RESUMO
BACKGROUND: Cardiac embolism is a common cause of ischemic stroke in young adults. Neurological complications associated with atrial myxoma most frequently include cerebral infarct due to embolus. Early complete resection of giant cardiac myxoma is the key to its treatment and prevention of stroke recurrence. CASE SUMMARY: A 42-year-old, previously healthy woman was admitted to the hospital with sudden-onset inability to speak and right-sided hemiplegia. While sweeping the floor 2 h prior to hospital admission, the patient developed sudden inability to express herself or understand what others were saying, accompanied by dyskinesia of the right limb, inability to walk or hold objects, and involuntary choreiform movements of the left upper limb. The patient was diagnosed with cerebral embolism and cardiac myxoma, complicated by left middle cerebral artery occlusion. The acute stroke was treated with intravenous thrombolytic therapy and arterial embolectomy as a bridging therapy to open resection of left atrial cardiac myxoma. The patient condition improved remarkably following initial thrombolysis and embolectomy and subsequently underwent emergency open resection of the atrial cardiac myxoma. She had no recurrence during 1-year follow-up. CONCLUSION: Strong consideration should be given to urgent intravenous thrombolysis (rt-PA, alteplase) in young adult stroke patients at the time of hospital admission. The present case demonstrated a highly successful outcome that combined thrombolysis and arterial embolus retrieval as a bridge to early complete resection of a giant cardiac myxoma for both stroke treatment and recurrence prevention.
RESUMO
BACKGROUND Our study aimed to identify key differentially expressed genes (DEGs) and miRNAs (DEmiRNAs) which can serve as potential biomarkers for diagnosis and therapy of Alzheimer's disease (AD). MATERIAL AND METHODS We performed miRNA and mRNA integrated analysis (MMIA) to identify DEGs and DEmiRNAs of AD. The AD-specific DEmiRNAs-targets interaction network was contrasted. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis were performed. Q-RT-PCR was used to verify the expression of selected DEGs and DEmiRNAs. RESULTS We conducted MMIA of AD based on 1 miRNA dataset and 3 mRNA datasets derived from the Gene Expression Omnibus (GEO) database; 1759 DEGs and 12 DEmiRNAs were obtained. DEGs of AD were significantly enriched in Huntington's disease and AD. LRP1, CDK5R1, PLCb2, NDUFA4, and DLG4 were 5 DEGs regulated by 4 DEmiRNAs, including miR-26b-5p, miR-26a-5p, miR-107, and miR-103a-3p. These 4 miRNAs were the top 4 miRNAs covering most DEGs. According to the qRT-PCR results, the expression of PLCß2, NDUFA4, DLG4, miR-107, and miR-103a-3p was consistent with our integrated analysis. CONCLUSIONS We concluded that LRP1, CDK5R1, PLCß2, NDUFA4, and DLG4 may play a role in AD regulated by miR-26b-5p, miR-26a-5p, miR-107, and miR-103a-3p. Our findings will contribute to identification of biomarkers and new strategies for drug design for AD treatment.
