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There is increasing evidence showing that adult stem cells are useful for tissue regeneration. Bone marrow mesenchymal stem cells (MSCs) are self-renewing and are potent in differentiating into multiple cells and tissues. To investigate the practicability of repairing burn wounds with tissue-engineered (TE) skin combined with bone MSCs, we established a burn wound model in the porcine skin. With a controlling temperature and time of the burning device to obtain different degrees of burn wounds, a deep dermal partial thickness burn was introduced to the porcine skin using a heated-brass contact injury at 100 degrees C for 20 s. Collagen-GAG scaffolds were utilized as the matrix; MSCs separated from pigs were seeded on them to form the skin equivalent. When grafted to the burn wounds, the TE skin containing MSCs showed better healing and keratinization, less wound contraction, and more vascularization. Grafts proliferated well and contributed to the neo-tissues. These data suggest that TE skin containing MSCs in a burn defect can accelerate wound healing and receive satisfactory effects.

Pancreatic cancer is the fourth leading cause of cancer related deaths in the United States. The prognosis remains dismal with little advance in treatment. Metformin is a drug widely used for the treatment of type II diabetes. Recent epidemiologic data revealed that oral administration of metformin is associated with a reduced risk of pancreatic cancer, suggesting its potential as a novel drug for this disease. Many studies have demonstrated the in vitro anticancer action of metformin, but the typically used concentrations were much higher than the in vivo plasma and tissue concentrations achieved with recommended therapeutic doses of metformin, and low concentrations of metformin had little effect on the proliferation of pancreatic cancer cells. We examined the effect of low concentrations of metformin on different subpopulations of pancreatic cancer cells and found that these selectively inhibited the proliferation of CD133+ but not CD24+CD44+ESA+ cells. We also examined the effect of low concentrations of metformin on cell invasion and in vivo tumor formation, demonstrating in vitro and in vivo anticancer action. Metformin was associated with a reduction of phospho-Erk and phospho-mTOR independent of Akt and AMPK phosphorylation. CD133+ pancreatic cancer cells are considered to be cancer stem cells that contribute to recurrence, metastasis and resistance to adjuvant therapies in pancreatic cancer. Our results provide a basis for combination of metformin with current therapies to improve the prognosis of this disease.

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