N, P and C removal simultaneously and microbial population numbers in a cyclic activated sludge system treating village and township domestic wastewater by altering the cycle times.

It was necessary to research an efficient treatment process suitable for township domestic wastewater. In this paper, the performance of the cyclic activated sludge system (CASS) system for simultaneous carbon (C), nitrogen (N) and phosphorus (P) removal was investigated by changing the operation cycle of the CASS reactor. Four operating conditions were set up, T1, T2, T3 and T4, with cycle times of 6, 8, 12 and 8 h (with carbon source), respectively. The results showed that the CASS system had good simultaneous removal of C, N and P. The highest removal rates of COD, TN, NH4+ -N and TP were 87.69, 72.99, 98.60 and 98.38%, respectively, at a cycle time of 8 h. The TN removal rate could be increased to 82.51% after the addition of carbon source. Microbial community analysis showed that Proteobacteria, Bacteroidetes and Candidatus Saccharibacteria were the main phylum-level bacteria. Their presence facilitated the effectiveness of the CASS process for nitrogen removal and phosphorus removal. Functional analysis of genes revealed that the abundance values of genes associated with C, N and P metabolism were higher when the treatment was effective.

Surgical ablation supplemented by ethanol injection for ventricular tachycardia refractory to percutaneous ablation.

BACKGROUND: A combination of endocardial and epicardial approaches has improved the overall success rate of ventricular tachycardia (VT) ablation in patients with cardiomyopathy. However, the origins of some VTs are truly intramural or close to coronary arteries, which makes this combined strategy either prone to failure or too risky. OBJECTIVES: This observational study aimed to explore the feasibility and efficacy of direct epicardial ablation combined with intramural ethanol injection via surgical approach for inaccessible intramural VTs or VTs too close to coronary arteries. METHODS: In four canines ventricular lesions produced by direct epicardial injection of ethanol were assessed. Six consecutive patients with recurrent VT refractory to catheter endocardial and epicardial RF ablation and that remained inducible after surgical epicardial mapping and RF ablation were included. Ethanol was injected by needle at the epicardial RF ablation sites. The primary outcome was freedom of sustained VT determined by device interrogation and periodical 24-h holter recordings subsequently. RESULTS: In an animal study, the lesions were homogenous and increased in size with the volume of ethanol injected. In all six patients, ethanol injection at the target sites in the anterior or lateral left ventricle abolished inducible VT. Over a median follow-up of 22 months (range, 6-65), all patients remained free of sustained VT. One patient died of pulmonary infection one year after the procedure. CONCLUSIONS: A hybrid strategy of surgical ablation combined with intramural ethanol injection is feasible and effective in patients with multiple failed percutaneous ablation attempts.

Tocilizumab for treating COVID-19: a systemic review and meta-analysis of retrospective studies.

OBJECTIVES: COVID-19 has become a global epidemic, and effective therapies have not been discovered up to now. We conducted this study to explore the effectiveness and safety of tocilizumab recently used for treating COVID-19. METHOD: A comprehensive search was conducted (up to September 27, 2020), and 19 eligible records were identified according to the inclusion and exclusion criteria. The data of the studies were extracted by 2 independent reviewers and were analyzed to evaluate the safety and availability of tocilizumab for treating COVID-19. RESULTS: Thirteen retrospective case-control studies (n = 2285 patients) and 6 retrospective single-armed studies (n = 208) were retrieved in this study. In the comparison of tocilizumab treatment group (TCZ) and standard treatment group (ST), significant associations with a lower risk of admission to ICU, use of ventilation, and mortality (OR, 95% CI: 0.53, 0.26~1.09; 0.66, 0.46~0.94; 0.44, 0.36~0.55) were found in the tocilizumab treatment group. What is more, patients treated with tocilizumab had better clinical improvement compared with the patients treated with ST (OR, 1.24; 95% CI, 0.96~1.62). After taking tocilizumab, the patients had lower C-reactive protein (CRP), white blood cell count (WBC), aspartate aminotransferase (AST) (WMD, 95% CI: - 99.66, - 156.24~- 43.09; - 0.95, - 1.8~- 0.11; - 12.58, - 18.88~-6.29) but higher troponin (WMD, 7.61; 95% CI, 3.06~12.15) than before. In addition, tocilizumab did not have significant influence on patients' neutrophil count (Neut), lymphocyte count (Lymp), platelet count (Plt), alanine aminotransferase (ALT), and creatine (WMD, 95% CI: - 0.29, - 2.91~2.33; 0.42, - 0.23~1.07; 5.2, - 2.85~13.25; 22.49, - 2.73~47.7; - 44.78, - 93.37~3.81). CONCLUSION: Tocilizumab may have potential effectiveness to treat COVID-19 according to the results of this study. However, more large-scale studies are needed for more accurate conclusions.

B-type Natriuretic Peptide and Other Risk Factors for Predicting Postoperative Atrial Fibrillation after Thoracic Surgery.

BACKGROUND: Postoperative atrial fibrillation (POAF) is associated with increased morality rate, prolonged hospitalization, and reduced long-term survival after surgery. Thus, prediction of POAF is important to assess surgical risk and provide prophylaxis. METHODS: It was a prospective study of 207 consecutive patients who underwent a routine preoperative laboratory testing before thoracic surgery from October 2016 to May 2017. Comprehensive data were collected. Then stepwise multivariate logistic regression analysis was adopted to identify significant risk factors associated with POAF from various variables. RESULTS: As results, three variables as follows: male gender, open thoracotomy, and B-type natriuretic peptide (BNP) exceeding 59 pg/mL were considered as independent risk factors associated with POAF (p < 0.05). CONCLUSION: In patients undergoing noncardiac thoracic surgery, we found that an elevated preoperative BNP level (with the level of 59 pg/mL as a cutoff), male gender, and open-chest surgeries were significant risk factors for POAF. The identification of patients who are prone to develop POAF will provide prevention strategies to reduce this complication.

Essential role of STX6 in esophageal squamous cell carcinoma growth and migration.

Abnormalities in endosomes, or dysregulation in their trafficking, play an important role directly in many diseases including oncogenesis. Syntaxin-6 (STX6) is involved in diverse cellular functions in a variety of cell types and has been shown to regulate many intracellular membrane trafficking events such as endocytosis, recycling and anterograde and retrograde trafficking. However, its expression pattern and biological functions in esophageal squamous cell carcinoma (ESCC) remained unknown. Here, we have found that the expression of STX6 was up-regulated in ESCC samples, its expression was significantly correlated with tumor size, histological differentiation, lymph node metastasis and depth. On one hand, STX6 silencing inhibited ESCC cells viability and proliferation in a p53-dependent manner. On the other hand, STX6 effect integrin trafficking and regulate ESCC cells migration. Taken together, our study revealed the oncogenic roles of STX6 in the progression of ESCC, and it might be a valuable target for ESCC therapy.

Oxidative stress and mitochondrial injury-mediated cytotoxicity induced by silver nanoparticles in human A549 and HepG2 cells.

OBJECTIVES: Considering the increasing applications of silver nanoparticles (AgNPs) in food- and cosmetic-related products worldwide, the aim of this study was to investigate the potential adverse health effects induced by AgNPs exposure in terms of cytotoxicity, oxidative stress, and mitochondrial injury in human A549 and HepG2 cells. METHODS: After a 48 h AgNPs treatment, the cell viability was measured by MTT assay. Oxidative damage was determined by assays of malondialdehyde (MDA), 8-epi-PGF2α and 8-hydroxy-2'-deoxyguanosine (8-oxo-dG). The protein expression of HSPA1A and HO-1 was analyzed by western blot analysis. Mitochondrial membrane potential (MMP) was detected by using JC-1 as fluorescent probes. The uptake and intracellular localization of AgNPs was measured by transmission electron microscopy (TEM), and cellular AgNPs was determined by inductively coupled plasma mass spectrometry (ICP-MS). RESULTS: A dose-dependent decrease in cell viability after AgNPs treatment was observed, which was associated correspondingly with oxidative damage as indicated by increases in MDA amount, 8-epi-PGF2α and 8-oxo-dG levels, HSPA1A and HO-1 expression, as well as mitochondrial injury as indicated by decreased MMP. The cellular uptake of AgNPs measured by ICP-MS analysis was correlated correspondingly with the oxidative damage and mitochondrial injury. CONCLUSIONS: The dose-dependent cytotoxicity induced by AgNPs may result from an interaction of oxidative stress, DNA damage and mitochondrial injury in A549 and HepG2 cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1691-1699, 2016.

The development of GADD45α luciferase reporter assays in human cells for assessing the genotoxicity of environmental pollutants.

OBJECTIVES: In order to assess the potential carcinogenic and genotoxic responses induced by environmental pollutants, genotoxicity test systems based on a GADD45α promoter-driven luciferase reporter in human A549 and HepG2 cells were established. MATERIALS AND METHODS: Four different types of environmental toxicants including DNA alkylating agents, precarcinogenic agents, DNA cross-linking agents and non-carcinogenic agents, and three environmental samples collected from a coke oven plant were used to evaluate the test systems. After treated with the tested agents and environmental samples for 12 h, the cell viabilities and luciferase activities of the luciferase reporter cells were determined, respectively. RESULTS: Methyl methanesulfonate, benzo[a]pyrene, formaldehyde and the extractable organic matter (EOM) from coke oven emissions in ambient air generally produced significant induction of relative luciferase activity in a similar dose-dependent manner in A549- and HepG2-luciferase cells. No significant increases in relative luciferase activity were observed in pyrene-treated A549- or HepG2-luciferase cells. Significant increase in relative luciferase activity was already evident after 2.5 µM benzo[a]pyrene, 5 µM formaldehyde, 0.006 µg/L bottom-EOM, 0.10 µg/L side-EOM or 0.06 µg/L top-EOM, where no cytotoxic damage was observed. Compared with the A549-luciferase cells, the tested pollutants produced higher induction of relative luciferase activity in HepG2-luciferase cells. DISCUSSION AND CONCLUSION: Therefore, the new genotoxicity test systems can detect different types of genotoxic agents and low concentrations of environmental samples. The luciferase reporter cells, especially the HepG2-luciferase cells, could provide a valuable tool for rapid screening of the genotoxic damage of environmental pollutants and their complex mixtures.

Increased expression of NF-AT3 and NF-AT4 in the atria correlates with procollagen I carboxyl terminal peptide and TGF-ß1 levels in serum of patients with atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. Unfortunately, the precise mechanisms and sensitive serum biomarkers of atrial remodeling in AF remain unclear. The aim of this study was to determine whether the expression of the transcription factors NF-AT3 and NF-AT4 correlate with atrial structural remodeling of atrial fibrillation and serum markers for collagen I and III synthesis. METHODS: Right and left atrial specimens were obtained from 90 patients undergoing valve replacement surgery. The patients were divided into sinus rhythm (n = 30), paroxysmal atrial fibrillation (n = 30), and persistent atrial fibrillation (n = 30) groups. NF-AT3, NF-AT4, and collagen I and III mRNA and protein expression in atria were measured. We also tested the levels of the carboxyl-terminal peptide from pro-collagen I, the N-terminal type I procollagen propeptides, the N-terminal type III procollagen propeptides, and TGF-ß1 in serum using an enzyme immunosorbent assay. RESULTS: NF-AT3 and NF-AT4 mRNA and protein expression were increased in the AF groups, especially in the left atrium. NF-AT3 and NF-AT4 expression in the right atrium was increased in the persistent atrial fibrillation group compared the sinus rhythm group with similar valvular disease. In patients with AF, the expression levels of nuclear NF-AT3 and NF-AT4 correlated with those of collagens I and III in the atria and with PICP and TGF-ß1 in blood. CONCLUSIONS: These data support the hypothesis that nuclear NF-AT3 and NF-AT4 participates in atrial structural remodeling, and that PICP and TGF-ß1 levels may be sensitive serum biomarkers to estimate atrial structural remodeling with atrial fibrillation.

ITGAM: A Pivotal Regulator in Macrophage Dynamics and Cardiac Function During Sepsis-Induced Cardiomyopathy.

BACKGROUND: Sepsis-induced cardiomyopathy (SIC) is a critical complication arising from sepsis characterized by reversible myocardial dysfunction. Despite the increasing attention to SIC in research, the underlying molecular mechanisms remain poorly comprehended. METHODS: In this study, we utilized bioinformatics to analyze RNA-sequencing (RNA-seq) and single-cell RNA-sequencing (scRNA-seq) data from the Gene Expression Omnibus (GEO) database to identify key immune cell populations and molecular markers associated with SIC. Our experimental approach combined in vitro and in vivo studies to investigate the roles of integrin alpha M (ITGAM) and intracellular adhesion molecule-1 (ICAM-1) in macrophage recruitment and phenotypic polarization, as well as their impact on cardiac function during SIC. RESULTS: The bioinformatics analysis disclosed significant alterations in gene expression and immune cell composition within the cardiac tissue during SIC, where macrophages emerged as the predominant immune cell type. Notably, ITGAM was identified as a key regulatory molecule that modulates macrophage function, driving the pathogenesis of SIC through its influence on the recruitment and functional reprogramming of these cells. In vitro experiments revealed that lipopolysaccharide (LPS) stimulation triggered an upregulation of ITGAM in macrophages and ICAM-1 in endothelial cells, underscoring their critical roles in immune cell mobilization and intercellular communication. The strategic administration of ITGAM-neutralizing antibodies to SIC mice resulted in a marked decrease in macrophage infiltration within the cardiac tissue, which was initially associated with an improvement in cardiac function. However, this intervention paradoxically resulted in an increased mortality rate during the later phases of SIC, underscoring the complex and dualistic function of ITGAM. CONCLUSION: This study provides new insights into the complex dynamics of immune cells within the cardiac environment during SIC, with a particular emphasis on the modulatory role of ITGAM in shaping macrophage behavior. The findings shed light on the reversible nature of myocardial dysfunction in SIC and emphasize the importance of targeted therapeutic strategies for the effective management of SIC.

Exploring Ferroptosis-Associated Gene Signatures as Diagnostic and Therapeutic Targets for Sepsis-Induced Cardiomyopathy.

BACKGROUND: Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis associated with high mortality rates. Despite its significance, the molecular mechanisms underlying SICM remain poorly understood, particularly the role of ferroptosis - a form of iron-dependent programmed cell death. METHODOLOGY: This study analyzed the GSE79962 dataset from the Gene Expression Omnibus, containing cardiac gene expression profiles from SICM patients and controls. A list of ferroptosis-related genes (FRGs) was retrieved from the FerrDb. We used the limma package in R for differential expression analysis, setting an adjusted P-value cutoff of <0.05 and a log2-fold change threshold of ±1 to identify differentially expressed ferroptosis-related genes (DE-FRGs). We applied machine learning algorithms for biomarker identification, including least absolute shrinkage and selection operator (LASSO) logistic regression and support vector machine with recursive feature elimination (SVM-RFE), implemented via the glmnet and e1071 packages in R, respectively. Gene set enrichment analysis (GSEA) was conducted using the GSEA package to investigate the biological pathways related to key DE-FRGs. RESULTS: After differential expression analysis, we identified 145 DE-FRGs. Functional enrichment analyses underscored the involvement of these genes in critical biological processes and pathways, such as lipid metabolism and insulin resistance. Machine learning approaches pinpointed five key DE-FRGs (NCOA4, GABARAPL1, GJA1, CISD1, CP), with strong predictive potential for SICM. Further analyses, including the construction of a ceRNA network, revealed intricate post-transcriptional regulatory mechanisms that may influence the expression of these key genes. CONCLUSIONS: Our findings highlight the central role of ferroptosis in SICM and identify potential biomarkers and therapeutic targets that could help refine diagnostic and treatment strategies. This study advances our understanding of the molecular underpinnings of SICM and sets the stage for future research aimed at mitigating this severe sepsis complication.

Association of urinary bisphenol A levels with heart failure risk in U.S. adults from the NHANES (2003-2016).

Introduction: Although heart failure (HF) has been linked to bisphenol A (BPA), few studies have investigated the cut-off values for the effects of urinary BPA levels on heart failure risk. The association between urinary BPA levels and HF prognosis has not been investigated. Methods: This study included 11,849 adults over 20 years old using information from the National Health and Nutrition Examination Survey (NHANES), which was conducted from 2003 to 2016. The relationship between urinary BPA levels and the risk of HF was determined via a multivariable logistic regression model, and restricted cubic spline (RCS) methods were used to determine the cut-off for the effect of BPA levels on HF risk. Based on the available NT-proBNP concentration data from the NHANES (2003-2004), multivariable linear regression was applied to determine the linear association between the NT-proBNP concentration and urinary BPA concentration. Results: The results revealed a positive correlation between a urinary BPA concentration in the fourth quartile and the occurrence of heart failure [OR 1.49, 95% CI (1.09, 2.04), p = 0.012]. A one-unit increase (1 ng/mg creatinine) in the ln-transformed BPA concentration was linked to a 15% increase in the incidence of HF [OR 1.15, 95% CI (1.03, 1.29), p = 0.014]. The cut-off urinary BPA concentration for HF risk was 1.51 ng/mg creatinine. There was a positive correlation between urinary BPA and NT-proBNP concentrations [ß = 0.093, 95% CI (0.014, 0.171), p = 0.02] in males, but there was no linear association [ß = 0.040, 95% CI (-0.033, 0.113), p = 0.283] in females. Discussion: Increased urinary BPA levels are linked to an increased risk of heart failure and poor prognosis. There is a significant increase in the risk of heart failure if the urinary concentration of BPA exceeds 1.51 ng/mg creatinine.

OPG/RANK/RANKL axis in stabilization of spontaneously restored sinus rhythm in permanent atrial fibrillation patients after mitral valve surgery.

OBJECTIVE: To investigate the expression of the osteoprotegerin (OPG)/receptor activator of nuclear factor-ĸB (RANK)/RANK ligand (RANKL) axis in the stabilization of spontaneously restored sinus rhythm (SR) in permanent atrial fibrillation (AF) patients after mitral valve (MV) surgery and study its clinical significance. METHODS: Clinical data, biopsies of right atrial appendages were collected from 135 permanent AF patients who spontaneously restored SR after conventional isolated MV replacement. A comparison was made between patients who had recurrence of AF within 7 days and patients with persistent SR for more than 7 days. RESULTS: AF patients had an increased expression of RANK, RANKL, and the RANKL/OPG ratio compared to SR patients, and the degree of fibrosis was lower in SR compared to AF in the atria. Moreover, the expressions of RANK, RANKL, and the RANKL/OPG ratio were positively correlated with the degree of fibrosis. CONCLUSION: These findings suggest that the OPG/RANK/RANKL axis plays important roles in the stabilization of restored SR after MV surgery by stimulating AF-related atrial remodeling in AF patients.

Maternal Serum tRNA-Derived Fragments (tRFs) as Potential Candidates for Diagnosis of Fetal Congenital Heart Disease.

BACKGROUND: Congenital heart disease (CHD) is one of the most predominant birth defects that causes infant death worldwide. The timely and successful surgical treatment of CHD on newborns after delivery requires accurate detection and reliable diagnosis during pregnancy. However, there are no biomarkers that can serve as an early diagnostic factor for CHD patients. tRNA-derived fragments (tRFs) have been reported to play an important role in the occurrence and progression of numerous diseases, but their roles in CHD remains unknown. METHODS: High-throughput sequencing was performed on the peripheral blood of pregnant women with an abnormal fetal heart and a normal fetal heart, and 728 differentially expressed tRFs/tiRNAs were identified, among which the top 18 tRFs/tiRNAs were selected as predictive biomarkers of CHD. Then, a quantitative reverse transcriptase polymerase chain reaction verified the expression of tRFs/tiRNAs in more clinical samples, and the correlation between tRFs/tiRNAs abnormalities and CHD was analyzed. RESULTS: tRF-58:74-Gly-GCC-1 and tiRNA-1:35-Leu-CAG-1-M2 may be promising biomarkers. Through further bioinformatics analysis, we predicted that TRF-58:744-GLy-GCC-1 could induce CHD by influencing biological metabolic processes. CONCLUSIONS: Our results provide a theoretical basis for the abnormally expressed tRF-58:74-Gly-GCC-1 in maternal peripheral blood as a new potential biomarker for the accurate diagnosis of CHD during pregnancy.

High­risk pathological subtype associated FAM83A­AS1 promotes malignancy and glycolysis of lung adenocarcinoma via miR­202­3p/HK2 axis.

According to the diverse cellular morphology, lung adenocarcinoma (LUAD) was classified into five pathological subtypes, referred to as follows: High­risk group (micropapillary and solid), intermediate­risk group (acinar and papillary) and low­risk group (epidic). Nevertheless, little is known about the biological function of long non­coding RNA (lncRNA) in the molecular determination of LUAD histologic patterns. Screening the transcriptional expression data from TCGA­LUAD, the differentially expressed lncRNA across the divergent pathological subtypes were explored. Pan­cancer analysis revealed the characteristic of FAM83A­AS1, which was also confirmed in the LUAD tissues. The function of FAM83A­AS1 was uncovered through the in vitro assays. RNA immunoprecipitation and dual­luciferase reporter assays were performed to explore the molecular mechanisms of FAM83A­AS1. In the present study, it was identified that the expression of FAM83A­AS1 was increased from the low­risk group to the high, which was associated with a poorer prognosis and higher risk of recurrence. Pan­cancer analysis revealed that FAM83A­AS1 was positively correlated with high tumor mutational burden. Additionally, FAM83A­AS1 promoted cell migration, invasion and growth of LUAD cancer cells. Mechanistically, FAM83A­AS1 sponged miR­202­3p to regulate the expression of hexokinase II (HK2) in post­transcription, which facilitated the malignancy and glycolysis. The present study uncovered the biological roles of FAM83A­AS1/miR­202­3p/HK2 axis in regulating malignancy and glycolysis of LUAD, which provided novel avenues to addressing the determination of histologic patterns.

Genome-wide analysis of RNA-binding proteins co-expression with alternative splicing events in mitral valve prolapse.

Objectives: We investigated the role and molecular mechanisms of RNA-binding proteins (RBPs) and their regulated alternative splicing events (RASEs) in the pathogenesis of mitral valve prolapse (MVP). Methods: For RNA extraction, we obtained peripheral blood mononuclear cells (PBMCs) from five patients with MVP, with or without chordae tendineae rupture, and five healthy individuals. High-throughput sequencing was used for RNA sequencing (RNA-seq). Differentially expressed genes (DEGs) analysis, alternative splicing (AS) analysis, functional enrichment analysis, co-expression of RBPs, and alternative splicing events (ASEs) analysis were conducted. Results: The MVP patients exhibited 306 up-regulated genes and 198 down-regulated genes. All down- and up-regulated genes were enriched in both Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Furthermore, MVP was closely associated with the top 10 enriched terms and pathways. In MVP patients, 2,288 RASEs were found to be significantly different, and four suitable RASEs (CARD11 A3ss, RBM5 ES, NCF1 A5SS, and DAXX A3ss) were tested. We identified 13 RNA-binding proteins (RBPs) from the DEGs and screened out four RBPs (ZFP36, HSPA1A, TRIM21, and P2RX7). We selected four RASEs based on the co-expression analyses of RBPs and RASEs, including exon skipping (ES) of DEDD2, alternative 3' splice site (A3SS) of ETV6, mutually exclusive 3'UTRs (3pMXE) of TNFAIP8L2, and A3SS of HLA-B. Furthermore, the selected four RBPs and four RASEs were validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and showed high consistency with RNA sequencing (RNA-seq). Conclusion: Dysregulated RBPs and their associated RASEs may play regulatory roles in MVP development and may therefore be used as therapeutic targets in the future.

Calcium- and integrin-binding protein-1 and calcineurin are upregulated in the right atrial myocardium of patients with atrial fibrillation.

AIMS: The aim of this study was to determine whether altered expression and distribution of calcium- and integrin-binding protein-1 (CIB1) is involved in the pathogenesis of different types of patients with atrial fibrillation (AF) associated with valvular heart disease (VHD). METHODS AND RESULTS: Right atrial specimens obtained from 65 patients undergoing valve replacement surgery were divided into three groups: sinus rhythm group (n= 24), paroxysmal atrial fibrillation group (PaAF; n= 10), and persistent atrial fibrillation group (PeAF; AF lasting >6 month; n= 31). The expression levels of mRNA and protein content for CIB1, calcineurin B, calcineurin A, and Na(+)-Ca(2+) exchanger-1 (NCX1) were measured. We also measured the combination of CIB1 with calcineurin B, L-type Ca(2+) channel, and NCX1 using immunoprecipitation. Expression of mRNA and protein content of CIB1, calcineurin B, calcineurin A, and NCX1 was increased in the AF group. Calcium- and integrin-binding protein-1 interacted with calcineurin B and L-type Ca(2+) channel. Surprisingly, CIB1 also combined with NCX1. CONCLUSIONS: The CIB1 and calcineurin expression was increased in AF atrial tissue and was related to the type of AF. This finding suggests that CIB1 may be involved in the pathogenesis of AF in VHD patients.

Comparison of catheter and surgical ablation of atrial fibrillation: A systemic review and meta-analysis of randomized trials.

OBJECTIVE: To compare both the beneficial and adverse effects of catheter ablation (CA) and surgical ablation (SA) on patients with atrial fibrillation (AF). METHODS: We searched MEDLINE and 4 additional databases for randomized controlled trials that compared CA with SA. Following data extraction, we conducted a meta-analysis to estimate the efficacy and safety of CA relative to SA. The primary end point of this study was the absence of AF during a 12-month follow-up period without the use of antiarrhythmic drugs. RESULTS: Seven trials comparing SA with CA met the inclusion criteria for efficacy outcome assessments. Following the meta-analysis, we obtained a summary odds ratio (OR) of achieving success 1 year after CA relative to SA was 0.37:1 (95% confidence interval [CI], 0.20-0.69). The result was robust in the subgroup analysis. CA was associated with a greater incidence of femoral vascular complications (OR, 5.81; 95% CI, 1.03-32.71), but a lower incidence of pneumothorax (OR, 0.09; 95% CI, 0.01-0.74) than SA. Statistically significant differences in the other safety outcomes were not observed between CA and SA. CONCLUSIONS: SA confers a moderate advantage over CA in 1-year efficacy outcomes and may be safely performed by experienced surgeons.

Aortic valve repair for the treatment of rheumatic aortic valve disease: a systematic review and meta-analysis.

Valvuloplasty for rheumatic aortic valve disease remains controversial. We conducted this study to explore whether aortic valvuloplasty is appropriate for the rheumatic population. A comprehensive search was conducted, and 7 eligible retrospective studies were identified from PubMed, Embase, Medline and Cochrane (up to April 7, 2020) according to the inclusion and exclusion criteria. The data for hospital mortality, 5-year survival, 5-year reoperation, aortic insufficiency grade (AIG) and aortic valve gradient (AVG) were extracted by 2 independent reviewers and were analysed to evaluate the safety and availability of aortic valvuloplasty for rheumatic patients. The heterogeneity of the results was estimated using the Q test and I2 statistics. The fixed pooling model was used when I2 ≤ 50%; otherwise, the random pooling model was selected. 7 articles with 418 patients were included. The pooled hospital mortality, 5-year survival and 5-year reoperation rates were 3.2%, 94.5% and 9.9%, respectively. The heterogeneities of the weighted mean differences (WMD) values of the AIG and AVG between preoperation and postoperation were extremely high (I2 = 81.5%, p < 0.001 in AIG, I2 = 97.6%, p = 0.003 in AVG). Subgroup analysis suggested that the AIG and AVG were improved by 3.03 grades (I2 = 0%, p < 0.001) and 3.16 mmHg (I2 = 0%, p < 0.001) in the European group, respectively. In the Asian group, the AIG and AVG were improved by 2.57 grades (I2 = 0%, p < 0.001) and 34.39 mmHg (I2 = 0%, p < 0.001), respectively. Compared with the values at discharge, the AIG was increased by 0.15 grades (I2 = 0%, p = 0.031) and the AVG was still decreased by 2.07 mmHg (I2 = 0%, p = 0.031) at the time of follow up. Valvuloplasty is safe and effective to treat rheumatic aortic insufficiency and stenosis, and the duration of maintenance required to improve stenosis was longer than that of insufficiency.

Functional analysis of differently expressed ferroptosis-related genes in patients with mitral valve prolapse.

Background: The prevalence of mitral valve prolapse (MVP) in heart valvular diseases is globally increasing. However, the understanding of its etiology and pathogenesis is limited. So far, the relationship between ferroptosis-related genes and long non-coding RNAs (lncRNAs) in MVP remains unexplored. This study investigates the potential pathogenesis of ferroptosis-related genes in MVP and provides a therapeutic target for the disease. Methods: Blood samples from patients with MVP and healthy volunteers were collected for transcriptomic sequencing to analyze the expression of ferroptosis-related differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs Co-expression network of ferroptosis-related DEGs and DElncRNAs. Furthermore, this work conducted GO and KEGG enrichment analyses. Results: CDKN2A, SLC1A4, ATF3, and other core genes related to the mitral valve prolapse were screened out. CDKN2A, SLC1A4, and ATF3 genes were at the core position of the network, regulated by numerous lncRNAs. Notably, these genes are primarily involved in the extracellular region and p53 signaling pathway. Conclusion: In summary, CDKN2A, SLC1A4, and ATF3 regulate the pathophysiological process of MVP and are potential therapeutic targets.

Association between polyfluoroalkyl chemical concentrations and leucocyte telomere length in US adults.

Exposure to some environmental chemicals is reportedly associated with the leucocyte telomere length (LTL), but the effects of the non-occupational exposure to polyfluoroalkyl chemical (PFCs) on the LTL are not well understood. Using data from 773 participants in the National Health and Nutrition Examination Survey (NHANES) conducted in 1999-2000, we analysed the association between blood PFC concentrations and LTL. Coefficients (betas) and 95% confidence intervals (CIs) for the blood PFC concentrations in association with the LTL were estimated using multivariate linear regression models after adjustment for age, gender, race, body mass index (BMI), poverty income ratio, educational level, white blood cell count, C-reactive protein and other PFCs. The results identified a strong positive association between the blood perfluorooctane sulfonic acid (PFOS) concentration and LTL in adults, and no associations were found between the LTL and other PFCs. In the linear regression models, each increment of one standard deviation (SD) in the base-10-logarithm-transformed PFOS concentration was associated with a 21-bp increase in the LTL in the fully adjusted model (P = 0.033). Moreover, serum PFOS was associated with the LTL mainly in females and individuals aged 40-50, as demonstrated by stratified analyses. These results provide epidemiological evidence showing that environment-related levels of serum PFOS are positively associated with the LTL in adults.