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The global incidence and prevalence of arrhythmias are continuously increasing. However, the precise mechanisms of underlying arrhythmogenesis and the optimal measures for effective treatment remain incompletely understood. The inducible form of heme oxygenase, known as heme oxygenase-1 (HO-1), is recognized as a potent antioxidant molecule capable of exerting anti-inflammatory and anti-apoptotic effects. Recent research indicates that HO-1 plays a role in preventing arrhythmias by mitigating cardiac remodeling, including electrical remodeling, ion remodeling, and structural remodeling. This review aimed to consolidate current knowledge regarding the involvement of HO-1 in arrhythmias and elucidate its underlying mechanisms of action. [ABSTRACT FROM AUTHOR]

Ventricular arrhythmias are the leading cause of sudden cardiac death in patients after myocardial infarction (MI). Connexin43 (Cx43) is the most important gap junction channel-forming protein in cardiomyocytes. Dysfunction of Cx43 contributes to impaired myocardial conduction and the development of ventricular arrhythmias. Following an MI, Cx43 undergoes structural remodeling, including expression abnormalities, and redistribution. These alterations detrimentally affect intercellular communication and electrical conduction within the myocardium, thereby increasing the susceptibility to post-infarction ventricular arrhythmias. Emerging evidence suggests that post-translational modifications play essential roles in Cx43 regulation after MI. Therefore, Cx43-targeted management has the potential to be a promising protective strategy for the prevention and treatment of post infarction ventricular arrhythmias. In this article, we primarily reviewed the regulatory mechanisms of Cx43 mediated post-translational modifications on post-infarction ventricular arrhythmias. Furthermore, Cx43-targeted therapy have also been discussed, providing insights into an innovative treatment strategy for ventricular arrhythmias after MI. [ABSTRACT FROM AUTHOR]

Ventricular arrhythmias are the leading cause of sudden cardiac death in patients after myocardial infarction (MI). Connexin43 (Cx43) is the most important gap junction channel-forming protein in cardiomyocytes. Dysfunction of Cx43 contributes to impaired myocardial conduction and the development of ventricular arrhythmias. Following an MI, Cx43 undergoes structural remodeling, including expression abnormalities, and redistribution. These alterations detrimentally affect intercellular communication and electrical conduction within the myocardium, thereby increasing the susceptibility to post-infarction ventricular arrhythmias. Emerging evidence suggests that post-translational modifications play essential roles in Cx43 regulation after MI. Therefore, Cx43-targeted management has the potential to be a promising protective strategy for the prevention and treatment of post infarction ventricular arrhythmias. In this article, we primarily reviewed the regulatory mechanisms of Cx43 mediated post-translational modifications on post-infarction ventricular arrhythmias. Furthermore, Cx43-targeted therapy have also been discussed, providing insights into an innovative treatment strategy for ventricular arrhythmias after MI. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study was to investigate the effects and mechanisms of SGLT2 inhibitor empagliflozin on diabetic coronary function.Methods: A rat diabetic model was established by injection of streptozotocin. Rats in the treated group were administered empagliflozin by gavage and rat coronary vascular tensions were measured after eight weeks. Large conductance calcium activated K+ channel currents were recorded using a patch clamp technique, while human coronary artery smooth muscle cells were used to explore the underlying mechanisms.Results: After incubation with empagliflozin (10, 30, 100, 300, 1000 μmol/L), the Δ relaxation % of rat coronary arteries were 2.459 ± 1.304, 3.251 ± 1.119, 6.946 ± 3.407, 28.36 ± 11.47, 86.90 ± 3.868, respectively. Without and with empagliflozin in the bath solution, BK channel opening probabilities at a membrane potential of +60 mV were 0.0458 ± 0.0517 and 0.3413 ± 0.2047, respectively (p < 0.05, n = 4 cells). After incubation with iberiotoxin, the Δ tensions of rat coronary arteries in the control (Ctrl), untreated (DM), low empagliflozin (10 mg/kg/d)-treated (DM+L-EMPA) and high empagliflozin (30mg/kg/d)-treated (DM+H-EMPA) group were 103.20 ± 5.85, 40.37 ± 22.12, 99.47 ± 28.51, 78.06 ± 40.98, respectively (p < 0.01 vs Ctrl, n = 3– 7; p < 0.001 vs DM+L-EMPA, n = 5– 7). Empagliflozin restored high glucose-induced downregulation of Sirt1, Nrf2, and BK-β 1, while the effect of empagliflozin disappeared in the presence of EX-527, a Sirt1 selective inhibitor.Conclusion: Empagliflozin has a vasodilation effect on the coronary arteries in a concentration-dependent manner and can activate BK channels via the Sirt1-Nrf2 mechanism. [ABSTRACT FROM AUTHOR]

Purpose: Diabetes mellitus is an independent risk factor for atrial fibrillation (AF), which may be related to accumulation of advanced glycation end products (AGEs). However, the mechanisms involved are not completely clear. Abnormality of gap junction proteins, especially connexin 43 (Cx43) and connexin 40 (Cx40) in atrial myocytes, is an important cause of increased susceptibility of AF. The aim of our work is to investigate the mechanism of dysregulated Cx43 and Cx40 in atrial myocytes of diabetic rats.Methods: We established a type 1 diabetic rat model by intraperitoneal injection of streptozotocin. HL-1 cells and primary rat atrial myocytes were treated with AGEs in vitro. Using Western blotting, immunofluorescence staining, immunohistochemistry, and lucifer yellow diffusion measurements, we investigated dysregulation of Cx43 and Cx40 and its mechanism in atrial myocytes of diabetic rats.Results: Accumulation of AGEs was found in diabetic rats. The expression of Cx43 and Cx40 was reduced in the atrium of diabetic rats, accompanied by the decrease of phosphorylated Adenosine 5'-monophosphate-activated protein kinase (p-AMPK). Similar results were found in cultured HL-1 cells and primary rat atrial myocytes, suggesting a role of AGEs on gap junction proteins. An AMPK agonist, 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR), reversed the down-regulated Cx43 expression induced by AGEs stimulation. More importantly, lucifer yellow diffusion assay showed that AGEs significantly affected gap junctional function, and these changes were reversed by AICAR.Conclusion: Thus, we conclude that AGEs cause dysregulation of Cx43 and Cx40 in diabetic atria via the AMPK pathway, thereby leading to gap junction dysfunction, which may contribute to the increased AF susceptibility in diabetes. [ABSTRACT FROM AUTHOR]

Background: Diabetes is associated with myocardial fibrosis, while the underlying mechanisms remain elusive. The aim of this study is to investigate the underlying role of calcineurin/nuclear factor of activated T cell 3 (CaN/NFATc3) pathway and the Enhancer of zeste homolog 2 (EZH2) in diabetes-related myocardial fibrosis. Methods: Streptozotocin (STZ)-injected diabetic rats were randomized to two groups: the controlled glucose (Con) group and the diabetes mellitus (DM) group. Eight weeks later, transthoracic echocardiography was used for cardiac function evaluation, and myocardial fibrosis was visualized by Masson trichrome staining. The primary neonatal rat cardiac fibroblasts were cultured with high-glucose medium with or without cyclosporine A or GSK126. The expression of proteins involved in the pathway was examined by western blotting. The nuclear translocation of target proteins was assessed by immunofluorescence. Results: The results indicated that high glucose treatment increased the expression of CaN, NFATc3, EZH2 and trimethylates lysine 27 on histone 3 (H3K27me3) in vitro and in vivo. The inhibition of the CaN/NFATc3 pathway alleviated myocardial fibrosis. Notably, inhibition of CaN can inhibit the nuclear translocation of NFATc3, and the expression of EZH2 and H3K27me3 protein induced by high glucose. Moreover, treatment with GSK126 also ameliorated myocardial fibrosis. Conclusion: Diabetes can possibly promote myocardial fibrosis by activating of CaN/NFATc3/EZH2 pathway. [ABSTRACT FROM AUTHOR]

Dilated cardiomyopathy (DCM) is characterized by the left ventricular dilatation and impaired myocardial systolic dysfunction with high mortality and morbidity. However, the underlying mechanisms remain elusive. We first identified the differentially expressed genes (DEGs) between the DCM and control group using two expression profiles from GSE3585 and GSE84796. Enrichment analysis was conducted to explore the potential mechanisms underlying DCM. A total of four algorithms, including key module of MCODE, degree, maximum neighborhood component (MNC), and maximal clique centrality (MCC), were used to identify the hub genes within Cytoscape. The correlation between hub genes and infiltrated immune cells was evaluated to determine potential immune-related genes. The expression analysis and diagnosis value analysis of potential immune-related genes were performed. Finally, the expression analysis with GSE57338 and relationship analysis with the comparative toxicogenomics database (CTD) were performed to identify the key immune-related genes in DCM. A total of 80 DEGs were screened for DCM. Enrichment analysis revealed that DEGs were involved in the immune-related pathological process. Immune infiltration analysis indicated a potentially abnormal immune response in DCM. Four up-regulated genes (COL1A2, COL3A1, CD53, and POSTN) were identified as potential immune-related genes. Finally, three genes (COL1A2, COL3A1, and POSTN) were determined as the key immune-related genes in DCM via expression analysis with a validation set (GSE57338) and relationship analysis with CTD. Our study suggested that the upregulated COL1A2, COL3A1, and POSTN might be the key immune-related genes for DCM. Further studies are needed to validate the underlying mechanisms. [ABSTRACT FROM AUTHOR]

Diabetes is a significant risk factor for arrhythmias. However, the pathophysiology of diabetes-related arrhythmias still needs to be elucidated, presumably associated with structural and electrical remodeling. There is growing evidence that inflammation and arrhythmias are intimately associated, which has spurred significant interest in exploring the regulatory links in diabetes. Recent research findings have revealed a vital role for the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling, and facilitated the occurrence of arrhythmias in diabetes, including NLRP3 inflammasome activation by multiple stressors and its downstream cytokines, interleukin-1β (IL-1β) and interleukin-18 (IL-18). This narrative review aims to summarize the complex interaction between NLRP3 inflammasomes signaling and diabetes-related arrhythmias. Articles regarding the role of NLRP3 inflammasome in diabetes-related arrhythmias and relevant mechanisms were selected. Relevant articles were selected from PubMed. The search terms were "NLRP3 inflammasome" and "diabetes" and "arrhythmia". Important references from selected articles were also retrieved. The role of NLRP3 inflammasome signaling in diabetes-induced arrhythmias may provide a new option for the prevention and treatment diabetes-related arrhythmias. [ABSTRACT FROM AUTHOR]

Objective: The relationship between different glycaemic variability (GV) indexes and adverse cardiovascular outcomes is not well understood. This study aims to determine whether GV is related to the occurrence of adverse cardiovascular events in patients with acute coronary syndrome (ACS). Methods: PubMed, EMBASE, and Web of Science were comprehensively searched from the establishment of databases to 29 June 2022. The relationship between two important GV indexes, including the mean amplitude of glycemic excursion (MAGE) and standard deviation (SD), and the adverse cardiovascular events in ACS patients were evaluated, respectively. Results: A total of 11 studies with 3709 ACS patients were included. Pooled results showed that patients with higher GV had significantly increased risk of adverse cardiovascular events, including MAGE (relative risk [RR] = 1.76, 95% CI: 1.40 to 2.22, p < 0.001, I2 = 25%) and SD (RR = 2.14, 95% CI: 1.73 to 2.66, p < 0.001, I2 = 0%). Conclusions: Increased GV is related to the poor prognosis in patients with ACS. Additionally, more well-designed studies comparing different indicators of GV with adverse cardiovascular events in ACS patients are still warranted. [ABSTRACT FROM AUTHOR]

Background: Age is an independent risk factor of the progress and prognosis of atrial fibrillation (AF). However, ablation outcomes between elderly and younger patients with AF remain elusive. Methods: Cochrane Library, Embase, PubMed, and Web of Science were systematically searched up to 1 April 2022. Studies comparing AF ablation outcomes between elderly and younger patients and comprising outcomes of AF ablation for elderly patients were included. Trial sequential analysis (TSA) was performed to adjust for random error and lower statistical power in our meta-analysis. Subgroup analysis identified possible determinants of outcome impact for elderly patients after ablation. Moreover, linear and quadratic prediction fit plots with confidence intervals were performed, as appropriate. Results: A total of 27 studies with 113,106 AF patients were eligible. Compared with the younger group, the elderly group was significantly associated with a lower rate of freedom from AF (risk ratio [RR], 0.95; p = 0.008), as well as a higher incidence of safety outcomes (cerebrovascular events: RR, 1.64; p = 0.000; serious hemorrhage complications: RR, 1.50; p = 0.035; all-cause death: RR, 2.61; p = 0.003). Subgroup analysis and quadratic prediction fit analysis revealed the follow-up time was the potential determinant of freedom from AF for elderly patients after AF ablation. Conclusions: Our meta-analysis suggests that elderly patients may have inferior efficacy and safety outcomes to younger patients with AF ablation. Moreover, the follow-up time may be a potential determinant of outcome impact on freedom from AF for elderly patients after AF ablation. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) has been highlighted as an important gasotransmitter in mammals. A growing number of studies have indicated that H2S plays a key role in the pathophysiology of vascular diseases and physiological vascular homeostasis. Alteration in H2S biogenesis has been reported in a variety of vascular diseases and H2S supplementation exerts effects of vasodilation. Accumulating evidence has shown vascular potassium channels activation is involved in H2S-induced vasodilation. This review aimed to summarize and discuss the role of H2S in the regulation of vascular tone, especially by interaction with different vascular potassium channels and the underlying mechanisms. [ABSTRACT FROM AUTHOR]

Objective: We aimed to screen out biomarkers for atrial fibrillation (AF) based on machine learning methods and evaluate the degree of immune infiltration in AF patients in detail. Methods: Two datasets (GSE41177 and GSE79768) related to AF were downloaded from Gene expression omnibus (GEO) database and merged for further analysis. Differentially expressed genes (DEGs) were screened out using "limma" package in R software. Candidate biomarkers for AF were identified using machine learning methods of the LASSO regression algorithm and SVM-RFE algorithm. Receiver operating characteristic (ROC) curve was employed to assess the diagnostic effectiveness of biomarkers, which was further validated in another independent validation dataset of GSE14975. Moreover, we used CIBERSORT to study the proportion of infiltrating immune cells in each sample, and the Spearman method was used to explore the correlation between biomarkers and immune cells. Results: 129 DEGs were identified, and CYBB, CXCR2, and S100A4 were identified as key biomarkers of AF using LASSO regression and SVM-RFE algorithm. Both in the training dataset and the validation dataset, CYBB, CXCR2, and S100A4 showed favorable diagnostic effectiveness. Immune infiltration analysis indicated that, compared with sinus rhythm (SR), the atrial samples of patients with AF contained a higher T cells gamma delta, neutrophils and mast cells resting, whereas T cells follicular helper were relatively lower. Correlation analysis demonstrated that CYBB, CXCR2, and S100A4 were significantly correlated with the infiltrating immune cells. Conclusions: In conclusion, this study suggested that CYBB, CXCR2, and S100A4 are key biomarkers of AF correlated with infiltrating immune cells, and infiltrating immune cells play pivotal roles in AF. [ABSTRACT FROM AUTHOR]

Six structurally related flavonoids including two flavones apigenin and luteolin, one isoflavone genistein, and three flavonols, galangin, kaempferol and quercetin, are affected differently as radical scavengers by presence of Ca(II). Except for apigenin showing no reaction with Ca(II), other flavonoids all coordinate with Ca(II) to form 1 : 2 Ca(II)‐flavonoid complexes confirmed by UV‐vis and mass spectra. Coordination with Ca(II) for luteolin with the 3′, 4′‐catechol group and for flavonols with 3‐hydroxyl and 4‐carbonyl significantly enhance the DPPH• scavenging efficiencies shown by stopped‐flow spectra. Addition of Ca(II) shows no effect on radical scavenging rate of Genistein, as an isomer of apigenin, although both containing the same 4‐carbonyl and 5‐hydroxyl as a potential chelating group as confirmed by mass spectra and cyclic voltammetry. The two structure elements, 3′, 4′‐catechol and the combination of 3‐hydroxyl and 4‐carbonyl, are identified as important factors for Ca(II) enhancement of radical scavenging of flavonoids. Coordination of Ca(II) to kaempferol forming a 1 : 2 Ca(II)‐kaempferol complex at 3,4 site shows the most significant enhancement in radical scavenging efficiency by a factor of 4.4 compared to other investigated flavonoids. [ABSTRACT FROM AUTHOR]

Diabetic coronary arterial disease is a leading cause of morbidity and mortality in diabetic patients. The impaired function of large-conductance calcium-activated potassium channels (BK channels) is involved in diabetic coronary arterial disease. Many studies have indicated that the reduced BK channel expression in diabetic coronary artery is attributed to ubiquitin-mediated protein degradation by the ubiquitin–proteasome system. This review focuses on the influence and the mechanisms of BK channel regulation by E3 ubiquitin ligases in diabetic coronary arterial disease. Thus, BK channels regulated by E3 ubiquitin ligase may play a pivotal role in the coronary pathogenesis of diabetic mellitus and, as such, is a potentially attractive target for therapeutic intervention. [ABSTRACT FROM AUTHOR]

Aim: Glucose fluctuations may be responsible for, or further the onset of arterial hypertension, but the exact mechanisms remain unclear. The purpose of this study was to investigate the mechanisms behind and related to aortic fibrosis and aortic stiffening induced by glucose fluctuations. Methods: Sprague-Dawley rats were injected with streptozotocin (STZ) and randomly divided into three treatment groups: controlled STZ-induced diabetes (C-STZ); uncontrolled STZ-induced diabetes (U-STZ); and STZ-induced diabetes with glucose fluctuations (STZ-GF). After 3 weeks, rat blood pressure (BP) was tested, and aortic fibrosis was detected by using the Masson trichrome staining technique. Levels of p38 mitogen-activated protein kinase (p38 MAPK), runt-related transcription factor 2 (Runx2), collagen type 1 (collagen I), and NADPH oxidases were determined by Western blot.Rat vascular smooth muscle cells in vitro were used to explore underlying mechanisms. Results: The systolic BP of diabetic rats in the C-STZ, U-STZ, and STZ-GF groups was 127.67 ± 6.53, 150.03 ± 5.24, and 171.63 ± 3.53 mm Hg, respectively (p< 0.05). The mean BP of diabetic rats in the three groups was 91.20 ± 10.07, 117.29 ± 4.28, and 140.58 ± 2.14 mm Hg, respectively (p< 0.05). The diastolic BP of diabetic rats in the three groups was 73.20 ± 12.63, 101.93 ± 5.79, and 125.37 ± 4.62 mm Hg, respectively (p< 0.05). The ratios of fibrosis areas in the aortas of the three groups were 11.85 ± 1.23, 29.00 ± 0.87, and 48.36 ± 0.55, respectively (p< 0.05). The expressions of p38 MAPK, Runx2, and collagen I were significantly increased in the STZ-GF group. In vitro, applications of inhibitors of reactive oxygen species (ROS) and p38 MAPK successfully reversed glucose fluctuations that would have possibly induced aortic fibrosis. Conclusions: Blood glucose fluctuations aggravate aortic fibrosis via affecting the ROS/p38 MAPK /Runx2 signaling pathway. [ABSTRACT FROM AUTHOR]

Accumulating evidence indicates the occurrence and development of diabetic complications relates to not only constant high plasma glucose, but also glucose fluctuations which affect various kinds of molecular mechanisms in various target cells and tissues. In this review, we detail reactive oxygen species and their potentially damaging effects upon glucose fluctuations and resultant downstream regulation of protein signaling pathways, including protein kinase C, protein kinase B, nuclear factor-κB, and the mitogen-activated protein kinase signaling pathway. A deeper understanding of glucose-fluctuation-related molecular mechanisms in the development of diabetic complications may enable more potential target therapies in future. [ABSTRACT FROM AUTHOR]

Aim: Docosahexaenoic acid (DHA) is known to activate the vascular large-conductance calcium-activated potassium (BK) channels and has protective effects on the cardiovascular system. However, the underlying mechanisms through which DHA activates BK channels remain unclear. In this study, we determined such mechanisms by examining the effects of different concentrations of DHA on BK channels in freshly isolated rat coronary arterial smooth muscle cells (CASMCs) using patch clamp techniques. Methods and Results: We found that BK channels are the major potassium currents activated by DHA in rat CASMCs and the effects of DHA on BK channels are concentration dependent with a bimodal distribution. At concentrations of <1 μM, DHA activated whole-cell BK currents with an EC50 of 0.24 ± 0.05 μM and the activation effects were abolished by pre-incubation with SKF525A (10 μM), a cytochrome P450 (CYP) epoxygenase inhibitor, suggesting the role of DHA-epoxide. High concentrations of DHA (1-10 μM) activated whole-cell BK currents with an EC50 of 2.38 ± 0.22 μM and the activation effects were unaltered by pre-incubation with SKF525A. Single channel studies showed that the open probabilities of BK channels were unchanged in the presence of low concentrations of DHA, while significantly increased with high concentrations of DHA. In addition, DHA induced a dose-dependent increase in cytosolic calcium concentrations with an EC50 of 0.037 ± 0.01 μM via phospholipase C (PLC)--inositol triphosphate (IP3)--Ca2+ signal pathway, and inhibition of this pathway reduced DHA-induced BK activation. Conclusion: These results suggest that DHA can activate BK channels by multiple mechanisms. Low concentration DHA-induced BK channel activation is mediated through CYP epoxygenase metabolites, while high concentration DHA can directly activate BK channels. In addition, DHA at low and high concentrations can both activate BK channels by elevated cytosolic calcium through the PLC--IP3--Ca2+ signal pathway. [ABSTRACT FROM AUTHOR]

Aim: The objective of this study was to examine the effects of n-3 polyunsaturated fatty acids (n-3 PUFAs) on coronary arterial large conductance Ca2+ -activated K+ (BK) channel function in coronary smooth muscle cells (SMCs) of streptozotocin- induced diabetic rats. Methods: The effects of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on coronary BK channel open probabilities were determined using the patch clamp technique. The mRNA and protein expressions of BK channel subunits were measured using qRTPCR and Western blots. The coronary artery tension and coronary SMC Ca2+ concentrations were measured using a myograph system and fluorescence Ca2+ indicator. Results: Compared to nondiabetic control rats, the BK channel function was impaired with a reduced response to EPA and DHA in freshly isolated SMCs of diabetic rats. Oral administration of n-3 PUFAs had no effects on protein expressions of BK channel subunits in nondiabetic rats, but significantly enhanced those of BK-β 1 in diabetic rats without altering BK-a protein levels. Moreover, coronary ring tension induced by iberiotoxin (a specific BK channel blocker) was increased and cytosolic Ca2+ concentrations in coronary SMCs were decreased in diabetic rats, but no changes were found in nondiabetic rats. Conclusions: n-3 PUFAs protect the coronary BK channel function and coronary vasoreactivity in diabetic rats as a result of not only increasing BK-β 1 protein expressions, but also decreasing coronary artery tension and coronary smooth muscle cytosolic Ca2+ concentrations. [ABSTRACT FROM AUTHOR]

These authors contributed equally: Feng Li, Tong-Yue Du and Li-Da Wu. Correction to: I Scientific Reports i https://doi.org/10.1038/s41598-022-26277-w, published online 01 February 2023 The original version of this Article contained an error in the order of the author names, which was incorrectly given as Feng Li, Tong-Yue Du, Li-Da Wu, Lei Zhang, Huan-Huan Liu, Zhen-Ye Zhang, Jie Zhang, Zhi-Yuan Zhang, Ling-Ling Qian, Jian-Feng Hao & Ru-Xing Wang. [Extracted from the article]

Background: There are no reports regarding entire gastric fundic and esophageal varices evaluated with 64-row multidetector CT (MDCT). We attempt to clarify the feasibility of portal venography with this scanner in evaluation of these varices. Methods: A total of 33 patients, with clinically confirmed gastric fundic and esophageal varices secondary to posthepatitic cirrhosis, underwent thoracicoabdominal triphasic enhancement scans using 64-row MDCT along with conventional angiographic portography. CT portography and conventional portography were compared by statistical agreement to determine whether CT maximum intensity projection (CT-MIP) portography is useful in evaluation of entire gastric fundic and esophageal varices. Results: CT-MIP portography demonstrated gastric fundic and esophageal varices, and the inflowing and outflowing vessels of the varices. Gastric fundic varices were shown in 32 cases (97.0%), and esophageal varices were in 27 (81.8%). The inflowing vessels including the left gastric vein and posterior gastric vein/short gastric vein were illustrated in 31 (94.0%) and 17 (51.5%) cases, respectively. The outflowing vessels including the azygos vein, hemiazygos vein, and gastro-renal shunts were seen in 30 (90.9%), 8 (24.2%), and 12 (36.4%) cases, respectively. Findings of CT-MIP portography and conventional angiographic portography were in close agreement (Kappa value ranged from 0.621 to 1.000). Conclusion: CT-MIP venography with 64-row MDCT could be considered as a method for detecting entire gastric fundic and esophageal varices developed from posthepatitic cirrhosis. [ABSTRACT FROM AUTHOR]

Corrigendum: Radical Scavenging Efficiency of Flavonoids Increased by Calcium(II) Binding: Structure-Activity Relationship Antioxidant, Flavonoid, Radical scavenging, Calcium(II), Metal-flavonoid complex Keywords: Antioxidant; Calcium(II); Flavonoid; Metal-flavonoid complex; Radical scavenging EN Antioxidant Calcium(II) Flavonoid Metal-flavonoid complex Radical scavenging 10323 10323 1 10/19/21 20211013 NES 211013 GRAPH Conflict of interest The authors declare no conflict of interest. [Extracted from the article]

Sn(II) binds to kaempferol (HKaem, 3,4′,5,7-tetrahydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one) at the 3,4-site forming [Sn(II)(Kaem)2] complex in ethanol. DPPH• scavenging efficiency of HKaem is dramatically decreased by SnCl2 coordination due to formation of acid inhibiting deprotonation of HKaem as ligands and thus reduces the radical scavenging activity of the complex via a sequential proton-loss electron transfer (SPLET) mechanism. Moderate decreases in the radical scavenging of HKaem are observed by Sn(CH3COO)2 coordination and by contact between Sn and HKaem, in agreement with the increase in the oxidation potential of the complex compared to HKaem, leading to a decrease in antioxidant efficiency for fruits and vegetables with Sn as package materials. [ABSTRACT FROM AUTHOR]