Prediction of the left ventricular mass index in hypertensive patients using the product of red cell distribution width and mean corpuscular volume.

The product of red cell distribution width (RDW) and mean corpuscular volume (MCV) has been identified as an indicator of target organ damage in cases of hypertension. However, the role of the RDW-MCV product in assessing carotid alteration, renal damage, and left ventricular hypertrophy in patients with hypertension has not been elucidated. In this cross-sectional study, a total of 1115 participants with hypertension were included. The RDW and MCV at admission were measured using an automated hematology analyzer. Organ damage was determined by the left ventricular mass index (LVMI), carotid intima-media thickness, and estimated glomerular filtration rate. The prevalence rates of carotid alteration and left ventricular hypertrophy were 57.0% and 18.0%, respectively. A higher RDW-MCV product and RDW were observed in hypertensive patients who developed carotid alteration. After adjusting for potential confounding factors, the correlations of the RDW-MCV product (P = .285) and RDW (P = .346) with carotid alteration were not significant. Moreover, the analysis of variance showed no significant correlation between RDW and LVMI (P = .186). However, the RDW-MCV product was higher in individuals with a high LVMI compared to those with a normal LVMI. Multivariable linear regression analysis revealed that the RDW-MCV product was independently associated with the LVMI (ß = 2.519, 95% CI: 0.921-4.116; P = .002), but not the estimated glomerular filtration rate (ß = -0.260, 95% CI: -2.031-1.511; P = .773). An elevated RDW-MCV product may be a predictor for left ventricular hypertrophy in patients with hypertension.

The m6A demethylase fat mass and obesity-associated protein mitigates pyroptosis and inflammation in doxorubicin-induced heart failure via the toll-like receptor 4/NF-κB pathway.

Background: Doxorubicin (Dox) can induce cardiotoxicity, thereby restricting the utility of this potent drug. Herein, the study ascertained the mechanism of the N6-methyladenosine (m6A) demethylase fat mass and obesity-associated protein (FTO) in pyroptosis and inflammation during Dox-induced heart failure (HF). Methods: Serum samples were collected from HF patients for detection of the expression of FTO and toll-like receptor 4 (TLR4). Dox-treated H9C2 cardiomyocytes were chosen for in vitro HF modeling, followed by measurement of FTO and TLR4 expression. Cardiomyocytes were detected for viability, apoptosis, spatial distribution of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), and the levels of lactic dehydrogenase, inflammatory factors, oxidative stress markers, and pyroptosis-related proteins. The m6A levels of mRNA were examined. RNA immunoprecipitation (RIP) and mRNA stability measurement were used to determine mRNA and protein expression, and RNA m6A dot blot and methylated-RIP assay were performed to detect m6A methylation levels. The expression of p-NF-κB p65 and p-IκB-α was measured by western blotting. Results: In the serum of HF patients, FTO was elevated while TLR4 was decreased. Dox treatment reduced FTO expression and increased m6A methylation levels and TLR4 expression in H9C2 cells. Overexpression of FTO and knockdown of TLR4 reduced apoptosis, cytotoxicity, inflammation, pyroptosis, oxidative stress, NLRP3 co-localization, and fluorescence intensity in Dox-induced H9C2 cells. Mechanistically, FTO resulted in reduced binding activity of YTHDF1 to TLR4 mRNA via m6A demethylation of TLR4, thus declining TLR4, p-NF-κB p65, and p-IκB-α expression. TLR4 knockdown counteracted the effects of FTO knockdown on Dox-induced H9C2 cells. Conclusions: FTO alleviated Dox-induced HF by blocking the TLR4/NF-κB pathway.

Sirtuin 2 Exerts Regulatory Functions on Radiation-Induced Myocardial Fibrosis in Mice by Mediating H3K27 Acetylation of Galectin-3 Promoter.

Background: Sirtuin 2 (SIRT2) and galectin-3 have been shown to protect the heart against fibrosis. However, their impacts on radiation-induced myocardial fibrosis (RIMF) remain to be elucidated. To deepen this understanding, the current study sought to explore the effects of SIRT2 and galectin-3 on RIMF and the underlying mechanisms. Methods: Galectin-3 knockout mice were obtained, and a radiation-induced heart damage (RIHD) mouse model was induced by local radiation exposure to the heart. Lentivirus transfection was then performed, and heart function, fibrosis of heart tissues, and levels of SIRT2, galectin-3, and fibrosis-related markers collagen type-I/-III and matrix metalloproteinase (MMP)2/MMP9 were respectively assessed by echocardiography, hematoxylin-eosin and Masson staining, reverse transcription-quantitative polymerase chain reaction, Western blot, and immunofluorescence staining. Additionally, Western blot and chromatin immunoprecipitation were used to test H3K27 acetylation levels and the binding of H3K27ac to galectin-3, respectively. Results: After radiation exposure, heart tissues from the galectin-3 knockout mice had a smaller fibrotic area compared to normal mice, with reduced expression levels of collagen type-I/-III and MMP2/MMP9. SIRT2 was down-regulated and galectin-3 was up-regulated after RIHD treatment. The histone deacetylase inhibitor sirtinol promoted galectin-3 expression and H3K27 acetylation in a time-dependent manner, and increased H3K27ac enrichment in the galectin-3 promoter. Overexpression of SIRT2 down-regulated H3K27ac, collagen type-I/-III, and MMP2/MMP9 expression levels, and reduced the fibrotic area in mouse heart tissues. However, these effects were reversed by the additional overexpression of galectin-3. Conclusions: SIRT2 facilitates deacetylation of H3K27 to inhibit galectin-3 transcription, thus ameliorating RIMF in mice.

The active pulling technique to solve microcatheter-uncrossable lesions in retrograde chronic total occlusion percutaneous coronary intervention.

BACKGROUND: It is not uncommon to encounter retrograde microcatheter-uncrossable lesions in retro-recanalization of Chronic Total Occlusion (CTO) cases, existing solutions were time-consuming or complicated to operate. Therefore, the present study aimed to propose and evaluate the feasibility, safety of a novel technique termed Active Pulling retrograde microcatheter crossing Technique (APT) during retrograde CTO percutaneous coronary intervention (PCI). METHODS: We retrospectively collected retrograde CTO-PCI cases from February 2017 to April 2023, only cases with the retrograde wire successfully crossed the CTO lesion were analyzed. The baseline clinical characteristics, angiographic characteristics, procedural details, and in-hospital major adverse cardiac events (MACEs) were compared. RESULTS: A total of 80 CTO cases were divided into the APT group and the non-APT group according to whether the APT was applied in the procedure. The APT group had a higher rate of device success than the non-APT group (100% vs. 85%, P = 0.013), with shorter duration (5.3 ± 3.8 vs. 18.6 ± 5.9 min, P < 0.001) and a smaller number of retrograde microcatheters were used (P < 0.001). In the APT group, the average air kerma radiation exposure was lower (2.7 ± 1.2 vs. 4.3 ± 1.7 Gy, P < 0.001), the fluoroscopy time (69.0 ± 15.0 vs. 88.1 ± 18.9 min, P < 0.001) and the procedure time (116.2 ± 22.2 vs. 131.6 ± 28.7 min, P = 0.009) was shorter than the non-APT group. The technical success rate of both groups reached 100% while the procedure success rate was higher in the APT group than the non-APT group (100% vs. 85%, P = 0.13). CONCLUSIONS: The APT is an easy and safe technique that can greatly improve procedural efficiency without adding other instruments, and allows the retrograde microcatheter to quickly crossing the CTO body after successful retrograde wire externalization.

From Porphyrin-Like Rings to High-Density Single-Atom Catalytic Sites: Unveiling the Superiority of p-C2N for Bifunctional Oxygen Electrocatalysis.

With effective utilization of the catalytic site, single-atom catalysts (SACs) supported by nitrogen atoms surrounding built-in pores of two-dimensional (2D) materials, such as porphyrin/phthalocyanine-based covalent organic frameworks, have been highly promising electrocatalysts in the oxygen evolution reaction (OER) and oxygen reduction reaction (ORR) processes for the air electrode of the metal-air battery. However, the number of stable single-atom anchoring sites, i.e., accessible single-atom metal sites, has been concerning as a result of the appearance of heterogeneous or large and even supersized pores in substrate materials. 2D porous graphitic carbon nitride (PGCN) with a stronger stability and smaller component is regarded as a more potential alternative owing to similar controllability and designability. In this work, inspired by the robust coordinated TM-N4 environment of porphyrin/phthalocyanine molecules, novel p-C2N with a high density of porphyrin-like organic units is rationally designed. In well-designed p-C2N, a higher homogeneity and uniformity of coordination sites can enhance the electrocatalytic activity in the whole catalytic material and better prevent SACs from sintering and agglomerating into thermodynamically stable nanoclusters. Utilizing density functional theory (DFT), the stability of the p-C2N monolayer, TM@p-C2N, and OER/ORR catalytic activities of TM@p-C2N (TM including Mn, Fe, Co, Ni, Cu, Ru, Rh, Pd, Ag, Os, Ir, Pt, and Au) are systematically evaluated. Among them, Ir@p-C2N (0.31 V of the OER and 0.36 V of the ORR), Co@p-C2N (0.47 and 0.22 V), and Rh@p-C2N (0.55 and 0.27 V) are screened as promising SACs for the bifunctional ORR and OER. The proposal of p-C2N guides a new direction for the development of TM-N-C-based SAC bifunctional electrocatalysts.

Penta-MP5 (M = B, Al, Ga, In) monolayers as high-performance photocatalysts for overall water splitting.

Two-dimensional (2D) phosphorus-rich phosphides generally preserve the excellent electronic properties of phosphorene, making them promising photocatalysts for water splitting. Despite tremendous efforts in the search for potential photocatalysts in 2D phosphides, few known 2D phosphides fully meet the requirements for photocatalytic water splitting. Herein, we systemically investigate a set of penta-MP5 (M = B, Al, Ga, and In) monolayers by first-principles calculations and identify them as potential photocatalysts for water splitting. These penta-MP5 monolayers are found to feature favorable bandgaps of about 2.70 eV with appropriate band edge positions, a high carrier mobility of 1 × 104 cm-2 V-1 s-1, an excellent optical absorption coefficient (OAC) of 1 × 105 cm-1, and a good solar-to-hydrogen (STH) efficiency of 8%. Meanwhile, free energy calculations indicate that these penta-MP5 monolayers present both hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) photocatalytic activities under light conditions. All these excellent properties demonstrate that penta-MP5 monolayers are suitable candidates as photocatalysts for promising applications in overall water splitting.

INTRA-AORTIC BALLOON PUMP REDUCES 30-DAY MORTALITY IN EARLY-STAGE CARDIOGENIC SHOCK COMPLICATING ACUTE MYOCARDIAL INFARCTION ACCORDING TO SCAI CLASSIFICATION.

ABSTRACT: Background: Cardiogenic shock complicating acute myocardial infarction (AMICS) remains a high 30-day mortality. Mechanical circulatory support devices are increasingly used in AMICS, but their effects on mortality vary partly because of shock severity. Aims: This study aimed to evaluate the association between intra-aortic balloon pump (IABP) and 30-day mortality in patients with early-stage AMICS. Methods: We retrospectively analyzed patients with ST-segment elevation myocardial infarction (STEMI) based on a multicenter clinical trial (NCT04996901). Patients were stratified by IABP use, and shock severity was classified according to the Society for Cardiovascular Angiography and Interventions (SCAI) SHOCK stages. The primary outcome was 30-day all-cause mortality. The association between IABP and 30-day mortality was evaluated across shock stages using propensity score matching, weighting, and logistic regression. Results: Five thousand three hundred forty-three patients were included, and 299 received IABP. The SCAI SHOCK stage was associated with 30-day mortality (odds ratio [OR], 20.19; 95% confidence interval [CI], 13.60-29.97; P < 0.001). In the 580 matched patients, a significant interaction between IABP and 30-day mortality at different shock stages was observed ( P = 0.005). Intra-aortic balloon pump was associated with lower 30-day mortality among patients with shock stage A/B (5.8% vs. 1.2%; OR, 0.19; 95% CI, 0.03-0.73; P = 0.034) but not stage C/D/E (29.3% vs. 38.1%; OR, 1.49; 95% CI, 0.84-2.65; P = 0.172). These results were confirmed by sensitivity analyses of the weighted cohort. Conclusions: Intra-aortic balloon pump reduced 30-day mortality in patients with early-stage AMICS. The SCAI SHOCK stage provides risk stratification for patients with STEMI and helps identify those who may respond well to IABP.

RNA methylation reading protein YTHDF2 relieves myocardial ischemia-reperfusion injury by downregulating BNIP3 via m6A modification.

BNIP3 is reported to be involved in hypoxia-induced mitochondrial defect and cell death in cardiomyocytes. However, little is known about the specific function and molecular mechanism of BNIP3-mediated mitophagy in myocardial ischemia-reperfusion injury (MIRI). Herein, this study explored the mechanism regulating BNIP3-modulated mitophagy in MIRI. Rat cardiomyocytes (H9c2 cells) underwent transfection and hypoxia/reoxygenation (H/R) treatment, followed by cell viability and apoptosis detection. Gain-of-function assays were conducted in rats before MIRI modeling, followed by the monitoring of cardiac changes and the evaluation of cardiac function, myocardial infarction area, and apoptosis in myocardial tissues. The levels of creatine kinase MB (CK-MB), cardiac troponin I (cTnI), lactic dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), p62, and LC3 II/LC3 I were tested in rat serum or H9c2 cells. The co-localization of LC3 and TOMM20 was analyzed. The interaction of BNIP3 with YTHDF2 was assessed. H/R treatment decreased cell viability and p62 and SOD levels while elevating cell apoptosis, the levels of CK-MB, cTnI, LDH, MDA, ROS, and LC3 II/LC3 I, the number of autophagosomes, and the co-localization of LC3 and TOMM20 in cardiomyocytes, which were neutralized by downregulating BNIP3 or upregulating YTHDF2. Moreover, upregulation of YTHDF2 repressed myocardial injury and mitophagy in MIRI rats. Mechanistically, YTHDF2 mediated BNIP3 expression by recognizing methylated BNIP3. Upregulation of BNIP3 counteracted the suppressive effect of YTHDF2 overexpression on H/R-induced injury and mitophagy in cardiomyocytes. The RNA methylation reading protein YTHDF2 ameliorated MIRI by downregulating BNIP3 via m6A modification.

Analysis of risk factors for postoperative acute cerebral infarction in patients with type B aortic dissection.

OBJECTIVE: To study risk factors of postoperative acute cerebral infarction (PACI) in patients with type B aortic dissection (TB-AD). METHODS: The data of 36 patients with TB-AD and PACI undergoing endovascular aortic repair (EVAR) from Mar 2018 and Mar 2021 were collected as the PACI group retrospectively. The data of 114 TB-AD patients without PACI were collected as the control group retrospectively. The medical history, surgery-related indicators, general data, imaging data and laboratory test results (D-dimer (D-D), preoperative serum creatinine and preoperative white blood cell count) were compared. Then, logistic regression was applied to analyze risk factors for PACI in TB-AD patients. RESULTS: The surgery time, blood loss and hospital stay of patients in the PACI group were determined to be obviously higher/longer when comparing to those in the control group. Aortic arch radius of curvature and length of proximal anchoring zone showed no significant difference between the two groups. Pearson correlation analysis indicated that D-D level after surgery was positively related to white blood cell count and serum creatinine level in TB-AD patients. Binary logistic regression analysis showed that operation time, emergency surgery, preoperative D-D and preoperative serum creatinine level were independent risk factors for PACI after EVAR in the patients with TB-AD (P < 0.05). CONCLUSION: There are many independent risk factors for PACI after EVAR in patients with TB-AD, and preoperative D-D level and serum creatinine level should be given attention.

C3N2: the missing part of highly stable porous graphitic carbon nitride semiconductors.

Two-dimensional (2D) porous graphitic carbon nitrides (PGCNs) with semiconducting features have attracted wide attention because of built-in pores with various active sites, large surface area, and high physicochemical stability. However, only a few PGCNs have been synthesized, covering a 1.23-3.18 eV band gap. We systematically investigate two new 2D PGCN monolayers, T-C3N2 and H-C3N2, including possible pathways for their experimental synthesis. Based on first-principles calculations, the mechanical, electronic, and optical properties of T-C3N2 and H-C3N2 have been systematically investigated. These two architectural frameworks exhibit contrasting mechanical characteristics owing to their structural differences. Both T-C3N2 and H-C3N2 monolayers are predicted to be intrinsic semiconductors. Exceptionally, the stacking bilayers of T-C3N2 can transform into a rare 2D nodal-line semimetal structure. The narrow bandgap (0.35 eV) of the T-C3N2 monolayer and its extraordinary transformation in the bilayer electronic structure fill the vacancy of PGCNs as electronic devices in the middle/long wave infrared region. C3N2 structures possess ultrahigh anisotropic carrier mobilities (×104 cm2 V-1 s-1) and exceptional absorption coefficients (×105 cm-1) in the near-infrared and visible light regions, suggesting its possible optoelectronic applications. The findings expand the scope of 2D PGCNs and offer guides for their experimental realization.

Thioredoxin Reductase 2 Synergizes with Cytochrome c, Somatic to Alleviate Doxorubicin-Induced Oxidative Stress in Cardiomyocytes and Mouse Myocardium.

Doxorubicin (DOX) may cause multiple side effects, which include cardiotoxicity. Hence, to ascertain the impact of thioredoxin reductase 2 (TXNRD2) and cytochrome c, somatic (CYCS) on DOX-induced oxidative stress (OS) in cardiomyocytes and mouse myocardium, this study was implemented. DOX was utilized to treat cardiomyocytes and mice, and TXNRD2 and CYCS expression in cell supernatant and mouse myocardial tissues was detected. TXNRD2 and/or CYCS were overexpressed in DOX-induced cardiomyocytes and mice. In cardiomyocytes, cell viability and the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and glutathione (GSH) were measured. In mice, pathologic changes of the heart, ejection fraction (EF), fractional shortening (FS), and heart weight (HW) /tibial length (TL) ratio, and the contents of lactic dehydrogenase (LDH), creatine kinase-MB (CK-MB), and cardiac troponin I (cTnI) were analyzed. To assess the binding between TXNRD2 and CYCS, coimmunoprecipitation and glutathione S-transferase pull-down assays were performed. TXNRD2 and CYCS were downregulated in DOX-treated cardiomyocytes and mice. Mechanistically, TXNRD2 interacted with CYCS. Overexpression of TXNRD2 or CYCS augmented viability and SOD, CAT, and GSH levels but reduced ROS and MDA contents in DOX-induced cardiomyocytes, which was further facilitated by simultaneous overexpression of TXNRD2 or CYCS. Moreover, TXNRD2 or CYCS upregulation improved the pathologic changes in myocardial tissues, along with increases in EF, FS, and HW/TL ratio of the heart and SOD, CAT, and GSH levels and decreases in LDH, CK-MB, cTnI, ROS, and MDA levels. TXNRD2 coordinated with CYCS to alleviate DOX-induced OS in cardiomyocytes and mouse myocardium.

A semiconductor Sc2S3 monolayer with ultrahigh carrier mobility for UV blocking filter application.

For humans, ultraviolet (UV) light from sun is harmful to our eyes and eye-related cells. This detrimental fact requires scientists to search for a material that can efficiently absorb UV light while allowing lossless transmission of visible light. Using an unbiased first-principles swarm intelligence structure search, we explored two-dimensional (2D) Sc-S crystals and identified a novel Sc2S3 monolayer with good thermal and dynamical stability. The optoelectronic property simulations revealed that the Sc2S3 monolayer has a wide indirect bandgap (3.05 eV) and possesses an ultrahigh carrier mobility (2.8 × 103 cm2 V-1 s-1). Remarkably, it has almost transparent visible light absorption, while it exhibits an ultrahigh absorption coefficient up to × 105 cm-1 in the ultraviolet region. Via the application of biaxial strain and thickness modulation, the UV light absorption coefficients of Sc2S3 can be further improved. These findings manifest an attractive UV blocking optoelectronic characteristic of the Sc2S3 configuration as a prototypical nanomaterial for the potential application in UV blocking filters.

MiR-30a-5p Promotes Vein Graft Restenosis by Inhibiting Cell Autophagy through Targeting ATG5.

OBJECTIVE: The aim of the study was to investigate the role of miR-30a-5p in restenosis of rats following vein grafting and the underlying mechanism. METHODS: Vein graft rat models were established and perfused with miR-30a-5p antagomir and si-ATG5 to probe the regulation of miR-30a-5p/ATG5 on intimal hyperplasia. Human saphenous vein smooth muscle cells (HSVSMCs) were obtained from the great saphenous veins of patients undergoing coronary artery bypass grafting and subjected to assays for autophagy, proliferation, and migration after gain and loss of function of miR-30a-5p and/or ATG5. The binding of miR-30a-5p and ATG5 was confirmed by RIP and dual-luciferase reporter assays. RESULTS: MiR-30a-5p expression gradually increased, ATG5 expression gradually decreased, and the intima was increasingly thickened during restenosis of grafted veins. Knockdown of miR-30a-5p in rats repressed the restenosis of vein grafts, while a deficiency of ATG5 reversed the effect of miR-30a-5p inhibition. Upregulation of miR-30a-5p enhanced the proliferation and migration of HSVSMCs and inhibited the autophagy, while downregulation of miR-30a-5p or overexpression of ATG5 showed opposite effects. ATG5 is a target gene of miR-30a-5p. CONCLUSION: MiR-30a-5p exacerbates vein graft restenosis by repressing ATG5 expression and inhibiting autophagy.

The potential function of SP1 and CPPED1 in restenosis after percutaneous coronary intervention.

OBJECTIVES: Impacts of molecular pathways have been discussed recently on restenosis after percutaneous coronary intervention (PCI). Hence, this study aimed to explore the impact of calcineurin-like phosphoesterase domain containing 1 (CPPED1) and specificity protein 1 (SP1) on restenosis after PCI. METHODS: A carotid balloon injury rat model was established, followed by western blot analysis of SP1 and CPPED1 expression in carotid artery (CA) tissues. After SP1 and CPPED1 were overexpressed, the neointimal hyperplasia and luminal stenosis were assessed. In addition, EPC underwent hypoxia/reoxygenation (H/R) treatment to construct an endothelial injury cell model. Then, cell proliferation, apoptosis, intracellular reactive oxygen species (ROS), and Ca2+ concentration were detected with cell counting kit-8 (CCK-8), flow cytometry, Chloromethyl-2'7'-dichlorofluorescein diacetate (CM-H2DCFDA) penetrant, and Fluo-4 AM staining, respectively. The binding relationship between SP1 and CPPED1 was verified by dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. RESULTS: SP1 and CPPED1 were lowly expressed in the model rats with carotid balloon injury. Mechanistically, SP1 bound to the promoter region of CPPED1 to activate CPPED1 expression. Overexpressing SP1 or CPPED1 lowered neointimal formation and restenosis rate, thus promoting the recovery of carotid balloon injury in rats. Meanwhile, SP1 and CPPED1 upregulation reduced ROS levels, Ca2+ concentration, and apoptosis of EPCs, accompanied by accelerated EPC viability. CONCLUSIONS: SP1 or CPPED1 overexpression reduced neointimal formation and restenosis rate in carotid balloon injury.

Salmonella pathogenicity island 1 knockdown confers protection against myocardial fibrosis and inflammation in uremic cardiomyopathy via down-regulation of S100 Calcium Binding Protein A8/A9 transcription.

BACKGROUND/AIM: Uremic cardiomyopathy (UCM) is a characteristic cardiac pathology that is commonly found in patients with chronic kidney disease. This study dissected the mechanism of SPI1 in myocardial fibrosis and inflammation induced by UCM through S100A8/A9. METHODS: An UCM rat model was established, followed by qRT-PCR and western blot analyses of SPI1 and S100A8/A9 expression in myocardial tissues. After alterations of SPI1 and S100A8/A9 expression in UCM rats, the blood specimens were harvested from the cardiac apex of rats. The levels of creatine phosphokinase-MB (CK-MB), blood creatinine, blood urea nitrogen (BUN), and inflammatory cytokines (interleukin [IL]-6, IL-1ß, and tumor necrosis factor-α [TNF-α]) were examined in the collected blood. Collagen fibrosis was assessed by Masson staining. The expression of fibrosis markers [transforming growth factor (TGF)-ß1, α-smooth muscle actin (SMA), Collagen 4a1, and Fibronectin], IL-6, IL-1ß, and TNF-α was measured in myocardial tissues. Chromatin immunoprecipitation and dual-luciferase reporter gene assays were conducted to test the binding relationship between SPI1 and S100A8/A9. RESULTS: S100A8/A9 and SPI1 were highly expressed in the myocardial tissues of UCM rats. Mechanistically, SPI1 bound to the promoter of S100A8/A9 to facilitate S100A8/A9 transcription. S100A8/A9 or SPI1 knockdown reduced myocardial fibrosis and inflammation and the levels of CK-MB, blood creatinine, and BUN, as well as the expression of TGF-ß1, α-SMA, Collagen 4a1, Fibronectin, IL-6, TNF-α, and IL-1ß in UCM rats. CONCLUSION: SPI1 knockdown diminished S100A8/A9 transcription, thus suppressing myocardial fibrosis and inflammation caused by UCM.

A new phosphorene allotrope: the assembly of phosphorene nanoribbons and chains.

Phosphorene allotrope monolayers such as blue and red phosphorus are being designed and synthesized to be used in the optoelectronics field due to their tunable bandgap and high mobility. Using the organic molecule self-assembly method similar to the synthesis of graphene allotropes, a novel phosphorene allotrope, P567 monolayer, with five-, six-, and seven-membered rings is designed through the assembly of black phosphorus chains and blue phosphorene nanoribbons. Ab initio molecular dynamics, phonon dispersion, and elastic constants demonstrate the dynamic, thermal, and mechanical stability of the P567 monolayer. Additionally, the first-principles calculations show that the P567 monolayer is an indirect bandgap semiconductor with moderate bandgap and high anisotropic mobility (4.47 × 103 cm2 V-1 s-1). Compared with black phosphorene, the suitable band edge position and higher optical absorption coefficient (105 cm-1) make the P567 monolayer more likely to be used as a photocatalytic hydrolysis material. The P567 monolayer is a viable candidate for use in innovative optoelectronic devices and the assembly method provides a rational approach to designing phosphorus allotropes with high photocatalytic efficiency.

Vinpocetine and coenzyme Q10 combination alleviates cognitive impairment caused by ionizing radiation by improving mitophagy.

OBJECTIVE: This research was designed to ascertain the effect and mechanism of vinpocetine (VIN) and coenzyme Q10 (CoQ10) combination on cognitive impairment induced by ionizing radiation (IR). METHODS: Cognitive impairment in mice was induced by 9-Gy IR, and they were intraperitoneally injected with VIN, CoQ10, or VIN + CoQ10. Then novel object recognition and Morris water maze tests were used to detect cognitive function. The number of hippocampal neurons and BrdU+Dcx+ cells was observed by Nissl and immunofluorescence staining. Mitochondrial respiratory complex I, adenosine triphosphate (ATP), and mitochondrial membrane potential (MMP) were evaluated, as well as oxidative stress injury. Mitophagy in hippocampal neurons was evaluated by observing the ultrastructure of hippocampal neurons and assessing the expression of mitophagy-related proteins. RESULTS: IR reduced novel object discrimination index, the time for platform crossing, and the time spent in platform quadrant, in addition to neuron loss, downregulated levels of mitochondrial respiratory complex I, ATP, and MMP, aggravated oxidative stress injury, increased expression of LC3 II/I, Beclin1, PINK1, and parkin, and decreased P62 expression. VIN or CoQ10 treatment mitigated cognitive dysfunction, neurons loss, mitochondrial damage, and oxidative stress injury, and enhanced mitophagy in hippocampal neurons. VIN and CoQ10 combination further protected against IR-induced cognitive dysfunction than VIN or CoQ10 alone. CONCLUSION: VIN combined with CoQ10 improved neuron damage, promoted mitophagy, and ameliorated cognitive impairment in IR mice.

Exploring a novel two-dimensional metallic Y4C3 sheet applied as an anode material for sodium-ion batteries.

As novel "post lithium-ion batteries" and promising alternatives to lithium-ion batteries (LIBs) suffering from the limited Li resources, sodium-ion batteries (SIBs) are nowadays emerging and show bright prospects in large-scale energy storage applications due to abundant Na resources. However, a lack of suitable anode materials has become a key obstacle for the development of SIBs. Here we explore the potential of the two-dimensional (2D) Y-C space and identify a novel anode material for SIBs, a new Y4C3 sheet with P3̄m1 crystal symmetry, by means of first-principles swarm structure calculations. This Y4C3P3̄m1 structure has rather good kinetic and thermodynamic stability, possesses intrinsic metallicity, and remains metallic after adsorbing Na atoms, ensuring good electrical conductivity during the SIB cycle. Remarkably, a Y4C3 sheet as an anode for SIBs possesses the essential properties of a high specific capacity (∼752 mA h g-1), a low barrier energy (∼0.1 eV), and suitable open-circuit voltage (0-0.15 V). These characteristics are comparable and even superior to those of another known 2D Y2C anode material, indicating that the Y4C3 sheet can act as an appealing new candidate as an anode material for SIBs and offering new insights into the 2D Y-C space.

CircSAMD4A aggravates H/R-induced cardiomyocyte apoptosis and inflammatory response by sponging miR-138-5p.

Hypoxia/reoxygenation (H/R)-induced myocardial cell injury is the main cause of acute myocardial infarction (AMI). Many proofs show that circular RNA plays an important role in the development of AMI. The purpose of this study was to investigate the role of circSAMD4A in H/R-induced myocardial injury. The levels of circular SAMD4A (circSAMD4A) were detected in the heart tissues of AMI mice and H/R-induced H9C2 cells, and the circSAMD4A was suppressed in AMI mice and H/R-induced H9C2 cells to investigate its' function in AMI. The levels of circSAMD4A and miR-138-5p were detected by real-time quantitative PCR, and MTT assay was used to detect cell viability. TUNEL analysis and Annexin V-FITC were used to determine apoptosis. The expression of Bcl-2 and Bax proteins was detected by Western blot. IL-1ß, TNF-α and IL-6 were detected by ELISA kits. The study found that the levels of circSAMD4A were up-regulated after H/R induction and inhibition of circSAMD4A expression would reduce the H/R-induced apoptosis and inflammation. MiR-138-5p was down-regulated in H/R-induced H9C2 cells. circSAMD4A was a targeted regulator of miR-138-5p. CircSAMD4A inhibited the expression of miR-138-5p to promote H/R-induced myocardial cell injury in vitro and vivo. In conclusion, CircSAMD4A can sponge miR-138-5p to promote H/R-induced apoptosis and inflammatory response.

A Novel Clinical Scoring Model for Interventional Therapy in Chronic Total Occlusion of the Coronary Artery.

OBJECTIVE: With the rapid development of technology and experience, the current percutaneous coronary intervention of chronic total occlusion (CTO-PCI) preoperative scoring model needs to be updated. This study aimed to evaluate the clinical value of the operator-CTO score in predicting the outcome of interventional therapy for chronic total occlusion of the coronary artery. METHODS: The data of 144 lesions in 130 patients with CTO were analyzed prospectively. The CTO procedures were performed by 10 operators with different skills and experiences. Before the procedures, J-CTO, progress, ORA, recharge, and operator-CTO scores were determined. Then, the clinical, imaging, and procedural data of patients in different operator-CTO score groups and between different operators were compared. The final focus was on comparing the predictive ability of each score on the outcome of CTO-PCI. RESULTS: The overall technical and procedural success rates were 90.9% and 88.9%, respectively. A decreasing trend in the technical success of CTO-PCI was observed according to the operator-CTO score hierarchy of "easy (≤2 points), moderate (3 points), difficult (4 points), and extremely difficult (≥5 points)" (99.0%, 87.5%, 53.8%, and 25.0%, respectively). All five scoring models were well calibrated, and the area under the curve (AUC) for the operator-CTO score was 0.901 (95% CI: 0.821-0.982, P < 0.01), larger than the AUC for the remaining four scoring models, showing excellent ability to predict technical outcomes. CONCLUSION: The operator-CTO score is a new clinical scoring tool that can predict the outcome of CTO-PCI and can be used to grade the difficulty of the procedure, with the potential to work well with a broad group of operators.