ObjectiveTo study absorbed mechanism of free bone auto-graft in cranium.MethodsTwenty-four adult New Zealand rabbits were randomly divided into two groups of twelve each. Cranium graft or rib graft was implanted on each side of the cranium. The onlay graft was harvested at the 12th and 24th week, and the collagen fibers were scrutinized under scanning electron microscope. ResultsThe number of the bone collagen fibrils at twenty- fourth week was more than that of the twelfth week, the arrangement of collagen fibrils at the twenty- fourth week was more regular than that of the twelfth week, and the collagen fibrils of the cranium graft were more numberous and regular than those of the rib graft observed at the twelfth week, but they were similar at twenty - fourth week. ConclusionRemoding time of cranium graft is shorter than that of rib graft, but bone remoding of both cranium and rib has finished in 24th week after operated.

OBJECTIVETo explore a feasible method to repair full-thickness skin defects with tissue engineered techniques.

METHODSThe skin specimens were cut from the Changfeng hybrid swines' abdomen, then keratinocytes and fibroblasts were isolated and harvested by trypsin, EDTA and type II collagenase. The cells were seeded in petri dishes for primary culture. When the cells were in logarithmic growth phase, they were treated with dispase II (keratinocytes) or trypsin (fibroblasts) to separate them from the floor of the tissue culture dishes. A biodegradable material-pluronic F-127 was prefabricated and mixed with these cells, and then the cells-pluronic compounds were seeded evenly into polyglycolic acid (PGA). Tinally the constructs were replanted to autologous animals to repair full-thickness skin defects. Histological changes were observed in 1, 2, 4 and 8 weeks postsurgery.

RESULTSThe cells-pluronic F-127-PGA compounds could repair autologous full-thickness skin defects. Histologically, the tissue engineered skin was similar to normal skin with stratified epidermis overlying a moderately thick collageneous dermis.

CONCLUSIONTissue engineered skin can repair autologous full-thickness skin defects with primary-cultured keratinocytes and fibroblasts as seed cells and PGA as a cell carrier.

Animals ; Female ; Fibroblasts ; physiology ; Male ; Polyglycolic Acid ; pharmacology ; Skin Transplantation ; Skin, Artificial ; Swine ; Tissue Engineering

Background::We previously reported that activation of the cell cycle in human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) enhances their remuscularization capacity after human cardiac muscle patch transplantation in infarcted mouse hearts. Herein, we sought to identify the effect of magnesium lithospermate B (MLB) on hiPSC-CMs during myocardial repair using a myocardial infarction (MI) mouse model.Methods::In C57BL/6 mice, MI was surgically induced by ligating the left anterior descending coronary artery. The mice were randomly divided into five groups ( n = 10 per group); a MI group (treated with phosphate-buffered saline only), a hiPSC-CMs group, a MLB group, a hiPSC-CMs + MLB group, and a Sham operation group. Cardiac function and MLB therapeutic efficacy were evaluated by echocardiography and histochemical staining 4 weeks after surgery. To identify the associated mechanism, nuclear factor (NF)-κB p65 and intercellular cell adhesion molecule-1 (ICAM1) signals, cell adhesion ability, generation of reactive oxygen species, and rates of apoptosis were detected in human umbilical vein endothelial cells (HUVECs) and hiPSC-CMs. Results::After 4 weeks of transplantation, the number of cells that engrafted in the hiPSC-CMs + MLB group was about five times higher than those in the hiPSC-CMs group. Additionally, MLB treatment significantly reduced tohoku hospital pediatrics-1 (THP-1) cell adhesion, ICAM1 expression, NF-κB nuclear translocation, reactive oxygen species production, NF-κB p65 phosphorylation, and cell apoptosis in HUVECs cultured under hypoxia. Similarly, treatment with MLB significantly inhibited the apoptosis of hiPSC-CMs via enhancing signal transducer and activator of transcription 3 (STAT3) phosphorylation and B-cell lymphoma-2 (BCL2) expression, promoting STAT3 nuclear translocation, and downregulating BCL2-Associated X, dual specificity phosphatase 2 (DUSP2), and cleaved-caspase-3 expression under hypoxia. Furthermore, MLB significantly suppressed the production of malondialdehyde and lactate dehydrogenase and the reduction in glutathione content induced by hypoxia in both HUVECs and hiPSC-CMs in vitro. Conclusions::MLB significantly enhanced the potential of hiPSC-CMs in repairing injured myocardium by improving endothelial cell function via the NF-κB/ICAM1 pathway and inhibiting hiPSC-CMs apoptosis via the DUSP2/STAT3 pathway.