Objectives:To study the pathological behavior and the value of transforming growth factor β1(TGF-β1) in predicting prognosis in pulmonary hypertension associated with congenital heart disease.　Methods:Lung tissues from 29 patients with congenital heart diseases associated with pulmonary hypertension were examined by surgical biopsy of the lung. All samples were examined for the expression and localization of TGF-β1 by immunohistochemical technique with anti-TGF-β1 antibody.　Results:Twenty-six out of 29 showed positive staining of intracellular endotheliocyte TGF-β1(89.65%),16 samples showed extracellular matrix TGF-β1 staining(55.17%).Statistically, there was significant difference between Ⅰ～Ⅱ and Ⅲ～Ⅵ pathological degrees in extracellular matrix(P<0.05).　Conclusions: TGF-β1 plays an important biological role in the formation of pulmonary hypertension after congenital heart disease. It is conductive in predicting prognosis.

Objective The three-dimensional finite element model of the normal ankle joint was established to simulate the changes of stress and displacement under stress from different directions and of different magnitudes so as to provide a theoretical basis for the biomechanical mechanism of the ankle joint injury.Methods Spiral CT scan was performed on the left ankle of a 30 year old healthy male volunteer to obtain the original CT image data.The three-dimensional digital model of ankle joint generated by Mimics and Geomagic softwares was imported into the software Ansys.The three-dimensional finite element model of ankle joint with complete anatomical structure was obtained after the main steps of meshing,central node,element linking and module loading using finite element method.Stress from different directions and of different magnitudes were loaded unto the model.The stress changes were measured by foot stress distribution measurement system.The stress changes,displacement change distribution,the stress peak value of heel are,metatarsal stress,and plantar contact stress area as well as the maximum,minimum,and contact are of the tibial articular surface contact stress were compared between the finite element model and the volunteer himself to verify the consistency.Results For the finite element model of normal ankle joint,the plantar peak stress was [(0.33 ± 0.10) MPa],the metatarsal stress was [(0.13 ± 0.21)MPa],the foot contact stress area was [(78.60 ±0.32)mm2],the tibial articular surface maximum contact stress was [(2.72 ± 0.10) MPa],the minimum contact stress was [(1.35 ±0.12)MPa],and the contact stress area was [(79.1 ± 0.14)mm2].For the volunteer,double foot plantar peak stress was [(0.35 ± 0.12)MPa],the metatarsal stress [(0.13 ±0.16)MPa],the foot contact stress area was [(77.3 ± 0.42)mm2],the tibial articular surface maximum contact stress was [(2.79 ± 0.23) MPa],the minimum contact stress was [(1.37 ± 0.20) MPa],and the contact stress area was [(79.10 ±0.14)mm2] (P ＜0.05).Therefore,the three finite element model of ankle joint was basically consistent with the real human ankle joint because of the similiar distribution,trend,and values.Conclusion The three-dimensional finite element model of normal ankle joint can objectively reflect the anatomical structure and biomechanical characteristics of the joint,which is of great value to understand the changes of the internal mechanics and ankle joint injury.

Background and Objectives: The search for a suitable alternative for urethral defect is a challenge in the field of urethral tissue engineering. Induced pluripotent stem cells (iPSCs) possess multipotential for differentiation. The in vitro derivation of urothelial cells from mouse-iPSCs (miPSCs) has thus far not been reported. The purpose of this study was to establish an efficient and robust differentiation protocol for the differentiation of miPSCs into urothelial cells. Methods: and Results: Our protocol made the visualization of differentiation processes of a 2-step approach possible. We firstly induced miPSCs into posterior definitive endoderm (DE) with glycogen synthase kinase-3β (GSK3β) inhibitor and Activin A. We investigated the optimal conditions for DE differentiation with GSK3β inhibitor treatment by varying the treatment time and concentration. Differentiation into urothelial cells, was directed with all-trans retinoic acid (ATRA) and recombinant mouse fibroblast growth factor-10 (FGF-10). Specific markers expressed at each stage of differentiation were validated by flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR) assay, immunofluorescence staining, and western blotting Assay. The miPSC-derived urothelial cells were successfully in expressed urothelial cell marker genes, proteins, and normal microscopic architecture. Conclusions We built a model of directed differentiation of miPSCs into urothelial cells, which may provide the evi-dence for a regenerative potential of miPSCs in preclinical animal studies.