No genetic causality between obesity and benign paroxysmal vertigo: A two-sample Mendelian randomization study.

Objective: We applied Mendelian randomization to explore the causal relationship between obesity and benign paroxysmal vertigo (BPV). Methods: We chose two types of obesity diseases. Obesity due to excessive calories and other or unspecified obesity from the FinnGen database. We used genomic significance (p < 5 × 10-8) to obtain independent single nucleotide polymorphisms (SNPs) as instrumental variables. Similarly, genome-wide association study data for the disease BPV were selected from the FinnGen database. R was then used to test the data for multiplicity and heterogeneity, as well as to detect the effect of individual SNPs on the results. Random effects inverse variance weighting was used as the main statistical analysis. Results: First, by analyzing, we found an outlier in obesity due to excessive calories (rs12956821). Outliers were then removed, and the statistical results were analyzed without heterogeneity (p > 0.05) and horizontal pleiotropy (p > 0.05), as well as individual SNPs having no effect on the results. Meanwhile, random-effects IVW results showed obesity due to excessive calories (p = 0.481; OR = 0.941), and other or unspecified obesity (p = 0.640; OR = 0.964). Conclusions: The present study did not find a causal relationship between the above two obesity types and BPV at the genetic level.

Advanced Architectures of Air Electrodes in Zinc-Air Batteries and Hydrogen Fuel Cells.

The air electrode is an essential component of air-demanding energy storage/conversion devices, such as zinc-air batteries (ZABs) and hydrogen fuel cells (HFCs), which determines the output power and stability of the devices. Despite atom-level modulation in catalyst design being recently achieved, the air electrodes have received much less attention, causing a stagnation in the development of air-demanding equipment. Herein, the evolution of air electrodes for ZABs and HFCs from the early stages to current requirements is reviewed. In addition, the operation mechanism and the corresponding electrocatalytic mechanisms of ZABs are summarized. In particular, by clarifying the air electrode interfaces of ZABs at different scales, several approaches to improve the air electrode in rechargeable ZABs are reviewed, including innovative electrode structures and bifunctional oxygen catalysts. Afterward, the operating mechanisms of proton-exchange-membrane fuel cells (PEMFCs) and anion-exchange-membrane fuel cells (AEMFCs) are explained. Subsequently, the strategies employed to enhance the efficiency of the membrane electrode assembly (MEA) in PEMFCs and AEMFCs, respectively, are highlighted and discussed in detail. Last, the prospects for air electrodes in ZABs and HFCs are considered by discussing the main challenges. The aim of this review is to facilitate the industrialization of ZABs and HFCs.

Impact of supplement of Qingke flours on physiochemical properties, sensory and in vitro starch digestibility of wheat bread and its enhancement by bread quality improvers.

The aim is to upgrade the formulation to produce wheat bread with lower starch digestibility by supplemented with Qingke flour. Physiochemical properties of multi-scale Qingke flours were examined to select the most satisfied Qingke flour for breadmaking. Data showed multi-scale Qingke samples differed in total starch content, water/oil binding capacity, freeze-thaw stability, but had similar swelling capacity and thermodynamic properties. Addition of Qingke flours significantly reduced the total in vitro starch digestion of bread from 80% to 41% and decreased the rapidly digested starch content from 53% to 27%. However, Qingke flours caused a worse bread quality, texture and sensory e.g. lower bread specific volume (4.26-3.3 mL/g), larger hardness (398-1170 g) and chewiness (296-707 mJ). Meanwhile, hydroxypropyl methylcellulose, sodium stearoyl lactylate and transglutaminase could improve the bread quality and sensory. Lastly, results revealed Qingke-supplemented bread could generate new volatile compounds, hence having a different aroma compared to original wheat bread.

Application of respiratory sensing technique in CT-guided radiofrequency ablation of liver malignancies.

Objective: This study aimed to examine the effectiveness and safety of respiratory sensing methods in nonvascular interventional therapy of liver tumors. Materials and Methods: In this study, 64 patients with primary liver cancer or liver metastasis were retrospectively analyzed. According to two widely used clinical techniques to limit respiratory movement-breath holding and respiratory sensing technology-they were randomly allocated into two groups: respiratory gated and respiratory training. We aimed to compare the application and effect of these two techniques in the nonvascular interventional therapy of liver tumors. Results: The puncture times of the respiratory-gated and respiratory training groups were 5.34 ± 2.47 and 8.41 ± 3.63 min, respectively. Puncture errors were 10.00 ± 2.65 and 12.81 ± 8.57 mm, respectively. Puncture adjustment times were 3.06 ± 1.26 and 4.87 ± 1.69 times, respectively, and the differences were statistically significant (P < 0.01). Conclusions: Respiratory sensing technology has been effectively used to assist in puncturing liver malignant tumors using a radiofrequency (RF) ablation (RFA) system that is guided by computed tomography (CT) scans. It is superior to the classical breath-holding step puncture technique in terms of puncture time, puncture error, and puncture needle adjustment times.

Erratum: PI3K/Akt/HIF-1α signaling pathway mediates HPV-16 oncoprotein-induced expression of EMT-related transcription factors in non-small cell lung cancer cells: Erratum.

[This corrects the article DOI: 10.7150/jca.26112.].

IL-6/gp130/STAT3 signaling contributed to the activation of the PERK arm of the unfolded protein response in response to chronic ß-adrenergic stimulation.

Prolonged activation of the PERK branch of the unfolded protein response (UPR) promotes cardiomyocytes apoptosis in response to chronic ß-adrenergic stimulation. STAT3 plays a critical role in ß-adrenergic functions in the heart. However, whether STAT3 contributed to ß-adrenoceptor-mediated PERK activation and how ß-adrenergic signaling activates STAT3 remains unclear. This study aimed to investigate whether STAT3-Y705 phosphorylation contributed to the PERK arm activation in cardiomyocytes and if IL-6/gp130 signaling was involved in the chronic ß-AR-stimulation-induced STAT3 and PERK arm activation. We found that the PERK phosphorylation was positively associated with STAT3 activation. Wild-type STAT3 plasmids transfection activated the PERK/eIF2α/ATF4/CHOP pathway in cardiomyocytes while dominant negative Y705F STAT3 plasmids caused no obvious effect on PERK signaling. Stimulation with isoproterenol produced a significant increase in the level of IL-6 in the cardiomyocyte's supernatants, while IL-6 silence inhibited PERK phosphorylation but failed to attenuate STAT3 activation in response to isoproterenol stimulation. Gp130 silence attenuated isoproterenol-induced STAT3 activation and PERK phosphorylation. Inhibiting IL-6/gp130 pathway by bazedoxifene and inhibiting STAT3 by stattic both reversed isoproterenol-induced STAT3-Y705 phosphorylation, ROS production, PERK activation, IRE1α activation, and cardiomyocytes apoptosis in vitro. Bazedoxifene (5 mg/kg/day by oral gavage once a day) exhibited similar effect as carvedilol (10 mg/kg/day by oral gavage once a day) on attenuating chronic isoproterenol (30 mg/kg by abdominal injection once a day, 7 days) induced cardiac systolic dysfunction, cardiac hypertrophy and fibrosis in C57BL/6 mice. Meanwhile, bazedoxifene attenuates isoproterenol-induced STAT3-Y705 phosphorylation, PERK/eIF2α/ATF4/CHOP activation, IRE1α activation, and cardiomyocytes apoptosis to a similar extend as carvedilol in the cardiac tissue of mice. Our results showed that chronic ß-adrenoceptor-mediated stimulation activated the STAT3 and PERK arm of the UPR at least partially via IL-6/gp130 pathway. Bazedoxifene has great potential to be used as an alternative to conventional ß-blockers to attenuate ß-adrenoceptor-mediated maladaptive UPR.

Electron-Donors-Acceptors Interaction Enhancing Electrocatalytic Activity of Metal-Organic Polymers for Oxygen Reduction.

Catalysts with metal-Nx sites have long been considered as effective electrocatalysts for oxygen reduction reaction (ORR), yet the accurate structure-property correlations of these active sites remain debatable. Report here is a proof-of-concept method to construct 1,4,8,11-tetraaza[14]annulene (TAA)-based polymer nanocomposites with well-managed electronic microenvironment via electron-donors/acceptors interaction of altering electron-withdrawing ß-site substituents. DFT calculation proves the optimal -Cl substituted catalyst (CoTAA-Cl@GR) tailored the key OH* intermediate interaction with Co-N4 sites under the d-orbital regulation, hence reaching the top of ORR performance with excellent turnover frequency (0.49 e s-1 site-1 ). The combination of in situ scanning electrochemical microscopy and variable-frequency square wave voltammetry techniques contribute the great ORR kinetics of CoTAA-Cl@GR to the relatively high accessible site density (7.71×1019  site g-1 ) and fast electron outbound propagation mechanism. This work provides theoretical guidance for rational design of high-performance catalysts for ORR and beyond.

Erratum: Cytochalasin H Inhibits Angiogenesis via the Suppression of HIF-1α Protein Accumulation and VEGF Expression through PI3K/AKT/P70S6K and ERK1/2 Signaling Pathways in Non-Small Cell Lung Cancer Cells: Erratum.

[This corrects the article DOI: 10.7150/jca.29933.].

Transcranial magnetic stimulation-based closed-loop modality for activity of daily living gain in spinal cord injury: a retrospective study using propensity score matching analysis.

BACKGROUND: Although transcranial magnetic stimulation (TMS)-based closed-loop (TBCL) modality was seldom recommended for functional restoring following spinal cord injury (SCI), several studies recently came to a positive suggestion. AIM: To explore the independent factors which influence activity of daily living (ADL) gain, and systematically investigate the efficacy of TBCL for ADL gain. DESIGN: A retrospective observational study. SETTING: The First Affiliated Hospital of Guangxi Medical University. POPULATION: SCI patients with neurological dysfunction. METHODS: A total of 768 patients who received TBCL (N.=548) or sole rehabilitation (SR, N.=220) were enrolled. Analysis on propensity score matching was also performed. Finally, the cumulative inefficiencies between TBCL and SR within entire patient population, matched-patients as well as subgroup on per SCI clinical characteristics were performed. RESULTS: Multivariate analysis showed that thoracolumbar injury, single/double injury, incomplete injury, no neurogenic bladder, no neurogenic intestinal and no respiratory disorder, as well as TBCL strategy were independent positive factors for ADL gain. Meanwhile, TBCL strategy was the outstanding positive factor. TBCL caused a lower cumulative inefficiency over SR at 1, 90 and 180 days (83.2% vs. 86.8%, 54.0% vs. 63.6%, and 38.3% vs. 50.9%, respectively; all P<0.05). Propensity matching also found TBCL caused a lower cumulative inefficiency over SR after 1, 90 and 180 days (82.4% vs. 86.4%, 51.1% vs. 62.5%, and 33.5% vs. 49.4%, respectively; all P<0.05). Subgroup analysis showed that TBCL caused a greater ADL gain regardless of injured site, segments of injury and injured extent, as well as whether concurrent with neurogenic bladder, neurogenic intestinal and respiratory disorder (all P<0.05). Further, TBCL was more effective in 180-days overall ADL gain within each subgroup (all P<0.05), except the subgroup whether concurrent with respiratory disorder (P>0.05). CONCLUSIONS: Our study indicates that TBCL strategy was the most outstanding independent positive factors for ADL gain. Further, TBCL is a better choice than SR in ADL gain for SCI-relevant neurological dysfunctions in case of adequate stimuli distance and individual temperature, regardless of discrepancy of clinical feature. CLINICAL REHABILITATION IMPACT: This study helps to improve everyday management for rehabilitative intervention on SCI. For another thing, the present study may be good for neuromodulation practice on function restoring in SCI rehabilitation clinics.

Notopterol Ameliorates Hyperuricemia-Induced Cardiac Dysfunction in Mice.

Notopterol is a naturally occurring furanocoumarin compound found in the root of Notopterygium incisum. Hyperuricemia involves the activation of chronic inflammation and leads to cardiac damage. Whether notopterol has cardioprotective potential in hyperuricemia mice remains elusive. The hyperuricemic mouse model was constructed by administration of potassium oxonate and adenine every other day for six weeks. Notopterol (20 mg/kg) and allopurinol (10 mg/kg) were given daily as treatment, respectively. The results showed that hyperuricemia dampened heart function and reduced exercise capacity. Notopterol treatment improved exercise capacity and alleviated cardiac dysfunction in hyperuricemic mice. P2X7R and pyroptosis signals were activated both in hyperuricemic mice and in uric acid-stimulated H9c2 cells. Additionally, it was verified that inhibition of P2X7R alleviated pyroptosis and inflammatory signals in uric acid-treated H9c2 cells. Notopterol administration significantly suppressed expression levels of pyroptosis associated proteins and P2X7R in vivo and in vitro. P2X7R overexpression abolished the inhibition effect of notopterol on pyroptosis. Collectively, our findings suggested that P2X7R played a critical role in uric acid-induced NLRP3 inflammatory signals. Notopterol inhibited pyroptosis via inhibiting the P2X7R/NLRP3 signaling pathway under uric acid stimulation. Notopterol might represent a potential therapeutic strategy against pyroptosis and improve cardiac function in hyperuricemic mice.

STAT3 signaling promotes cardiac injury by upregulating NCOA4-mediated ferritinophagy and ferroptosis in high-fat-diet fed mice.

High-fat diet (HFD) intake provokes obesity and cardiac anomalies. Recent studies have found that ferroptosis plays a role in HFD-induced cardiac injury, but the underlying mechanism is largely unclear. Ferritinophagy is an important part of ferroptosis that is regulated by nuclear receptor coactivator 4 (NCOA4). However, the relationship between ferritinophagy and HFD-induced cardiac damage has not been explored. In this study, we found that oleic acid/palmitic acid (OA/PA) increased the level of ferroptotic events including iron and ROS accumulation, upregulation of PTGS2 mRNA and protein levels, reduced SOD and GSH levels, and significant mitochondrial damage in H9C2 cells, which could be reversed by the ferroptosis inhibitor ferrostatin-1 (Fer-1). Intriguingly, we found that the autophagy inhibitor 3-methyladenine mitigated OA/PA-induced ferritin downregulation, iron overload and ferroptosis. OA/PA increased the protein level of NCOA4. Knockdown of NCOA4 by SiRNA partly reversed the reduction in ferritin, mitigated iron overload and lipid peroxidation, and subsequently alleviated OA/PA-induced cell death, indicating that NCOA4-mediated ferritinophagy was required for OA/PA-induced ferroptosis. Furthermore, we demonstrated that NCOA4 was regulated by IL-6/STAT3 signaling. Inhibition or knockdown of STAT3 effectively reduced NCOA4 levels to protect H9C2 cells from ferritinophagy-mediated ferroptosis, whereas STAT3 overexpression by plasmid appeared to increase NCOA4 expression and contribute to classical ferroptotic events. Consistently, phosphorylated STAT3 upregulation, ferritinophagy activation, and ferroptosis induction also occurred in HFD-fed mice and were responsible for HFD-induced cardiac injury. In addition, we found evidence that piperlongumine, a natural compound, effectively reduced phosphorylated STAT3 levels to protect cardiomyocytes from ferritinophagy-mediated ferroptosis both in vitro and in vivo. Based on these findings, we concluded that ferritinophagy-mediated ferroptosis was one of the critical mechanisms contributing to HFD-induced cardiac injury. The STAT3/NCOA4/FTH1 axis might be a novel therapeutic target for the treatment of HFD-induced cardiac injury.

Efficiency and safety of high-power ablation guided by Lesion size index: An ex vivo porcine heart study.

BACKGROUND: Although Lesion size index (LSI) has been reported to highly predict radiofrequency lesion size in vitro, its accuracy in lesion size and steam pop estimation has not been well investigated for every possible scenario. METHODS: Initially, radiofrequency ablations were performed on porcine myocardial slabs at various power, CF, and time settings with blinded LSI. Subsequently, radiofrequency power at 20, 30, 40, 50, and 60 W was applied at CF values of 5, 10, 20, and 30 g to reach target LSIs of 4, 5, 6, and 7. Lesion size and steam pops were recorded for each ablation. RESULTS: Lesion size was positively correlated with LSI regardless of power settings (p < 0.001). The linear correlation coefficients of lesion size and LSI decreased at higher power settings. At high power combined with high CF settings (50 W/20 g), lesion depth and LSI showed an irrelevant correlation (p = 0.7855). High-power ablation shortened ablation time and increased the effect of resistive heating. LSI could predict the risk of steam pops at high-power settings with the optimal threshold of 5.65 (sensitivity, 94.1%; specificity, 46.1%). The ablation depth of the heavy heart was shallower than that of the light heart under similar ablation settings. CONCLUSIONS: LSI could predict radiofrequency lesion size and steam pops at high power settings in vitro, while synchronous high power and high CF should be avoided. Lighter hearts require relatively lower ablation settings to create appropriate ablation depth.

ATF3/SPI1/SLC31A1 Signaling Promotes Cuproptosis Induced by Advanced Glycosylation End Products in Diabetic Myocardial Injury.

Cuproptosis resulting from copper (Cu) overload has not yet been investigated in diabetic cardiomyopathy (DCM). Advanced glycosylation end products (AGEs) induced by persistent hyperglycemia play an essential role in cardiotoxicity. To clarify whether cuproptosis was involved in AGEs-induced cardiotoxicity, we analyzed the toxicity of AGEs and copper in AC16 cardiomyocytes and in STZ-induced or db/db-diabetic mouse models. The results showed that copper ionophore elesclomol induced cuproptosis in cardiomyocytes. It was only rescued by copper chelator tetrathiomolybdate rather than by other cell death inhibitors. Intriguingly, AGEs triggered cardiomyocyte death and aggravated it when incubated with CuCl2 or elesclomol-CuCl2. Moreover, AGEs increased intracellular copper accumulation and exhibited features of cuproptosis, including loss of Fe-S cluster proteins (FDX1, LIAS, NDUFS8 and ACO2) and decreased lipoylation of DLAT and DLST. These effects were accompanied by decreased mitochondrial oxidative respiration, including downregulated mitochondrial respiratory chain complex, decreased ATP production and suppressed mitochondrial complex I and III activity. Additionally, AGEs promoted the upregulation of copper importer SLC31A1. We predicted that ATF3 and/or SPI1 might be transcriptional factors of SLC31A1 by online databases and validated that by ATF3/SPI1 overexpression. In diabetic mice, copper and AGEs increases in the blood and heart were observed and accompanied by cardiac dysfunction. The protein and mRNA profile changes in diabetic hearts were consistent with cuproptosis. Our findings showed, for the first time, that excessive AGEs and copper in diabetes upregulated ATF3/SPI1/SLC31A1 signaling, thereby disturbing copper homeostasis and promoting cuproptosis. Collectively, the novel mechanism might be an alternative potential therapeutic target for DCM.

Cirsiliol regulates mitophagy in colon cancer cells via STAT3 signaling.

BACKGROUND: Mitophagy is a type of selective autophagy for dysfunctional mitochondria and plays a key role in tumorigenesis and cancer progression. However, whether mitophagy plays a role in colon cancer remains unclear. Cirsiliol is a natural product and has been found to exert anti-cancer effects in multiple tumors. The effects of cirsiliol in the tumorigenesis and progression of colon cancer remain unknown. METHODS: CCK8 assay, plate cloning assay, and cell scratch assay were performed to determine cell viability, colony formation, and wound healing abilities of HCT116 and SW480 cells. JC-1 staining, H2DCFDA staining, and Mito-Tracker Red staining were carried out to evaluate mitochondrial membrane potential (Δψm), intracellular reactive oxygen species (ROS) level, and mitochondrial morphology. Molecular docking technology was utilized to predict interaction of cirsiliol and signal transducer and activator of transcription 3 (STAT3). Immunofluorescence staining was used to measure nuclear translocation of STAT3. The protein levels of phosphorylated STAT3 (Y705), total STAT3, and mitophagy proteins were detected by western blot. RESULTS: In this study, we first found that cirsiliol inhibited cell viability, colony formation, and wound healing abilities of HCT116 and SW480 colon cancer cells. Moreover, cirsiliol suppressed Δψm, increased ROS production, and disrupted mitochondrial morphology via inhibiting the levels of mitophagy proteins including PINK1, Parkin, BNIP3, and FUNDC1. Application of mitophagy activator improved the levels of mitophagy-related proteins, and ameliorated Δψm and ROS levels. According to the result of molecular docking, we found that cirsiliol potentially bound to the SH2 domain of STAT3, the key domain for the functional activation of STAT3. Moreover, it was found that cirsiliol inhibited constitutive and IL­6­induced STAT3 phosphorylation and nuclear translocation by western blot and immunofluorescence analysis. Comparing with cirsiliol group, we found that overexpression of STAT3 restored the expressions of mitophagy proteins. CONCLUSIONS: Cirsiliol targets STAT3 to inhibit colon cancer cell proliferation by regulating mitophagy.

Myocardial protection of S-nitroso-L-cysteine in diabetic cardiomyopathy mice.

Diabetic cardiomyopathy (DCM) is a severe complication of diabetes mellitus that is characterized by aberrant myocardial structure and function and is the primary cause of heart failure and death in diabetic patients. Endothelial dysfunction plays an essential role in diabetes and is associated with an increased risk of cardiovascular events, but its role in DCM is unclear. Previously, we showed that S-nitroso-L-cysteine(CSNO), an endogenous S-nitrosothiol derived from eNOS, inhibited the activity of protein tyrosine phosphatase 1B (PTP1B), a critical negative modulator of insulin signaling. In this study, we reported that CSNO treatment induced cellular insulin-dependent and insulin-independent glucose uptake. In addition, CSNO activated insulin signaling pathway and promoted GLUT4 membrane translocation. CSNO protected cardiomyocytes against high glucose-induced injury by ameliorating excessive autophagy activation, mitochondrial impairment and oxidative stress. Furthermore, nebulized CSNO improved cardiac function and myocardial fibrosis in diabetic mice. These results suggested a potential site for endothelial modulation of insulin sensitivity and energy metabolism in the development of DCM. Data from these studies will not only help us understand the mechanisms of DCM, but also provide new therapeutic options for treatment.

Infralimbic medial prefrontal cortex signalling to calbindin 1 positive neurons in posterior basolateral amygdala suppresses anxiety- and depression-like behaviours.

Generalization is a fundamental cognitive ability of organisms to deal with the uncertainty in real-world situations. Excessive fear generalization and impaired reward generalization are closely related to many psychiatric disorders. However, the neural circuit mechanism for reward generalization and its role in anxiety-like behaviours remain elusive. Here, we found a robust activation of calbindin 1-neurons (Calb 1) in the posterior basolateral amygdala (pBLA), simultaneous with reward generalization to an ambiguous cue after reward conditioning in mice. We identify the infralimbic medial prefrontal cortex (IL) to the pBLACalb1 (Calb 1 neurons in the pBLA) pathway as being involved in reward generalization for the ambiguity. Activating IL-pBLA inputs strengthens reward generalization and reduces chronic unpredictable mild stress-induced anxiety- and depression-like behaviours in a manner dependent on pBLACalb1 neuron activation. These findings suggest that the IL-pBLACalb1 circuit could be a target to promote stress resilience via reward generalization and consequently ameliorate anxiety- and depression-like behaviours.

Endocardial Radiofrequency Ablation vs. Septal Myectomy in Patients With Hypertrophic Obstructive Cardiomyopathy: A Systematic Review and Meta-Analysis.

Background: Septal myectomy (SM) has been the gold standard therapy for most patients with hypertrophic obstructive cardiomyopathy (HOCM). Endocardial radiofrequency ablation of septal hypertrophy (ERASH) is a novel treatment for septal reduction. We aimed to assess the efficacy and safety between two treatment strategies. Methods: We searched PubMed, Web of Science, Cochrane Library, and Embase databases to identify relevant studies published up to March 2021. Random-effect models were used to calculate standardized mean difference (SMD) and 95% confidence intervals (CIs) for resting left ventricular outflow tract gradient (LVOTG) and septal thickness. Results: Twenty-five studies are included in this review, eighteen studies for SM and seven studies for ERASH. During follow-up, there were significant reductions of the mean resting LVOTG in adults (SM groups: SMD = -3.03, 95% CI [-3.62 to -2.44]; ERASH groups: SMD = -1.95, 95% CI [-2.45 to -1.45]) and children (SM groups: SMD = -2.67, 95% CI [-3.21 to -2.12]; ERASH groups: SMD= -2.37, 95% CI [-3.02 to -1.73]) after the septal reduction therapies. For adults, SM groups contributed to more obvious reduction than ERASH groups in interventricular septal thickness (SM groups: SMD = -1.82, 95% CI [-2.29 to -1.34]; ERASH groups: SMD = -0.43, 95% CI [-1.00 to 0.13]). The improvement of the New York Heart Association class was similar in the two groups (SM groups: 46.4%; ERASH groups: 46.7%). The periprocedural mortality in SM and ERASH were 1.1 and 1.8%, respectively. Conclusions: This systematic review suggests that SM is superior to ERASH in the treatment of HOCM. But for the patients who are at risk for open cardiac surgeries or prefer a less invasive approach, ERASH might be an optional approach.

Simultaneously Integrate Iron Single Atom and Nanocluster Triggered Tandem Effect for Boosting Oxygen Electroreduction.

Atomically nitrogen-coordinated iron atoms on carbon (FeNC) catalysts are emerging as attractive materials to substitute precious-metal-based catalysts for the oxygen reduction reaction (ORR). However, FeNC usually suffers from unsatisfactory performance due to the symmetrical charge distribution around the iron site. Elaborately regulating the microenvironment of the central Fe atom can substantially improve the catalytic activity of FeNC, which remains challenging. Herein, N/S co-doped porous carbons are rationally prepared and are verified with rich Fe-active sites, including atomically dispersed FeN4 and Fe nanoclusters (FeSA-FeNC@NSC), according to systematically synchrotron X-ray absorption spectroscopy analysis. Theoretical calculation verifies that the contiguous S atoms and Fe nanoclusters can break the symmetric electronic structure of FeN4 and synergistically optimize 3d orbitals of Fe centers, thus accelerating OO bond cleavage in OOH* for improving ORR activity. The FeSA-FeNC @NSC delivers an impressive ORR activity with half-wave-potential of 0.90 V, which exceeds that of state-of-the-art Pt/C (0.87 V). Furthermore, FeSA-FeNC @NSC-based Zn-air batteries deliver excellent power densities of 259.88 and 55.86 mW cm-2 in liquid and all-solid-state flexible configurations, respectively. This work presents an effective strategy to modulate the microenvironment of single atomic centers and boost the catalytic activity of single-atom catalysts by tandem effect.

Deciphering the Precursor-Performance Relationship of Single-Atom Iron Oxygen Electroreduction Catalysts via Isomer Engineering.

Single atom Fe-nitrogen-carbon (Fe-N-C) catalysts have high catalytic activity and selectivity for the oxygen reduction reaction (ORR), and are possible alternatives for Pt-based materials. However, the reasonable design and selection of precursors to establish their relationship with Fe-N-C catalyst performance is still a formidable task. Herein, precursors with controllable structures are easily achieved through isomer engineering, with the purpose of regulating the active site density and microscopic morphology of the final electrocatalyst. As-proof-of-concept, phenylenediamine isomers-based polymers are used as precursors to fabricate Fe-N-C catalysts. The Fe-PpPD-800 derived from p-phenylenediamine shows that the best ORR activity with a half-wave potential (E1/2 ) reaches 0.892 V vs reversible hydrogen electrode (RHE), which is better than the counterparts derived from o-phenylenediamine (Fe-PoPD-800) and m-phenylenediamine (Fe-PmPD-800), even surpassing commercial Pt/C (E1/2  = 0.881 V vs RHE). Furthermore, the self-made zinc-air battery based on Fe-PpPD-800 achieves high power density and specific capacity up to 242 mW cm-2 and 873 mA h gZn -1 respectively, a stable open circuit voltage of 1.45 V, and excellent cycling stability. This work not only proves the practicability of adjusting the catalytic activity of single-atom catalysts through isomer engineering, but also provides an approach to understand the relationship between precursors and target catalysts performance.