Enhanced Capacity Retention of Li3V2(PO4)3-Cathode-Based Lithium Metal Battery Using SiO2-Scaffold-Confined Ionic Liquid as Hybrid Solid-State Electrolyte.

Li3V2(PO4)3 (LVP) is one of the candidates for high-energy-density cathode materials matching lithium metal batteries due to its high operating voltage and theoretical capacity. However, the inevitable side reactions of LVP with a traditional liquid-state electrolyte under high voltage, as well as the uncontrollable growth of lithium dendrites, worsen the cycling performance. Herein, a hybrid solid-state electrolyte is prepared by the confinement of a lithium-containing ionic liquid with a mesoporous SiO2 scaffold, and used for a LVP-cathode-based lithium metal battery. The solid-state electrolyte not only exhibits a high ionic conductivity of 3.14 × 10-4 S cm-1 at 30 °C and a wide electrochemical window of about 5 V, but also has good compatibility with the LVP cathode material. Moreover, the cell paired with a solid-state electrolyte exhibits good reversibility and can realize a stable operation at a voltage of up to 4.8 V, and the discharge capacity is well-maintained after 100 cycles, which demonstrates excellent capacity retention. As a contrast, the cell paired with a conventional liquid-state electrolyte shows only an 87.6% discharge capacity retention after 100 cycles. In addition, the effectiveness of a hybrid solid-state electrolyte in suppressing dendritic lithium is demonstrated. The work presents a possible choice for the use of a hybrid solid-state electrolyte compatible with high-performance cathode materials in lithium metal batteries.

Glutamatergic Neurons in the Zona Incerta Modulate Pain and Itch Behaviors in Mice.

Emerging evidence suggest that parvalbumin neurons in zona incerta (ZI) modulate pain and itch behavior in opposite manners. However, the role of ZI glutamatergic neurons, a unique incertal neuronal subpopulation residing in the caudal division, in pain and itch modulation remains unknown. In the present study, by combining chemogenetic manipulation, fiber photometry, and behavioral tests, we proved that incertal glutamatergic neurons served as an endogenous negative diencephalic modulator for both pain and itch processing. We demonstrated that ZI vesicular glutamate transporter 2 (VGluT2) neurons exhibited increased calcium signal upon hindpaw withdrawal in response to experimental mechanical and thermal stimuli. Behavioral tests further showed that pharmacogenetic activation of this specific type of neurons reduced nocifensive withdrawal responses in both naïve and inflammatory pain mice. Similar neural activity and modulatory role of ZI VGluT2 neurons were also observed upon histaminergic and non-histaminergic acute itch stimuli. Together, our study would expedite our understandings of brain mechanisms underlying somatosensory processing and modulation, and supply a novel therapeutic target for the management of chronic pain and itch disorders.

Long Non-coding RNA LOXL1-AS1 Facilitates Colorectal Cancer Progression via Regulating miR-1224-5p/miR-761/HK2 Axis.

Colorectal cancer (CRC) is one of the most common cancers worldwide. Long non-coding RNAs (lncRNAs) play crucial roles in the development of malignant tumors. The present study aimed to explore the function and potential mechanism of lncRNA LOXL1 antisense RNA 1 (LOXL1-AS1) in CRC. The abundance of LOXL1-AS1, miR-1224-5p, miR-761, and hexokinase 2 (HK2) was detected by quantitative real-time PCR or western blot assay. Cell proliferation was assessed by Cell Counting Kit-8 and colony formation assays. Cell apoptosis, invasion, and migration were examined by flow cytometry, transwell assay, and wound healing assay. Glycolysis was evaluated by detecting glucose consumption, lactate production, and ATP/ADP ratios. Xenograft assay was used for in vivo tumor growth analysis. LOXL1-AS1 and HK2 levels were increased, while miR-1224-5p and miR-761 levels were reduced in CRC tissues and cells. Knockdown of LOXL1-AS1 suppressed CRC cell proliferation, invasion, migration, and glycolysis, and induced cell apoptosis. Silencing of LOXL1-AS1 blocked tumor growth in vivo. Moreover, LOXL1-AS1 accelerated CRC cell progression by absorbing miR-1224-5p/miR-761. Besides, miR-1224-5p and miR-761 inhibited CRC cell progression via targeting HK2. LOXL1-AS1 contributed to CRC progression via modulating miR-1224-5p/miR-761/HK2 pathway.

CDK9 is up-regulated and associated with prognosis in patients with papillary thyroid carcinoma.

ABSTRACT: Papillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy but shows excellent prognosis. We investigated the clinical significance of cyclin-dependent kinase 9 (CDK9) in patients with PTC.This prospective observational study included 192 patients with PTC, who visited our hospital between August 2018 and February 2020. We obtained 93 tissue samples from patients with benign thyroid disease during the same period as controls. Immunohistochemical evaluation and reverse transcription-quantitative polymerase chain reaction assay were performed to evaluate CDK9 expression. Patients' demographic and clinical characteristics were analyzed.Delphian lymph node (DLN) metastasis in patients with PTC was associated with clinicopathological characteristics. CDK9 expression was up-regulated in patients with PTC, and those with DLN metastasis showed higher CDK9 expression. We also observed that tumor size, capsule invasion, tumor-node-metastasis classification (TNM) stage, and multifocality were the risk factors for DLN metastasis in patients with PTC. Additionally, CDK9 expression was strongly associated with tumor size, capsule invasion, TNM stage, and multifocality and weakly associated with the number of metastatic DLN.CDK9 is up-regulated in patients with PTC and associated with prognosis in these patients.

Gasless endoscopic thyroidectomy via modified areola approach with a simple flap-lifting technique.

Objective: Studies have shown that carbon dioxide (CO2) insufflation during endoscopic thyroidectomy is associated with many risks. Recently, we have designed a simple lifting tool using Kirschner wire. We aimed to use this tool for flap-lifting in modified areola approach endoscopic thyroidectomy and compare it with conventional CO2 insufflation. Methods: In a prospective study, patients who underwent endoscopic thyroidectomy via modified areola approach were randomly assigned into gasless (n = 20) or CO2 groups (n = 22). Pre-operative variables included age, gender, tumor diameter, and clinical diagnosis. Intra-operative hemodynamic monitoring included mean arterial pressure, heart rate, pulse oximetry, end-tidal carbon dioxide (ET-CO2) and arterial pH. Other intra-operative details included total operative time, operative blood loss, conversion from endoscopic surgery to open surgery, intra-operative events, and endoscope video score. Postoperatively, the hospital stay, drainage volume, and complications were recoded. Results: Patient characteristics were not different between the two groups. During the operation, ET-CO2 levels were significantly higher in the CO2 group (P < 0.05), whereas arterial pH levels were significantly lower (P < 0.05). The CO2 group had longer operation time and higher endoscope clarity VAS score than gasless group. Hospital stay, drainage volume, and postoperative complications did not differ significantly between the two groups (P > 0.05). Conclusions: The gasless endoscopic thyroidectomy we performed via our Kirschner wire hook was safe, feasible, and yielded good results.

A Positive Feedback Loop of lncRNA MIR31HG-miR-361-3p -YY1 Accelerates Colorectal Cancer Progression Through Modulating Proliferation, Angiogenesis, and Glycolysis.

BACKGROUND: Colorectal cancer (CRC) is a common malignant tumor with high metastatic and recurrent rates. This study probes the effect and mechanism of long non-coding RNA MIR31HG on the progression of CRC cells. MATERIALS AND METHODS: Quantitative real-time PCR (qRT-PCR) was used to analyze the expression of MIR31HG and miR-361-3p in CRC tissues and normal tissues. Gain- or loss-of-function assays were conducted to examine the roles of MIR31HG, miR-361-3p and YY1 transcription factor (YY1) in the CRC progression. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and colony formation experiment were conducted to test CRC cell proliferation. CRC cell invasion was determined by Transwell assay. The glucose detection kit and lactic acid detection kit were utilized to monitor the levels of glucose and lactate in CRC cells. The glycolysis level in CRC cells was examined by the glycolytic stress experiment. Western blot was performed to compare the expression of glycolysis-related proteins (PKM2, GLUT1 and HK2) and angiogenesis-related proteins (including VEGFA, ANGPT1, HIF1A and TIMP1) in HUVECs. The binding relationships between MIR31HG and miR-361-3p, miR-361-3p and YY1 were evaluated by the dual-luciferase reporter assay and RNA immunoprecipitation (RIP). RESULTS: MIR31HG was up-regulated in CRC tissues and was associated with poorer prognosis of CRC patients. The in-vitro and in-vivo experiments confirmed that overexpressing MIR31HG heightened the proliferation, growth, invasion, glycolysis and lung metastasis of CRC cells as well as the angiogenesis of HUVECs. In addition, MIR3HG overexpression promoted YY1 mRNA and protein level, and forced overexpression of YY1 enhanced MIR31HG level. Overexpressing YY1 reversed the tumor-suppressive effect mediated by MIR31HG knockdown. miR-361-3p, which was inhibited by MIR31HG overexpression, repressed the malignant behaviors of CRC cells. miR-361-3p-mediated anti-tumor effects were mostly reversed by upregulating MIR31HG. Further mechanism studies illustrated that miR-361-3p targeted and negatively regulated the expression of YY1. CONCLUSION: This study reveals that MIR31HG functions as an oncogenic gene in CRC via forming a positive feedback loop of MIR31HG-miR-361-3p-YY1.

Circ-MFN2 Positively Regulates the Proliferation, Metastasis, and Radioresistance of Colorectal Cancer by Regulating the miR-574-3p/IGF1R Signaling Axis.

Numerous studies have shown that the expression of circular RNA (circRNA) is closely related to the malignant progression of cancer. However, the role of circ-MFN2 in colorectal cancer (CRC) is unclear. Our study aims to explore the role and mechanism of circ-MFN2 in CRC progression. The relative expression levels of circ-MFN2, microRNA (miR)-574-3p and insulin-like growth factor 1 receptor (IGF1R) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was determined using 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The colony number and radioresistance of cells were assessed using colony formation assay. Moreover, the migration and invasion of cells were measured using transwell assay. Tumor xenograft model was constructed to evaluate the effect of circ-MFN2 knockdown on CRC tumor growth. Furthermore, dual-luciferase reporter assay was used to verify the interaction between miR-574-3p and circ-MFN2 or IGF1R. In addition, the protein level of IGF1R was evaluated by western blot (WB) analysis. Circ-MFN2 expression was elevated in CRC tissues and cells. Knockdown of circ-MFN2 restrained the proliferation, migration, invasion, and radioresistance of CRC cells in vitro. Furthermore, silenced circ-MFN2 also reduced the tumor volume and weight of CRC in vivo. MiR-574-3p could be sponged by circ-MFN2, and its inhibitor reversed the suppression effect of circ-MFN2 silencing on CRC progression. Moreover, IGF1R was a target of miR-574-3p, and its overexpression reversed the inhibition effect of miR-574-3p mimic on CRC progression. In addition, circ-MFN2 could positively regulate IGF1R expression by sponging miR-574-3p. Our results revealed that circ-MFN2 promoted the proliferation, metastasis and radioresistance of CRC through regulating the miR-574-3p/IGF1R axis, suggesting that circ-MFN2 might be a novel therapeutic biomarker for CRC.

Surgical Treatment of a Giant Pleomorphic Adenoma of the Submandibular Gland: A Case Report.

Pleomorphic adenomas (PAs) are the most common benign salivary neoplasms. PAs are generally slow-growing but may sometimes become aggressive and grow rapidly within a short period of time. Here, we report the case of an 83-year-old Chinese woman with an anterior neck mass that had been growing over the past 30 years. She felt uncomfortable because the mass had grown quite rapidly in the past year. The final diagnosis of a PA of the left submandibular gland was confirmed by histopathological and immunohistochemical examinations after surgical resection. Our patient recalled a history of an excision of a neck mass 40 years prior to presentation at another hospital. Based on our imaging findings and surgical findings, we speculate that the neck mass 40 years prior may also have been a PA. Our case reminds us the rare recurrence possibility of PAs, and early and thorough resection may have a good prognosis. In addition, to the best of our knowledge, this is the largest PA of the submandibular gland reported to date.

ALKBH5 promotes colon cancer progression by decreasing methylation of the lncRNA NEAT1.

Colon cancer is the third leading cause of cancer-related deaths all around the world. LncRNA methylation has been verified to participate in some kinds of malignancies. The aim of this study was to investigate the function of NEAT1 in colon cancer and further explore the potential mechanism between NEAT1 and ALKBH5. Differential expression of lncRNAs between colon cancer tissues and normal tissues was identified using ArrayStar lncRNA microarrays. The levels of NEAT1 and ALKBH5 expression in colon cancer tissues and cells were measured using qRT-PCR. MTT, transwell migration assays and qRT-PCR were performed to detect cell proliferation and migration. Flow cytometry and qRT-PCR was used for apoptosis analysis. Then, m6A RNA immunoprecipitation was performed to detect methylated NEAT1 in colon cancer cells. The results showed NEAT1 was remarkably enhanced in colon cancer tissues and correlated with poor prognosis. Knockdown of NEAT1 inhibited cell proliferation and migration, induced cell apoptosis in colon cancer cell lines. Besides, ALKBH5 could upregulate NEAT1 expression by demethylation. In addition, ALKBH5 knockdown suppressed malignant behavior of colon cancer partially through NEAT1 in vitro and vivo. In a word, we observed NEAT1 expression level was up-regulated in colon cancer tissues and cells. ALKBH5 knockdown suppressed malignant behavior of colon cancer partially through NEAT1 by demethylation in vitro and vivo, suggesting that ALKBH5-NEAT1 axis maybe potential therapeutic target for colon cancer treatment.