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.

[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.

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.

Killer or helper? The mechanism underlying the role of adenylate activated kinase in sound conditioning.

Objective: To investigate whether sound conditioning influences auditory system protection by activating adenylate activated kinase (AMPK), and if such adaption protects ribbon synapses from high-intensity noise exposure. Materials and methods: CBA mice (12 weeks old) were randomly divided into four groups (n = 24 mice per group): control, sound conditioning (SC), sound conditioning plus noise exposure (SC+NE), and noise exposure (NE). Hearing thresholds were assessed before testing, after sound conditioning, and 0, 3, 7, and 14 days after 110 dB noise exposure. Amplitudes and latencies of wave I at 90 dB intensity were assessed before test, after conditioning, and at 0 and 14 days after 110 dB noise exposure. One cochlea from each mouse was subjected to immunofluorescence staining to assess synapse numbers and AMPK activation, while the other cochlea was analyzed for phosphorylated adenylate activated kinase (p-AMPK) protein expression by western blot. Results: There was no significant difference in auditory brainstem response (ABR) threshold between SC and control mice. The degree of hearing loss of animals in the two SC groups was significantly reduced compared to the NE group after 110 dB noise exposure. Animals in the SC group showed faster recovery to normal thresholds, and 65 dB SPL sound conditioning had a stronger auditory protection effect. After sound conditioning, the amplitude of ABR I wave in the SC group was higher than that in the control group. Immediately after noise exposure (D0), the amplitudes of ABR I wave decreased significantly in all groups; the most significant decrease was in the NE group, with amplitude in 65SC+NE group significantly higher than that in the 85SC+NE group. Wave I latency in the SC group was significantly shorter than that in the control group. At D0, latency was prolonged in the NE group compared with the control group. In contrast, there was no significant difference in latency between the 65SC+NE and 85SC+NE groups. Further, at D14, there was no significant difference between the NE and control groups, while latency remained significantly shorter in the 65SC+NE and 85SC+NE groups compared with controls. Number of ribbon synapses in SC mice did not differ significantly from that in controls. After 110 dB noise exposure, there were significantly more ribbon synapses in the SC+NE group than the NE group. Ribbon synapses of all groups were recovered 14 days after the noise exposure, while the SC group had a shorter recovery time than the non-SC groups (p < 0.05). AMPK was highly activated in the SC group, and p-AMPK expression was detected; however, after 110 dB noise exposure, the strongest protein expression was detected in the NE group, followed by the SC+NE groups, and the lowest protein expression was detected in the control group. Conclusion: Sound conditioning animals were more noise resistant and recovered hearing faster than non-SC animals. Further, 65 dB SPL SC offered better hearing protection than 85 dB SPL SC. Early AMPK activation may protect hearing by increasing ATP storage and reducing the release of large quantities of p-AMPK, which could help to inhibit synapse damage.

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.