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Seeking for extremely active and durable bifunctional electrocatalysts towards the overall water splitting possesses a strategic significance on the development of sustainable and clean energy for the replacement of fossil fuels. Ir-based nanomaterials are deemed as one of the most high-efficiency oxygen evolution reaction electrocatalysts while the hydrogen evolution reaction performance is unfavorable. In this work, we report a one-pot hydrothermal synthesis of N-doped graphene anchored Ir nanoparticles (Ir/N-rGO) with ultrasmall particle size (∼2.0 nm). Apart from the predictably superior OER performance, the resultant Ir/N-rGO also displays excellent hydrogen evolution reaction (HER) performance, requiring merely 76 and 260 mV overpotentials to achieve the current density of 10 mA cm-2 towards HER and OER, respectively. When applied as the bifunctional electrodes for overall water splitting, Ir/N-rGO needs a lower overpotential (1.74 V) to achieve a current density of 50 mA cm-2 in alkaline solution, exceeding that of Pt/C and RuO2 couple (1.85 V). Thus, the as-fabricated Ir/N-rGO has a commendable prospect in the practical application of alkaline water electrocatalysis.

Coronary slow flow is taken to be indicative of delayed filling of terminal vessels of the coronary arteries in the absence of coronary stenosis, as detected using coronary angiography. Patients suffering from coronary slow flow typically experience recurrent chest pain, thereby markedly affecting their quality of life. The etiology and pathogenesis of coronary slow flow, which is gradually attracting clinical attention, have yet to be sufficiently established, although it is currently believed that they may be associated with endothelial dysfunction in the coronary arteries, inflammatory response, abnormalities in microvascular reserve function, subclinical atherosclerosis, blood cell and platelet abnormalities, and genetic factors. In this review, we provide a brief overview of recent progress in research on the pathogenesis of coronary slow flow with a view toward elucidating the possible underlying pathogenesis and identify targets and directions for the treatment of this condition.

Qing Zhu,1 Cuiting Zhao,1 Yonghuai Wang,1 Xinxin Li,1 Yixue Xue,2– 4 Chunyan Ma1 1Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Neurobiology, School of Life Sciences, China Medical University, Shenyang, People’s Republic of China; 3Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang, People’s Republic of China; 4Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang, People’s Republic of ChinaCorrespondence: Chunyan MaDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical University, No. 155 Nanjingbei Street, Shenyang, Liaoning, 110001, People’s Republic of ChinaTel +86 2483282129Email cmu1h_mcy@126.comBackground: Coronary slow flow (CSF) is an angiographic phenomenon characterized by delayed coronary opacification with normal or near-normal epicardial coronary arteries. The pathogenesis of CSF is closely related to inflammatory response. Accumulating evidence shows that long non-coding RNAs (lncRNAs) play an important role in cardiovascular disease. However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown.Patients and Methods: Forty CSF patients and forty control subjects were included in the study and underwent coronary angiography, Seattle angina questionnaire (SAQ) and echocardiography. The plasma levels of the inflammatory factors soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were determined by ELISA. The expression levels of NEAT1, miR-148b-3p and ICAM-1 in cells were measured by qRT-PCR or Western blotting. Cell proliferation was measured by 5‐Ethynyl‐2ʹ‐deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by apoptosis assay. The relationship between NEAT1 and miR-148b-3p was verified by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and avidin-biotin pull-down assay. The relationship between ICAM-1 and miR-148b-3p was verified by luciferase reporter gene assay and avidin-biotin pull-down assay.Results: This study showed that plasma sICAM-1, miR-148b-3p, and NEAT1 as independent predictors of a CSF diagnosis. Furthermore, plasma NEAT1 level showed superior diagnostic ability for CSF compared with sICAM-1 and miR-148b-3p. It was also shown that high expression of NEAT1 in oxygen-glucose deprivation (OGD)-treated human umbilical vein endothelial cells (HUVECs) functions as a competing endogenous RNA (ceRNA). By specifically binding miR-148b-3p, it weakened the negative regulatory effects of miR-148b-3p on the ICAM-1 target gene leading to upregulated expression of ICAM-1. This interaction was also shown to inhibit HUVEC proliferation and enhance apoptosis.Conclusion: This study demonstrated for the first time the important mechanism of action of the NEAT1/miR-148b-3p/ICAM-1 axis in the progression of CSF disease, and indicated the potential of NEAT1, miR-148b-3p, and ICAM-1 as a new target for the diagnosis and treatment of CSF.Keywords: coronary slow flow, ncRNA, inflammation, biomarkers, cell biology

Cryoballoon ablation (CBA) is recommended for patients with symptomatic drug refractory paroxysmal atrial fibrillation (pAF). However, substantial atrial fibrillation (AF) recurrence is common during follow-up. Searching for a potential biomarker representing both myocardial injury and inflammation to identify patients at high risk of AF recurrence after CBA is very meaningful for postoperative management of AF patients.To evaluate the clinical efficacy of high-mobility group box 1 (HMGB1) protein released from the left atrium to predict AF recurrence in pAF patients after CBA at 1-year follow-up.We included 72 pAF patients who underwent CBA. To determine the expression levels of HMGB1, left atrial blood samples were collected from the patients before CBA and after the procedure through the transseptal sheath. Patients were followed up for AF recurrence for 1 year.A total of 19 patients of the 72 experienced AF recurrence. The level of postoperative HMGB1 (HMGB1post) was higher in the AF recurrence group than in the AF non recurrence group (p = .03). However, no differences were noted in the levels of other biomarkers such as preoperative high-sensitivity C-reactive protein (hs-CRP), postoperativehs-CRP, and preoperative HMGB1 between the two groups. Multiple logistic regression analysis revealed that a higher level of serum HMGB1post was associated with AF recurrence (odds ratio: 5.29 [1.17-23.92], p = .04). Receiver operating characteristic analysis revealed that HMGB1post had a moderate predictive power for AF recurrence (area under the curve: 0.68; sensitivity: 72%; and specificity: 68%). The 1-year AF-free survival was significantly lower in patients with a high HMGB1post level than in those with a low HMGB1post level (hazard ratio: 3.81 [1.49-9.75], p = .005).In pAF patients who under went CBA, the level of HMGB1 after CBA was associated with AF recurrence and demonstrated a moderate predictive power. Thus, we offer a potential biomarker to identify pAF patients at high risk of AF recurrence.

Background Shear wave elastography (SWE) directly quantifies the local arterial wall stiffness by calculating the elastic modulus. However, whether carotid wall elastic modulus can predict obstructive coronary artery disease (CAD) is not well known. We aimed to investigate the value of carotid wall elastic modulus measured using SWE in identifying obstructive CAD. Materials and methods We prospectively enrolled 61 patients without carotid plaque referred for clinically indicated coronary angiography. Twenty-seven (44.3%) patients were diagnosed with obstructive CAD (≥50% coronary stenosis). The elastic modulus of common carotid artery was quantified using SWE. Ankle--brachial index (ABI) and echocardiographic global cardiac calcium score (GCCS) were measured. Results Patients with obstructive CAD had significantly higher elastic modulus than those without obstructive CAD. The maximum elastic modulus (EMmax) was independently associated with obstructive CAD after adjusting for the Framingham risk score, ABI, and GCCS. EMmax had the highest area under the curve (AUC) to identify obstructive CAD (AUC 0.70; P = 0.003). In the nested models, the model based on the Framingham risk score and ABI (χ2 = 3.74) improved by adding GCCS (χ2 = 9.95) and further improved by adding EMmax (χ2 = 15.86). Adding EMmax to the combined ABI and GCCS model increased integrated discrimination index from 0.10 to 0.19. Conclusion Carotid wall elastic modulus measured using SWE is a useful predictor of obstructive CAD in patients without carotid plaque. We demonstrated the incremental and independent value of carotid wall elastic modulus in identifying obstructive CAD compared with clinical risk factors and other imaging predictors, including ABI and GCCS. Video abstract Please see the video, in Supplemental Digital Content 1, http://links.lww.com/HJH/B551 for more insights from the authors.

Aims: Sweroside, a secoiridoid glucoside extracted from Swertia pseudochinensis Hara, is reported to possess antioxidant and anti-inflammatory activities. However, whether sweroside has a protective effect on myocardial ischemia–reperfusion (IR) injury is yet to be elucidated. The present study aimed to confirm the cardioprotective effect of sweroside and to identify its underlying mechanism.Methods and Results: H9c2 cells were pretreated with sweroside and then underwent hypoxia–reoxygenation. Cell Counting Kit-8, creatine kinase-myocardial band (CK-MB) and lactate dehydrogenase (LDH) assays were conducted to detect cell viability and myocardial injury, respectively. The Langendorff method was used to induce myocardial IR injury ex vivo. Triphenyltetrazolium chloride staining was performed to detect myocardial infarct size, while protein expression was analyzed using western blotting. Overall, the results indicated that sweroside pretreatment dose-dependently led to a significant enhancement in cell viability, a decrease in release of CK-MB and LDH, a reduction in infarct size, and an improvement in cardiac function. Additionally, sweroside pretreatment caused a marked suppression of oxidative stress, as evidenced by the fact that sweroside decreased the accumulation of reactive oxygen species and malondialdehyde, while enhancing the activities of superoxide dismutase and glutathione peroxidase. Moreover, sweroside was found to notably repress pyroptosis, as sweroside blocked pore formation in the cell membrane, inhibited caspase-1 and interleukin (IL)-1β activity, and decreased the expression levels of NLR family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD, cleaved caspase-1, and IL-1β. Mechanistically, it was found that sweroside inhibited Kelch-like ECH-associated protein 1 (Keap1) and induced nuclear factor E2-associated factor 2 (Nrf2) nuclear translocation. Furthermore, the inhibition of oxidative stress and pyroptosis by sweroside could be abrogated via the inhibition of Nrf2 expression, which suggested that the protective effect induced by sweroside was Nrf2-dependent.Conclusions: The present study demonstrated that sweroside pretreatment could protect against myocardial IR injury by inhibiting of oxidative stress and NLRP3 inflammasome-mediated pyroptosis partially via modulation of the Keap1/Nrf2 axis.

Background Left atrial (LA) volume (LAV) is one of the recommended key variables for evaluating left ventricular (LV) diastolic function. However, only LA anteroposterior diameter (LAAP) is available in numerous large-scale existing databases. Therefore, this study aimed to validate whether LV diastolic function could be evaluated with estimated LAV from LAAP. Methods A total of 552 inpatients with sinus rhythm were consecutively enrolled. LAV was measured by biplane Simpson’s disk summation method. LV diastolic function was evaluated according to the 2016 proposed recommendations. Best-fitting regression models of LAAP index (LAAPI)–LAV index (LAVI) were developed and equations with the highest F-value were chosen in the first 276 subjects (derivation set), and concordance for evaluating LV diastolic function between using estimated and observed LAVI was verified in the remaining 276 subjects (validation set). Results In the derivation set, the linear model has the highest F-value in all subjects and in the subjects with normal or depressed LV ejection fraction. In the validation set, using the linear equation (LAVI = 2.05 × LAAPI − 13.86), the higher area under curve and narrower range of difference were shown between estimated LAVI and observed LAVI, respectively. Further, concordance for diagnosis (overall proportion of agreement, 88.4%; κ = 0.79) and grading (overall proportion of agreement, 84.8%; κ = 0.74) of LV diastolic dysfunction was substantial between using estimated and observed LAVI. Conclusions LV diastolic function can be evaluated with estimated LAVI from LAAPI, which might provide a surrogate method when the direct measurement of LAV is not available.

Background Coronary slow flow phenomenon (CSFP) involves the delayed opacification of the coronary distal vessel, in the absence of an obstructive lesion in the epicardial coronary artery during angiography. Since the link between left atrial (LA) function and decreased left ventricular function is still unclear, we evaluated LA function using real-time three-dimensional echocardiography (RT3DE) in patients with CSFP, and subsequently determined the incremental value of RT3DE. Methods This study enrolled 60 patients with CSFP and 45 control subjects. CSFP was diagnosed based on thrombolysis in myocardial infarction frame count (TFC). The LA phasic volume and function was evaluated by both two-dimensional echocardiography (2DE) and RT3DE. Results The LA maximal volume (Volmax), pre-systolic volume (Volp), and minimal volume (Volmin) increased, but LA total and active ejection fraction decreased in patients with CSFP. Based on our results, Volmax, Volp, Volmin, and LA total and active ejection fraction correlated with TFC, and with the number of arteries involved. The LA total ejection fraction by RT3DE was the only independent predictor for CSFP (odds ratio, 0.64 [95% confidence interval, 0.49–0.83]; P = 0.001). Also, the LA total ejection fraction by RT3DE demonstrated good predictive power for CSFP, with a cut-off value of 54.15% (area under curve, 0.85; sensitivity, 84%; specificity, 83%). Conclusions The LA reservoir and contractile function decreased in the patients with CSFP and correlated with coronary flow rate and with the number of arteries involved. The LA total ejection fraction by RT3DE can independently predict CSFP, and RT3DE demonstrated incremental value for evaluating LA phasic function in the patients with CSFP compared to 2DE.

Slow coronary flow (SCF) is an angiographic entity characterized by delayed coronary opacification without an evident obstructive lesion in the epicardial coronary artery. However, patients with SCF have decreased left ventricular (LV) global longitudinal strain (GLS). SCF is associated with inflammation, and soluble endothelial protein C receptor (sEPCR) is a potential biomarker of inflammation. Therefore, under evaluation herein, was the relationship between SCF and sEPCR and the predictive value of sEPCR and LV GLS for SCF was investigated.Twenty-eight patients with SCF and 34 controls were enrolled. SCF was diagnosed by the thrombolysis in myocardial infarction frame count (TFC). The plasma level of sEPCR was quantified using enzyme-linked immunosorbent assay. LV GLS was measured by two-dimensional speckle-tracking echocardiography.Plasma sEPCR was significantly higher in patients with SCF than in controls and was positively correlated with the mean TFC (r = 0.67, p0.001) and number of involved vessels (r = 0.61, p0.001). LV GLS was decreased in patients with SCF compared to that in controls. sEPCR level (OR = 3.14, 95% CI 1.55-6.36, p = 0.001) and LV GLS (OR = 1.44, 95% CI 1.02-2.04, p = 0.04) were independent predictors of SCF. sEPCR predicted SCF (area under curve [AUC]: 0.83); however, sEPCR9.63 ng/mL combined with LV GLS-14.36% demonstrated better predictive power (AUC: 0.89; sensitivity: 75%; specificity: 91%).Patients with SCF have increased plasma sEPCR and decreased LV GLS. sEPCR may be a useful potential biomarker for SCF, and sEPCR combined with LV GLS can better predict SCF.

Bicuspid aortic valve (BAV) is a common congenital cardiac malformation, frequently combined with ascending aorta dilation. However, isolated abnormalities of the aortic arch are less frequent in BAV patients. Here, we present a rare case of BAV combined with right-sided aortic arch aneurysm, aberrant left subclavian artery, and Kommerell's diverticulum, diagnosed by echocardiography and computed tomography angiography. The patient was followed-up regularly because of the life-threatening risks of aortic arch aneurysms.

Background Coronary slow flow (CSF) refers to coronary arteries with no obvious stenosis but have slow coronary flow without effective treatment. The main cause of CSF is endothelial dysfunction. The long non-coding RNA (lncRNA) MALAT1 is involved in regulating endothelial dysfunction, but its role in CSF endothelial dysfunction is still unclear. Methods We included 41 CSF patients and 37 controls in the study, who all underwent coronary angiography, echocardiography, and brachial artery flow-mediated dilatation (FMD) examination. Human umbilical vein endothelial cells (HUVECs) stimulated by oxygen–glucose deprivation were used as CSF-induced HUVECs. Plasma endothelin-1 (ET-1) concentrations were determined by enzyme-linked immunosorbent assay (ELISA). The expression levels of MALAT1, miR-181b-5p, myocyte enhancer factor 2A (MEF2A), and ET-1 were measured by qRT-PCR or western blotting. Cell proliferation was determined by 5-ethynyl-2′-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assays. Apoptosis was examined by flow cytometry. The relationship between miR-181b-5p and MALAT1 or MEF2A was verified by dual-luciferase reporter assay. MEF2A binding directly to the ET-1 promoter region was verified via chromatin immunoprecipitation (ChIP) assay. Results MALAT1 and ET-1 were increased, and miR-181b-5p was decreased in the peripheral blood of the CSF patients, and could be used as predictors of CSF. In the CSF-induced HUVECs, MALAT1 was highly expressed, and MALAT1 knockdown improved endothelial function. In contrast, miR-181b-5p was downregulated in the CSF-induced HUVECs, and miR-181b-5p overexpression improved endothelial function. While MEF2A was highly enriched in CSF-induced HUVECs, MEF2A knockdown reduced ET-1 and increased the endothelial function of CSF-induced HUVECs as a transcriptional regulator of ET-1. MALAT1 modulated MEF2A expression positively by sponging miR-181b-5p. Conclusions Endothelial function is reduced in CSF. MALAT1 participates in regulating CSF endothelial dysfunction through the miR-181b-5p–MEF2A–ET-1 axis, and could provide a new target for CSF treatment.

Palmitic acid (PA) can induce lipotoxic damage to cardiomyocytes, although its precise mechanism of action has not been completely elucidated. Growth arrest‑specific transcript 5 (GAS5) is a long noncoding RNA that serves a regulatory role in several pathological processes, including tumorigenesis, stroke, cardiac fibrosis and osteoarthritis; however, its role in PA‑induced myocardial injury remains elusive. The present study aimed to explore the role and underlying mechanism of GAS5 on PA‑induced myocardial injury. The expression of GAS5 in PA‑treated cardiomyocytes (H9c2 cells) was detected by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), and its effects on PA‑induced myocardial injury were measured by Cell Counting Kit‑8 and lactate dehydrogenase (LDH) assays. The activities of cytokines and nuclear factor (NF)‑κB were also detected by enzyme‑linked immunosorbent assay, while interactions between GAS5 and microRNA (miR)‑26a were evaluated by luciferase reporter assay and RT‑qPCR. The regulation of GAS5 on high mobility group box 1 (HMGB1) expression was detected by RT‑qPCR and western blotting. The results demonstrated that GAS5 was significantly upregulated in cardiomyocytes following treatment with PA. GAS5‑knockdown increased the viability of PA‑treated cardiomyocytes and reduced the activity of LDH, tumor necrosis factor‑α and interleukin‑1β. Furthermore, the present study identified that GAS5 specifically binds to miR‑26a, and a reciprocal negative regulation exists between the two. The present study also demonstrated that GAS5 downregulation inhibited HMGB1 expression and NF‑κB activation, while these suppressive effects were mediated by miR‑26a. In conclusion, the present study demonstrated that PA can induce GAS5 expression and that the downregulation of GAS5 alleviated PA‑induced myocardial inflammatory injury through the miR‑26a/HMGB1/NF‑κB axis. These data may provide a novel insight into the mechanism of myocardial lipotoxic injury.

// Hongyun Chen 1 , Shuang Liu 2 , Zhihong Zong 3 , Cuiting Zhao 2 , Guangyuan Li 2 , Yonghuai Wang 2 , Guoxian Qi 1 , Jun Yang 2 and Chunyan Ma 2 1 Department of Geriatric Cardiology, First Hospital of China Medical University, Shenyang, Liaoning, China 2 Department of Cardiovascular Ultrasound, First Hospital of China Medical University, Shenyang, Liaoning, China 3 China Medical University, Shenyang, Liaoning, China Correspondence to: Chunyan Ma, email: cmu1h_mcy@126.com Keywords: cardiac resynchronization therapy (CRT); SERCA2A; endo-CRT; epi-CRT; dyssynchronous heart failure Received: March 29, 2017 Accepted: December 29, 2017 Published: January 02, 2018 ABSTRACT The aims of the present study were to compare the effects of endocardial cardiac resynchronization therapy (endo-CRT) and epicardial CRT (epi-CRT) on cardiac contractile function and to delineate the underlying molecular mechanisms. Twenty-four adult mongrel canines were divided into four groups: sham-operation control group (CT, n = 6), dyssynchronous heart failure (DHF) group ( n = 6), epi-CRT group ( n = 6), and endo-CRT group ( n = 6). The global and local left ventricle (LV) systolic function, dyssynchrony and myocardium calcium handling molecular mRNA and protein levels were measured. Compared to CT group, we found the global and local LV function, dyssynchrony and SERCA2A decreased in DHF group and increased in CRT groups, particularly in endo-CRT group at LV lateral wall (pacing site). Therefore, endo-CRT appears to be an effective procedure in the treatment of DHF, which might be mediated by upregulating the mRNA and protein expression of SERCA2A in the LV at the pacing and remote site.

Gum arabic, an inexpensive dispersant widely used in the food industry, has great potential for application in building materials. In order to find out the dispersion effect of gum arabic and the factors influencing the holding capacity of gum arabic in cement during hydration, rheological properties of cement paste with added gum arabic were assessed in this paper. The results show that 0.10–0.60 wt% of gum arabic positively affects dispersion, whereas lower dosages have negligible effect. High speed mixing is required to maintain the dispersion stability of gum arabic in cement paste. The optimum dosage of gum arabic to achieve best disperse-holding capacity of cement paste was 0.3 wt%, and the minimum water–cement ratio needed to obtain a dispersion effect was 0.28.