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Background: Non‐small‐cell lung cancer (NSCLC) often presents at later stages, typically associated with poor prognosis. Autophagy genes play a role in the progression of tumors. This study investigated the clinical relevance, prognostic value, and biological significance of RBBP4 in NSCLC. Methods: We assessed RBBP4 expression using the GSE30219 and TCGA NSCLC datasets and NSCLC cells, exploring its links with clinical outcomes, tumor immunity, and autophagy genes through bioinformatics analysis after transcriptome sequencing of RBBP4‐knockdown and control PC9 cells. We identified differentially expressed genes (DEGs) and conducted Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway enrichment, and protein–protein interaction network analyses. The significance of autophagy‐related DEGs was evaluated for diagnosis and prognosis using the GSE30219 dataset. Experiments both in vivo and in vitro explored the biological mechanisms behind RBBP4‐mediated autophagic cell death in NSCLC. Results: RBBP4 overexpression in NSCLC correlates with a poorer prognosis. Eighteen types of immune cell were significantly enriched in cultures that had low RBBP4 expression compared high expression. DEGs associated with RBBP4 are enriched in autophagy pathways. Transcriptomic profiling of the PC9 cell line identified autophagy‐related DEGs associated with RBBP4 that exhibited differential expression in NSCLC, suggesting prognostic applications. In vitro experiments demonstrated that RBBP4 knockdown induced autophagy and apoptosis in PC9 cells, promoting cell death, which was inhibited by 3‐MA. In vivo, targeted siRNA against RBBP4 significantly reduced tumor development in PC9 cell‐injected nude mice, elevating autophagy‐related protein levels and inducing apoptosis and necrosis in tumor tissues. Conclusion: In NSCLC, RBBP4 upregulation correlates with poor prognosis and altered immunity. Its knockdown induces autophagic cell death in NSCLC cells. These results indicate RBBP4 as a potential NSCLC diagnostic marker and its autophagy modulation as a prospective therapeutic target. [ABSTRACT FROM AUTHOR]

Background: Exposure to some special events, also called stroke triggers, can precipitate the onset of ischemic stroke (IS). Previous studies have presented preliminary hypotheses about sexual intercourse as a trigger of IS in predisposed individuals, but the mechanisms of IS associated with sexual intercourse are still not well defined. This literature review summarizes the etiologies and mechanisms of IS associated with sexual intercourse. Further studies on stroke triggers are warranted, and early recognition and appropriate preventive strategies directed against the short-term risks posed by stroke triggers may complement the long-term risk factor reduction approach. Methods: Articles were selected from PubMed (1946–2021) and Web of Science Core Collection (1990–2021) using the following search terms: ischemic stroke, ischaemic stroke, stroke, cerebral infarction, cerebral ischemia, cerebral embolism, embolism, sexual intercourse, sexual activity, intercourse, coitus, coition, and coital. Results: A total of 20 studies, which included 26 patients with IS associated with sexual intercourse, were included. This literature review found that IS associated with sexual intercourse is not rare but has not received enough attention, and paradoxical embolization and postcoital arterial dissection are common etiologies. Other etiologies include drug usage (such as sexual adjuvant drugs and illicit drugs), paroxysmal sympathetic hyperactivity, and reversible cerebral vasoconstriction syndrome. Discussion/Conclusion: Sexual intercourse should be considered an important trigger for IS. Clinicians should be aware that IS associated with sexual intercourse is not subjective but may be a warning sign of multiple etiologies and mechanisms. [ABSTRACT FROM AUTHOR]