Improved whale swarm algorithm for solving material emergency dispatching problem with changing road conditions.

To overcome the problem of easily falling into local extreme values of the whale swarm algorithm to solve the material emergency dispatching problem with changing road conditions, an improved whale swarm algorithm is proposed. First, an improved scan and Clarke-Wright algorithm is used to obtain the optimal vehicle path at the initial time. Then, the group movement strategy is designed to generate offspring individuals with an improved quality for refining the updating ability of individuals in the population. Finally, in order to maintain population diversity, a different weights strategy is used to expand individual search spaces, which can prevent individuals from prematurely gathering in a certain area. The experimental results show that the performance of the improved whale swarm algorithm is better than that of the ant colony system and the adaptive chaotic genetic algorithm, which can minimize the cost of material distribution and effectively eliminate the adverse effects caused by the change of road conditions.

Changes in Heart Rate after Pulmonary Vein Isolation in Patients with Paroxysmal Atrial Fibrillation and Sinus Bradycardia.

This study aimed to evaluate the effect of circumferential pulmonary vein isolation (CPVI) on autonomic nervous function and prognosis in patients with paroxysmal atrial fibrillation (AF) with or without sinus bradycardia.A total of 66 patients with paroxysmal AF accompanied by sinus bradycardia and who underwent CPVI were recruited as the sinus bradycardia group. A total of 91 patients with paroxysmal AF but without sinus bradycardia and who underwent catheter ablation were selected as the control group. After surgical contraindications were eliminated, CPVI was performed by three-dimensional mapping system. 24-hour dynamic electrocardiogram was used to observe the changes of heart rate before and 2 days after surgery.A total of 45 (68%) and 51 (56%) patients in the sinus bradycardia and control groups, respectively, maintained sinus rhythm. There was an increase in heart rate after CPVI in both groups. The standard deviation of normal-to-normal (NN) intervals (SDNN), standard deviation of the average NN intervals (SDANN), low frequency (LF), and LF/high frequency (HF) in the sinus bradycardia and control groups decreased after CPVI (P < 0.01). Moreover, SDANN was higher in patients with sinus bradycardia treated by successful ablation than in those with recurrence (P < 0.01), while SDNN, a standard statistical measure of heart rate variability (rMSSD), LF, and HF were significantly lower in patients with sinus bradycardia (P < 0.05).CPVI was able to produce a significant reduction effect on vagal nerve and sympathetic activity regardless of whether patients with paroxysmal AF had sinus bradycardia. Moreover, CPVI exerted a certain influence on the success rate of AF catheter ablation.

Associations between KCNQ1OT1 genetic variation rs10766212 and susceptibility to colorectal cancer and clinical stage in a Chinese Han population.

KCNQ1OT1 has been linked to the development and progression of colorectal cancer (CRC). As a result, functional polymorphisms in the KCNQ1OT1 gene may have a role in CRC formation and progression. The goal of this study was to see if the rs10766212 polymorphism on the KCNQ1OT1 gene was linked to CRC susceptibility and clinical stage in a Chinese Han population. The case-control research comprised a total of 576 CRC patients and 606 healthy controls. The genotype of the rs10766212 polymorphic locus was determined using the Sanger sequencing technique. We found that the KCNQ1OT1 rs10766212 polymorphism was not related to CRC susceptibility; however, it was connected with the clinical stage of CRC. Patients with CRC who had the rs10766212 T allele had a lower risk of stage III/IV tumors than those who had the rs10766212 C allele. Furthermore, CRC tissues with the rs10766212 CC genotype showed a significant negative connection between KCNQ1OT1 and hsa-miR-622 expression. The luciferase assay showed that the rs10766212 C allele might contribute to the adsorption of KCNQ1OT1 on hsa-miR-622. In conclusion, the rs10766212 polymorphism altering hsa-miR-622 binding is linked to the clinical stage of CRC and may serve as a biomarker for predicting CRC progression in the Chinese Han population. However, better-designed studies are still needed to confirm the current findings.

TP73-AS1 rs3737589 Polymorphism is Associated With the Clinical Stage of Colorectal Cancer.

Objective: TP73-AS1 can promote the occurrence and development of a variety of tumors, including colorectal cancer (CRC). The current study aimed to investigate the association between a potentially functional genetic polymorphism (rs3737589 T > C) on the TP73-AS1 gene and the susceptibility and clinical stage of CRC in a Chinese Han population. Methods: The polymorphic genotyping was performed by the SNaPshot method. The real-time quantitative PCR method and the luciferase assay were used separately to explore genotype-tissue expression and the function of the genetic polymorphism. Results: A total of 576 CRC patients and 896 healthy controls were included in the current study. The rs3737589 polymorphism was not associated with CRC susceptibility but was associated with the CRC stage (CC vs. TT: OR = 0.25, 95% CI = 0.12 - 0.54, P=0.0003; C vs. T: OR = 0.69, 95% CI = 0.53-0.89, P=0.006; and CC vs. (TC + TT): OR = 0.26, 95% CI = 0.12-0.56, P=0.0004). CRC patients carrying the rs3737589 CC genotype or C allele were less likely to have stage III/IV tumors than those carrying the rs3737589 TT genotype or T allele. The expression of TP73-AS1 was lower in CRC tissues with the rs3737589 CC genotype compared to those with the TT genotype. Bioinformatics analysis and the luciferase assay revealed that the C allele could promote the binding of miR-3166 and miR-4771 to TP73-AS1. Conclusion: The TP73-AS1 gene rs3737589 polymorphism affecting miRNAs binding is associated with the CRC stage and may serve as a biomarker for predicting CRC progression.

KRAS G12D mutation eliminates reactive oxygen species through the Nrf2/CSE/H 2S axis and contributes to pancreatic cancer growth.

In pancreatic cancer, KRAS G12D can trigger pancreatic cancer initiation and development. Rapid tumor growth is often accompanied by excess intracellular reactive oxygen species (ROS) production, which is unfavorable to tumor. However, the regulation of intracellular ROS levels in KRAS mutant pancreatic cancer remains unclear. In this study, we establish BxPC3 stable cell strains expressing KRAS wild type (WT) and G12D mutation and find unchanged ROS levels despite higher glycolysis and proliferation viability in KRAS mutant cells than KRAS WT cells. The key hydrogen sulfide (H 2S)-generating enzyme cystathionine-γ-lyase (CSE) is upregulated in KRAS mutant BxPC3 cells, and its knockdown significantly increases intracellular ROS levels and decreases cell glycolysis and proliferation. Nuclear factor erythroid 2-related factor 2 (Nrf2) is activated by KRAS mutation to promote CSE transcription. An Nrf2 binding site (‒47/‒39 bp) in the CSE promoter is verified. CSE overexpression and the addition of NaHS after Nrf2 knockdown or inhibition by brusatol decreases ROS levels and rescues cell proliferation. Our study reveals the regulatory mechanism of intracellular ROS levels in KRAS mutant pancreatic cancer cells, which provides a potential target for pancreatic cancer therapy.

Early prediction of clinical scores for left ventricular reverse remodeling using extreme gradient random forest, boosting, and logistic regression algorithm representations.

Objective: At present, there is no early prediction model of left ventricular reverse remodeling (LVRR) for people who are in cardiac arrest with an ejection fraction (EF) of ≤35% at first diagnosis; thus, the purpose of this article is to provide a supplement to existing research. Materials and methods: A total of 109 patients suffering from heart attack with an EF of ≤35% at first diagnosis were involved in this single-center research study. LVRR was defined as an absolute increase in left ventricular ejection fraction (LVEF) from ≥10% to a final value of >35%, with analysis features including demographic characteristics, diseases, biochemical data, echocardiography, and drug therapy. Extreme gradient boosting (XGBoost), random forest, and logistic regression algorithm models were used to distinguish between LVRR and non-LVRR cases and to obtain the most important features. Results: There were 47 cases (42%) of LVRR in patients suffering from heart failure with an EF of ≤35% at first diagnosis after optimal drug therapy. General statistical analysis and machine learning methods were combined to exclude a number of significant feature groups. The median duration of disease in the LVRR group was significantly lower than that in the non-LVRR group (7 vs. 48 months); the mean values of creatine kinase (CK) and MB isoenzyme of creatine kinase (CK-MB) in the LVRR group were lower than those in the non-LVRR group (80.11 vs. 94.23 U/L; 2.61 vs. 2.99 ng/ml; 27.19 vs. 28.54 mm). Moreover, AUC values for our feature combinations ranged from 97 to 94% and to 87% when using the XGBoost, random forest, and logistic regression techniques, respectively. The ablation test revealed that beats per minute (BPM) and disease duration had a greater impact on the model's ability to accurately forecast outcomes. Conclusion: Shorter disease duration, slightly lower CK and CK-MB levels, slightly smaller right and left ventricular and left atrial dimensions, and lower mean heart rates were found to be most strongly predictive of LVRR development (BPM).

lncRNA PCAT1 might coordinate ZNF217 to promote CRC adhesion and invasion through regulating MTA2/MTA3/Snai1/E-cadherin signaling.

LncRNA prostate cancer-associated transcript 1 (PCAT1) is a well-known oncogene, but the mechanisms of exosomes PCAT1 in colorectal cancer (CRC) remain largely unknown. Thus, the mechanisms of exosomes lncRNA PCAT1 were investigated. The expressions of exosomes lncRNA PCAT1 in tissues from stage 0-I and stage II-III CRC patients, and intestinal epithelial cell line FHC and two CRC cell lines, HT29 and HCT8 were measured by real-time quantitative PCR. The effects of lncRNA PCAT1 on adhesion and invasion of two CRC cell lines were investigated by cell-matrix adhesion and transwell assays. In addition, the target of PCAT1 (ZNF217) was validated using an RNA immune precipitation assay. Finally, the protein levels of MTA2, MTA3, SNAI1, and E-cadherin in normal participants, stage 0-I and stage II-III CRC patients, as well as two cell lines with stable ZNF217 knockdown were investigated by western blotting. The plasma exosomal lncRNA PCAT1 was found to be significantly increased in the CRC tissues and cell lines. In addition, lncRNA PCAT1 knockdown significantly inhibited the adhesion and invasion of HT29 and HCT8 cells. RIP assay results showed lncRNA PCAT1 could target ZNF217, and downregulation of lncRNA PCAT1 could decrease the protein expressions of ZNF217 in two CRC cells lines. Moreover, ZNF217 knockdown significantly decreased MTA2, MTA3, and SNAI1 expressions, but increased E-cadherin expressions in both CRC cells lines. Exosomal lncRNA PCAT1 can promote the adhesion and invasion of CRC cells, and PCAT1 overexpression may lead to ZNF217 upregulation that regulates EMT-related MTA2/MTA3/Snai1/E-cadherin signaling.

HAND2-AS1 rs2276941 Polymorphism Affecting the Binding of hsa-miR-1275 Is Associated with the Risk of Colorectal Cancer.

Genetic variants in several long noncoding RNA genes have been implicated in the occurrence and development of colorectal cancer (CRC). In this study, we explored the association between HAND2-AS1 gene rs2276941 polymorphism and the risk and clinical stage of CRC. A direct sequencing method was used to detect the rs2276941 polymorphism in 576 CRC patients and 864 healthy individuals. Real-time quantitative PCR technology was used to explore the expression of HAND2-AS1 and hsa-miR-1275 in colorectal tissues with different rs2276941 genotypes. Dual-luciferase reporter assay was used to assess the function of the rs2276941 polymorphism. We found that the rs2276941 polymorphism was associated with a decreased risk of CRC (TT vs. CC, OR = 0.38, 95% CI = 0.16-0.89, p = 0.03; TT vs. [CC+CT], OR = 0.40, 95% CI = 0.17-0.94, p = 0.03). Furthermore, a significant negative correlation was observed between the expression of HAND2-AS1 and hsa-miR-1275 in colorectal tissues with rs2276941 TT genotype. Functional experimental results showed that the rs2276941 T allele might promote the binding of HAND2-AS1 to hsa-miR-1275. The current study results suggested that HAND2-AS1 gene rs2276941 polymorphism affecting the binding of hsa-miR-1275 was associated with CRC risk and might serve as a CRC susceptibility biomarker.

Evaluating Common NOS1AP Variants in Patients with Implantable Cardioverter Defibrillators for Secondary Prevention : Evaluating SNPs in NOS1AP.

BACKGROUND: Recent research has found that single nucleotide polymorphisms (SNPs) in the nitric oxide synthase 1 adaptor protein (NOS1AP) gene are associated with altered QT intervals and sudden cardiac death (SCD). However, the clinical utility and implications of NOS1AP SNPs remain unclear. Thus, this study aimed to explore the influence of NOS1AP SNPs in patients with implantable cardioverter defibrillator (ICD) for secondary prevention. METHODS: We conducted a case-control study to evaluate the most studied SNPs in NOS1AP (rs12143842, rs10494366, rs12567209, and rs16847548) in patients with ICD for secondary prevention. Patients were followed for up to 36 months from the time of ICD implantation. ICD interrogation data at 3 and 12 months, including rapid ventricular arrhythmia episodes and appropriate therapies, were then analyzed.  RESULTS: A significant association was observed between rs10494366 and ICD recipients who experienced appropriate therapies. After a mean follow-up time of 31.70 ± 9.15 months, we detected significant differences among the three rs10494366 genotype groups in the distribution of ICD shocks and appropriate therapies, as well as in the correlation of rs10494366 and ICD shocks. According to Kaplan-Meier and Cox regression analyses, patients with the TT genotype had a higher risk of SCD than those with the GG genotype. CONCLUSIONS: The present study revealed that NOS1AP SNP rs10494366 was associated with appropriate therapies. Specifically, the TT genotype increased ICD shocks and SCD risk in patients with ICD for secondary prevention for the first time.

ARID1A Downregulation Predicts High PD-L1 Expression and Worse Clinical Outcome in Patients With Gallbladder Cancer.

BACKGROUND: Recent studies have confirmed that AT-rich interactive domain-containing protein 1A (ARID1A) plays a critical role in tumorigenesis, but its role in gallbladder cancer (GBC) remains unclear. METHODS: In total, 224 patients from Zhongshan Hospital were recruited for this retrospective study. The clinicopathological and baseline characteristics of the patients were collected. Bioinformatics analysis was performed to reveal variations in genes and signaling pathways, and ARID1A and PD-L1 expression and the number of PD1+ tumor-infiltrating lymphocytes (TILs) were measured by immunohistochemical staining. RESULTS: ARID1A expression was negatively correlated with overall survival in patients with GBC, and multivariate analysis identified ARID1A as an independent prognostic factor for overall survival. A heatmap and gene set enrichment analysis suggested that cytotoxic T lymphocyte signatures and immune-related signaling pathways were downregulated in ARID1A low tumors. Subsequent immunohistochemical staining confirmed that ARID1A expression was negatively correlated with PD-L1 expression and PD1+ TILs in the tumor microenvironment. The Kaplan-Meier analysis suggested that high ARID1A expression combined with low PD-L1 expression or low PD1+ TIL counts is associated with the best prognosis in patients with GBC. CONCLUSION: ARID1A inactivation can lead to a worse prognosis in patients with GBC, potentially by mediating immune evasion through the PD1/PD-L1 pathway.

VPS9D1-AS1 gene rs7206570 polymorphism associated with the clinical stage of colorectal cancer and binding with hsa-miR-361-3p.

VPS9D1-AS1 is a long non-coding RNA that can operate as a competitive endogenous RNA and plays an essential role in the occurrence and development of malignancies, including colorectal cancer (CRC). In this study, we investigated whether a putative functional polymorphism (rs7206570) in the VPS9D1-AS1 gene is linked to the risk and clinical stage of CRC. Sanger sequencing method was used to detect the rs7206570 polymorphism in 500 CRC patients and 500 healthy individuals. Quantitative real-time PCR technology was used to detect the expression of VPS9D1-AS1 and hsa-miR-361-3p in colorectal tissues with different rs7206570 genotypes. The dual-luciferase reporter assay was used to examine whether the rs7206570 polymorphism affects hsa-miR-361-3p binding. The rs7206570 polymorphism was not associated with CRC risk, but was associated with the clinical stage of CRC. CRC patients with rs7206570 A allele were less likely to have high-stage CRC. Furthermore, there was a significant negative correlation between the expression of VPS9D1-AS1 and hsa-miR-361-3p in CRC tissues with rs7206570 GG genotype. Dual-luciferase reporter assay showed that the rs7206570 A allele presumably hinders the binding of VPS9D1-AS1 to hsa-miR-361-3p. In conclusion, VPS9D1-AS1 gene rs7206570 polymorphism affecting hsa-miR-361-3p binding was associated with the clinical stage of CRC, which might be able to assist in the preoperative staging of CRC.

The association of PRNCR1 rs1456315 polymorphism with the risk of colorectal cancer.

A recent meta-analysis found a link between the PRNCR1 rs1456315 polymorphism and cancer risk. In the current study, we further investigated the association of this polymorphism with the risk and clinical stage of colorectal cancer (CRC). A total of 416 CRC patients and 416 healthy individuals were genotyped by Sanger sequencing. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Furthermore, a pooled analysis with 872 CRC cases and 1141 controls was performed by Stata 12.0 software. In both the case-control study and the pooled analysis, there was no significant link between the rs1456315 polymorphism and CRC risk. However, there was a significant link between the rs1456315 polymorphism and the clinical stage of CRC. CRC patients carrying the rs1456315 G allele were more likely to have a high-stage tumor. Further bioinformatics analysis showed that the rs1456315 polymorphism could influence the binding of miRNA to PRNCR1. In conclusion, the findings suggest that the rs1456315 polymorphism is linked to CRC clinical stage and might be used as a biomarker to predict CRC progression.

The Association of MEG3 Gene rs7158663 Polymorphism With Cancer Susceptibility.

Although the association of MEG3 gene rs7158663 polymorphism with cancer susceptibility has been investigated, the findings are inconsistent. The aim of this study was to analyze the association between the rs7158663 polymorphism and cancer susceptibility through a case-control study and meta-analysis. In a case-control study with 430 colorectal cancer (CRC) cases and 445 healthy controls, the rs7158663 polymorphism was genotyped by direct sequencing. STATA software was used to calculate the pooled odds ratio and 95% confidence interval in a meta-analysis including 4,649 cancer cases and 5,590 controls. Both the case-control study and meta-analysis showed that the rs7158663 polymorphism was associated with increased susceptibility to CRC. Individuals carrying the AA or GA genotype were more likely to develop CRC than those carrying the rs7158663 GG genotype. Interestingly, MEG3 expression was significantly lower in colorectal tissues of the AA or GA genotype compared to those of the rs7158663 GG genotype. In addition, the meta-analysis suggested that the rs7158663 polymorphism was also associated with increased susceptibility to breast cancer and gastric cancer. Bioinformatics analysis showed that the rs7158663 A allele contributed to the binding of hsa-miR-4307 and hsa-miR-1265 to MEG3. In conclusion, the current findings suggest that the MEG3 gene rs7158663 polymorphism may serve as a genetic marker for predicting the risk of cancers, such as breast cancer, gastric cancer and CRC. However, the sample size of the current study is still insufficient, especially in the subgroup analysis. Therefore large and well-designed studies are needed to validate our findings.

LINC00355 triggers malignant progression of hepatocellular carcinoma via the sponge effect on miR-217-5p with the involvement of the Wnt/ß-catenin signaling.

PURPOSE: To uncover the biological role of LINC00355 in regulating the proliferative and apoptotic potentials in hepatocellular carcinoma (HCC), and the underlying mechanism. METHODS: LINC00355 levels in HCC tissues and cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). After knockdown of LINC00355 or miR-217-5p in Hub7 and Hep3B cells, proliferative and apoptotic potentials were assessed by cell counting kit-8 (CCK-8), colony formation assay and flow cytometry. The interaction between LINC00355 and miR-217-5p was determined by dual-luciferase reporter assay and Pearson correlation test. Western blot analysis was conducted to illustrate the regulatory effects of LINC00355 and miR-217-5p on the Wnt/ß-catenin signaling. RESULTS: LINC00355 was upregulated in HCC tissues and cell lines. Knockdown of LINC00355 reduced viability in Hub7 and Hep3B cells, which was much pronounced on days 3 and 4. Clonality was attenuated by transfection of shLINC00355 as well. In addition, apoptosis rate increased by knockdown of LINC00355 in HCC cells. Protein levels of ß-catenin, GSK3ß, c-myc and cyclin D1 were downregulated in Hub7 and Hep3B cells transfected with shLINC00355. MiR-217-5p was the target gene binding LINC00355. It displayed exactly opposite regulations on HCC cell phenotypes and protein levels of vital genes in the Wnt/ß-catenin signaling to those of LINC00355. CONCLUSIONS: LINC00355 is upregulated in HCC specimens, LINC00355 triggers proliferative rate and inhibits apoptosis in HCC cells by negatively regulating miR-217-5p and activating the Wnt/ß-catenin signaling.

Cystic Duct Carcinoma: A New Classification System and the Clinicopathological Features of 62 Patients.

BACKGROUND: Cystic duct carcinoma (CDC) is a rare biliary malignancy with a low incidence and poor prognosis. However, the clinical landscape of the disease has not been clarified and no widely applicable classification system has been developed. METHODS: Sixty-two patients with CDC were included in this retrospective study, and a new classification system was established using imaging data. Blood indices, radiological characteristics, pathological features, surgical procedures, and overall survival data were collected. The efficacy of the new classification in predicting resectability was evaluated using receiver operating characteristic (ROC) curves, and K-means clustering and t-distributed stochastic neighbor embedding were applied to verify the conclusion. RESULTS: The pT stage of patients with type II CDC was significantly worse than that of type I. Patients with type II CDC were more likely to experience distant metastasis and invasion of the nervous system, vascular system, and liver. The resectability of patients with type II CDC was significantly worse than that of patients with type I CDC. Patients with type II CDC had worse prognoses. ROC curve analysis and K-means clustering revealed that the new classification could better categorize patients with CDC than currently available systems. CONCLUSION: Patients with type II CDC have significantly worse clinicopathological outcomes. The new classification system has better accuracy in grouping patients with CDC.

Left Bundle Branch Area Pacing vs. Biventricular Pacing for Cardiac Resynchronization Therapy: A Meta-Analysis.

Background: Left bundle branch area pacing (LBBAP) is a recently proposed method for conduction system pacing. We performed a meta-analysis of controlled studies to compare the clinical outcome in patients who received LBBAP vs. biventricular pacing (BVP) for cardiac resynchronization therapy (CRT). Methods: PubMed, Embase, and Cochrane's Library databases were searched for relevant controlled studies. A random-effect model incorporating the potential heterogeneity was used to synthesize the results. Results: Four non-randomized controlled studies including 249 patients with heart failure (HF) for CRT were included, and the patients were followed for 6-12 months. Compared with BVP, LBBAP was associated with significantly shortened QRS duration [mean difference (MD): -29.18 ms, 95% confidence interval (CI): -33.55-24.80, I 2 = 0%, P < 0.001], improved left ventricular ejection fraction (MD: 6.93%, 95% CI: 4.69-9.17, I 2 = 0%, P < 0.001), reduced left ventricular end-diastolic dimension (MD: -2.96 mm, 95% CI: -5.48 to -0.44, I 2 = 0%, P = 0.02), and improved New York Heart Association class (MD: -0.54, 95% CI: -0.84 to -0.24, I 2 = 65%, P < 0.001). Moreover, patients who received LBBAP were more likely to achieve echocardiographic [odds ratio (OR): 5.04, 95% CI: 2.17-11.69, I 2 = 0%, P < 0.001] and clinical (OR: 7.33, 95% CI: 1.62-33.16, I 2 = 0%, P = 0.01) CRT responses. Conclusion: Current evidence from non-randomized studies suggests that LBBAP appears to be a promising method for CRT, which is associated with more remarkable improvements of symptoms and cardiac function in HF patients with indication for CRT.

The effect of coronary slow flow on left atrial structure and function.

The coronary slow flow phenomenon (CSFP) is common in coronary angiography, however its impact on left atrial (LA) function is still controversial. This study aims to evaluate the LA structure and function of patients with CSFP using two-dimensional speckle tracking echocardiography (2D-STE). Consecutive patients scheduled for coronary angiography from January 2016 to September 2017 were enrolled in this study. Patients' demographic data, clinical histories, laboratory and angiographic findings were collected and recorded. Diagnostic criteria for CSFP is based on Beltrame et al. proposed in 2012. Meanwhile 139 patients who have no significant stenosis (≤ 40%) and normal blood flow were selected as control. All patients received an echocardiographic examination 24 h before coronary angiography. LA structure and function were measured with echocardiography and 2D-STE. Our results showed that among the 1,954 patients who had received coronary angiography, 512 patients were included in the analysis after the exclusion criteria was implemented. Of those, 101 patients met the CSFP criteria (5.5%). CSFP is mainly seen in LAD (~ 70%). There was no statistical difference in baseline characteristics between the CSFP group and control group, except for a higher proportion of smokers in the CSFP group (P = 0.001). The percentage of monocytes is an independent risk factor for the occurrence of CSFP (P = 0.036) after binary logistic regression analysis. The LA global longitudinal strain (LA-GLS, represents reservoir functions) decreased and LA strain rate at late diastole (LA-SRa, represents booster function) increased in patients with CSFP compared to the control group (P < 0.05). Correlation test of continuous variables by Pearson test suggested that LA-GLS was negatively correlated with TIMI frame count (TFC). We concluded that the percentage of monocytes is an independent risk factor for the CSFP; the LA reservoir and booster functions were impaired in patients with CSFP; LA-GLS is negatively correlated with TFC.

Predictors of Permanent Pacemaker Implantation in Patients After Transcatheter Aortic Valve Replacement in a Chinese Population.

Background: Permanent pacemaker (PPM) implantation is the main complication of transcatheter aortic valve replacement (TAVR). Few studies have evaluated the requirement for PPM implantation due to ECG changes following TAVR in a Chinese population. Objective: Our study aimed to evaluate the incidence and predictors of PPM implantation in a cohort of Chinese patients with TAVR. Methods: We retrospectively evaluated 39 consecutive patients with severe native aortic stenosis referred for TAVR with a self-expandable prosthesis, the Venus A valve (Venus MedTech Inc., Hangzhou, China), from 2019 to 2021 at the Heart Center of Affiliated Zhongshan Hospital of Dalian University. Predictors of PPM implantation were identified using logistic regression. Results: In our study, the incidence of PPM implantation was 20.5%. PPM implantation occurs with higher risk in patients with negative creatinine clearance (CrCl), dyslipidemia, high Society of Thoracic Surgeons (STS) Morbimortality scores, and lead I T wave elevation. TAVR induced several cardiac electrical changes such as increased R wave and T wave changes in lead V5. The main independent predictors of PPM implantation were new-onset left bundle branch block (LBBB) (coef: 3.211, 95% CI: 0.899-7.467, p = 0.004) and lead I T wave elevation (coef: 11.081, 95% CI: 1.632-28.083, p = 0.016). Conclusion: New-onset LBBB and lead I T wave elevation were the main independent predictors of PPM implantation in patients undergoing TAVR. Clinical indications such as negative CrCl, dyslipidemia, high STS Morbimortality scores, and an increased T wave elevation before TAVR should be treated with caution to decrease the need for subsequent PPM implantation.

The IL-17A rs2275913 polymorphism is associated with colorectal cancer risk.

OBJECTIVE: The association of the IL-17A rs2275913 polymorphism with the risk of colorectal cancer (CRC) has been previously reported. However, the results are inconsistent. In this study, we comprehensively assessed the effect of the rs2275913 polymorphism on CRC risk. METHODS: The rs2275913 polymorphism of 208 CRC patients and 312 age- and gender-matched healthy controls was genotyped by the polymerase chain reaction-restriction fragment length polymorphism method, and then analyzed by logistic regression. In addition, a pooled analysis based on five single-center studies was performed using Stata 12.0 software. RESULTS: Logistic regression analysis indicated that the IL-17A rs2275913 polymorphism was associated with CRC risk (GA vs. GG: OR = 1.53, 95% CI = 1.02-2.28; AA vs. GG: OR = 1.89, 95% CI = 1.11-3.20; GA+AA vs. GG: OR = 1.62, 95% CI = 1.11-2.37; A vs. G: OR = 1.38, 95% CI = 1.07-1.77). Further pooled analysis also indicated a statistically significant association between the rs2275913 polymorphism and CRC risk in Asians and Northern Africans. CONCLUSION: This study suggested that the IL-17A rs2275913 polymorphism may act as a biomarker for predicting CRC risk. However, further functional research should be performed to clarify the role of the rs2275913 polymorphism in the etiology of CRC.

Sex-Specific Differences in the Association of Metabolically Healthy Obesity With Hyperuricemia and a Network Perspective in Analyzing Factors Related to Hyperuricemia.

Background: Although obesity is a well-known risk factor for hyperuricemia, it remains unclear whether obese subjects with metabolically healthy status have a decreased the risk of hyperuricemia and whether sex modifies the association of metabolically healthy obesity (MHO) with hyperuricemia risk. We aimed to investigate the sex-specific association between MHO and other obesity phenotypes and hyperuricemia, and to use Bayesian networks to determine and visualize the interactions among hyperuricemia and its related factors. Methods: This study was conducted using data from the China Health and Nutrition Survey 2009. Hyperuricemia was defined as serum uric acid ≥ 420 µmol/L in men and ≥ 360 µmol/L in women according to the guidelines. Body mass index (BMI) was used to define normal weight, overweight, and obese status in subjects, and metabolic health state was defined by the Adult Treatment Panel (ATP)-III and Visceral Adiposity Index (VAI) criteria, respectively. Subjects were categorized into six phenotypes according to their metabolic health and BMI level status. Results: Of the 7,364 Chinese adult individuals included, the prevalence of hyperuricemia among MHO women was only 8.5% (95% CI 4.8 to 14.3%), but increased to 30.7% among MUO women, whereas the highest prevalence among men was found in the MUOW phenotype (39.4%, 95% CI 35.4 to 43.6%), compared to 15.4% for male subjects with MHO. After adjusting for confounders, the MHO phenotype was significantly associated with an increased risk of hyperuricemia compared with their MHNW counterparts in women (OR: 1.95, 95% CI: 1.02-3.74) whereas a significant association was not found in men (OR: 1.46, 95% CI: 0.8-2.68). A complex network structure was established by BNs and then used to find connections between hyperuricemia and its related factors, as well as their interrelationships. By using BN reasoning, the probability of having hyperuricemia was 0.076 among MHO men, while it reached 0.124 in MHO women. Conclusions: In conclusion, our results demonstrated that the MHO phenotype was significantly associated with the risk of hyperuricemia only in women, not in men. This sex-specific differences in the association may suggest a favorable condition of MHO for Chinese men with respect to hyperuricemia risk, meanwhile more attention should be paid to the increased risk of hyperuricemia among MHO women.