Objective To study the safety and efficacy of accessory hepatic vein (AHV) stenting to treat primary Budd-Chiari syndrome (BCS).Methods The clinical data of 20 BCS patients with AHV ostial stenosis or occlusion were retrospectively analyzed.These 20 patients underwent balloon dilation and AHV stenting.Thirteen patients underwent AHV stenting via the right jugular vein approach,5 patients via the right femoral vein approach,and 2 patients via the percutaneous transhepatic combined with the right femoral vein approach.On follow-up,patency of the AHV stent was evaluated by color Doppler ultrasound.The cumulative primary and secondary patency rates were assessed with the Kaplan-Meier curves.Results AHV stenting was successful in 20 patients.Angiography showed that the AHV was patent after stenting.The mean pressure gradient between the AHV and the inferior vena cava reduced from (19.2 ± 4.8) cmH2O (1 cmH2O =0.098 kPa) before treatment to (4.5 ± 1.9) cmH2O after treatment (t =7.119,P ＜ 0.01).During the procedure,rupture of the AHV caused by balloon dilation occurred in one patient.This was treated successfully by a covered stent placement.On follow-up from 1 to 80 months [(32.1 ±27.4) months]after treatment for the 20 patients,re-stenosis of the AHV were found in 5 patients.They were treated successfully with re-dilation.The cumulative 1-,3-,and 5-year primary patency rates were 100％,85.1％ and 74.5％,respectively.The cumulative 1-,3-,and 5-year secondary patency rates were 100％,90.9％ and 90.9％,respectively.One patient died of hepatic failure 3 years after the treatment.Conclusion AHV stenting was a safe and efficacious treatment for BCS and it provided good mid-and long-term results.

Objective: To investigate the effect of casein kinase 2 interacting protein-1 (CKIP-1) on craniofacial soft tissues and hard tissues, to provide the basis for the study and treatment of craniomaxillofacial related diseases. Methods: 6-month- old male CKIP-1 knockout (KO) mice were selected as the experimental group, and wild-type (WT) mice were selected as the control group. The craniomaxillofacial hard tissues (parietal bone, nasal bone, incisors and molars) were analyzed through micro- CT, and the morphological changes of maxillofacial soft tissues (nasal cartilage, lip mucosa and tongue) were analyzed through HE staining and toluidine blue staining. Results: CKIP-1 negatively regulated bone mass of cancellous bone of cranial and maxillofacial bones and dentin mineralization. Compared with the WT mice, the thickness of the parietal baffle layer increased by 93% in KO mice, while cortical bone showed no significant difference between the two groups. The nasal cancellous bone thickness increased by 160% in KO-mice, while cortical bone showed no significant difference between the two groups; the enamel thickness was normal, but the pulp cavity became smaller and the dentin thickness increased by 48%. Compared with the WT mice, the HE staining and toluidine blue staining analyses of the soft tissues revealed that the thickness of the alar cartilage plate of KO mice increased by 57%, and local ossification was found within the cartilage plate. The thickness of the keratinized layer of the labial mucosa increased by 170% in KO mice and the muscle fiber diameter of the lingual muscle increased by 45%. Conclusion CKIP-1 genes have different effects on the growth and development of various soft and hard tissues in the maxillofacial region of mice.