDD) are prone to developing ventricular arrhythmias. Moreover, the Sigma-1 receptor not only plays a crucial role in MDD but has also been shown to have antiarrhythmic properties. The Sigma-1 receptor is a common receptor related to depression and ventricular arrhythmias. We analyzed the effects of the Sigma-1 receptor on depression and ventricular repolarization-related ion remodeling in MDD rats. MDD was induced in rats by chronic unpredictable mild stress (CUMS), and 28 days later, the rats were subjected to behavior tests. Protein expression was measured by western blotting, and cardiac morphological changes were observed by Masson staining. Electrophysiological measurement of the myocardium was performed with the whole-cell patch-clamp technique. Compared with the control rats, the MDD rats exhibited lower transient outward potassium current (Ito) and L-type calcium current (ICa-L) amplitudes. On the other hand, a trend of depolarization of Ito and hyperpolarization of ICa-L was observed in the MDD rats. Thus, we investigated the effect of fluvoxamine, a Sigma-1 receptor agonist, on Ito and ICa-L. Fluvoxamine enhanced Ito and altered its current kinetics, as shown by acceleration of activation and recovery from inactivation. In contrast, fluvoxamine inhibited the Ca2+ by hyperpolarizing the steady-state activation of ICa-L. All these effects were blocked by BD1047. Taken together, our results indicate that Sigma-1 receptor modulates the functions of Ito and ICa-L to possibly exert antiarrhythmic effects.

High levels of circulating catecholamines are related to raise risk of cardiac arrhythmias. In addition, our recent studies have suggested that pinocembrin could decrease the susceptibility to arrhythmias in several rat models, including chronic ischemic heart failure, myocardial infarction and depression. In this research, the effects of pinocembrin on ventricular fibrillation (VF) susceptibility were investigated in rats treated with isoproterenol (ISO) and further explored the possible mechanism.Cardiac remodeling was induced by intraperitoneally injection ISO (5 mg/kg) 7 days. Simultaneously, Rats were received pinocembrin (5 mg/kg) or saline by tail vein injection. The effects of pinocembrin were evaluated by electrocardiogram parameters, ventricular electrophysiological parameters, echocardiographic, western blot, ventricular histology, biochemical examinations. In vitro, we cultured H9C2 cardiomyocytes to further define the mechanisms.Compared with ISO group, pinocembrin remarkably decreased VF inducibility rate, attenuated the shortening of QT and corrected QT (QTc) interval, action potential duration (APD), ventricular effective refractory period (ERP), and increased the protein levels of Kv4.2 and Kv4.3 and Cav1.2 and decreased phosphorylated CaOur data demonstrate that pinocembrin decreases ventricular electrical remodeling, ion remodeling, ventricular fibrosis, hypertrophy and suppresses isoproterenol-induced oxidative stress. The findings shown that pinocembrin mediates antiarrhythmic effects in rats with isoproterenol-induced cardiac remodeling related to Nrf2/HO-1 pathway.

Background MicroRNAs (miRNAs) have been identified as important participants in the development of atherosclerosis (AS). The present study explored the role of miR-128-3p in the dysfunction of vascular smooth muscle cells (VSMCs) and the underlying mechanism. Methods Human VSMCs and ApoE knockout (ApoE−/−) C57BL/6J mice were used to establish AS cell and animal models, respectively. Expression levels of miR-128-3p, forkhead box O4 (FOXO4) and matrix metallopeptidase 9 (MMP9) were detected using qRT-PCR and Western blot, respectively. CCK-8, BrdU, and Transwell assays as well as flow cytometry analysis were performed to detect the proliferation, migration and apoptosis of VSMCs. Levels of inflammatory cytokines and lipids in human VSMCs, mice serum and mice VSMCs were also determined. The binding site between miR-128-3p and 3′UTR of FOXO4 was confirmed using luciferase reporter gene assay. Results MiR-128-3p was found to be decreased in AS patient serum, ox-LDL-treated VSMCs, AS mice serum and VSMCs of AS mice. Transfection of miR-128-3p mimics suppressed the proliferation and migration of VSMCs, accompanied by the promoted apoptosis and the decreased levels of inflammatory cytokines. Further experiments confirmed the interaction between miR-128-3p and FOXO4. Augmentation of FOXO4 or MMP9 reversed the effects of miR-128-3p. Besides, miR-128-3p inhibited triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) but increased high-density lipoprotein cholesterol (HDL-C) in the serum of AS mice. Conclusion MiR-128-3p repressed the proliferation and migration of VSMCs through inhibiting the expressions of FOXO4 and MMP9.

Background: Upright T wave in lead aVR (TaVR) has recently been reported to be associated with cardiovascular death and mortality in general population and in patients with prior cardiovascular disease (CVD). However, the evidence for the predictive ability of TaVR in patients with ischemic stroke (IS) is lacking. Methods: A total of 625 consecutive patients with IS (mean age: 66 ± 12 years; 379 male) were enrolled in this study between January 2013 and December 2014. Patients were divided into upright TaVR (≥0 mV; n = 201) and negative TaVR ( 450 ms, higher rate of negative T in lead II, higher rate of negative T in lead V6, higher rate of ST depression, and longer QTc duration. During the mean follow-up period of 20.0 ± 5.8 months, 29 (4.6%) patients experienced all-cause death and 12 (1.9%) patients experienced cardiovascular death, the primary end point. Concomitantly, 94 (15%) patients experienced recurrence of IS, the secondary end point. After adjusting for clinical covariates, upright TaVR was independently associated with all-cause death [hazard ratio (HR): 2.88, 95% confidence intervals (CI): 1.07-7.73], cardiovascular death (HR: 3.04, 95% CI: 1.07-8.64), and IS recurrence (HR: 1.86, 95% CI: 1.08-3.20). Conclusions: Upright TaVR in patients with IS is associated with increased mortality and recurrence of IS. Key words: T wave in lead aVR; Ischemic stroke; Prognosis

Mg/Al dissimilar joints with favourable static and dynamic mechanical properties were obtained utilising ultrasonic spot welding and ultrasonic spot weld bonding technology. The fatigue behaviour, ...

Aim Recent studies have shown that, with its excellent anti-inflammatory and antioxidant effects, pinocembrin can reduce the occurrence of arrhythmia in myocardial infarction rats. However, whether it can alleviate lipopolysaccharide (LPS)-induced myocardial injury in rats has not been reported. Therefore, the purpose of this study was to investigate whether pinocembrin could alleviate myocardial injury and arrhythmia in rats with sepsis. Materials and methods Rats were intraperitoneally injected with LPS to simulate animal sepsis, and the caudal vein was injected with pinocembrin or normal saline for intervention. Transthoracic echocardiography, inflammatory factors, electrophysiological recording, histological analysis, and western-blot analysis were performed. Key findings Compared with the control group, the rats in the LPS group had myocardial injury and cardiac dysfunction, and the incidence of ventricular arrhythmia increased. In addition, LPS resulted in the increase of p-c-Jun N-terminal kinase (JNK), p-p38 proteins in the myocardium, the levels of inflammatory factors in the blood and the apoptosis rate of left ventricular cardiomyocytes. And all these adverse effects were eliminated, thus confirming that pinocembrin has an excellent protective effect on the heart. Significance Reducing the inflammatory response and cell apoptosis by inhibiting p38/JNK mitogen-activated protein kinase (MAPK) signaling pathway, pinocembrin can alleviate myocardial injury, cardiac dysfunction, and ventricular arrhythmia induced by LPS.

Objective: Previous studies of ambient air pollutants and ventricular arrhythmias in patients with implantable cardioverter-defibrillator (ICD) have yielded mixed results, and the association between air pollution and ventricular arrhythmias in these patients remains unclear. This study aimed to assess and quantify the association between exposure to major air pollutants [CO, inhalable particles (PM10), SO2, fine particulate matter (PM2.5), O3, and NO2] and the presence of ventricular arrhythmia in patients with ICD. Methods: The Medline, PubMed, Web of Science, Global Health Library, Virtual Health Library, Population Information Online (POPLINE), and New York Academy of Medicine Grey Literature Report databases were searched to identify studies analyzing the association between ventricular arrhythmias in patients with ICD and the abovementioned main air pollutants. Pooled estimates were generated using a random-effects model or fixed-effects model, according to the value of heterogeneity. Heterogeneity within studies was assessed using Cochran's Q and I2 statistics. Funnel plots, Egger's regression test, and Begg's rank correlation method were used to evaluate publication bias. Sensitivity analyses were also conducted to evaluate the potential sources of heterogeneity. Results: After a detailed screening of 167 studies, seven separate studies were identified. Ventricular arrhythmias in patients with ICD were found to be positively, but not significantly, associated with CO, PM10, SO2, PM2.5, and NO2, with a pooled estimate [odds ratio (OR) associated with each 10 μg/m3 increase in pollutant concentration, except for CO, which was associated with each 1 mg/m3 increase in concentration] of 1.03 [95% confidence interval (CI): 0.92-1.17, P = 0.59] for CO, 1.01 (95%CI: 0.97-1.05, P = 0.55) for PM10, 1.09 (95%CI: 0.95-1.24, P = 0.22) for SO2, 1.07 (95%CI: 0.95-1.21, P = 0.25) for PM2.5, and 1.06 (95%CI: 0.98-1.14, P = 0.16) for NO2. No increased risk of ventricular arrhythmias in patients with ICD was found to be associated with O3 (OR = 1.00; 95%CI: 0.98-1.01, P = 0.56). Conclusions: The results of this study provide little evidence that ambient air pollutants affect the risk of ICD discharges for treating ventricular arrhythmias. Key words: Air pollutants; Ventricular arrhythmia; Implantable cardioverter-defibrillator; Systematic review

Major depression is an important clinical factor in ventricular arrhythmia. Patients diagnosed with major depression overexpress N-methyl-d-aspartate receptors (NMDARs). Previous studies found that chronic NMDAR activation increases susceptibility to ventricular arrhythmias. We aimed to explore the mechanisms by which NMDAR activation may increase susceptibility to ventricular arrhythmias. Male rats were randomly assigned to either normal environments as control (CTL) group or 4 wk of chronic mild stress (CMS) to produce a major depression disorder (MDD) model group. After 4 wk of CMS, depression-like behaviors were measured in both groups. Varying doses (1–100 μM) of NMDA and 10 μM NMDA antagonist (MK-801) were perfused through ventricular myocytes isolated from MDD rats to measure the L-type calcium current ( ICa-L) and transient outward potassium current ( Ito). Structural remodeling was assessed using serial histopathology including Masson’s trichrome dye. Electrophysiological characteristics were evaluated using Langendorff perfusion. Depression-like behaviors were observed in MDD rats. MDD rats showed longer action potential durations at 90% repolarization and higher susceptibility to ventricular arrhythmias than CTL rats. MDD rats showed lower ICa-L and Ito current densities than CTL rats. Additionally, NMDA reduced both currents in a concentration-dependent manner, whereas there was no significant impact on the currents when perfused with MK-801. MDD rats exhibited significantly more fibrosis areas in heart tissue and reduced expression of Kv4.2, Kv4.3, and Cav1.2. We observed that acute NMDAR activation led to downregulation of potassium and L-type calcium currents in a rat model of depression, which may be the mechanism underlying ventricular arrhythmia promotion by depression.

This study aimed to evaluate the effects of the sigma-1 receptor (S1R) on atrial fibrillation (AF) susceptibility in rats.Rats were randomly assigned into three groups for intraperitoneal treatment with saline (CTL group), BD1047 (an antagonist of the S1R, BD group) or BD1047 plus fluvoxamine (an agonist of the S1R, BD + F group) for 4 weeks. The heart rate variability (HRV) and atrial electrophysiological parameters were measured via the PowerLab system and analyzed by LabChart 8.0 software. Atrial histology was determined with Masson staining. The protein levels of connexin (Cx) 40, Cav1.2, S1R, eNOS, p-eNOS, and p-AKT were detected by western blot assays.Our results showed that BD1047 significantly shortened the atrial effective refractory period (ERP) and action potential duration (APD), increased AF inducibility and duration, augmented sympathetic activity, depressed parasympathetic activity, and reduced heart rate variability (HRV) compared with the CTL group. Masson staining also showed a significant increase in atrial fibrosis in the BD group. Furthermore, the expressions of S1R, Cx40, Cav1.2, p-eNOS, and p-AKT were dramatically reduced in the BD group compared with the CTL group (all P 0.01). However, fluvoxamine administration mitigated most of the abovementioned alterations.Our findings indicated that S1R inhibition contributed to atrial electrical remodeling, cardiac autonomic remodeling and atrial fibrosis, which could be attenuated by fluvoxamine, thus providing new insights into the relationship between the S1R and AF.

The unique photoelectric properties of phosphorene typically include anisotropy, hence the nondestructive and rapid identification of its crystal orientation is a key point to the investigation and application of phosphorene. Currently, the orientation identification by analyzing the Ag1 mode based on parallel-polarized Raman has severe requirements for the applicable Raman system. Therefore, it is necessary to develop a more general, convenient, and accurate method for determining the crystal orientation of phosphorene. In this paper, a method of orientation identification was proposed by using a Raman system without an analyzer and quantifying the correlation between the intensities of Ag1 and Ag2 modes with the change of the incident polarization direction. By using mechanically peeled phosphorene as specimens, Raman measurements were carried out under the Raman configurations of both parallel polarization and with no analyzer. The results show that the crystal orientation of phosphorene can be accurately identified by quantifying the Raman intensities of both Ag1 and Ag2 modes using the Raman system without an analyzer.

Myofibroblast transdifferentiation is an important feature of cardiac fibrosis. Previous studies have indicated that microRNA‑216a (miR‑216a) is upregulated in response to transforming growth factor‑β (TGF‑β) in kidney cells and can activate Smad3; however, its role in myofibroblast transdifferentiation remains unclear. The present study aimed to investigate the role of miR‑216a in TGF‑β‑induced myofibroblast transdifferentiation, and to determine the underlying mechanisms. Adult mouse cardiac fibroblasts were treated with TGF‑β to induce myofibroblast transdifferentiation. An antagomir and agomir of miR‑216a were used to inhibit or overexpress miR‑216a in cardiac fibroblasts, respectively. Myofibroblast transdifferentiation was evaluated based on the levels of fibrotic markers and α‑smooth muscle actin expression. The miR‑216a antagomir attenuated, whereas the miR‑216a agomir promoted TGF‑β‑induced myofibroblast transdifferentiation. Mechanistically, miR‑216a accelerated myofibroblast transdifferentiation via the AKT/glycogen synthase kinase 3β signaling pathway, independent of the canonical Smad3 pathway. In addition, it was observed that miR‑216a activated AKT via the downregulation of PTEN. In conclusion, miR‑216a was involved in the regulation of TGF‑β‑induced myofibroblast transdifferentiation, suggesting that targeting miR‑216a may aid in developing effective interventions for the treatment of cardiac fibrosis.

The present study aimed to assess the effect of sigma-1 receptor (S1R) stimulation on ventricular remodeling and susceptibility to ventricular arrhythmias (VAs) after myocardial infarction (MI) in rats. Wild-type male rats were placed into one of the following four treatment groups. For four weeks, animals in the Sham group and MI group received intraperitoneal (i.p.) injections of 0.9% saline (1 ml/kg/day); those in the MI + F group received fluvoxamine (FLV) (0.3 mg/kg/day); and those in the MI + F + BD group received FLV plus BD1047 (0.3 mg/kg/day). After that, the ventricular electrophysiological parameters were measured via the langendorff system. Ventricular fibrosis quantification was determined with Masson staining. Cardiac function was evaluated by echocardiography. The protein levels of S1R, connexin (Cx)43, Cav1.2, Kv4.2, Kv4.3, tyrosine hydroxylase (TH), nerve growth factor (NGF), growth-associated protein 43 (GAP43) were detected by Western blot assays. Our results indicated that fluvoxamine significantly prolonged the ventricular effective refractory period (ERP), shortened action potential duration (APD), reduced susceptibility to VAs after MI. Masson staining showed a decrease in ventricular fibrosis in the MI + F group. Furthermore, the contents of Cx43, S1R, Cav1.2, Kv4.2, Kv4.3 were increased in the MI + F group compared with the MI group (all P 0.05). The contents of TH, NGF, GAP43 were reduced in the MI + F group compared with the MI group. (all P 0.05). However, BD1047 reduces all of these effects of FLV. The results suggest that S1R stimulation reduces susceptibility to VAs and improves cardiac function by improving myocardial fibrosis, lightning sympathetic remodeling, electrical remodeling, gap junction remodeling and upregulating S1R content.

Aim The purpose of the study was to investigate what effects the sigma-1 receptor (S1R) could exert on the cardiac myocyte ion channels in a rodent model of depression and to explore the underlying mechanisms since depression is an independent risk factor for cardiovascular diseases including ventricular arrhythmias (VAs). Materials and methods To establish the depression model in rats, chronic mild unpredictable stress (CMUS) for 28 days was used. The S1R agonist fluvoxamine was injected intraperitoneally from the second week to the last week for 21 days in total, and the effects were evaluated by patch clamp, western blot analysis, and Masson staining. Key findings We demonstrated that depression was improved after treatment with fluvoxamine. In addition, the prolongation of the corrected QT (QTc) interval under CMUS that increased vulnerability to VAs was significantly attenuated by stimulation of S1R due to the decreased amplitude of L-type calcium current (ICa-L) and the restoration of reduced transient outward potassium current (Ito) resulting from CMUS induction. The S1R also decelerated Ito inactivation and accelerated Ito recovery by activating Ca2+/calmodulin-dependent kinase II. Moreover, the stimulation of S1R ameliorated the structural remodeling as the substrate for maintenance of VAs. All these effects were abolished by the administration of S1R antagonist BD1047, which verified the roles for S1R. Significance Activation of S1R could decrease the vulnerability to VAs by inhibiting ICa-L and restoring Ito, in addition to ameliorating the CMUS-induced depressive symptoms and structural remodeling.

The present study aimed to assess the effect of sigma-1 receptor (S1R) stimulation on autonomic nerve dysfunction and susceptibility to atrial fibrillation (AF) in a rat depression model. Male rats were randomly divided into one of the following four treatment groups: saline [control (CTL)]; saline + intragastric administration of SA4503, an agonist of S1R (CTS); chronic unpredictable mild stress (CUMS) to produce depression (MDD); and CUMS + intragastric administration of SA4503 (MDS). Depression-like behaviors, such as reduced sucrose preference, decreased body weight gain, and increased immobility time during forced swimming, improved in the MDS group after 4 wk of SA4503 treatment. Compared with rats in the CTL group, rats in the MDD group showed significantly augmented sympathetic activity, reduced parasympathetic activity, decreased heart rate variability, and lowered S1R expression in the atrium and hippocampus (all P < 0.01). However, rats in the MDS group showed mitigated aforementioned alterations and improved electrical remodeling compared with rats in the MDD group (all P < 0.01). Furthermore, rats in the MDS group showed shortened activation latencies, increased effective refractory periods, and lowered frequency of AF incidence duration and fibrosis compared with rats in the MDD group (all P < 0.01). The results indicate that S1R stimulation reduces sympathetic activity and susceptibility to AF by improving depressive behaviors, modulating cardiac autonomic nerve balance, lightening nerve remodeling, and upregulating S1R and ion channel protein expression. NEW & NOTEWORTHY Chronic stimulation of the sigma-1 receptor (S1R) ameliorates depression-induced autonomic nerve dysfunction by modulating the imbalance between overactivated sympathetic activity and decreased vagal activity. Chronic S1R stimulation alleviates atrial electrical remodeling, fibrosis, and susceptibility to atrial fibrillation (AF). The S1R agonist may target the underlying mechanisms related to AF occurrence. The results indicate that the S1R could be a potential clinical target for atrial arrhythmia, especially when it is combined with major depressive disorders.