Superhydrophilicity boron-doped cobalt phosphide nanosheets decorated carbon nanotube arrays self-supported electrode for overall water splitting.

Transition metal borides (TMBs) or phosphides (TMPs) have attracted great attention to the design of bifunctional electrocatalysts for energy storage. The superaerophobicity and superhydrophilicity of the catalytic electrode surface are crucial factors to determine the reaction process of the gas electrode. Herein, we report a self-supported electrode of carbon nanotube (CNTs) array grown on carbon cloth (CC) modulated together by boron-doped cobalt phosphide (CoP-B/CNTs/CC). The electrode requires the overpotential of 73.8 mV and 189.5 mV at the current density of ±10 mA cm-2 for hydrogen and oxygen evolution reactions in an alkaline electrolyte (1.0 M KOH), respectively, meanwhile maintaining outstanding long-term durability for more than 300 h. The excellent activity of CoP-B/CNTs/CC is attributed to boron doping regulating its electronic structure and further enriching active sites. The attractive stability of CoP-B/CNTs/CC is due to the unique geometric structure of the self-supported electrode. Furthermore, the superaerophobicity and superhydrophilicity of the electrode surface also accelerate the reaction process of the gas electrode. Expectedly, water splitting cells assembled using CoP-B/CNTs/CC electrodes as cathode and anode, respectively, require a cell voltage of 1.54 V at 10 mA cm-2, which is lower than that of the Pt/C/CC||RuO2/CC couple (1.69 V at 10 mA cm-2). Importantly, CoP-B/CNTs/CC||CoP-B/CNTs/CC achieve stable cell voltage under the step current changes (10 mA cm-2, 50 mA cm-2, and 100 mA cm-2) over 300 h. This work highlights a new path to understanding the effects of the static and dynamic behavior of bubbles on the surface of self-supporting electrodes on catalytic performance.

Silencing FHL2 inhibits bleomycin-induced pulmonary fibrosis through the TGF-ß1/Smad signaling pathway.

OBJECTIVE: This study aimed to investigate the inhibiting effects of FHL2 and Arbutin on cell fibrosis and their possible mechanisms. METHODS: The mRNA expression of FHL2 in pulmonary fibrosis tissues was analyzed by bioinformatics. TGF⁃ß1 induced fibrosis of mouse lung fibroblast (Mlg) and mouse primary pulmonary fibroblast (PPF) in rat's lung fibroblasts. FHL2 siRNA was transfected into Mlg and mouse PPF cells to inhibit FHL2. FHL2, α-smooth muscle actin (α-SMA), collagen 1 (Col I), and Fibronectin (Fn) were detected by qRT-PCR. Western blot expression levels of Smad3, p-Smad3, Smad2, and p-Smad2 proteins in cells. High-throughput drug screening for FHL2 inhibitors and the inhibitory effect of Arbutin on pulmonary fibrosis were validated in cellular and animal models of pulmonary fibrosis. RESULTS: The mRNA expression of FHL2 in lung fiber tissue was increased. Meanwhile, the decrease of FHL2 expression significantly inhibited the cellular fibrosis morphological changes of rat's lung fibroblasts (Mlgs) and primary lung fibroblasts (PPFs). The expression levels of α⁃SMA, Col I, and Fn were decreased. High-throughput screening showed that Arbutin targeted FHL2. Arbutin alleviated bleomycin (BLM)-induced pulmonary fibrosis in rats by inhibiting FHL2 and then the TGF-ß1/Smad signaling pathway. CONCLUSION: Inhibition of FHL2 can effectively reduce the fibrosis process induced by TGF⁃ß1 and bleomycin, and then inhibit the fibrosis.

CoP2/Co2P Encapsulated in Carbon Nanotube Arrays to Construct Self-Supported Electrodes for Overall Electrochemical Water Splitting.

Electrocatalytic water splitting is a desirable and sustainable strategy for hydrogen production yet still faces challenges due to the sluggish kinetics and rapid deactivation of catalysts in the oxygen evolution process. Herein, we utilized the metal-catalyzed growth technology and phosphating process to fabricate self-supported electrodes (CoxPy@CNT-CC) composed of carbon nanotube (CNT) arrays grown on carbon cloth (CC); thereinto, cobalt-based phosphide nanoparticles (CoxPy) are uniformly encapsulated in the cavity of the CNTs. After further optimization, when the nanoparticles are in the composite phase (CoP2/Co2P), CoP2/Co2P@CNT-CC served as catalytic electrodes with the highest activity and stability for electrocatalytic water splitting in an alkaline medium (1.0 M KOH). The as-prepared CoP2/Co2P@CNT-CC integrates the advantages of the abundant active sites and confinement effect of CNTs, imparting promising electrocatalytic activities and stability in catalyzing both hydrogen evolution reaction and oxygen evolution reaction. Remarkably, electrocatalytic water splitting cells assembled using CoP2/Co2P@CNT-CC electrodes as the cathode and anode, respectively, require a cell voltage of 1.55 V at 10 mA cm-2, which is lower than that of the commercially noble Pt/C/CC and RuO2/CC catalyst couple (1.68 V). Besides, a CoP2/Co2P@CNT-CC||CoP2/Co2P@CNT-CC system shows outstanding durability for a period of 100 h at 10 mA cm-2. This work may provide new ideas for designing bifunctional electrocatalysts for applications in electrocatalytic water splitting.

Short- (30-90 days) and mid-term (1-3 years) outcomes and prognostic factors of patients with esophageal cancer undergoing surgical treatments.

BACKGROUND: The factors influencing the prognosis of patients with esophageal cancer vary among studies and are still poorly known. AIM: To determine the factors associated with survival in patients with esophageal cancer. METHODS: This retrospective study included patients with esophageal cancer admitted between January 2017 and March 2020 at Heping Hospital Affiliated to Changzhi Medical College. All patients were treated according to the available guidelines. Follow-up was censored in October 2020. Univariable and multivariable Cox regression analyses were used to determine the independent risk factors for overall survival (OS). RESULTS: In total, 307 patients were included. Their median age was 64 (range, 44-79) years, 63.5% were male, and the median disease course was 2 (0.1-36) months. The median tumor size was 3 (0-10) cm. Most patients were T3 (29.6%), N0 (70.0%). Most tumors were grade 2 (48.2%), and 87.3% were squamous cell carcinoma. The in-hospital mortality was 16.9%, the 30-day mortality was 19.9%, and the 90-day mortality was 25.4%. The cumulative OS rates at the last follow-up were 82.1% (95%CI: 67.7%-96.5%) for stage 0/I/II and 47.4% (95%CI: 16.5-78.6%) for stage III/IVA (P < 0.001). The multivariable analysis showed that creatinine levels (HR = 1.02, 95%CI: 1.00-1.03, P = 0.050), pTNM III/IVA (HR = 4.19, 95%CI: 2.19-8.01, P < 0.001), adjuvant radiotherapy and/or chemotherapy (HR = 0.23, 95%CI: 0.11-0.49), and the Comprehensive Complication Index (CCI) (HR = 1.02, 95%CI: 1.004-1.03, P = 0.011) were independently associated with OS. CONCLUSION: The survival of patients with esophageal cancer is poor, especially those with pTNM III/IVA. pTNM stage III/IVA, CCI, and adjuvant therapy (radiotherapy and/or chemotherapy) are independently associated with OS.

mmu-microRNA-92a-3p attenuates pulmonary fibrosis by modulating Cpeb4-mediated Smad2/3 signaling pathway.

Pulmonary fibrosis (PF) is a chronic lung disorder, in which the mechanism of mmu-microRNA (miR)-92a-3p is not elucidated clearly. The present work was proposed to disclose mmu-miR-92a-3p-focused mechanism in PF with cytoplasmic polyadenylation element-binding protein 4 (Cpeb4)/Smad2/3 axis. PF was induced in mice by the intratracheal injection of bleomycin (BLM). Then, the BLM-treated mice were injected with mmu-miR-92a-3p- and/or Cpeb4-related adenovirus vectors. mmu-miR-92a-3p, Cpeb4, and Smad2/3 expression in lung tissues were examined. Alveolar cell apoptosis and collagen deposition in lung tissues and inflammatory factors in serum were observed. The interaction between mmu-miR-92a-3p and Cpeb4 was explored. Lowly expressed mmu-miR-92a-3p and highly expressed Cpeb4 and Smad2/3 were manifested in BLM-induced PF mice. BLM-induced PF mice exhibited enhanced inflammation, alveolar cell apoptosis, and collagen deposition, which would be attenuated by upregulating mmu-miR-92a-3p or downregulating Cpeb4. mmu-miR-92a-3p targeted Cpeb4. Upregulating mmu-miR-92a-3p or downregulating Cpeb4 inactivated the Smad2/3 signaling pathway in BLM-induced PF mice. It is elaborated that mmu-miR-92a-3p attenuates the process of PF by modulating Cpeb4-mediated Smad2/3 signaling pathway, renewing the molecular mechanism of PF.

Effect of silencing C-erbB-2 on esophageal carcinoma cell biological behaviors by inhibiting IGF-1 pathway activation.

OBJECTIVE: C-erbB-2 has been confirmed to be an oncogene that participates in cell growth, differentiation and division of tumors. We are wondered if its silenced expression can exert an anti-tumor effect. Therefore, this study is conducted to investigate the mechanism of C-erbB-2 silencing and IGF-1 pathway on esophageal carcinoma (EC) cell biological behaviors. METHODS: The objects of study were 84 EC patients from Heping Hospital Affiliated to Changzhi Medical College, with the collection of EC tissue and adjacent normal tissue (> 5 cm away from cancer tissue). C-erbB-2 protein expression in EC tissues was detected by immunohistochemistry. Human EC cell line Eca-109 was purchased from Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. Based on different transfection protocols, EC cells with logarithmic growth phase of 3-5 passages were divided into blank control group, oe-C-erbB-2 NC group, siRNA C-erbB-2 NC group, oe-C-erbB-2 group, siRNA C-erbB-2 group, OSI-906 group, Rg5 group, Rg5 + siRNA C-erbB-2 NC group and Rg5 + siRNA C-erbB-2 group. Cell proliferation was detected by MTT assay; cell cycle distribution and apoptosis by flow cytometry; C-erbB-2, IGF-1, IGF-1R and Akt mRNA and protein expressions by qRT-PCR and western blot; and cell invasion and migration by Transwell assay and scratch test. Tumor growth was observed in male BALB/c nude mice (Shanghai Experimental Animal Center) based on Eca109 cell implantation, raising, and measurement. RESULTS: C-erbB-2, IGF-1, IGF-1R and Akt expression were higher in EC tissues than those in adjacent tissues (all P < 0.05). Compared with blank control group, both si-C-erbB-2 and OSI-906 groups had decreased IGF-1, IGF-1R and Akt mRNA and protein expressions, decreased cell proliferation, migration and invasion, prolonged G0/G1 phase, shortened S phase, increased cell apoptosis, and inhibited tumor growth (all P < 0.05); while opposite trends were detected in C-erbB-2 vector and Rg5 groups (all P < 0.05), without statistical differences in siRNA C-erbB-2 + Rg5 group (all P > 0.05). CONCLUSION: Silencing C-erbB-2 expression may inhibit EC cell proliferation, promote cell apoptosis and block cell cycle progression by inhibiting IGF-1 pathway activation. The beneficial effect of silencing C-erbB-2 expression can be reversed by promoting the activation of IGF-1 pathway. Findings in our study may provide potential reference for understanding the molecular mechanism of EC and supply possible axis for preventing the development of EC from the perspective of molecular biology.

MiR-216a-3p regulates the proliferation, apoptosis, migration, and invasion of lung cancer cells via targeting COPB2.

Effect of miR-216a-3p on lung cancer hasn't been investigated. Here, we explored its effects on lung cancer. MiR-216a-3p expression in lung cancer tissues and cells was detected by RT-qPCR. The target gene of miR-216a-3p was predicted by bioinformatics and confirmed by luciferase-reporter assay. After transfection, cell viability, migration, invasion, proliferation, and apoptosis were detected by MTT, scratch, transwell, colony formation, and flow cytometry. The expressions of COPB2 and apoptosis-related factors were detected by RT-qPCR or western blot. MiR-216a-3p was low-expressed and COPB2 was high-expressed in lung cancer tissues and cells. MiR-216a-3p targeted COPB2 and regulated its expression. MiR-216a-3p inhibited lung cancer cell viability, migration, invasion, and proliferation, while promoted apoptosis. Effect of miR-216a-3p on lung cancer was reversed by COPB2. MiR-216a-3p regulated proliferation, apoptosis, migration, and invasion of lung cancer cells via targeting COPB2.

Prediction of Overall Survival of Patients with Completely Resected Non-Small Cell Lung Cancer: Analyses of Preoperative Spirometry, Preoperative Blood Tests, and Other Clinicopathological Data.

PURPOSE: Risk stratification of patients with non-small cell lung cancer (NSCLC) is crucial to select the appropriate treatments, but available models for patients with complete resection are unsatisfactory. The purpose of this study was to determine a prediction model based on clinical information, routine physical and blood tests, and molecular markers. PATIENTS AND METHODS: This was a retrospective cohort study of patients who underwent surgical resection for lung cancer between 2009 to 2013. Potential prognostic factors were used to build a full prediction model based on a multivariable Cox regression analysis. A nomogram was constructed. The risk stratification cutoffs for clinical use were determined based on the model. RESULTS: A total of 368 NSCLC patients with R0 resection were included. The final multivariable model indicated that low diffusing capacity of the lung for carbon monoxide (HR=1.66, 95% CI: 1.18-2.34), high platelet-to-lymphocyte ratio (HR=1.42, 95% CI: 1.04-1.95), histology type of squamous cell carcinoma and others (squamous cell carcinoma vs adenocarcinoma, HR=1.40, 95% CI: 1.01-1.96; others vs adenocarcinoma, HR=2.36, 95% CI: 1.15-4.84; P trend=0.001), N>0 status (HR=1.96, 95% CI: 1.42-2.70), high serum carcinoembryonic antigen levels (HR=1.61, 95% CI: 1.13-2.27), and postoperative chemotherapy (HR=0.53, 95% CI: 0.33-0.87) were independently associated with poor OS. The patients were classified into four risk groups according to the nomogram, and the OS was different among the four groups (P<0.05). CONCLUSION: A nomogram was successfully constructed based on a multivariable analysis, and the nomogram can discriminate the OS of patients with NSCLC based on risk categories, but external validation is still necessary.

A nomogram to predict prognosis in patients undergoing sublobar resection for stage IA non-small-cell lung cancer.

INTRODUCTION: This study aimed to develop a practical nomogram to predict prognosis in patients who are undergoing sublobar resection for stage IA non-small-cell lung cancer (NSCLC). Data from Surveillance, Epidemiology, and End Results (SEER) databases were used to construct the nomogram. METHODS: Data from patients undergoing sublobar resection for stage IA NSCLC diagnosed between 2004 and 2014 were extracted from the SEER database. Factors that may predict the outcome were identified using the Kaplan-Meier method and the Cox proportional-hazards model. A nomogram was constructed to predict the 3- and 5-year overall survival (OS) and lung cancer-specific survival (LCSS) rates of these patients. The predictive accuracy of the nomogram was measured using the concordance index (C-index) and calibration curve. RESULTS: A total of 4,866 patients were selected for this study. Using univariate and multivariate analyses, eight independent prognostic factors associated with OS were identified, including sex (P<0.001), age (P<0.001), race (P=0.043), marital status (P=0.009), pathology (P=0.004), differentiation (P<0.001), tumor size (P<0.001), and surgery (P=0.001), and five independent prognostic factors associated with LCSS were also identified, including sex (P<0.001), age (P<0.001), differentiation (P<0.001), tumor size (P<0.001), and surgery (P=0.011). A nomogram was established based on these results and validated using the internal bootstrap resampling method. The C-index of the established nomogram for OS and LCSS was 0.649 (95% CI: 0.635-0.663) and 0.640 (95% CI: 0.622-0.658), respectively. The calibration curves for probability of 3-, and 5-year OS and LCSS rates demonstrated good agreement between the nomogram prediction and actual observation. CONCLUSION: This innovative nomogram delivered a relatively accurate individual prognostic prediction for patients undergoing sublobar resection for stage IA NSCLC.

Icaritin Attenuates Myocardial Ischemia and Reperfusion Injury Via Anti-Inflammatory and Anti-Oxidative Stress Effects in Rats.

Icaritin (ICT) is a traditional Chinese medicinal herb proved to be neuroprotective and exerts promoting effects on cardiac differentiation. However, its role in cardioprotection against myocardial ischemia/reperfusion (MI/R) injury remains largely unknown. This study aimed to investigate the effects of ICT treatment on MI/R injury and the underlying mechanisms. Rats were subjected to 30 min of myocardial ischemic insult followed by 3 h of reperfusion. ICT (3, 10, and 30 mg/kg) was administered intraperitoneally 10 min before reperfusion. ICT treatment at the dose of 10 and 30 mg/kg improved cardiac function and limited infarct size following MI/R. Meanwhile, ICT reduced plasma creatine kinase (CK), lactate dehydrogenase (LDH) activities and cardiomyocyte apoptosis in I/R heart tissue. Moreover, ICT treatment not only inhibited the pro-inflammatory cytokine TNF-α production and increased the anti-inflammatory cytokine IL-10 level in myocardium but also reduced the increase in the generation of superoxide content and malondialdehyde (MDA) formation and simultaneously increased the anti-oxidant capability in I/R hearts. Furthermore, ICT treatment increased Akt phosphorylation and inhibited PTEN expression in I/R hearts. PI3K inhibitor wortmannin inhibited ICT-enhanced Akt phosphorylation, and blunted ICT-mediated anti-oxidative and anti-inflammatory effects and cardioprotection. Our study indicated for the first time that ICT reduces inflammation and oxidative stress and protects against MI/R injury in rats, which might be via a PI3K-Akt-dependent mechanism.