Quantitative proteomics analysis revealed the potential role of lncRNA Ftx in cardiomyocytes.

OBJECTIVE: This study aims to decode the proteomic signature of cardiomyocytes in response to lncRNA Ftx knockdown and overexpression via proteomic analysis, and to study the biological role of lncRNA Ftx in cardiomyocytes.  METHODS: The expression level of the lncRNA Ftx in cardiomyocytes cultured in vitro was intervened, and the changes in protein levels in cardiomyocytes were quantitatively detected by liquid chromatography-mass spectrometry. The key molecules and pathways of the lncRNA-Ftx response were further examined by GO, KEGG, and protein interaction analysis. RESULTS: A total of 2828 proteins are quantified. With a 1.5-fold change threshold, 32 upregulated proteins and 49 downregulated proteins are identified in the lncRNA Ftx overexpression group, while 67 up-regulated proteins and 54 down-regulated proteins are identified in the lncRNA Ftx knockdown group. Functional clustering analysis of differential genes revealed that the lncRNA Ftx is involved in regulating cardiomyocyte apoptosis and ferroptosis and improving cellular energy metabolism. In addition, Hub genes such as ITGB1, HMGA2, STAT3, GSS, and LPCAT3 are regulated downstream by lncRNA Ftx. CONCLUSION: This study demonstrates that lncRNA Ftx plays a vital role in cardiomyocytes and may be involved in the occurrence and development of various myocardial diseases. It provides a potential target for clinical protection of the myocardium and reversal of myocardial fibrosis.

Non-Radical Activation of Peracetic Acid by Powdered Activated Carbon for the Degradation of Sulfamethoxazole.

Environmental-friendly and low-cost catalysts for peracetic acid (PAA) activation are vital to promote their application for micropollutant degradation in water. In this study, powdered activated carbon (PAC) was reported to improve the degradation of sulfamethoxazole (SMX). The improvement of SMX degradation in the PAC/PAA system was expected to be because of the PAA activation rather than the co-existing H2O2 activation. Non-radical oxidation pathways, including the mediated electron-transfer process and singlet oxygen (1O2), were evidenced to play the dominant roles in the degradation of micro-organic pollutants. The graphitization of PAC, persistent free radicals, and electron-donating groups like C-OH were proposed to contribute to the activation of PAA. High SMX degradation could be achieved in the acidic and neutral conditions in the PAC/PAA system. Overall, higher dosages of PAC (0-0.02 g/L) and PAA (0-100 µM) benefited the degradation of SMX. The presence of HCO3- could lower the SMX degradation significantly, while Cl-, PO43-, and humic acid (HA) only reduced the SMX degradation efficiency a little. Overall, this study offered an efficient non-radical PAA activation method using PAC, which can be effectively used to degrade micro-organic pollutants.

Early and Intermediate-Term Results for the Combined Superior Approach Correction of Supracardiac Total Anomalous Pulmonary Venous Connection in Neonatal Patients.

BACKGROUND: There are different surgical approaches used for repairing a supracardiac total anomalous pulmonary venous connection (TAPVC), with different results. This retrospective study evaluated the outcomes of surgical repair for supracardiac TAPVC through the combined superior approach in neonatal patients. METHODS: Medical records were retrospectively reviewed and 21 neonates who underwent supracardiac TAPVC repair with the combined superior approach between July 2014 and January 2020 were identified. There were 13 males and eight females. RESULTS: The patients' median age was 20.6±8.9 days (range, 3-27). The median weight was 3.1±0.39 kg (range, 2.5-3.7) The median aortic cross-clamp and cardiopulmonary bypass times were 49.3±19.5 minutes (range, 27-86) and 91.1±23.7 minutes (range, 57-146). They were two deaths during the intensive care unit stay. One (1) patient died 2 months after discharge, the other remaining patients had no pulmonary venous obstruction (PVO) at the 6-month and intermediate-term follow-ups. CONCLUSIONS: The combined superior approach is a useful method for repair of neonatal critical supracardiac TAPVC. This technique may be more helpful in preventing early postoperative anastomotic stenosis and contribute to an improved patient outcome.

Serum miR-1297: a promising diagnostic biomarker in esophageal squamous cell carcinoma.

We aimed to value the diagnostic potential of serum miR-1297 in esophageal squamous cell cancer (ESCC). Its expression level was detected in 156 pairs of patients with ESCC and healthy volunteers using quantitative real-time polymerase chain reaction (qRT-PCR) method. It was statistically decreased in ESCC patients compared with healthy controls. AUC based on serum miR-1297 was 0.840 ± 0.035 in discovery group and 0.837 ± 0.034 in validation group. Further analysis on early-stage patients revealed that the AUC was 0.819 ± 0.053 in discovery group and 0.814 ± 0.044 in validation group. Its sensitivity and specificity were promising. In conclusion, serum miR-1297 can serve as an ideal indicator for the diagnosis of ESCC.

Lobulated Hemangioma as a Rare Cause of Tricuspid Regurgitation.

Introduction: Cardiac hemangioma is one of the rarest tumors, with only a few cases described. Unlike other cardiac tumors, its symptoms are nonspecific, making misdiagnosis easy. Cardiac hemangioma can present with various clinical manifestations, including valve disorder, arrhythmia, pericardial effusion, and embolism. Echocardiography is the most direct examination, and surgical resection the simplest and most effective treatment. Patients and methods: We present a new case of lobulated cardiac hemangioma causing tricuspid regurgitation and discuss the clinical features, diagnosis, and treatment of this rare tumor. Results: After surgical resection and tricuspid valve replacement, the patient recovered well. Conclusion: For cardiac hemangiomas involving the tricuspid valve, tumor resection combined with valve surgery is an effective treatment option.

The Effects of Perineural Dexamethasone on Rebound Pain After Nerve Block in Patients With Unicompartmental Knee Arthroplasty: A Randomized Controlled Trial.

OBJECTIVES: A single nerve block provides excellent analgesia in a short time, but rebound pain after the nerve block dissipates has attracted researchers' attention. The aim of this study was to evaluate the effect of perineural dexamethasone on rebound pain after sciatic nerve block and femoral nerve block in patients undergoing unicompartmental knee arthroplasty (UKA). METHODS: In a double-blinded fashion, we recruited 72 patients undergoing UKA, each of whom received sciatic and femoral nerve block. Patients were randomly assigned to 2 groups (n=36): X (ropivacaine only) and D (ropivacaine combined with dexamethasone). The primary outcome was the incidence of rebound pain. The secondary outcomes were rebound pain score, the duration of rebound pain, the duration of nerve block, pain score, sufentanil consumption and rescue analgesic, patient-controlled intravenous analgesia, distance walked, sleep quality score, C-reactive protein levels, and adverse effects. RESULTS: Compared with group X, the incidence of rebound pain in group D was higher, the rebound pain score was higher and the duration of the nerve block was prolonged ( P <0.05). At 12, 16, and 20 hours postoperatively, the pain scores at rest in group D were lower. At 32 and 36 hours postoperatively, the pain scores at rest in group D were higher ( P <0.05). Furthermore, patients in group D had lower levels of C-reactive protein after surgery ( P <0.05). DISCUSSION: The addition of dexmedetomidine to ropivacaine for UKA effectively prolonged the duration of nerve block and decreased C-reactive protein levels, but increased the incidence of rebound pain and rebound pain score, and had no beneficial effects on the postoperative analgesia.

Nonfunctioning benign cardiac pheochromocytoma.

PURPOSE: Nonfunctioning benign cardiac pheochromocytoma is one of the rarest tumors and only a few cases have been described before. We present a rare case of nonfunctioning benign cardiac pheochromocytoma and a review of the literature with special emphasis on diagnosis and treatment. METHODS: Different from the other cardiac pheochromocytomas, its symptoms and signs are so nonspecific that it is easy to make a misdiagnosis or missed diagnosis. One patient with nonfunctioning benign cardiac pheochromocytoma was treated surgically and relevant cases data were collected. Clinical features, diagnosis and treatment of pheochromocytoma were discussed. RESULTS: The presented case was cured by surgery. The prognosis for patients of benign cardiac pheochromocytomas was excellent, but for those of malignant ones was very poor. CONCLUSION: Reviewing the few reported cases, most nonfunctioning benign cardiac pheochromocytomas can be cured completely by operation with good prognosis.

Nestin servers as a promising prognostic biomarker in non-small cell lung cancer.

Lung cancer is currently the leading cause of cancer-related death worldwide and it is important to identify the predictive and/or prognostic markers for the cancer. Nestin, a proliferative and multipotent biomarker has been reported to be associated with prognosis in non-small cell lung cancer (NSCLC) in a few studies. In the present study, we retrospectively recruited 153 patients with NSCLC. Nestin protein expression in tumor samples was determined by immunohistochemistry staining. Nestin expression was related with tumor differentiation (P=0.036), lymphatic metastasis (N stage, P=0.011), and p-TNM stage (P=0.013), while there was no significant association between Nestin expression level and age, smoking habits, gender, histologic type, and T stage. Nestin was an independent prognostic factor for overall survival in NSCLC with an adjusted hazard ratio of 2.701 (95% CI, 1.616-4.513, P<0.001) after controlling the confounding factors. Then we determined the effects of Nestin on cell proliferation, colony formation, invasion, and apoptosis by knockout of Nestin with a new developed method, CRISPR/Cas9 mediated genome editing. It was observed that knockout of Nestin caused enhancement of cancer cell apoptosis and inhibition of cell proliferation, colony formation, and invasion in A549 and H1299 cell lines. Furthermore, we examined the expression of epithelial-mesenchymal transition (EMT) related biomarkers such as E-cadherin and Vimentin in Nestin-depleted lung cancer cells and knockout of Nestin was found to inhibit EMT, suggesting the involvement of Nestin mediated EMT signaling in lung cancer. The finding above demonstrated that Nestin might serve as a prognostic factor and therapeutic target in NSCLCs.

Association of SOX2 and Nestin DNA amplification and protein expression with clinical features and overall survival in non-small cell lung cancer: A systematic review and meta-analysis.

Up to now, the prognosis of non-small cell lung cancer (NSCLC) is poor. With progress of cancer biology, a number of genes have been investigated for predicting prognosis of NSCLC, such as cancer stem cell markers SRY (sex determining region Y)-box 2 (SOX2) and Nestin. Recently, a series of studies have been performed to examine the associations of SOX2 and Nestin with clinical parameters and prognosis in NSCLC, however, the results were not consistent. In the present study, we conducted a systematic review and meta-analysis to summarize the associations. Four English databases (PubMed, ISI web of science, Embase, and Ovid) were used to search the relevant studies with the last date of November 10, 2015. The pooling analyses were stratified by DNA amplification and protein expression. The pooling ORs or HRs were used to assess the strength of the associations. Finally, we included 19 articles for SOX2 and six articles for Nestin according to the inclusion and exclusion criteria. The pooling analyses revealed that there were significant associations between SOX2 DNA amplification and clinical features of NSCLC, gender, smoking status, squamous cell cancer (SCC) histology, and differentiations. And significant associations were also identified between SOX2 protein expression and clinical parameters, smoking status and SCC histology. For Nestin, its protein expression was correlated with lymph node metastasis and stage. Simultaneously, we found that high/positive SOX2 alterations, either DNA amplification or protein expression, were favorable for overall survival (OS) in NSCLC. On the contrary, high/positive Nestin protein expression was poor for OS.

Notch2 as a promising prognostic biomarker for oesophageal squamous cell carcinoma.

We aimed to examine Notch2 expression in oesophageal squamous cell carcinoma (ESCC) patients and to evaluate its prognostic potential. Immunohistochemical (IHC) staining, quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis were utilized to investigate the Notch2 expression status and prognostic value. Furtherly, CCK8 and clonogenic assays were conducted to determine if Notch2 inhibition by shRNA could lead to a decrease in the proliferation and survival of ESCC cells. A notably higher Notch2 expression level was found in ESCC tissues at the mRNA (P < 0.0001) and protein levels (IHC: P = 0.004; western blot: P = 0.021). Log-rank analysis demonstrated that Notch2 overexpression was significantly associated with worse overall survival (OS) (29.1% vs. 49.1%; P = 0.013) and progression-free survival (PFS) (15.3% vs. 34.4%; P = 0.006) rates in ESCC patients. The multivariate analysis revealed Notch2 as an independent prognostic factor for OS and PFS (P = 0.002 and 0.006, resp.). Besides, in vitro assays showed that OD450 values and colony formations were significantly reduced in Notch2-shRNA group (all P < 0.0001). In conclusion, these results show that Notch2 is up-regulated in ESCC tissues and could serve as a promising biomarker for identifying individuals with poor prognostic potential.

Prognostic and diagnostic potential of isocitrate dehydrogenase 1 in esophageal squamous cell carcinoma.

We aimed to investigate the pattern of expression and clinical significance of isocitrate dehydrogenase 1(IDH1) in esophageal squamous cell carcinoma (ESCC). The IDH1 expression was determined by quantitative real-time polymerase chain reaction, immunohistochemistry, and Western blot analysis using 38 pairs of frozen tissues. Enzyme-linked immunosorbent assay was employed to measure 67 pairs of serum samples from patients and their controls to evaluate its diagnostic value. Immunohistochemistry analysis of 111 formalin-fixed paraffin embedded tissue samples was conducted for explaining its prognostic value. After shRNA transfection, CCK8 and clonal efficiency assays were carried on for verifying the function of IDH1 in vitro. Increased expression at mRNA (P < 0.001) and protein levels (immunohistochemistry: P < 0.001, Western blot analysis: P < 0.001) were observed. Similarly, the IDH1 expression in serum from patients with ESCC was significantly upregulated relative to that from healthy controls (P < 0.001). Kaplan-Meier curve indicated that IDH1 upregulation predicted worse overall survival (OS) and progression-free survival (PFS). Univariate and multivariate analyses identified IDH1 expression as an independent prognostic factor for OS and PFS. Furthermore, OD450 values and colony numbers were decreased in sh-IDH1 groups (all P < 0.05). In conclusion, IDH1 is upregulated in patients with ESCC and can be used as a good potential biomarker for diagnosis and prognosis.

Role of adenovirus-mediated retinoblastoma 94 in the treatment of human non-small cell lung cancer.

Non­small cell lung cancer (NSCLC) remains the leading cause of cancer­related mortality despite the fact that great advances have been made in therapeutic treatment methods. Therefore, in the present study, the role of adenovirus-mediated retinoblastoma 94 (Ad­RB94) gene therapy in NSCLC was investigated. Following treatment with Ad­RB94, the proportion of A549 cells in the G2/M phase was increased. In the mouse xenograft model, the overexpression of RB94 inhibited the tumor growth compared with the control group and the Ad-­LacZ-treated group. In the transplanted tumors, the overexpression of RB94 induced the apoptosis of tumors as well as an increase in the mRNA levels of cyclinB1. In conclusion, the results of the present study suggested that RB94 may effectively inhibit NSCLC tumor cell growth by inducing G2/M cell cycle arrest and apoptosis, indicating that RB94 may be a promising candidate for adjuvant therapy with radiation or chemotherapy in NSCLC.

Peroxisome proliferator-activated receptor ß/δ activation in adult hearts facilitates mitochondrial function and cardiac performance under pressure-overload condition.

Peroxisome proliferator-activated receptor ß/δ (PPARß/δ) is an essential transcription factor in myocardial metabolism. This study aims to investigate the effects of PPARß/δ activation in the adult heart on mitochondrial biology and oxidative metabolism under normal and pressure-overload conditions. We have investigated the effects of cardiac constitutively active PPARß/δ in adult mice using a tamoxifen-inducible transgenic approach with Cre-LoxP recombination. The expression of PPARß/δ mRNA and protein in cardiomyocytes of adult mice was substantially increased after short-term induction. In these mice, the cardiac expression of key factors involved in mitochondrial biogenesis, such as PPARγ coactivator-1, endogenous antioxidants Cu/Zn superoxide dismutase, and catalase, fatty acid, and glucose metabolism, such as carnitine palmitoyltransferase Ib, carnitine palmitoyltransferase II, and glucose transporter 4, were upregulated. Subsequently, myocardial oxidative metabolism was elevated concomitant with an increased mitochondrial DNA copy number and an enhanced cardiac performance. Moreover, activation of PPARß/δ in the adult heart improved cardiac function and resisted progression to pathological development in mechanical stress condition. We conclude that PPARß/δ activation in the adult heart will promote cardiac performance along with transcriptional upregulation of mitochondrial biogenesis and defense, as well as oxidative metabolism at basal and pressure-overload conditions.