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BackgroundAneurysms of an aberrant splenic artery originating from the superior mesenteric artery (SMA) are extremely rare; however, they are clinically important because possible rupture could be catastrophic. The methods of treatment for this condition include surgical resection, minimally invasive techniques (include laparoscopic technique) and endovascular therapy. The purpose of this study is to evaluate the efficacy of coils embolization combined with covered stents to treat aberrant splenic artery aneurysm (SAA).Cases PresentationWe report four consecutive cases of aberrant SAA that the aberrant splenic artery was embolized with coils and the superior mesenteric artery was excluded with a covered stent and an up-to-date review of all previous cases in the field. A follow-up computed tomography performed 6 to 12 months postoperatively showed persistent exclusion with marked shrinkage of the aneurysm sac.ConclusionsThe authors believe although early results are promising, further careful follow-up will be needed to determine the long-term clinical efficacy, safety and applicability of this approach.

Abstract. Endothelial progenitor cells (EPCs) participate in angiogenesis by differentiating into endothelial cells (ECs)and may be developed to treat ischemia/reperfusion injury. MicroRNAs (miRs) are a type of non-coding RNA that are 18-25 nucleotides in length and serve a role in angiogenesis. It has been demonstrated that miR-138 regulates hypoxia-induced EC dysfunction. However, to the best of our knowledge, the exact role of miR-138 in the regulation of hypoxia-induced EPCs has not previously been reported. In the present study, data collected from an MTT assay indicated that hypoxia treatment enhanced EPC proliferation, which was accompanied by an upregulation of hypoxia-inducible factor 1α (HIF-1α) expression. miR-138 overexpression inhibited hypoxia-induced EPC proliferation and induced cell cycle arrest at the G1 stage. A mechanistic investigation revealed that miR-138 negatively regulated HIF-1α protein levels but did not affect HIF-1α mRNA levels in EPCs. Moreover, results from a dual luciferase reporter assay demonstrated that HIF-1α was a direct target of miR-138 in EPCs. Furthermore, upregulation of miR-138 suppressed the hypoxia-induced upregulation of HIF-1α. Downstream factors of HIF-1α were also investigated and it was observed that the upregulation of miR-138 inhibited the hypoxia-induced upregulation of vascular endothelial growth factor, as well as the activity of mitogen-activated protein kinase and AKT signaling in EPCs. In summary, the present study suggested that miR-138 inhibits hypoxia-induced EPC proliferation, possibly by inhibiting HIF-1α-mediated signaling.

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It is beneficial that we treat RAAAs in the diagnosed hospital. The reasons are: 1) to avoid the development of unstable state of aneurysm after rupturing of stable state; 2) the time interval from initial symptoms to operation will be shortened.