RESUMO
BACKGROUND: Dextroversion is defined as the presence of dextrocardia with situs solitus, dextro-loop ventricles, and normally related great arteries. Dextrocardia can pose technical challenges when interventional treatments are required. However, the challenges posed by dextroversion can be amplified due to the disruption of typical anatomical relationships, the unpredictable positioning and boundaries of cardiac structures resulting from the shift, and the pathological processes influencing rotation. CASE SUMMARY: A 73-year-old woman with cardiac dextroversion suffered from a recurrence of atrial fibrillation after her radiofrequency catheter ablation and Despite the cessation of antiarrhythmic medications, there were episodes of sinus pauses and symptomatic bradycardia, with heart rates dropping as low as 28 beats per minute. CONCLUSION: Dextroversion makes the implantation of leadless pacemakers more challenging, and appropriate adjustments in fluoroscope angles may be crucial for intracardiac operations. Additionally, when advancing delivery systems, attention should be paid to rotational direction during valve-crossing procedures; changes in the perspective of posture angle between normal cardiac position and dextroversion can serve as references.
RESUMO
Neuroinflammation hinders repair of the central nervous system (CNS). Stem cell transplantation is a very promising approach for treatment of CNS injuries. However, it is difficult to select seed cells that can both facilitate nerve regeneration and improve the microenvironment in the CNS. In this study, we isolated multilineage-differentiating stress-enduring (Muse) cells from bone marrow mesenchymal stem cells. We explored the anti-inflammatory effect and mechanism of Muse cells in vitro by coculture of Muse cells with lipopolysaccharide-stimulated microglia. Our results showed that Muse cells effectively reduced the transcription and secretion of tumor necrosis factor α and interleukin-1ß and increased the expression of transforming growth factor-ß and interleukin-10 in microglia. In addition, Muse cells decreased the number of M1 microglia and increased the proportion of M2 microglia in an inflammatory environment more effectively than bone marrow mesenchymal stem cells. We also show that Muse cells inhibited the protein expression of toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein (MyD88) and inhibited the expression of the phosphorylated forms of transcription factor p65, nuclear factor (NF)-κB inhibitor alpha, and p38 mitogen-activated protein kinase (MAPK) in microglia. Therefore, we suggest Muse cells cause antineuroinflammatory effects by inhibition of the TLR4/MyD88/NF-κB and p38 MAPK signaling pathways in microglia. Our results shed light on the function of Muse cells in relation to CNS diseases and provide insight into the selection of seed cells.
