First-principles study on the effect of torsional deformation on WSe2 as an anode material for calcium ion batteries.

CONTEXT: In this paper, the effects of torsional deformation on the electronic properties of intrinsic WSe2 system and Ca-adsorbed WSe2 system were systematically studied by first-principles method. The results show that Ca can be stably adsorbed on the vacancy (H site) of WSe2 surface in all deformation systems, and the adsorption energy of the system without deformation is the highest. Intrinsic WSe2 is a semiconductor with a direct band gap of 1.53 eV. The torsional deformation makes WSe2 change from a direct band gap semiconductor to an indirect band gap semiconductor and finally to a metal property. The adsorption of Ca makes the conduction band of WSe2 move down and increases the number of peaks in the conduction band region. The new density of state peaks are mainly derived from the contribution of W-d, Se-p, and d orbitals of adsorbed atoms in each adsorption system. Mulliken charge analysis shows that Ca transfers most of the valence electrons to the substrate, and the torsional deformation changes the amount of transferred charge. The twist deformation reduces the diffusion barrier of Ca on WSe2 surface from 0.20 to 0.14 eV. The above results provide a basis for the improved application of WSe2 in ion batteries. METHODS: In this study, all the first-principles calculations are based on Materials Studio 8.0 software package. The generalized gradient approximation (GGA) functional Perdew-Burke-Ernzerhof (PBE) is used for the electron exchange correlation interactions in all systems. The optimization algorithm uses Broyden-Fletcher-Goldfarb-Shanno (BFGS) to optimize the model structure and calculate the energy. The measured cutoff energy is optimized to 450 eV, and the radius of the vacuum layer in the Z-axis direction is 20 Å. The K-point of 7 × 7 × 1 is selected by Monkhorst-Pack method. The structural optimization criterion is selected, the convergence radius of the force is 0.01 eV/Å, and the displacement radius between atoms is within 0.001 Å distance. The energy convergence radius of each atom is less than 1.0 × 10-6 eV/atom.

lncRNA Oip5-as1 inhibits excessive mitochondrial fission in myocardial ischemia/reperfusion injury by modulating DRP1 phosphorylation.

BACKGROUND: Aberrant mitochondrial fission, a critical pathological event underlying myocardial ischemia/reperfusion (MI/R) injury, has emerged as a potential therapeutic target. The long non-coding RNA (lncRNA) Oip5-as1 is increasingly recognized for its regulatory roles, particularly in MI/R injury. However, its precise mechanistic role in modulating mitochondrial dynamics remains elusive. This study aims to elucidate the mechanistic role of Oip5-as1 in regulating mitochondrial fission and evaluate its therapeutic potential against MI/R injury. METHODS: To simulate in vitro MI/R injury, HL-1 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R). Lentiviral vectors were employed to achieve overexpression or knockdown of Oip5-as1 in HL-1 cells by expressing Oip5-as1 or shRNA targeting Oip5-as1, respectively. The impact of Oip5-as1 on mitochondrial dynamics in HL-1 cells was assessed using CCK-8 assay, flow cytometry, immunofluorescence staining, and biochemical assays. MI/R injury was induced in mice by ligating the left anterior descending coronary artery. Conditional knockout mice for Oip5-as1 were generated using the CRISPR/Cas9 genome editing technology, while overexpression of Oip5-as1 in mice was achieved via intramyocardial administration of AAV9 vectors. In mice, the role of Oip5-as1 was evaluated through echocardiographic assessment, histopathological staining, and transmission electron microscopy. Furthermore, Western blotting, RNA pull-down, RNA immunoprecipitation, and co-immunoprecipitation assays were conducted to investigate Oip5-as1's underlying mechanisms. RESULTS: The expression levels of Oip5-as1 are significantly decreased in MI/R-injured HL-1 cells and myocardium. In HL-1 cells undergoing H/R injury, overexpression of Oip5-as1 attenuated excessive mitochondrial fission, preserved mitochondrial functionality, and reduced cellular apoptosis, while knockdown of Oip5-as1 exhibited the opposite effects. Furthermore, in a mouse model of MI/R injury, overexpression of Oip5-as1 diminished mitochondrial fission, myocardial infarct size and improved cardiac function. However, knockout of Oip5-as1 exacerbated myocardial injury and cardiac dysfunction, which were significantly reversed by treatment with a mitochondrial division inhibitor-1 (Mdivi-1). Mechanistically, Oip5-as1 selectively interacts with AKAP1 and CaN proteins, inhibiting CaN activation and subsequent DRP1 dephosphorylation at Ser637, thereby constraining DRP1's translocation to the mitochondria and its involvement in mitochondrial fission. CONCLUSIONS: Our study underscores the pivotal role of Oip5-as1 in mitigating excessive mitochondrial fission during MI/R injury. The findings not only enhance our comprehension of the molecular mechanisms underlying MI/R injury but also identify Oip5-as1 as a potential therapeutic target for ameliorating MI/R injury.

Unexplained Left Ventricular Hypertrophy Diagnosed as a Cardiac Variant of Late-Onset Fabry Disease: A Case Report.

The cardiac variant of Fabry disease (FD) has high rates of missed diagnosis and misdiagnosis due to the lack of systemic symptoms. Here, we report a case of a 68-year-old female with delayed-onset FD presenting as concentric left ventricular hypertrophy (LVH) with right bundle branch block, atrial fibrillation, and diastolic dysfunction, which was first presented with coronary artery spasm. Early cardiac-specific signs are crucial for diagnosing this disease due to the lack of extracardiac indications and the late onset of symptoms. This case raises a new red flag that patients with unexplained LVH and its atypical electrocardiographic (ECG) manifestations accompanied by diastolic dysfunction should be considered for FD. We also recommend further refinement of examinations associated with Fabry disease, which will contribute to the early diagnosis and treatment of the disease.

Highly Effective Hybrid Copper(I) Iodide Cluster Emitter with Negative Thermal Quenched Phosphorescence for X-Ray Imaging.

The low efficiency triplet emission of hybrid copper(I) iodide clusters is a critical obstacle to their further practical optoelectronic application. Herein, we present an efficient hybrid copper(I) iodide cluster emitter (DBA)4 Cu4 I4 , where the cooperation of excited state structure reorganization and the metallophilicity interaction enables ultra-bright triplet yellow-orange emission with a photoluminescence quantum yield over 94.9 %, and the phonon-assisted de-trapping process of exciton induces the negative thermal quenching effect at 80-300 K. We also investigate the potential of this emitter for X-ray imaging. The (DBA)4 Cu4 I4 wafer demonstrates a light yield higher than 104  photons MeV-1 and a high spatial resolution of ≈5.0 lp mm-1 , showing great potential in practical X-ray imaging applications. Our new copper(I) iodide cluster emitter can serve as a model for investigating the thermodynamic mechanism of photoluminescence in hybrid copper(I) halide phosphorescence materials.

Insights into research on myocardial ischemia/reperfusion injury from 2012 to 2021: a bibliometric analysis.

BACKGROUND: Numerous studies on myocardial ischemia/reperfusion (MI/R) injury have been undertaken in recent years. Hotspots and developmental trends in MI/R research are being rapidly updated. However, there has been no bibliometric analysis that systematically evaluates existing literature on MI/R injury. Our study explores developments in MI/R research over the past decade, and provides a reference for future research. MATERIALS AND METHODS: Both experimental and clinical publications on MI/R injury from 2012 to 2021 were retrieved from the Web of Science Core Collection database. The CiteSpace and VOSviewer tools were used to perform a bibliometric analysis. RESULTS: A total of 8419 papers were analyzed. The number of annual publications demonstrated an overall upward trend, rising from 629 publications in 2012 to 1024 publications in 2021. China, the USA, Germany, England, and Italy were the top five contributors to MI/R studies. The Fourth Military Medical University in China contributed the most publications (188, 2.23%), while the University College London in England cooperated the most with relevant research institutions. Derek J Hausenloy (University College London), Derek M Yellon (University College London), and Gerd Heusch (University of Essen Medical School) were the top three most active and influential scholars according to the H-index. Among the top 10 journals with the most publications, Basic Research in Cardiology had the highest impact factors. The top three co-cited journals were Circulation, Circulation Research, and Cardiovascular Research. According to a co-cited reference analysis, MI/R research can be divided across 10 major subfields of mitophagy, cardioprotection, inflammation, remote ischemic preconditioning, long non-coding RNA, melatonin, postconditioning, mitochondria, microvascular obstruction, and ferroptosis. After 2018, the keywords with strongest citation bursts included extracellular vesicles, long non-coding RNA, cell proliferation, microRNA, mitochondrial quality control, mitophagy, biomarker, and mitochondrial biogenesis. CONCLUSIONS: The present study reveals the influential authors, cooperating institutions, and main research foci in the field of MI/R injury in the past decade. The latest hotspots are a more in-depth insight into the molecular mechanisms underlying MI/R injury, such as mitochondrial quality control, non-coding RNAs, cell proliferation, and extracellular vesicles.

Case report: A case of isolated cardiac sarcoidosis diagnosed by multimodal imaging and endomyocardial biopsy.

Due to its low incidence, isolated cardiac sarcoidosis (ICS) is often missed or misdiagnosed. Herein, we describe a case of ICS in a 52-year-old male patient. Advanced imaging, including cardiac magnetic resonance (CMR) and fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET), could not only screen high-risk patients for establishing diagnosis, but also guide endomyocardial biopsy (EMB) for improving cardiac disease detection rate. This case highlights the importance of multimodal imaging for screening and necessity of EMB for diagnosis.

PM2.5-Induced Programmed Myocardial Cell Death via mPTP Opening Results in Deteriorated Cardiac Function in HFpEF Mice.

PM2.5 exposure can induce or exacerbate heart failure and is associated with an increased risk of heart failure hospitalization and mortality; however, the underlying mechanisms remain unclear. This study focuses on the potential mechanisms underlying PM2.5 induction of cardiomyocyte programmed necrosis as well as its promotion of cardiac function impairment in a mouse model of heart failure with preserved ejection fraction (HFpEF). HFpEF mice were exposed to concentrated ambient PM2.5 (CAP) (CAP group) or filtered air (FA) (FA group) for 6 weeks. Changes in myocardial pathology and cardiac function were documented for comparisons between the two groups. In vitro experiments were performed to measure oxidative stress and mitochondrial permeability transition pore (mPTP) dynamics in H9C2 cells following 24 h exposure to PM2.5. Additionally, co-immunoprecipitation was conducted to detect p53 and cyclophilin D (CypD) interactions. The results showed exposure to CAP promoted cardiac function impairment in HFpEF mice. Myocardial pathology analysis and in vitro experiments demonstrated that PM2.5 led to mitochondrial damage in cardiomyocytes and, eventually, their necrosis. Moreover, our experiments also suggested that PM2.5 increases mitochondrial reactive oxygen species (ROS), induces DNA oxidative damage, and decreases the inner mitochondrial membrane potential (ΔΨm). This indicates the presence of mPTP opening. Co-immunoprecipitation results showed a p53/CypD interaction in the myocardial tissue of HFpEF mice in the CAP group. Inhibition of CypD by cyclosporin A was found to reverse PM2.5-induced mPTP opening and H9C2 cell death. In conclusion, PM2.5 induces mPTP opening to stimulate mitochondria-mediated programmed necrosis of cardiomyocytes, and it might exacerbate cardiac function impairment in HFpEF mice.

All-Inorganic Manganese-Based CsMnCl3 Nanocrystals for X-Ray Imaging.

Lead-based halide perovskite nanomaterials with excellent optical properties have aroused great attention in the fields of solar cells, light-emitting diodes, lasing, X-ray imaging, etc. However, the toxicity of lead prompts researchers to develop alternatives to cut down the usage of lead. Herein, all-inorganic manganese-based perovskite derivatives, CsMnCl3 nanocrystals (NCs), with uniform size and morphology have been synthesized successfully via a modified hot-injection method. These NCs have a direct bandgap of 4.08 eV and a broadband emission centered at 660 nm. Through introducing modicum lead (1%) into the CsMnCl3 NCs, the photoluminescence intensity greatly improves, and the quantum yield (PLQY) increases from 0.7% to 21%. Furthermore, the CsMnCl3 :1%Pb NCs feature high-efficiency of X-ray absorption and radioluminescence, which make these NCs promising candidates for X-ray imaging.

Halogen Bonding: A New Platform for Achieving Multi-Stimuli-Responsive Persistent Phosphorescence.

Monotonous luminescence has always been a major factor limiting the application of organic room-temperature phosphorescence (RTP) materials. Enhancing and regulating the intermolecular interactions between the host and guest is an effective strategy to achieve excellent phosphorescence performance. In this study, intermolecular halogen bonding (CN⋅⋅⋅Br) was introduced into the host-guest RTP system. The interaction promoted intersystem crossing and stabilized the triplet excitons, thus helping to achieve strong phosphorescence emission. In addition, the weak intermolecular interaction of halogen bonding is sensitive to external stimuli such as heat, mechanical force, and X-rays. Therefore, the triplet excitons were easily quenched and colorimetric multi-stimuli responsive behaviors were realized, which greatly enriched the luminescence functionality of the RTP materials. This method provides a new platform for the future design of responsive RTP materials based on weak intermolecular interactions between the host and guest molecules.

Improvement of Al2O3 on the multi-pollutant control performance of NOx and chlorobenzene in vanadia-based catalysts.

We compared the influences of Al2O3 and SiO2 on a traditional V2O5-MoO3/TiO2 for the simultaneous removal of NOx and chlorobenzene (CB). The Al2O3 doping catalyst considerably broadens the active temperature window with higher NOx reduction and CB oxidation efficiencies than the SiO2 doping one and the V2O5-MoO3/TiO2. Furthermore, its resistance to SO2 was preserved and the quantities of polychlorinated byproducts also decreased. The increase in activity at low temperatures could be due to the promotion of vanadia reducibility via interactions between V2O5 and Al2O3. Moreover, the high temperature activity could be due to the additional surface acidities provided by Al2O3, in which the Lewis acid sites played the predominant role in both NH3 adsorptions and CB de-chlorination compared to the Brønsted acid sites. Finally, we proposed that Al2O3 is an effective addition for vanadia-based catalyst in NOx and CB simultaneous removal from stationary sources.

Genetic Mapping and Identification of the Candidate Genes for Mottled Rind in Cucumis melo L.

The rind appearance of melon is one of the most vital commercial quality traits which determines the preferences and behavior of consumers toward the consumption of melon. In this study, we constructed an F2 population derived from SC (mottled rind) and MG (non-mottled rind) lines for mapping the mottled rind gene(s) in melon. Genetic analysis showed that there were two dominant genes (CmMt1 and CmMt2) with evidence of epistasis controlling the mottled rind. Meanwhile, the phenotypic segregation ratio implied that the immature rind color had an epistatic effect on the mottled rind, which was regulated by CmAPRR2. A Kompetitive Allele-Specific PCR (KASP) DNA marker (CmAPRR2 SNP(G/T) ) was developed and shown to co-segregate with rind color, confirming that CmAPRR2 was CmMt1. Using bulked segregant analysis sequencing and KASP assays, CmMt2 was fine-mapped to an interval of 40.6 kb with six predicted genes. Functional annotation, expression analysis, and sequence variation analyses confirmed that AtCPSFL1 homolog, MELO3C026282, was the most likely candidate gene for CmMt2. Moreover, pigment content measurement and transmission electron microscopy analysis demonstrated that CmMt2 might participate in the development of chloroplast, which, in turn, decreases the accumulation of chlorophyll. These results provide insight into the molecular mechanism underlying rind appearance and reveal valuable information for marker-assisted selection breeding in melon.

Effects of SGLT-2 inhibitors on health-related quality of life and exercise capacity in heart failure patients with reduced ejection fraction: A systematic review and meta-analysis.

OBJECTIVE: Improving health-related quality of life (HRQoL) and exercise capacity is an important goal of treatment in heart failure (HF). However, evidence for the effects of sodium-glucose cotransporter-2 (SGLT-2) inhibitors on the improvement of HRQoL and exercise capacity seems to be conflicted. We performed a systematic review and meta-analysis to evaluate the effects of SGLT-2 inhibitors on HRQL and exercise capacity in patients with heart failure and reduced ejection fraction (HFrEF). METHODS: All studies (up to March 20, 2021) evaluating the effects of SGLT-2 inhibitors on HRQoL and exercise capacity in patients with HFrEF were initially searched from four electronic search engines: PubMed, Web of Science, Cochrane Library, and SinoMed. All statistical analyses were performed with RevMan 5.4. RESULTS: We included 9 articles describing 7 trials with 9428 patients. SGLT-2 inhibitors group exhibited significant improvement in HRQoL assessed by Kansas City Cardiomyopathy Questionnaires (KCCQ) (MD: 2.13, 95% CI: 1.11 to 3.14, p < 0.001) and the rate of KCCQ-overall summary score improvement≥5 points (RR 1.15, 95%CI 1.08 to 1.21, P < 0.001) compared with placebo. No significant difference was observed in exercise capacity assessed by 6-min walk test distance between SGLT-2 inhibitors and placebo (MD 24.45, 95%CI -22.82 to 71.72, P = 0.31). CONCLUSIONS: Our meta-analysis demonstrates that SGLT-2 inhibitors significantly improve HRQoL, and supports the concept that SGLT-2 inhibitors do not significantly improve exercise capacity in patients with HFrEF. Studies with larger sample sizes and longer follow-up duration are needed to determine whether the treatment with SGLT-2 inhibitors may improve exercise ability. PROSPERO: CRD42021248346.

Combined treatment with valsartan and fluvastatin to delay disease progression in nonpermanent atrial fibrillation with hypertension: A clinical trial.

BACKGROUND: Atrial fibrillation (AF) is a complex cardiac arrhythmia in clinical practice with increasing incidence. However, the effects of statins on patients with AF are not quite clear. HYPOTHESIS: To investigate the protective effect of calcium channel blocker (CCB) and valsartan combined fluvastatin on hypertension (HTN) patients with nonpermanent AF. METHODS: In three and a half years, 189 cases of patients diagnosed as HTN combining nonpermanent AF by eight medical centers, were recruited and randomly assigned to four groups with varied treatments: CCB group; CCB + statin group; valsartan group; and valsartan + statin group. The four groups were followed up for 24 months. The 7-day Holter ultrasound echocardiography (UCG) and biochemical indexes were completed at preset time nodes respectively. RESULTS: After 24 months of follow-up, 178 patients completed the study. Compared with CCB group, the blood lipid level, inflammatory index, ultrasonic index and electrocardiographic measurement results of CCB + statin group, valsartan group and valsartan + statin group were improved in different degrees and had statistical significance (P < .05 or P < .01). Furthermore, the improvement trend of CCB + statin group and valsartan + statin group was more obvious. CONCLUSIONS: The results indicated that valsartan can reduce AF load and recurrence rate, and delay the progression of nonpermanent AF to permanent AF in multiple ways, and the effect of combination of valsartan and fluvastatin is more significant. These results provide a new direction for the integrated upstream control strategy of AF.

lncRNA Oip5-as1 attenuates myocardial ischaemia/reperfusion injury by sponging miR-29a to activate the SIRT1/AMPK/PGC1α pathway.

OBJECTIVES: Myocardial ischaemia/reperfusion (MI/R) injury is associated with adverse cardiovascular outcomes after acute myocardial infarction. However, the molecular mechanisms underlying MI/R injury are unclear. This study investigated the role of long non-coding RNA (lncRNA) Oip5-as1 in regulating mitochondria-mediated apoptosis during MI/R injury. MATERIALS AND METHODS: Sprague-Dawley rats were subjected to MI/R induced by ligation of the left anterior descending coronary artery followed by reperfusion. H9c2 cells were incubated under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions to mimic in vivo MI/R. RT-qPCR and Western blot were used to evaluate gene and protein levels. CCK-8 assay, biochemical assay and flow cytometric analysis were performed to assess the function of Oip5-as1. The dual-luciferase gene reporter assay and RIP assay were conducted as needed. RESULTS: Oip5-as1 expression was downregulated in the hearts of rats with MI/R and in H9c2 cells treated with OGD/R. Oip5-as1 overexpression alleviated reactive oxygen species-driven mitochondrial injury and consequently decreased apoptosis in MI/R rats and H9c2 cells exposed to OGD/R. Mechanistically, Oip5-as1 acted as a competing endogenous RNA of miR-29a and thus decreased its expression. Inhibition of miR-29a reduced the oxidative stress and cytotoxicity induced by OGD/R. Overexpression of miR-29a reversed the anti-apoptotic effect of Oip5-as1 in H9c2 cells treated with OGD/R. Further experiments identified SIRT1 as a downstream target of miR-29a. Oip5-as1 upregulated SIRT1 expression and activated the AMPK/PGC1α pathway by targeting miR-29a, thus reducing the apoptosis triggered by OGD/R. However, these effects were reversed by a selective SIRT1 inhibitor, EX527. CONCLUSIONS: Oip5-as1 suppresses miR-29a leading to activation of the SIRT1/AMPK/PGC1α pathway, which attenuates mitochondria-mediated apoptosis during MI/R injury. Our findings thus provide new insights into the molecular mechanisms of MI/R injury.

Weighted Gene Co-Expression Network Analysis Identifies Critical Genes in the Development of Heart Failure After Acute Myocardial Infarction.

Background: The development of heart failure (HF) remains a common complication following an acute myocardial infarction (AMI), and is associated with substantial adverse outcomes. However, the specific predictive biomarkers and candidate therapeutic targets for post-infarction HF have not been fully established. We sought to perform a weighted gene co-expression network analysis (WGCNA) to identify key modules, hub genes, and possible regulatory targets involved in the development of HF following AMI. Methods: Genes exhibiting the most (top 50%) variation in expression levels across samples in a GSE59867 dataset were imported to the WGCNA. Gene Ontology and pathway enrichment analyses were performed on genes identified in the key module by Metascape. Gene regulatory networks were constructed using the microarray probe reannotation and bioinformatics database. Hub genes were screened out from the key module and validated using other datasets. Results: A total of 10,265 most varied genes and six modules were identified between AMI patients who developed HF within 6 months of follow-up and those who did not. Specifically, the blue module was found to be the most significantly related to the development of post-infarction HF. Functional enrichment analysis revealed that the blue module was primarily associated with the inflammatory response, immune system, and apoptosis. Seven transcriptional factors, including SPI1, ZBTB7A, IRF8, PPARG, P65, KLF4, and Fos, were identified as potential regulators of the expression of genes identified in the blue module. Further, non-coding RNAs, including miR-142-3p and LINC00537, were identified as having close interactions with genes from the blue module. A total of six hub genes (BCL3, HCK, PPIF, S100A9, SERPINA1, and TBC1D9B) were identified and validated for their predictive value in identifying future HFs. Conclusions: By using the WGCNA, we provide new insights into the underlying molecular mechanism and molecular markers correlated with HF development following an AMI, which may serve to improve risk stratification, therapeutic decisions, and prognosis prediction in AMI patients.

Construction of a CQDs/Ag3PO4/BiPO4 Heterostructure Photocatalyst with Enhanced Photocatalytic Degradation of Rhodamine B under Simulated Solar Irradiation.

A carbon quantum dot (CQDs)/Ag3PO4/BiPO4 heterostructure photocatalyst was constructed by a simple hydrothermal synthesis method. The as-prepared CQDs/Ag3PO4/BiPO4 photocatalyst has been characterized in detail by X-ray diffraction, field-emission scanning electron microscopy, transmission electron microscopy, X-ray photoelectron spectroscopy, ultraviolet-visible spectroscopy, and photoelectrochemical measurements. It is demonstrated that the CQDs/Ag3PO4/BiPO4 composite is constructed by assembling Ag3PO4 fine particles and CQDs on the surface of rice-like BiPO4 granules. The CQDs/Ag3PO4/BiPO4 heterostructure photocatalyst exhibits a higher photocatalytic activity for the degradation of the rhodamine B dye than that of Ag3PO4, BiPO4, and Ag3PO4/BiPO4. The synergistic effects of light absorption capacity, band edge position, separation, and utilization efficiency of photogenerated carriers play the key role for the enhanced photodegradation of the rhodamine B dye.

Etiologic impact on difference on clinical outcomes of patients with heart failure after cardiac resynchronization therapy: A systematic review and meta-analysis.

OBJECTIVE: To compare long-term clinical outcomes between patients with heart failure due to non-ischemic cardiomyopathy (NICM) and those due to ischemic cardiomyopathy (ICM) after cardiac resynchronization therapy (CRT). METHODS AND RESULTS: EMbase, PubMed, and Cochrane Library were searched for published studies up to December 2017. Twenty-one observational studies with 12,331 patients were enrolled in the present meta-analysis. The results demonstrated that the all-cause mortality in NICM patients was significantly lower than that in ICM patients (RR 1.37, 95% CI 1.16-1.61). In terms of echocardiographic parameters, NICM patients exhibited statistically significant improvement in left ventricular ejection fraction (LVEF) (MD 2.70, 95%CI -4.13 to -1.28), and a significant decrement in left ventricular end-systolic volume (LVESV) (MD 10.41,95% CI 2.10-18.73) and left ventricular end diastolic diameter (LVEDD) (MD 7.63, 95% CI 2.59-12.68) as compared with ICM patients. No significant difference was observed in the improvement of New York Heart Association Functional Classification (MD 0.05, 95% CI -0.05 to 0.15), pulmonary arterial systolic pressure (PASP) (MD -0.61, 95% CI -4.36 to 3.14), and severity of mitral regurgitation (MD 0.00, 95% CI -0.08 to 0.07) between the 2 groups. CONCLUSIONS: Our meta-analysis illustrated that patients with HF due to NICM tended to have better clinical outcomes and LV reverse remodeling as compared with those due to ICM. This finding may help clinicians select patients who respond favorably to CRT, though further research is required to clarify the potential confounding factors and underlying mechanisms for this phenomenon.

Upstream therapeutic strategies of valsartan and fluvastatin on hypertensive patients with non-permanent atrial fibrillation.

AIM: To investigate the upstream therapeutic effects of fluvastatin and valsartan on hypertensive patients with non-permanent atrial fibrillation (AF). METHODS: A total of 189 patients who were admitted to outpatient and inpatient department from eight medical centers in China, diagnosed as hypertension with non-permanent AF, were divided into four groups randomly: the CCBs group (group A, n = 45); CCB + fluvastatin group (group B, n = 48); valsartan group (group C, n = 46); valsartan + fluvastatin group (group D, n = 50). The four groups were followed up for 24 months. The blood routine, biochemical examination, echocardiography, high sensitive C-reactive protein (hs-CRP), N-terminal pro-brain natriuretic peptide (NT-proBNP), the maintenance rate of sinus rhythm, and the recurrence of paroxysmal AF or persistent AF incidence were observed in these groups before and after 24 months' treatment. RESULTS: After 24 months of follow-up, there were 178 cases of patients who have completed the study. (a) There was no significant difference in blood routine, liver, and renal function in each group (P > 0.05). (b) The blood lipids level in groups B and D was significantly reduced after treatment (P < 0.01). There was no significant difference of hs-CRP level in group A (P > 0.05). The left ventricular remodeling was significantly alleviated in group C and group D (P < 0.05). The NT-ProBNP level was significantly decreased in group D (P < 0.05). (c) The sinus rhythm maintenance rate of group B, group C, and group D was higher than group A (77.78%, 70.45%, 79.17% vs 43.90%), the occurrence of persistent AF was significantly lower than group A (11.11%, 14.29%, 8.33% vs 31.71%; P < 0.05). CONCLUSIONS: CCB plus fluvastatin and valsartan can reduce the recurrence rate of non-permanent AF and to delay the progression from non-permanent AF to permanent AF in patients with hypertension. The combined application of valsartan and fluvastatin is more effective than valsartan or CCB alone in the upstream therapies of AF.

Network pharmacology-based identification of major component of Angelica sinensis and its action mechanism for the treatment of acute myocardial infarction.

Background: To decipher the mechanisms of Angelica sinensis for the treatment of acute myocardial infarction (AMI) using network pharmacology analysis. Methods: Databases were searched for the information on constituents, targets, and diseases. Cytoscape software was used to construct the constituent-target-disease network and screen the major targets, which were annotated with the DAVID (Database for Annotation, Visualization and Integrated Discovery) tool. The cardioprotective effects of Angelica sinensis polysaccharide (ASP), a major component of A. sinensis, were validated both in H9c2 cells subjected to simulated ischemia by oxygen and glucose deprivation and in rats with AMI by ligation of the left anterior coronary artery. Results: We identified 228 major targets against AMI injury for A. sinensis, which regulated multiple pathways and hit multiple targets involved in several biological processes. ASP significantly decreased endoplasmic reticulum (ER) stress-induced cell death both in vitro and in vivo In ischemia injury rats, ASP treatment reduced infarct size and preserved heart function. ASP enhanced activating transcription factor 6 (ATF6) activity, which improved ER-protein folding capacity. ASP activated the expression of p-AMP-activated protein kinase (p-AMPK) and peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α). Additionally, ASP attenuated levels of proinflammatory cytokines and maintained a balance in the oxidant/antioxidant levels after AMI. Conclusion:In silico analysis revealed the associations between A. sinensis and AMI through multiple targets and several key signaling pathways. Experimental data indicate that ASP protects the heart against ischemic injury by activating ATF6 to ameliorate the detrimental ER stress. ASP's effects could be mediated via the activation of AMPK-PGC1α pathway.

Sensitive miRNA markers for the detection and management of NSTEMI acute myocardial infarction patients.

BACKGROUND: NSTEMI patients will benefit greatly with better biomarker screening to detect and prognose the disease. Using miRNAs, we evaluated the clinical utility in acute myocardial infarction (AMI) patients during disease onset and therapy. METHODS: A total of 145 NSTEMI patients and 30 healthy volunteers with no history of cardiovascular disease (CVD) were recruited. miRNA levels in plasma were measured during disease manifestation and serially during treatment phase. Levels of multiple candidates (miR-1, miR-133, miR-208, miR-499) were analysed. The miRNA levels were directly compared between NSTEMI and healthy volunteers. RESULTS: Cardiac related miRNAs levels demonstrated significant increase compared with healthy controls. miR-499 exhibited the highest elevation with more than 6.03-fold change compared with healthy participants. Conventional cTnT measurements were in good agreement to miRNA relative expressions. In serial measurements, miR-499 demonstrated large fluctuations and could be linked to the secondary complications. In contrast, miR-133 showed insignificant variations in mean levels during serial sampling. CONCLUSIONS: miRNA is a potentially sensitive biomarker for NSTEMI AMI patients for disease detection and treatment monitoring. The sensitivities were comparable to cTnT for diagnostic accuracy and patients with sustained or higher levels were correlated to secondary complications.