The ipsilateral peroneus longus tendon (PLT) was utilized as an autograft for anterior cruciate ligament (ACL) reconstruction of patients with acute ACL rupture and grade III medial collateral ligament (MCL) injury. We investigated the efficacy and safety of this alternative autograft compared with autologous hamstring tendon (HT). Biomechanical testing of the graft options was performed and compared with the native ACL. Thirty-eight patients with acute ACL ruptures and grade III MCL injuries were treated with ACL reconstruction with a doubled autologous PLT or quadrupled autologous HT. Knee stability and function was evaluated clinically with the Lachman test and KT-2000 arthometer as well as subjectively with functional scores. Effects on the donor ankle were evaluated by biomechanical testing. The ultimate tensile strengths of doubled PLT and quadrupled HT were significantly higher than that of the native ACL and the ultimate tensile strength of doubled PLT was comparable with that of quadrupled HT. There were no significant differences in clinical or functional scores between the two groups. There were no significant differences in pre- and postoperative biomechanical testing of the donor ankle. PLT is a suitable alternative autograft for an ACL reconstruction in patients with a concomitant grade III MCL injury without a significant biomechanical disadvantage to the ankle donor site.
There is limited information on the relation between sleep duration and incident atrial fibrillation. We aimed to investigate this association in a Chinese population using cohort data from a study in Kailuan. The analysis included 87,693 participants (age range, 18–98 years) free of atrial fibrillation at the baseline survey. Participants were divided into three categories according to self-reported sleep duration: ≤6.0 hours, 7 hours (ref), ≥8.0 hours. Atrial fibrillation diagnosis was made on a standard 12-lead electrocardiogram and via self-reported history. Cox proportional hazards models were used to calculate hazard ratio (HR) and confidence interval (CI) for atrial fibrillation, according to sleep duration. During median follow-up of 7.89 (range, 6.36–8.57) years, 322 cases of atrial fibrillation had occurred. Using 7 hours of sleep as the reference group, multivariable adjusted HRs (95% CI) for atrial fibrillation were 1.07 (0.75–1.53), 1.0 (ref), and 1.50 (1.07–2.10), from lowest to highest category of sleep duration. Secondary analysis showed no evidence of interactions between sleep duration and sex and snoring on the risk of incident atrial fibrillation (p = 0.75/0.25). We conclude long sleep duration may be a potential predictor/marker for incident atrial fibrillation.
MicroRNAs (miRNAs) are key regulators of multiple cancers, including non-small cell lung carcinoma (NSCLC). The aim of this study was to determine the expression pattern of miR-769-5p in NSCLC and to investigate its biological role during tumorigenesis. We showed that miR-769-5p was significantly downregulated and predicted poor prognosis in NSCLC compared with corresponding normal tissues. We then investigated its function and found that miR-769-5p significantly inhibited cell proliferation, migration and invasion in vitro and reduced tumor growth and metastasis in vivo. Furthermore, we explored the molecular mechanisms by which miR-769-5p contributes to NSCLC suppression and identified TGFBR1 as a direct target gene of miR-769-5p. Finally, we showed that TGFBR1 had opposite effects to those of miR-769-5p on lung cancer cells, suggesting that miR-769-5p might inhibit lung tumorigenesis by silencing TGFBR1. Taken together, our results demonstrated that miR-769-5p plays a pivotal role in NSCLC by inhibiting cell proliferation, migration and invasion by targeting TGFBR1.
DNA methylation is the best-studied epigenetic mechanism for regulating gene transcription and maintaining genome stability. Current research progress of transcriptional regulation by DNA methylation mostly focuses on promoter region where hypomethylated CpG islands are present transcriptional activity, as hypermethylated CpG islands generally result in gene repression. Recently, the DNA methylation patterns across the gene body (intragenic methylation) have increasingly attracted attention towards their role in transcriptional regulation and efficiency, due to the improvement of numerous genome-wide DNA methylation profiling studies. However, the function and mechanism of gene body methylation is still unclear. In this study, we revealed that the methylation level of METTL7A, a seldom studied gene, was downregulated in thyroid cancer compared to normal thyroid cells in vivo and in vitro. Moreover, we determined the methylation level of one CpG site at the exon of the METTL7A gene body impacted the transcriptional activity. Through generating a mutation of this CpG site (CG to CC) of METTL7A exogenous vector artificially in vitro, we observed higher RNA polymerase II recruitment and a declined enrichment of methyl-CpG binding protein-2 in gene body of METTL7A, in papillary thryoid cancer cells (BCPAP) compared to normal thryoid cells. Finally, we revealed that EZH2, a subunit of polycomb repressor complex 2, dominant in thyroid cancer, might be responsible for regulating gene body methylation of METTL7A. Our study depicted the DNA methylation patterns and the transcriptional regulatory mechanism of the gene body in thyroid cancer. Furthermore, this study provides new insight into potential future avenues, for therapies targeting cancer.
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