Immediate Repair With a Self-Gripping Retromuscular Mesh for Abdominal Wall Defect Following Tumor Resection.

Background: Prosthetic repair is always employed after large abdominal wall tumor resection, while chronic pain is one of the mesh-related complications after traumatic fixation. The objective of this research was to evaluate the outcomes of retromuscular repair with self-gripping mesh after abdominal wall tumor resection.Methods: The study was a monocentric retrospective analysis following STrengthening the Reporting of OBservational studies in Epidemiology (STROBE) statements of all patients with abdominal wall tumor >5 cm in diameter undergoing tumor excision and retromuscular repair with self-gripping mesh. Demographic, operative, early postoperative, and follow-up data were noted. Visual Analog Scale, ranging from 0 (no pain) to 10 (very severe pain), was used to estimate the wound pain.Results: 24 patients were included in this study, and the defect following tumor resection was 26.9±10.0 cm2. There was no tumor recurrence or incisional hernia in median follow-up of 20 months, and the mean VAS score was 0.4. Three had foreign body feeling and no one suffered chronic pain.Conclusions: Immediate repair with a self-gripping retromuscular mesh can be considered as an effective way to treat an abdominal wall defect after resecting an abdominal wall tumor.

Efficacy on radiofrequency ablation according to the types of benign thyroid nodules.

Percutaneous radiofrequency ablation (RFA) has been recommended as minimally invasive treatment for patients with symptomatic benign thyroid nodules (BTNs) because of the large number of clinical applications. This retrospective observational study sought to evaluate the clinical outcomes of RFA for BTNs. From 2014 to 2019, a sample size of 1289 patients treated by RFA were 262 ones with solid nodules and 1027 ones with cystic-solid nodule, respectively. The efficacy including the nodule maximal diameter reduction ratio (MDRR), the volume reduction ratio (VRR) and the cosmetic scores reduction ratio (CSRR). The results of the nodule MDRR and VRR in the cystic-solid nodule group were significantly better than those in the solid nodule group at the 3rd and 6th month, and the CSRR in the two groups showed statistically significant difference at the 3rd month. In a word, RFA is an effective method for symptomatic benign solid or cystic-solid nodules. The achieved MDRR and VRR in the cystic-solid nodule group were significantly better than those in the solid nodule group at the 3rd and 6th month.

Incidence and Risk Factors of Postoperative Bleeding in Patients Undergoing Total Thyroidectomy.

Purpose: Our goal was to analyze postoperative bleeding in patients undergoing total thyroidectomy and to explore the possible risk factors. Materials and Methods: Patients undergoing total thyroidectomy were retrospectively enrolled, and the main study outcomes were postoperative bleeding and 30-day mortality. Univariate and multivariate analyses were used to determine the independent risk factors for postoperative bleeding. Results: A total of 31,706 patients were enrolled for analysis during January 2010 and December 2018 from the Affiliated First Hospital of Zhengzhou University. Benign and malignant disease was reported in 4,521 and 27,185 patients, respectively. Postoperative bleeding occurred in 48 patients with benign disease and in 263 patients with malignant disease. There was one bleeding site in 243 patients. The branch of the superior thyroid artery was the most common arterial bleeding site, occurring in 124 patients, and the anterior jugular vein was the most common venous bleeding site, occurring in 85 patients. Multivariable analysis confirmed that hypertension, diabetes, BMI, and disease pathology were independent factors affecting postoperative bleeding in patients with benign disease and that hypertension, diabetes, BMI, operation time, tumor stage, and tracheotomy were independent factors affecting postoperative bleeding in patients with malignant disease. In patients with postoperative bleeding, there were 5 deaths; in patients without postoperative bleeding, there were 42 deaths, and the difference was significant (p < 0.001). Conclusions: Compared with malignant disease patients, benign disease patients have a similar postoperative bleeding rate. A previous history of chemotherapy or radiotherapy has no significant effect on postoperative bleeding.

Effect of Graves' disease on the prognosis of differentiated thyroid carcinoma: a meta-analysis.

PURPOSE: Several studies have reported different findings on the prognosis of differentiated thyroid carcinoma combined with Graves' disease. To assess the effect of Graves' disease on differentiated thyroid carcinoma, a meta-analysis was undertaken. METHODS: PubMed, OVID and the Cochrane Library were systematically searched for trials published prior to Oct. 2018. Studies containing data on the outcomes of Graves' disease with differentiated thyroid carcinoma were included. Summary estimates of the prevalence of recurrence/disease progression/persistence and mortality as well as odds ratios and weighted mean differences were calculated with a random-effects model. RESULTS: Of the 916 related articles found, 13 fulfilled the inclusion criteria. The recurrence/disease progression/persistent rate was not significantly different between the Graves' disease group and the non-Graves' disease group (P = 0.86). However, the analysis of three studies with K-M curves or HRs showed that there was a significant difference between the two groups (P = 0.04). Subgroup analysis showed that the contradictory results could be due to the location/race assessed in the studies. Graves' disease almost acted as a risk factor (OR = 1.77, 95%C.I. = 0.99-3.16) for differentiated thyroid carcinoma in European studies. When heterogeneous studies were excluded, the analyses show that GD was a risk factor for recurrence/disease progression/persistence (P = 0.03, OR = 1.75, 95%C.I. = 1.04-2.95). The overall mortality rate was significantly higher in the Graves' disease group than in the non-Graves' disease group (P = 0.02, OR = 2.93, 95%C.I. = 1.17-7.37). CONCLUSIONS: Graves' disease acts as a risk factor for the prognosis of differentiated thyroid carcinoma. The recurrence/disease progression/persistent rate may be affected by TSAbs in a specific location/race and with a genetic immunization background. However, the histotypes and subtypes may play an important role in mortality rate.

Long noncoding RNA AURKAPS1 potentiates malignant hepatocellular carcinoma progression by regulating miR-142, miR-155 and miR-182.

The mitotic serine/threonine kinase aurora kinase-A (AURKA) has been identified as carcinogenic in hepatocellular carcinoma (HCC). AURKAPS1, a long non-coding RNA (lncRNA), is the pseudo-gene of AURKA, which play important roles in the cancer. Its underlying functions and mechanisms in liver cancer progression remain largely unknown. The mRNA expression of AURKAPS1 in HCC tumor tissues was significantly higher, which is associated with tumor size and TNM stage. The high expression of AURKAPS1 promotes cell movement, migration and invasion. AURKAPS1 can increases the protein expression of RAC1, promotes the activation of ERK, and enhance the formation of membrane ruffles by binding with miR-182, miR-155 and miR-142 competively. Thus, AURKAPS1 could be a useful marker, and the combination of AURKAPS1/miRNAs (miR-142, miR-155 and miR-182) may be a new theoretical basis for the treatment of HCC.

MiR-23a-3p-regulated abnormal acetylation of FOXP3 induces regulatory T cell function defect in Graves' disease.

This study aims to investigate the mechanism of miR-23a-3p in regulating Treg dysfunction in Graves' disease (GD). The percentage of Treg cells and interleukin (IL)-17+ T cells were determined by flow cytometry. The expression of forkhead box P3 (FOXP3), sirtuin 1 (SIRT1), RAR-related orphan receptor gamma t (RORγt) and miR-23a-3p was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or Western blot. CD4+ T cells were treated with SIRT1 specific inhibitor EX-527 or left untreated. MiR-23a-3p mimic or inhibitor were transfected into CD4+ T cells. Acetylation expression of FOXP3 was analyzed by immunoprecipitation. The suppressive function of Treg was analyzed by the carboxyfluorescein succinimidyl ester (CFSE) assay. The results showed that GD patients have significantly less Treg cells and more IL-17+ T cells. FOXP3 and miR-23a-3p were significantly down-regulated meanwhile SIRT1 and RORγt were up-regulated in GD patients. FOXP3 acetylation level of the GD group was lower than that of control groups. After EX-527 treatment, the percentage of Treg cells, expression and acetylation level of FOXP3 were significantly increased in the GD group. GD Tregs exhibited weaker suppressive activity, miR-23a-3p mimic suppressed SIRT1 expression and suppressive-activity of Tregs whereas it promoted the expression and acetylation level of FOXP3 in the GD group. Our findings suggest that the Treg function defect in GD patients is mediated by the abnormal acetylation of FOXP3, which is regulated by miR-23a-3p via targeting SIRT1.

TGF-ß secreted by tumor-associated macrophages promotes proliferation and invasion of colorectal cancer via miR-34a-VEGF axis.

Tumor-associated macrophages (TAMs) were reported to be involved in colorectal cancer (CRC) progression. However, its biological role and underlying mechanism in CRC remained to be elucidated. In this study, the expressions of the macrophage marker CD68 and transforming growth factor ß1 (TGF-ß1) in CRC tumor tissues and adjacent tissues were detected by immunohistochemistry. The expression levels of miR-34a, TGF-ß1 and vascular endothelial growth factor (VEGF) in CRC tumor tissues and peripheral blood macrophages were measured by quantitative real-time PCR (qRT-PCR) and western blot. TGF-ß1 levels in culture supernatant were detected by ELISA. The cell proliferation and invasion of human CRC cell lines CL187 and HCT116 were determined by MTT assay and Transwell assay, respectively. The results showed that the expression of miR-34a was downregulated whereas TGF-ß1 and VEGF were upregulated in CRC tumor tissues and peripheral blood macrophages. TGF-ß1 secreted by TAMs promoted the proliferation and invasion of CRC cells. TGF-ß1-mediated miR-34a downregulation contributed to the proliferation and invasion of CRC cells via upregulating VEGF. MiR-34a in vivo exerted anti-tumor effect in CRC via inhibiting VEGF expression. In conclusion, TGF-ß1 secreted by TAMs promoted CRC proliferation and invasion through regulating miR-34a/VEGF axis.

MicroRNA-155 attenuates late sepsis-induced cardiac dysfunction through JNK and ß-arrestin 2.

Cardiac dysfunction is correlated with detrimental prognosis of sepsis and contributes to a high risk of mortality. After an initial hyperinflammatory reaction, most patients enter a protracted state of immunosuppression (late sepsis) that alters both innate and adaptive immunity. The changes of cardiac function in late sepsis are not yet known. MicroRNA-155 (miR-155) is previously found to play important roles in both regulations of immune activation and cardiac function. In this study, C57BL/6 mice were operated to develop into early and late sepsis phases, and miR-155 mimic was injected through the tail vein 48 h after cecal ligation and puncture (CLP). The effect of miR-155 on CLP-induced cardiac dysfunction was explored in late sepsis. We found that increased expression of miR-155 in the myocardium protected against cardiac dysfunction in late sepsis evidenced by attenuating sepsis-reduced cardiac output and enhancing left ventricular systolic function. We also observed that miR-155 markedly reduced the infiltration of macrophages and neutrophils into the myocardium and attenuated the inflammatory response via suppression of JNK signaling pathway. Moreover, overexpression of ß-arrestin 2 (Arrb2) exacerbated the mice mortality and immunosuppression in late sepsis. Furthermore, transfection of miR-155 mimic reduced Arrb2 expression, and then restored immunocompetence and improved survival in late septic mice. We conclude that increased miR-155 expression through systemic administration of miR-155 mimic attenuates cardiac dysfunction and improves late sepsis survival by targeting JNK associated inflammatory signaling and Arrb2 mediated immunosuppression.

Long non-coding RNA NEAT1 promotes malignant progression of thyroid carcinoma by regulating miRNA-214.

The long non­coding RNA nuclear enrich abundant transcript 1 (NEAT1) has been identified to be carcinogenic in various cancers and elevated NEAT1 expression was tightly linked to tumorigenesis and progression. However, the mechanism has not been revealed in progression of thyroid cancer. Tumor xenograft mouse model was established and tumor size was evaluated. Arg­1, NEAT1 and miR­214 expression in CBMs, TAMs, BMDMs and RAW 264.7 cell lines were detected. TPC­1 cells were subjected to si­NEAT1 transfection in vitro for cell viability study. A direct target of miRNA­214 (ß­catenin) was assessed, cell survival and invasion in TAMs were investigated. NEAT1, Arg­1 was highly expressed and miRNA­214 had lower expression in patients with thyroid cancer. NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced ß­catenin (a direct target of miRNA­214) protein expression. Furthermore, NEAT1 significantly accelerated thyroid cancer cell growth and metastasis in vitro and increased tumor size in vivo. Upregulation of NEAT1 decreased the expression of miRNA­214, presenting a reciprocal repression correlation. In conclusion, these results suggest that high expression of NEAT1 promoted the onset of thyroid carcinoma. In addition, NEAT1 promoted the malignant progression of thyroid cancer through regulating miRNA­214 expression, which adds to our understanding of the molecular mechanisms in thyroid carcinoma.

MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23.

OBJECTIVES: Vascular calcification is one the major characteristics in patients with various types of chronic inflammatory disorders. MiRNAs have been shown to be involved in many normal biological functions as well as diseases; however, their role in vascular calcification has not received much attention. MATERIALS AND METHODS: In the current study, we built a vascular calcification rat model using vitamin D3 plus nicotine and analyzed miRNA expression profile by miRNA chip assay. Potential target of one selected miRNA with sharpest variation in expression were predicted by both PicTar and TargetScan. The impact of the selected miRNA on the expression of the potential target on both mRNA and protein levels were measured by RT-PCR and Western blot, respectively. RESULTS: Our results identified 16 dysregulated miRNAs, among which miR-297a showed the sharpest variation. Further analysis focusing on miR-297a revealed that fibroblast growth factor 23 (FGF23) was a potential target of miR297a. Measurement of FGF23 and its regulator Klotho on both mRNA and protein levels demonstrated that FGF23 was significantly increased while Klotho was decreased in rats with vascular calcification. CONCLUSION: Our results indicated that FGF23 was target of miR-297a and decreased miR-297a in vascular calcification lead to the increase of FGF23, which together with Klotho might enhance vascular calcification. The findings of this study could provide valuable information for the understanding of mechanisms underlying miR-dependent vascular calcification as well as potential treatment target for the disease.

The BRAF V600E mutation predicts poor survival outcome in patients with papillary thyroid carcinoma: a meta analysis.

INTRODUCTION: There have been contradictory data on whether or not BRAF V600E mutation should be regard as a poor prognosis predictor of papillary thyroid carcinoma (PTC). To settle down the conflict, this metaanalysis is prepared to clarify the present prognostic role of BRAF V600E mutation in patients with PTC. METHODS AND MATERIALS: The relevant published researches were incorporated according to the defined inclusion/exclusion criteria from PubMed. The effect sizes of outcome parameters were estimated by hazard ratios (HRs). RESULTS: The current meta-analysis included 19 researches with a total of 6087 patients. We have found that patients with BRAF V600E mutation have a poor overall survival (the pooled HR=2.91, 95% confidence interval (CI): 1.35-6.29). Furthermore, subgroup analysis of the recurrence-free survival (RFS) of PTC patients by races indicated that BRAF V600E mutation predicts poor RFS of patients (the pooled HR=1.63, 95% CI: 1.37-1.93), both Caucasian (the pooled HR=1.57, 95% CI: 1.30-1.90) and Asian (the pooled HR=1.91, 95% CI: 1.28-2.87). CONCLUSIONS: The poor prognosis predicted role of BRAF V600E mutation in PTC was certified from the current meta-analysis. The BRAF V600E mutation may be used as a prognostic predictor of patients with PTC.