Risk factors of arytenoid dislocation after endotracheal intubation: A propensity-matched analysis.

Objective: Arytenoid dislocation (AD) after general anesthesia with endotracheal intubation (EI) is an iatrogenic injury that impairs patient function and requires reduction. We aimed to investigate the risk factors of AD following EI. Methods: This retrospective case-control study involved surgical adults who received EI for general anesthesia at a single institution from June 2010 to June 2020. Cases included all the patients who had AD. We used a ratio of 1:5 to identify patients in the propensity-matched control group. Results: Multivariate analysis of 49 cases with AD and 245 controls without AD demonstrated that the use of a nasogastric (NG) tube (odds ratio [OR], 23.9; 95% confidence interval [CI], 6.8-84.1), undergoing abdominal surgery (OR, 3.7; 95% CI, 1.2-11.9), and an operative time longer than 3 h (OR, 5.2; 95% CI, 2.1-12.9) were risk factors for AD. We did not find significant independent associations between AD and 40 years or older age, gender, body mass index, whether a laryngeal mask airway was used, endotracheal tube size, and EI performers' experience. Conclusion: The use of an NG tube, abdominal surgery, and longer operative time were risk factors for AD. Among these, the NG tube application showed a strong association with AD. Preventive measures of informing the patients of the increased risk and providing high-level patient monitoring can reduce the incidence of AD. Level of Evidence: III.

LINC00629, a KLF10-responsive lncRNA, promotes the anticancer effects of apigenin by decreasing Mcl1 stability in oral squamous cell carcinoma.

Apigenin, a naturally occurring flavonoid, is known to exhibit antitumor activity in many cancers. However, the regulatory mechanism of apigenin and the long noncoding RNAs (lncRNAs) altered upon apigenin treatment in oral squamous cell carcinoma (OSCC) remain unclear. In this study, we found that LINC00629 was significantly upregulated in response to apigenin treatment. Upregulated LINC00629 enhanced the growth-suppressive and proapoptotic effects of apigenin on OSCC cells by interacting with Mcl1 and facilitating its degradation. Subsequently, our data indicated that KLF10, an important transcription factor, directly bound to the promoter of LINC00629, facilitating its transcription and contributing to apigenin-induced LINC00629 expression. Collectively, these results suggest that the KLF10-LINC00629-Mcl1 axis plays an important role in the anticancer effects of apigenin.

[A case of Madelung's disease combined with laryngeal cancer].

Madelung's disease is a lipodystrophy of unknown etiology. This article reports a case of Madelung's disease complicated with laryngeal cancer. The clinical manifestations of the patient were progressive hoarseness and dyspnea, dysphagia, and diffuse symmetrical swelling of the neck, submental, and submandibular. Dynamic laryngoscopy revealed a giant cauliflower-like neoplasm in the throat, with the left vocal cord fixed. Laryngeal CT showed laryngeal carcinoma （transglottic type）, signs of lymph node metastasis in the left jugular chain region, and Madelung syndrome in the neck. Biochemical tests showed albumin 38.7 g/L, globulin 27.5 g/L, prealbumin 160 g/L, aspartate aminotransferase 14 IU/L, γ-transpeptidase 80 IU/L, alanine aminotransferase 7 IU/L, Creatinine 43 µmol/L. Preoperative pathology suggested squamous cell carcinoma. Admission diagnosis included laryngeal cancer （transglottic T4N1M0）, Ⅲ degree laryngeal obstruction, Madelung's disease and fatty liver. The patient recovered well after surgery.

MicroRNA-1469, a p53-responsive microRNA promotes Genistein induced apoptosis by targeting Mcl1 in human laryngeal cancer cells.

Genistein, a plant isoflavone, is reported to have therapeutic potentials in multiple cancers, However, the molecular mechanism underlying promoting cell apoptosis in laryngeal cancer remains unclear. In this study, we report that miR-1469 was induced by genistein in laryngeal cancer. Elevated miR-1469 promoted cell apoptosis and inhibited Mcl1 expression. In addition, we also observed that tumor suppressor p53 was increased under genistein treatment. Elevation of p53 promoted miR-1469 expression, leading to miR-1469 increase and Mcl1 decrease. Therefore, our findings suggest that genistein can suppress laryngeal cancer cell survival through p53 -miR-1469-Mcl1pathway.

LncRNAAC132217.4, a KLF8-regulated long non-coding RNA, facilitates oral squamous cell carcinoma metastasis by upregulating IGF2 expression.

Increasing evidence has revealed the aberrant expression of long non-coding RNAs (lncRNAs) in many cancer types, including oral squamous cell carcinoma (OSCC). However, limited investigations report metastasis-related lncRNAs in OSCC. Herein, we report the identification of dysregulated intergenic lncRNAs in the highly metastatic OSCC cell line, UM-SCC6H. One of the lncRNAs, termed AC132217.4, was remarkably upregulated and promoted cell migration and epithelial-mesenchymal transition (EMT) by upregulating IGF2 expression. Further mechanistic studies revealed that AC132217.4 interacted with the 3'UTR of IGF2 mRNA and increased its stability, leading to increased IGF2 levels. Thereafter, we found that KLF8 binds to the upstream sequence of AC132217.4, activating its expression at the transcriptional level, which accelerated OSCC metastasis via the AC132217.4-IGF2 axis both in vitro and in vivo. We also revealed that the expression level of AC132217.4 was increased in OSCC tissues, and this elevation correlated with KLF8 and IGF2 expression. Thus, our data demonstrate that the KLF8-AC132217.4-IGF2 signalling pathway plays a critical role in OSCC metastasis.