21:T52a,Objective: To investigate the correlation between cognitive function and quality of life in patients with moderate to severe OSAHS, and to further analyze the impact of cognitive domains on QoL in patients with OSAHS.Methods: Pearson analysis was applied to explore the correlation between MoCA score and SAQLI score. It was conducted by collecting the clinical characteristics of patients and the Epworth Sleepiness Scale and Sleep Quality Scale. T-test, a non-parametric test (Mann-Whitney) or chi-square test, and Pearson analysis were used to analyze the relationship between MoCA score and patient clinical characteristics, sleep variables, and SAQLI score.Results: The SAQLI score of the MCI group significantly decreased. Patients in the MCI group had a higher WHR, higher alcohol intake, and a history of hypertension were firmly related to the poor SAQLI (P < 0.05). The Epworth sleepiness scale (ESS) score increased in the MCI group, and the AHI and ODI elevated significantly, which was related to the poorer SAQLI as well (P < 0.05).Conclusion: Cognitive impairment in OSAHS patients is related to QoL reduction.Keywords: cognitive function; Montreal cognitive assessment; obstructive sleep apnea hypopnea syndrome; quality of life; sleep apnea quality of life index.22:T50c,Tuberous sclerosis complex (TSC), caused by loss-of-function mutations in the TSC1 or TSC2 gene, is characterized by benign tumor formation in multiple organs. Hyperactivation of mammalian target of rapamycin complex 1 (mTORC1) is the primary alteration underlying TSC tumors. By analyzing Tsc2-null mouse embryonic fibroblasts (MEFs) and rat uterine leiomyoma-derived Tsc2-null ELT3 cells, we detected evidence for the involvement of cyclooxygenase 2 (COX2) as a downstream target of mTORC1 in the development of TSC tumors. We showed that loss of TSC2 led to decreased COX2 expression through activation of an mTORC1/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Overexpression of COX2 promoted proliferation and tumoral growth of Tsc2-null cells. COX2 knockdown inhibited the proliferation of the control cells. COX2 enhanced Tsc2-null cell growth through upregulation of interleukin-6 (IL-6). In addition, rapamycin in combination with celecoxib, a COX2 inhibitor, strongly inhibited Tsc2-deficient cell growth. We conclude that downregulation of COX2 exerts a protective effect against hyperactivated mTORC1-mediated tumorigenesis caused by the loss of TSC2, and the combination of rapamycin and celecoxib may be an effective new approach to treating TSC.

	Year	Citations

About