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Objectives: Myocardial infarction without significant stenosis or occlusion of the coronary arteries carries a high risk of recurrent major adverse cardiovascular events and poor prognosis. This study aimed to investigate the association between body mass index and outcomes in patients with a suspected myocardial infarction with nonobstructive coronary artery disease (MINOCA). Methods: Patients were recruited at Bergmannsheil University Hospital from January 2010 to April 2021. The primary outcomes were in‐hospital and long‐term mortality. Secondary outcomes consisted of adverse events during hospitalization and during follow‐up. Results: A total of 373 patients were included in the study, with a mean follow‐up time of 6.2 years. The patients were divided into different BMI groups: < 25 kg/m² (n = 121), 25−30 kg/m² (n = 140), and > 30 kg/m² (n = 112). In‐hospital mortality was 1.7% versus 2.1% versus 4.5% (p = 0.368). However, long‐term mortality tended to be higher in the < 25 kg/m² group compared to the 25−30 and > 30 kg/m² groups (log‐rank p = 0.067). Subgroup analysis using Kaplan−Meier analysis showed a higher rate of cardiac cause of death in the < 25 kg/m² group compared to the 25−30 and > 30 kg/m² groups: 5.7% versus 1.1% versus 0.0% (log‐rank p = 0.042). No significant differences were observed in other adverse events between the different BMI groups during hospitalization and long‐term follow‐up. Conclusions: Patients with a BMI < 25 kg/m² who experience a suspected myocardial infarction without significant coronary artery disease may have higher all‐cause mortality and cardiovascular cause of death. However, further data are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

miR-132, a microRNA, has been reported to be down-regulated in several human cancers and is related with tumor progression; however, its function in non-small cell lung cancer (NSCLC) progression remains unclear. This study aimed to investigate the putative role of miR-132 in the metastasis of NSCLC. We determined the function of miR-132 in the migration and invasion of a NSCLC cell line in vitro using a miR-132 inhibitor and mimic. Our results showed overexpression of miR-132 significantly inhibited the migration and invasion of NSCLC cells in vitro . We then identified USP9X as a potential target of miR-132, and demonstrated miR-132 could regulate the expression of USP9X at both the mRNA and protein level. miR-132 could directly bind to the 3' untranslated region (3'-UTR) of USP9X. Inhibition of USP9X by its inhibitor WP1130 reduced the migration and invasion of NSCLC cells. Furthermore, USP9X inhibition also reversed the increased migration and invasion mediated by miR-132 inhibition. We found USP9X inhibition up-regulated expression of the epithelial-mesenchymal transition (EMT) marker E-cadherin, but down-regulated vimentin expression. A similar effect was seen with miR-132 overexpression, while the opposite effect occurred with miR-132 knockdown. USP9X inhibition reversed the miR-132 inhibitor-induced vimentin up-regulation and E-cadherin down-regulation. Taken together, these results indicate miR-132 prohibits the migration and invasion of NSCLC cells via targeting USP9X-induced EMT. Our data provides further evidence for the critical role of miR-132 and USP9X in regulating cell invasion and migration of NSCLC., Competing Interests: None.