Objective [WT5”BZ]To evaluate the interventional therapy for Budd Chiari syndrome in which inferior vena cava was segmentally stenotic or occlusive combined with obstruction of hepatic vein and thrombosis.[WT5”HZ] Methods [WT5”BZ] 13 cases with regional stricture or occlusion in inferior vena cava (8 cases with hepatic vein occlusion and 5 cases with thrombosis of inferior vena cava) were reviewed and the length of lesions ranged from 2?cm to 5?cm. For patients with IVC occlusion, atrial septum puncture was used, followed by 1 0～2 0?cm balloon dilation and implantation of metal stent. For patients with hepatic vein occlusion, RUPS 100 liver puncture apparatus was applied and followed by 0 5～1 0?cm balloon dilation. Postoperative anticoagulant therapy was used for 3 months.[WT5”HZ] Results [WT5”BZ]Procedures were successful in all cases. Shrinkage of the spleen and absorption of ascites were observed after operation. There were no relapse of symptoms, nor digestive tract bleeding during 3～26 months of follow up. [WT5”HZ]Conclusions [WT5”BZ] Thrombolytic therapy was very important before the repatency of the IVC for patients with thrombosis formation. The embedded in stent must be away from the orifice of accessory liver vein. Angioplasty of hepatic vein is essential for the interventional treatment of Budd Chiari syndrome. [WT5”HZ]

Cell Nucleus ; Cellular Senescence/genetics* ; CRISPR-Cas Systems/genetics*

Aging poses a major risk factor for cardiovascular diseases, the leading cause of death in the aged population. However, the cell type-specific changes underlying cardiac aging are far from being clear. Here, we performed single-nucleus RNA-sequencing analysis of left ventricles from young and aged cynomolgus monkeys to define cell composition changes and transcriptomic alterations across different cell types associated with age. We found that aged cardiomyocytes underwent a dramatic loss in cell numbers and profound fluctuations in transcriptional profiles. Via transcription regulatory network analysis, we identified FOXP1, a core transcription factor in organ development, as a key downregulated factor in aged cardiomyocytes, concomitant with the dysregulation of FOXP1 target genes associated with heart function and cardiac diseases. Consistently, the deficiency of FOXP1 led to hypertrophic and senescent phenotypes in human embryonic stem cell-derived cardiomyocytes. Altogether, our findings depict the cellular and molecular landscape of ventricular aging at the single-cell resolution, and identify drivers for primate cardiac aging and potential targets for intervention against cardiac aging and associated diseases.
Aged ; Animals ; Humans ; Aging/genetics* ; Forkhead Transcription Factors/metabolism* ; Myocytes, Cardiac/metabolism* ; Primates/metabolism* ; Repressor Proteins/metabolism* ; Transcriptome ; Macaca fascicularis/metabolism*