Lung cancer is the most frequent leading cause of cancer-related death all around the world, and about 60 000 patients with lung cancer die every year in China. The majority of lung cancer (approximately 85%) are diagnosed as non-small-cell lung cancer (NSCLC), and tumor metastasis is found in most NSCLC cases at diagnosis. 1,2 Although great advancements in the therapies such as radiation and chemotherapy have been made over the past decades, the 5-year survival rate of this malignancy remains unfavorable. Early diagnosis and accurate prognosis prediction can reduce the mortality of this disease and improve patients' survival time. 3,4 Therefore, it is of importance to identify novel and reliable biomarkers for early detection and prognosis prediction of NSCLC.

No abstract

No abstract

Objective: Systemic immune-inflammation index (SII) is a biomarker that reflect systemic inflammation. We aimed to assess the value of SII in prediction of shortterm outcomes in acute type A aortic dissection (ATAD) patients undergoing surgery.Method: All patients underwent surgery for ATAD at our institution from 2018 to 2020 (n = 324) were retrospectively reviewed and divided into low SII (<1582.6 × 10 9 /L) and high SII (≥1582.6 × 10 9 /L) group according to optimal cutoff values defined by receiver operating characteristic curve. Cox regression and Kaplan-Meier analyses were performed to illustrate the correlation between SII and postoperative short-outcomes, including 30-day mortality and main complications after surgery.Results: In total, 48 (14.8%) patients died in 30 days after ATAD surgery. And multivariable Cox analysis demonstrated that high preoperative SII was closely related with 30-day mortality (hazard ratio: 3.532, 95% confidence interval:1.719-7.255, p = .001). Furthermore, Kaplan-Meier analysis illustrated that the short-term mortality rate increased significantly in high SII group (p < .001). In addition, the incidence of main postoperative complications including major adverse cardiovascular events (p = .001) and multiorgan failure (p = .002) were higher in high SII group. However, the length of intensive unit stay (p = .909) and hospital stay (p = .836) presented no difference in two groups. Conclusion:The study indicated that SII was an available biomarker to predict postoperative short-term prognosis, but not length of stay in intensive care unit and hospital in ATAD patients. And SII may be applied to risk stratification and patient selection in ATAD patients before surgery.

Background Vascular aging is an important risk factor for various cardiovascular diseases. Transcription factor krüppel‐like factor 4 (KLF4) could regulate the phenotypic transformation of the vascular smooth muscle cell (VSMC) in the pathogenesis of aortic diseases. The present study aimed to explore the role and mechanism of KLF4 in angiotensin II (Ang II)‐induced VSMC senescence. Methods The VSMC senescence mouse model was induced by sustained release of Ang II (1.0 μg/kg/min) for 4 weeks. The premature senescent VSMCs were induced by Ang II (0.1 μmol/L) for 72 h. Cellular senescence was measured by senescence‐associated β‐galactosidase (SA‐β‐gal) activity and p53/p16 expression. The autophagic activity was evaluated by autophagic flux and autophagic marker expression. Results The expression of KLF4 was extremely increased in abdominal aorta tissues after 1‐week Ang II stimulation (p < .01) but began to decrease in later periods. Decreased expression of KLF4 was also detected in premature senescent VSMCs. Overexpression of KLF4 could enhance the antisenescence ability of VSMCs. Significantly decreased amounts of SA‐β‐gal‐positive cells and lower p53/p16 expression were detected in KLF4‐overexpressing VSMCs (p < .01). Next, telomerase reverse transcriptase (TERT) was identified as a direct downstream target of KLF4 in VSMCs. Overexpression of KLF4 in VSMCs prevented the decreased expression of TERT under Ang II stimulation condition, which could in turn, contribute to the enhanced autophagic activity, and ultimately to the improved antisenescence ability of VSMCs. Conclusions Our results demonstrated that overexpression of KLF4 prevented Ang II‐induced VSMC senescence by promoting TERT‐mediated autophagy. These findings provided novel potential targets for the prevention and therapy of vascular aging.