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]

Objective To explore development status in different types of the hand bone and its developmental characteristics with Poland syndrome.Methods There were 32 cases with Poland's syndrome who accepted bilateral hand X-ray examination in Department of Hand Surgery,Beijing Jishuitan Hospital from February 2013 to August 2014.There were 24 male and 8 female patients aged from 1.0 to 15.0 years with median age of 2.4 years.Right hand deformity was 23 cases and left hand deformity was 9 cases.According to Tanner-Whitehouse skeletal age scoring system,20 bones (radius and ulna,7 carpal bones,11 metacarpal and phalangeal bones) selected from the affected and contralateral limb respectively,were evaluated.Besides,hand deformity of the cases was classified into 5 types based on relevant literature.Each bone was given an individual age using the references of Greulich-Pyle chart.The average of all individual ages was taken as gross bone age,the average of individual ages of radius and ulna was taken as bone age of long bones,the average of individual ages of carpal bone was taken as bone age of carpal bones,and the average of individual age of metacarpal and phalangeal bones was taken as bone age of short bones.The delay of bone age was evaluated by correlation test,while the curve of cubic equation was used for analyzing the variance of skeletal development with age.Results The delay of long bone age of patients with Poland's syndrome in this study were 0-1.9 years ((0.5 ±0.5) years),0-2.2 years ((0.7 ±0.5)years) for carpal bone,0.5-2.0 years((0.6 ±0.4) years)for short bone and 0.1-1.7 years((0.6 ±0.4)years) for gross bone.Twelve cases in type Ⅱ hand deformity,15 cases in type Ⅲ and 5 cases in type Ⅳ.The delay of bone ages,including long bone age,carpal bone age,short bone age and gross bone age,was not related with gender and side(all P ＞ 0.05),but related with degree of deformity(F =3.663-12.971,P =0.000-0.038).Conclusion Compared with normal upper limb,the bone age in the affected limb in Poland's syndrome is delayed and it is correlated with gender,age and the extent of hand deformity and negative with side.

Objective To explore development status in different types of the hand bone and its developmental characteristics with Poland syndrome.Methods There were 32 cases with Poland's syndrome who accepted bilateral hand X-ray examination in Department of Hand Surgery,Beijing Jishuitan Hospital from February 2013 to August 2014.There were 24 male and 8 female patients aged from 1.0 to 15.0 years with median age of 2.4 years.Right hand deformity was 23 cases and left hand deformity was 9 cases.According to Tanner-Whitehouse skeletal age scoring system,20 bones (radius and ulna,7 carpal bones,11 metacarpal and phalangeal bones) selected from the affected and contralateral limb respectively,were evaluated.Besides,hand deformity of the cases was classified into 5 types based on relevant literature.Each bone was given an individual age using the references of Greulich-Pyle chart.The average of all individual ages was taken as gross bone age,the average of individual ages of radius and ulna was taken as bone age of long bones,the average of individual ages of carpal bone was taken as bone age of carpal bones,and the average of individual age of metacarpal and phalangeal bones was taken as bone age of short bones.The delay of bone age was evaluated by correlation test,while the curve of cubic equation was used for analyzing the variance of skeletal development with age.Results The delay of long bone age of patients with Poland's syndrome in this study were 0-1.9 years ((0.5 ±0.5) years),0-2.2 years ((0.7 ±0.5)years) for carpal bone,0.5-2.0 years((0.6 ±0.4) years)for short bone and 0.1-1.7 years((0.6 ±0.4)years) for gross bone.Twelve cases in type Ⅱ hand deformity,15 cases in type Ⅲ and 5 cases in type Ⅳ.The delay of bone ages,including long bone age,carpal bone age,short bone age and gross bone age,was not related with gender and side(all P ＞ 0.05),but related with degree of deformity(F =3.663-12.971,P =0.000-0.038).Conclusion Compared with normal upper limb,the bone age in the affected limb in Poland's syndrome is delayed and it is correlated with gender,age and the extent of hand deformity and negative with side.

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*