Objective To investigate the relationship between the plasma galectin-3 level and the severity of cerebral artery atherosclerosis as well as the prognosis of patients with large artery atherosclerosis (LAA) stroke.Methods According to the TOAST classification,105 patients with LAA stroke,50 patients with small artery occlusion (SAO) stroke,33 patients with asymptomatic cerebral artery stenosis,and 60 healthy controls were enrolled.The plasma galectin-3 level was measured using enzyme-linked immunosorbent assay.According to the number of cerebral arteries with atherosclerosis,the LAA group was divided into single-branch lesions group (n =30),double-branch lesions group (n =30) and multi-branch lesions group (n =45).Plasma galectin-3 levels were compared among the three subgroups,and the associations between galectin-3 and the severity of cerebral atherosclerosis were analyzed.The LAA group patients were followed up for three months,and the value of galectin-3 on predicting the prognosis of patients with LAA stroke was assessed using the receiver operating characteristic (ROC) curve and the modified Rankin scale (mRS) scores.Results The plasma galectin-3 level in LAA group ((13.64 ± 3.08) ng/ml) was significantly higher than in SAO group ((12.20 ± 2.88) ng/ml) and control group ((11.89 ± 2.93) ng/ml;t =2.790,3.617,P =0.006,0.000).Besides,the plasma galectin-3 level in asymptomatic stenosis group ((13.94 ± 2.89) ng/ml) was significantly higher than in SAO group and control group (t =2.695,3.238,P =0.009,0.002).However,the differences between asymptomatic stenosis group and LAA group,SAO group and control group were not statistically significant.In LAA group,the plasma galectin-3 level in multi-branch lesions group ((15.02 ±2.94) ng/ml) was significantly higher than in double-branch lesions group ((13.47 ± 2.88) ng,/ml) and single-branch lesions group ((11.73 ± 2.43) ng/ml;t =2.261,5.080,P =0.027,0.000).The plasma galectin-3 level in double-branch lesions group was significantly higher than in single-branch lesions group (t =2.532,P =0.014).The plasma galectin-3 level and the range of atherosclerosis and mRS scores were positively correlated (r =0.433,0.629;P =0.000,0.000).The area under the ROC curve of plasma galectin-3 level and prognosis was 0.812 (95％ CI O.726-0.897,P =0.000).Conclusions The plasma galectin-3 level was found associated with the severity of cerebral artery atherosclerosis,but not with acute onset of LAA and SAO stroke.Galectin-3 may be involved in the inflammatory pathogenesis and development of cerebral atherosclerosis,and may have the potential to become a plasma marker for evaluating the severity of cerebral artery atherosclerosis and judging the prognosis of patients with LAA stroke.

Purpose: Oligometastatic non–small cell lung cancer (NSCLC) patients have been increasingly regarded as a distinct group that could benefit from local treatment to achieve a better clinical outcome. However, current definitions of oligometastasis are solely numerical, which are imprecise because of ignoring the biological heterogeneity caused by genomic characteristics. Our study aimed to profile the molecular alterations of oligometastatic NSCLC and elucidate its potential difference from polymetastasis. Materials and Methods: We performed next-generation sequencing to analyze tumors and paired peripheral blood from 77 oligometastatic and 21 polymetastatic NSCLC patients to reveal their genomic characteristics and assess the genetic heterogeneity. Results: We found ERBB2, ALK, MLL4, PIK3CB, and TOP2A were mutated at a significantly lower frequency in oligometastasis compared with polymetastasis. EGFR and KEAP1 alterations were mutually exclusive in oligometastatic group. More importantly, oligometastasis has a unique significant enrichment of apoptosis signaling pathway. In contrast to polymetastasis, a highly enriched COSMIC signature 4 and a special mutational process, COSMIC signature 14, were observed in the oligometastatic cohort. According to OncoKB database, 74.03% of oligometastatic NSCLC patients harbored at least one actionable alteration. The median tumor mutation burden of oligometastasis was 5.00 mutations/Mb, which was significantly associated with smoking, DNA damage repair genes, TP53 mutation, SMARCA4 mutation, LRP1B mutation, ABL1 mutation. Conclusion Our results shall help redefine oligometastasis beyond simple lesion enumeration that will ultimately improve the selection of patients with real oligometastatic state and optimize personalized cancer therapy for oligometastatic NSCLC.