Quality of life in pregnancy after percutaneous closure of atrial septal defect guided by transthoracic echocardiography.

PURPOSE: We evaluated quality of life (QoL) in pregnant women who underwent transthoracic echocardiography-guided percutaneous closure of atrial septal defect (ASD). METHODS: A total of 45 pregnant women underwent transthoracic echocardiography-guided percutaneous closure of ASD. We assessed QoL using the 36-Item Short Form Survey (SF-36) and compared results between pre- and post-procedure patients, as well as between those with ASD and healthy women in their second and third trimesters of pregnancy. RESULTS: All patients showed improved right ventricular function and were classified as Class I, post-procedure. Mean SF-36 scores of the post-procedure group were better on all sub-scales than those of the pre-procedure group (p < 0.05), with the exception of role-emotional and mental health. Mean SF-36 scores for the pre-procedure group were also lower on all sub-scales than those of healthy pregnant controls (p < 0.05), with the exception of role physical, role emotional, and mental health. There was no difference between the post-procedure group and healthy pregnant controls. In a subgroup analysis, scores were better in some dimensions (social functioning and role emotional) for post-procedure patients in the 31-40 years of age group and the group on their second or third pregnancies than those of the 20-30 years of age group and the group on their first pregnancies (p < 0.05). CONCLUSION: After closure of ASD, QoL in pregnant women was improved. In a subgroup analysis, the younger women and those on their first pregnancy performed more poorly in some dimensions (social functioning and role emotional); this suggested that these groups should receive more proactive intervention.

Limited data was available on the general quality of life (QoL) in pregnant women with atrial septal defect (ASD), even though the condition could produce anxiety over health of the pregnancy and fetus. The percutaneous closure procedure was available for ASD during pregnancy; however, pregnant women were often concerned that the required X-rays would harm the fetus. A safe and effective procedure, percutaneous closure of ASD guided by transthoracic echocardiography, was widely used for this condition. This study used the 36-Item Short Form Survey (SF-36) to assess QoL in pregnant women with ASD pre- and post-procedure and compared the results to those of healthy pregnant women at a similar stage of pregnancy. Post-procedure QoL in pregnant women with ASD was improved; however, the younger women and those on their first pregnancy performed more poorly in some dimensions (social functioning and role emotional). Our results suggested that these groups should receive more proactive intervention.

Mid-term outcomes of right subaxillary approach versus median sternotomy incision for ventricular septal defect with patent ductus arteriosus.

BACKGROUND: This study aimed to evaluate and compare two surgical approaches to repair ventricular septal defect (VSD) with patent ductus arteriosus (PDA) and to explore the patients' health-related quality of life (HRQoL). METHODS: We conducted a retrospective study of all patients who had surgical repair of VSD and PDA between 2013 and 2015 using the right subaxillary approach (group A) or the median sternotomy incision (group B). The outcomes of both techniques were compared. Paediatric QoL Inventory 4.0 scale was applied to assess patients' HRQoL in the 6th postoperative year. Multiple linear regression analysis was performed to explore factors associated with higher HRQoL scores. RESULTS: A total of 128 patients were included (group A, n = 70 and group B, n = 58). Patients in group A were older and heavier than patients in group B. In group B, the diameters of VSD and PDA were larger and the pulmonary artery pressures were higher than those in group A (p < 0.001). No mortality occurred on a mean follow-up of 8.3 ± 1.2 years. Patients in group A had higher HRQoL scores than those in group B in terms of emotional and social functioning dimensions. The right subaxillary approach (OR: 3.56; 95% CI 1.65-5.46), higher parents' education level (OR: 1.62; 95% CI 0.65-2.31), and better family economic status (OR: 1.48; 95% CI 0.79-2.45) were associated with higher HRQoL scores. CONCLUSIONS: Younger and smaller patients receiving median sternotomy incisions due to large defects and pulmonary hypertension had lower HRQoL scores. The right subaxillary approach, higher parents' education level, and better family economic status were associated with higher HRQoL scores.

Outcomes of hemi- vs. total arch replacement in acute type A aortic dissection: A systematic review and meta-analysis.

Background: Acute type A aortic dissections (ATAAD) pose a challenge to surgeons due to high mortality, and decision making regarding the appropriate procedure is controversial. This study compared the outcomes of hemiarch and total arch replacement for ATAAD. Methods: The PubMed, Web of Science, Embase and Cochrane databases were searched for comparative studies on hemiarch versus total arch replacement that were published before May 1, 2022. Results: We included 23 observational studies with a total of 4,576 patients. Combined data analysis showed that early mortality (RR = 0.82; 95% CI: 0.70-0.97; P = 0.02), incidence of postoperative permanent neurological dysfunction (RR = 0.72; 95%CI:0.54∼0.94; P = 0.02), and incidence of renal failure and dialysis (RR = 0.82; 95%CI:0.71∼0.96; P = 0.01) were all lower for hemiarch than for total arch replacement. However, hemiarch replacement had a higher rate of late mortality (RR = 1.37; 95%CI:1.10∼1.71; P = 0.005). There were no statistically significant differences between the two groups in terms of re-operation for bleeding, aortic re-operation, or postoperative pneumonia. Conclusion: In this study, hemiarch replacement had better early outcomes but a higher late mortality rate than total arch replacement. Decisions regarding the extent of arch repair should be made according to location and extent of ATAAD and the experience of surgeons to ensure the most favorable prognosis. Systematic review registration: [INPLASY.COM], identifier [INPLASY202250088].

Upregulation of miR-222-3p alleviates the symptom of aortic dissection through targeting STAT3.

OBJECTIVE: This study sought to investigate the differentially expressed miRNAs in Aortic dissection (AD) and explore the downstream mechanisms in regulating AD. METHODS: Exosomes of AD patients and healthy people were isolated by differential centrifugation, and the differentially expressed miRNAs were evaluated by RNA sequencing. The downstream target of miR-222-3p was predicted by bioinformatics method and validated by dual-luciferase assay. Angiotensin II and Promethazine were used to establish AD mouse model and platelet-derived growth factor BB (PDGF-BB) was used to induce human vascular smooth muscle cells (HVSMCs) to elucidate the effect of miR-222-3p upregulation on AD in vivo and in vitro. The relative level of miR-222-3p was evaluated by RT-qPCR. The level of several proteins was investigated by Western blot. Immunofluorescence staining was used to detect the stress fiber formation. Cell migration was evaluated by wound healing and Transwell assay. The proliferation, cell cycle and apoptosis of HVSMCs were assessed by CCK-8 and flow cytometry, respectively. RESULTS: MiR-222-3p was downregulated in AD and PDGF-BB induced HVSMCs. The upregulation of miR-222-3p alleviated the symptom of AD in vivo by targeting STAT3, and inhibited stress fiber formation, abnormal migration, proliferation and apoptosis of HVSMCs induced by PDGF-BB by regulating the expression of α-SMA, SM22α, MMP2, MMP9 and p-Smad2. CONCLUSION: The upregulation of miR-222-3p attenuates the progression of AD. Our study provides a theoretical basis for exploring new strategies against AD.

LncRNA C9orf139 can regulate the progression of esophageal squamous carcinoma by mediating the miR-661/HDAC11 axis.

Increasing evidence has indicated that long non-coding RNAs (LncRNAs) play multiple functions in the development of cancer and function as indicators of diagnosis and prognosis. This aim of this study was to investigate the roles LncRNA C9orF139 had in the progression of esophageal squamous carcinoma (ESCC). We found C9orf139 was highly expressed in ESCC and knock down the expression of C9orf139 significantly suppressed cell proliferation, promoted apoptosis, and inhibited migration and invasion. C9orf139 was able to negatively regulate miR-661 expression. At the same time, HDAC11 expression was negatively regulated by miR-661. The C9orf139/miR-661/HDAC11 axis was further involved in regulating the expression of the NF-κB signaling pathway. The association between the C9orf139 knockdown and the reduced tumor growth and size was observed during in vivo study. C9orf139 is highly expressed in ESCC, and is thus qualified to be used as a potential diagnostic and prognostic marker for ESCC. Its promotion of ESCC progression is achieved by mediating the miR-661/HDAC11 axis.

Meta-Analysis: Shouldn't Prophylactic Corticosteroids be Administered During Cardiac Surgery with Cardiopulmonary Bypass?

Background: Corticosteroids can effectively inhibit systemic inflammation induced by cardiopulmonary bypass. Recently clinical trials and meta-analyses and current guidelines for cardiac surgery do not support corticosteroids prophylaxis during cardiac surgery because of an increase in myocardial infarction and no benefit for patients. The aim of this study is to determine whether specific corticosteroids dose ranges might provide clinical benefits without increasing myocardial infarction. Methods: The PubMed, Web of Science, Embase, Clinical Trials, and Cochrane databases were searched for randomized controlled trials (RCTs) published before August 1, 2021. Results: 88 RCTs with 18,416 patients (17,067 adults and 1,349 children) were identified. Relative to placebo and high-dose corticosteroids, low-dose corticosteroids (≤20 mg/kg hydrocortisone) during adult cardiac surgery did not increase the risks of myocardial infarction (odds ratio [OR]: 0.96, 95% confidence interval [CI]: 0.43-2.17; p = 0.93). However, low-dose corticosteroids were associated with lower risks of atrial fibrillation (OR: 0.58, 95% CI: 0.44-0.76; p < 0.0001) and kidney injury (OR: 0.29, 95% CI: 0.09-0.96; p = 0.04). Furthermore, low-dose corticosteroids significantly shortened the mechanical ventilation times (mean difference [MD]: -2.74 h, 95% CI: -4.14, -1.33; p = 0.0001), intensive care unit (ICU) stay (MD: -1.48 days, 95% CI: -2.73, -0.22; p = 0.02), and hospital stay (MD: -2.29 days, 95% CI: -4.51, -0.07; p = 0.04). Conclusion: Low-dose corticosteroids prophylaxis during cardiac surgery provided significant benefits for adult patients, without increasing the risks of myocardial infarction and other complications.

Genome-Wide Identification of Associations of Circulating Molecules With Spontaneous Coronary Artery Dissection and Aortic Aneurysm and Dissection.

Circulating proteins play functional roles in various biological processes and disease pathogenesis. The aim of this study was to highlight circulating proteins associated with aortic aneurysm and dissection (AAD) and spontaneous coronary artery dissection (SCAD). We examined the associations of circulating molecule levels with SCAD by integrating data from a genome-wide association study (GWAS) of CanSCAD and 7 pQTL studies. Mendelian randomization (MR) analysis was applied to examine the associations between circulating molecule levels and AAD by using data from UK Biobank GWAS and pQTL studies. The SCAD-associated SNPs in 1q21.2 were strongly associated with circulating levels of extracellular matrix protein 1 (ECM1) and 25 other proteins (encoded by CTSS, CAT, CNDP1, KNG1, SLAMF7, TIE1, CXCL1, MBL2, ESD, CXCL16, CCL14, KCNE5, CST7, PSME1, GPC3, MAP2K4, SPOCK3, LRPPRC, CLEC4M, NOG, C1QTNF9, CX3CL1, SCP2D1, SERPINF2, and FN1). These proteins were enriched in biological processes such as regulation of peptidase activity and regulation of cellular protein metabolic processes. Proteins (FGF6, FGF9, HGF, BCL2L1, and VEGFA) involved in the Ras signaling pathway were identified to be related to AAD. In addition, SCAD- and AAD-associated SNPs were associated with cytokine and lipid levels. MR analysis showed that circulating ECM1, SPOCK3 and IL1b levels were associated with AAD. Circulating levels of low-density lipoprotein cholesterol and small very-low-density lipoprotein particles were strongly associated with AAD. The present study found associations between circulating proteins and lipids and SCAD and AAD. Circulating ECM1 and low-density lipoprotein cholesterol may play a role in the pathology of SCAD and AAD.

Association of Circulating Cathepsin B Levels With Blood Pressure and Aortic Dilation.

Hypertension is a key risk factor for spontaneous coronary artery dissection (SCAD) and aortic dilation. Circulating proteins play key roles in a range of biological processes and represent a major source of druggable targets. The aim of this study was to identify circulating proteins that were associated with blood pressure (BP), SCAD and aortic dilation. We identified shared genetic variants of BP and SCAD in genome-wide association studies, searched for circulating protein affected by these variants and examined the association of circulating protein levels with BP, aortic aneurysm and dissection (AAD) and aortic diameters by integrating data from circulating protein quantitative trait loci (pQTL) studies and genome wide association study (GWAS) in individuals from the UK Biobank using two-sample Mendelian randomization analysis methods. Single nucleotide polymorphisms (SNPs) in JAG1, ERI1, ULK4, THSD4, CMIP, COL4A2, FBN1, FAM76B, FGGY, NUS1, and HNF4G, which were related to extracellular matrix components, were associated with both BP and SCAD. We found 49 significant pQTL signals among these SNPs. The regulated proteins were encoded by MMP10, IL6R, FIGF, MMP1, CTSB, IGHG1, DSG2, TTC17, RETN, POMC, SCARF2, RELT, and GALNT16, which were enriched in biological processes such as collagen metabolic process and multicellular organism metabolic process. Causal associations between BP and AAD and aortic diameters were detected. Significant associations between circulating levels of cathepsin B, a well-known prorenin processing enzyme, and BP and aortic diameters were identified by using several Mendelian randomization analysis methods and were validated by independent data. Conclusion: The present study identified the association between circulating cathepsin B and BP and aortic diameters. The findings indicated that BP-associated genetic variants may influence aortic dilation risk by circulating proteins that regulate BP.

PSRC1 May Affect Coronary Artery Disease Risk by Altering CELSR2, PSRC1, and SORT1 Gene Expression and Circulating Granulin and Apolipoprotein B Protein Levels.

OBJECTIVE: The aim of the study was to identify additional factors that contributed to coronary artery disease (CAD). METHODS: We conducted integrative analysis on publicly available data from genome-wide association studies and quantitative trait locus studies by employing Mendelian randomization methods to examine the associations of gene expression in liver cells and circulating protein levels with LDL-C and CAD. RESULTS: We found that the mRNA expression levels of CELSR2, PSRC1, SORT1, SYPL2, RHD, RHCE, ANGPTL3, ATXN7L2, DNAH11, FADS3, ST3GAL4, NYNRIN, CETP, EFCAB13, and SPTLC3 were significantly associated with LDL-C. The expression levels of SORT1, PSRC1, and CELSR2 in liver cells were significantly associated with CAD. Higher expression levels of SORT1, PSRC1, and CELSR2 in the liver were significantly associated with lower circulating LDL-C levels and CAD risk. PSRC1 variants were strongly associated with SORT1, PSRC1, and CELSR2 gene expression in liver cells. Higher circulating granulin and apolipoprotein B levels, which were strongly affected by PSRC1 variants, were significantly associated with higher LDL-C levels and CAD risk, with odds ratios of 1.15 (1.10-1.19) and 1.45 (1.21-1.74), respectively. CONCLUSION: This study showed that regulatory SNPs in PSRC1 may affect CAD risk by altering CELSR2, PSRC1, and SORT1 gene expression in liver cells and circulating granulins and apolipoprotein B proteins.

A narrative review of research advances in hypoxic pulmonary hypertension.

Background and Objective: Hypoxic pulmonary hypertension (HPH) is a pathological syndrome characterized by pulmonary vasoconstriction and pulmonary vascular remodeling caused by hypoxia, which eventually leads to right heart failure or death. There are 2 stages of onset of HPH: hypoxic pulmonary vasoconstriction (HPV) and hypoxic pulmonary vascular remodeling (HPVR). It is an important pathophysiological link in the pathogenesis of chronic obstructive pulmonary disease (COPD) and chronic mountain sickness (CMS), and its severity is closely related to the course and prognosis of COPD and CMS. However, there is a lack of systematic review on the diagnosis, pathogenesis and treatment of HPH. The objective of this paper is to review the diagnosis, pathogenesis, treatment of HPH. Methods: In this paper, the method of literature review is adopted to obtain the information about HPH. Based on the literature, comprehensive and systematic review is made. The diagnosis, pathogenesis, treatment of HPH are summarized. Key Content and Findings: Right heart catheterization is the gold standard for diagnosing HPH. Hypoxia-inducible factor, oxidative stress, metal metabolism, ion channel, inflammatory cytokines, cell apoptosis and vascular factors are the main pathogenesis of HPH. The treatment of HPH includes long-term oxygen therapy, statins, prostaglandins, phosphodiesterase inhibitor and ET receptor antagonists. Conclusions: Although great progress has been made in the pathophysiology and molecular biology of HPH, it is still unclear which factors play a leading role in the pathogenesis of HPH, and no breakthrough has been made in the treatment of HPH. It is believed that the specific mechanism will be revealed as the research continues, and earlier diagnosis and the development of more effective targeted drugs will be the focus of future research.

Partial upper sternotomy for extensive arch repair in older acute type A aortic dissection patients.

OBJECTIVES: The partial upper sternotomy (PUS) approach is acceptable for aortic valve replacement, and even aortic root operation. However, the efficiency of PUS for extensive arch repair of acute type A aortic dissection (AAAD) in older adult patients has not been well investigated. METHODS: Between January 2014 and December 2019, 222 older adult patients (≥ 65 years) diagnosed with AAAD went through extensive arch repair, among which 127 received PUS, and 95 underwent full sternotomy (FS). Logistic regression analysis was used to identify risk factors for early death, and negative binomial regression analysis was applied to explore risk factors related to post-operative ventilator-supporting time and intensive care unit stay time. RESULTS: Total early mortality was 8.1% (18/222 patients). The PUS group had shorter Cardiopulmonary bypass time (133.0 vs.155.0 min, P < 0.001), cross-clamp time (44.0 vs. 61.0 min, P < 0.001) and shorter selective cerebral perfusion time (11.0 vs. 21.0 min, P < 0.001) than the FS group. Left ventricle ejection fraction < 50% (odds ratio [OR] 17.05; 95% confidence interval [CI] 1.87-155.63; P = 0.012) and malperfusion syndromes (OR 65.83; 95% CI 11.53-375.86; P < 0.001) were related to early death. In the multivariate model, the PUS approach contributed to shorter ventilator-supporting time (incidence rate ratio [IRR] 0.76; 95% CI 0.64-0.91; P = 0.003), when compared with the FS group. CONCLUSIONS: The early results of emergency extensive arch repair of AAAD via PUS in older adult patients were satisfactory. However, the long-term results remain to be investigated.

miR-145 attenuates phenotypic transformation of aortic vascular smooth muscle cells to prevent aortic dissection.

BACKGROUND: miR-145 is closely related to vascular smooth muscle cells (VSMC) phenotype transformation; however, the regulatory mechanisms through which miR-145 regulates the VSMC phenotype transformation under mechanical stretching are unclear. In this study, we evaluated the roles of miR-145 in VSMCs subjected to mechanical stretching in aortic dissection (AD). METHODS: The expression of miR-145 in the aortic vessel wall of model animals and patients with AD was analyzed by quantitative polymerase chain reaction. miR-145-related protein-protein interaction networks and Wikipathways were used to analyze VSMC phenotypic transformation pathways regulated by miR-145. We used gain- and loss-of-function studies to evaluate the effects of miR-145 on VSMC differentiation under mechanical stretch induction and assessed whether Krüppel-like factor 4 (KLF4) was regulated by miR-145 in the aorta under mechanical stretch conditions. RESULTS: miR-145 was abundantly expressed in the walls of the normal human aorta, but was significantly downregulated in animal models and the walls of patients with dissection. We found that contractile phenotype-related proteins were downregulated in VSMCs subjected to mechanical stretching, whereas the expression of secreted phenotype-related proteins increased. miR-145 overexpression also downregulated contractile phenotype-related proteins in VSMCs and suppressed upregulation of phenotype-related proteins. Finally, under mechanical stretching, KLF4 expression was significantly increased in VSMCs, and overexpression of miR-145 blocked this effect. CONCLUSION: Our results confirmed that mechanical stretch-induced phenotypic transformation of VSMCs to promote AD via upregulation of KLF4; this mechanism was regulated by miR-145, which directly modulated KLF4 expression and VSMC differentiation.

Genome-Wide Identification of RNA Modifications for Spontaneous Coronary Aortic Dissection.

RNA modification plays important roles in many biological processes such as gene expression control. Genetic variants that affect RNA modification may have functional roles in aortic dissection. The aim of this study was to identify RNA modifications related to spontaneous coronary artery dissection (SCAD). We examined the association of RNA modification-associated single-nucleotide polymorphisms (RNAm-SNPs) with SCAD in summary data from a genome-wide association study (GWAS) of European descent (270 SCAD cases and 5,263 controls). Furthermore, we performed expression quantitative loci (eQTL) and protein quantitative loci (pQTL) analyses for the RNAm-SNPs using publicly available data. Functional enrichment and protein-protein interaction analyses were performed for the identified proteins. We found 11,464 unique RNAm-SNPs in the SCAD GWAS dataset, and 519 were nominally associated with SCAD. Nine RNAm-SNPs were associated with SCAD at p < 0.001, and among them, seven were N6-methyladenosine (m6A) methylation-related SNPs, one (rs113664950 in HLA-DQB1) was m7G-associated SNP, and one [rs580060 in the 3'-UTR of Mitochondrial Ribosomal Protein S21 (MRPS21)] was A-to-I modification SNP. The genome-wide significant SNP rs3818978 (SCAD association p = 5.74 × 10-10) in the 5'-UTR of MRPS21 was related to m6A modification. These nine SNPs all showed eQTL effects, and six of them were associated with circulating protein or metabolite levels. The related protein-coding genes were enriched in specific Gene Ontology (GO) terms such as extracellular space, extracellular region, defense response, lymphocyte migration, receptor binding and cytokine receptor binding, and so on. The present study found the associations between RNAm-SNPs and SCAD. The findings suggested that RNA modification may play functional roles in SCAD.

Identification of potential core genes in esophageal carcinoma using bioinformatics analysis.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a common human malignancy worldwide. The tumorigenesis mechanism in ESCC is unclear. MATERIALS AND METHODS: To explore potential therapeutic targets for ESCC, we analyzed 3 microarray datasets (GSE20347, GSE38129, and GSE67269) derived from the gene expression omnibus (GEO) database. Then, the GEO2R tool was used to screen out differently expressed genes (DEGs) between ESCC and normal tissue. Gene ontology function and kyoto encyclopedia of genes and genomes pathway enrichment analysis were performed using the database for annotation, visualization and integrated discovery to identify the pathways and functional annotation of DEGs. Protein-protein interaction of these DEGs was analyzed based on the search tool for the retrieval of interacting genes database and visualized by Cytoscape software. In addition, we used encyclopedia of RNA interactomes (ENCORI), gene expression profiling interactive analysis (GEPIA), and the human protein atlas to confirm the expression of hub genes in ESCC. Finally, GEPIA was used to evaluate the prognostic value of hub genes expression in ESCC patients and we estimated the associations between hub genes expression and immune cell populations (B Cell, CD8+ T Cell, CD4+ T Cell, Macrophage, Neutrophil, and Dendritic Cell) in esophageal carcinoma (ESCA) using tumor immune estimation resource (TIMER). RESULTS: In this study, 707 DEGs (including 385 upregulated genes and 322 downregulated genes) and 6 hub genes (cyclin B1 [CCNB1], cyclin dependent kinase 1 [CDK1], aurora kinase A [AURKA], ubiquitin conjugating enzyme E2C [UBE2C], cyclin A2 [CCNA2], and cell division cycle 20 [CDC20]) were identified. All of the 6 hub genes were highly expressed in ESCC tissues. Among of them, only CCNB1 and CDC20 were associated with stage of ESCC and all of them were not associated with survival time of patients. CONCLUSION: DEGs and hub genes were confirmed in our study, providing a thorough, scientific and comprehensive research goals for the pathogenesis of ESCC.

Insulin Resistance Promotes the Formation of Aortic Dissection by Inducing the Phenotypic Switch of Vascular Smooth Muscle Cells.

BACKGROUND: Insulin resistance (IR) plays a key role in the development of type 2 diabetes mellitus (T2DM) and is one of its most important characteristics. Previous studies have shown that IR and T2DM were independent risk factors for a variety of cardiovascular and cerebrovascular diseases. However, there are few studies on the relationship between IR and aortic dissection (AD). The goal of this research was to find evidence that IR promotes the occurrence of AD. METHODS: Through the statistical analysis, we determined the proportion of glycosylated hemoglobin (HbA1c) abnormalities (HbA1c > 5.7) in people with acute thoracic aortic dissection (ATAD) and compared the difference of messenger RNA (mRNA) and protein expression of GluT1 in the thoracic aorta of normal people and those with ATAD to find evidence that IR is a causative factor in AD. The mouse model of IR and AD and the IR model of human aortic vascular smooth muscle cells (HA-VSMC) were established. Real time-PCR (RT-PCR) and Western blotting were used to study the mRNA and protein expression. Hematoxylin and eosin (H&E), Masson, and elastic fiber staining, and immunofluorescence were used to study the morphological structure. RESULTS: The proportion of HbA1c abnormalities in patients with ATAD was 59.37%, and the mRNA and protein expression of GluT1 were significantly lower than that in normal people. Fasting glucose concentration (FGC), serum insulin concentration (SIC), and the homeostasis model assessment of insulin resistance (HOMA-IR) of mice was obviously increased in the high-fat diet group and the protein expressions of Glut1 and GluT4 were reduced, indicating that the mouse IR model was successfully established. The incidence of AD was different between the two groups (IR: 13/14, Ctrl: 6/14), and the protein expression of MMP2, MMP9, and OPN were upregulated and SM22 and α-SMA were downregulated in mice. The expressions of mRNA and protein of GluT1 and SM22 in HA-VSMCs with IR were reduced and OPN was increased. CONCLUSION: Combined results of clinical findings, mouse models, and cell experiments show that IR induced the phenotypic switching of vascular smooth muscle cells (VSMCs) from contractile to synthetic, which contributes to the occurrence of AD. It provides a basis for further research on the specific mechanism of how IR results in AD and a new approach for the prevention and treatment of AD.

Efficacy and safety of corticosteroids prophylaxis in cardiac surgery: A protocol for systematic review and meta-analysis.

BACKGROUND: Although corticosteroid prophylaxis in adult cardiac surgery has been studied extensively for 40 years, its role remains controversial, and the optimal dose remains uncertain. The objective of this meta-analysis was to estimate the clinical benefits and risks of corticosteroid use in cardiopulmonary bypass. METHODS: We will search Pubmed, Web of Science, Embase, Clinical Trials, and Cochrane Central Register of Controlled Trials for relevant clinical trials published in any language before August 1, 2020. Randomized controlled trials (RCTs) of interest which meet inclusion criteria published or unpublished will be included. We will divide the included studies into child and adult groups for analysis. If sufficient data are available, the included trials will be divided into 4 subgroups: ≤20 mg/kg (low dose), 20-40 mg/kg (slightly high dose), 40-100 mg/kg (high dose), and >100 mg/kg (ultra high dose) based on the equivalent hydrocortisone dose. INPLASY registration number: INPLASY2020100044. RESULTS: The results of this study will be published in a peer-reviewed journal. CONCLUSION: This study will compare the efficacy of tprophylactic corticosteroids for adults and children undergoing cardiac surgery with CPB. Due to the nature of the disease and intervention methods, randomized controlled trials may be inadequate, and we will carefully consider inclusion in high-quality, non-randomized controlled trials, but this may result in high heterogeneity and affect the reliability of the results.

A retrospective study of the relationship between the pathologic subtype and lymph node metastasis of lung adenocarcinomas of ≤3 cm diameter.

To analyze the relationship between pathologic subtype and lymph node metastasis for lung adenocarcinomas of ≤3 cm diameter.We retrospectively studied 384 patients with operable lung adenocarcinomas of ≤3 cm diameter that had been radically resected by lobectomy or anatomic segmentectomy with systematic nodal dissection, at the Fujian Medical University Union Hospital between March 2014 and March 2016.Lymph node metastasis pN1 + pN2 (pN+) was found in 2 of 104 (1.9%) patients with tumor diameter ≤1.0 cm, 12 of 159 (7.5%) patients with tumor diameter >1.0 cm but ≤2.0 cm, and 35 of 121 (28.9%) patients with tumor size >2.0 cm but ≤3.0 cm (P < .01). Lymph node metastasis pN+ was found in 19 of 53 (35.8%) patients with visceral invasion pleural (VIP) and 30 of 331 (9.0%) patients without VIP (P < .05). It was also found in 16 of 51 (31.3%) patients with high serum CEA concentrations and 28 of 297 (9.4%) patients with normal concentrations (P < .05). In a multivariate analysis, tumor diameter, VIP, high serum CEA concentration, and pathologic subtype were significant risk factors. The prevalences of lymph node metastasis pN+ were: 0.0% (0/2), 0.0% (0/89), 3.2% (1/31), 16.2% (34/209), 7.7% (1/13), 46.7% (7/15), 100% (4/4), and 11.8% (2/17) for adenocarcinoma in situ (AIS); minimally invasive adenocarcinoma (MIA); predominantly lepidic (LEP), acinar (ACI), papillary, solid (SOL), and micropapillary (MIP) tumors; and variants of invasive adenocarcinoma, respectively (P < .05). For predominant SOL and MIP tumors, the prevalences of lymph node involvement were significantly higher than for the other subtypes.We have shown that lymph node metastasis in patients with tumor diameter ≤3 cm differs according to lung adenocarcinoma subtype. AIS and MIA were not associated with lymph node metastasis; therefore, systematic nodal dissection may be unnecessary. The prevalence of lymph node metastasis rate was low for LEP, suggesting that systemic lymph node sampling is sufficient. In contrast, for other pathologic subtypes, including SOL and MIP, systematic lymph node dissection should be performed.

Vein-first vs artery-first surgical technique for lobectomy of non-small cell lung cancer: A protocol for systematic review and meta-analysis.

BACKGROUND: The operation of lung cancer may squeeze the tumor and further promote the spread of tumor cells to the circulation, which may be one of the reasons for the metastasis and recurrence of lung cancer. The potential risk of tumor cell dissemination can theoretically be minimized if the effluent veins were ligated first (via the vein-first [V-first] technique), instead of having the artery ligated first (via the artery-first [A-first] technique). However, this technical concept has not yet been widely accepted as a standard of surgical oncology in current guidelines owing to a lack of sufficient evidence. This systematic review and meta-analysis will be performed to determine which technique during lobectomy will achieve longer patient survival and be more beneficial for patients. METHODS: We will search PubMed, Web of Science, EMBASE, Cancerlit, the Cochrane Central Register of Controlled Trials, and Google Scholar databases for relevant clinical trials published in any language before October 1, 2020. Randomized controlled trials (RCTs), quasi-RCTs, propensity score-matched comparative studies, and prospective cohort studies of interest, published or unpublished, that meet the inclusion criteria will be included. Subgroup analysis of the type of operation, tumor pathological stage, and ethnicity will be performed. INPLASY registration number: INPLASY202050060. RESULTS: The results of this study will be published in a peer-reviewed journal. CONCLUSION: As far as we know, this study will be the first meta-analysis to compare the efficacy of the vein-first and artery-first surgical technique of lobectomy for patients diagnosed with resectable non-small cell lung cancer. Due to the nature of the disease and intervention methods, randomized controlled trials may be inadequate, and we will carefully consider inclusion in high-quality, non-randomized controlled trials, but this may result in high heterogeneity and affect the reliability of the results.

Loss of miR-204-5p Promotes Tumor Proliferation, Migration, and Invasion Through Targeting YWHAZ/PI3K/AKT Pathway in Esophageal Squamous Cell Carcinoma.

PURPOSE: MicroRNAs dysregulation has been confirmed in multiple malignancies. This paper reported the molecular mechanism of miR-204-5p in esophageal squamous cell carcinoma (ESCC). METHODS: miR-204-5p expression in 30 ESCC tumor tissues and 10 normal tissues was downloaded from RNA-seq data. ESCC tissues/normal tissues of 97 ESCC patients were collected. TE-1 and KYSE510 cells were transfected by miR-204-5p mimic, inhibitor, siYWHAZ or their corresponding controls. The phenotype of cells was detected by CCK-8 assay, transwell experiment, and flow cytometry. Luciferase reporter gene assay and RNA-binding protein immunoprecipitation (RIP) were performed to verify the targeting relationship between miR-204-5p and YWHAZ. miR-204-5p and YWHAZ expression in tissues/cells was detected by qRT-PCR and Western blot. Xenograft tumor experiment was performed. RESULTS: miR-204-5p expression was declined in ESCC patients and cells, which was indicated the poor outcome of patients. Compared with siNC group, TE-1 cells in miR-204-5p inhibitor group had higher OD450 value, less cell percentage in G1 phase, and more cell percentage in S phase, lower apoptosis percentage, and higher migration and invasion cell numbers. Moreover, KYSE510 cells of miR-204-5p mimic group showed lower OD450 value, more cell percentage in G1 phase and less cell percentage in S phase, higher apoptosis percentage, and lower migration and invasion cell numbers than control. YWHAZ was directly inhibited by miR-204-5p. Relative to siNC group, TE-1 cells of miR-inhibitor group exhibited higher YWHAZ protein expression, higher OD450 value, less cell percentage in G1 phase and more cell percentage in S phase, lower apoptosis percentage, higher migration and invasion cell numbers, and higher p-PI3K/PI3K and p-AKT/AKT protein expression, while siYWHAZ rescued the effects of miR-inhibitor. miR-204-5p up-regulation inhibited ESCC growth in vivo. CONCLUSION: miR-204-5p inhibits ESCC progression by targeted inhibition of YWHAZ/PI3K/AKT.

LGR6 is a potential diagnostic and prognostic marker for esophageal squamous cell carcinoma.

BACKGROUND: Leucine-rich repeat-coupled receptor 6 (LGR6) is a marker of the skin, nails, and other types of adult tissue stem cells and has been widely found to be related to the development and progression of a variety of cancer types. The clinical significance and biological function of LGR6 in esophageal squamous cell carcinoma (ESCC) have not been determined. METHODS: The expression of LGR6 at the transcriptional level was analyzed by searching the TCGA and UCSC data sets. Immunohistochemistry, WB, and q-PCR were used to detect the expression of LGR6 in ESCC and adjacent normal tissues. LGR6 PPI networks and KEGG pathways were used to analyze the potential biological functions of LGR6. RESULTS: The expression of LGR6 in ESCC tissues was significantly higher than that in normal tissues and was negatively correlated with the differentiation degree of ESCC and the prognosis of the patients but not closely correlated with the TNM stage of ESCC. PPI networks showed that LGR6 had a close interaction with RSPO1, RSPO2, RSPO3, and RSPO4. KEGG pathway analysis showed that LGR6 activated the Wnt/ß-catenin signaling pathway by binding with RSPO ligands to promote the progression of ESCC. CONCLUSION: LGR6 can serve as a potential diagnostic and prognostic marker for ESCC.