The present study is to enhance the critical heat flux (CHF) in pool boiling from a flat square heater immersed in nanofluid (water mixed with extremely small amount of nanosized particles). The test results show that the enhancement of CHF was drastic when nanofluid is used as a cooling liquid instead of pure water. The experiment was performed to measure and compare pool boiling curves of pure water and nanofluid at the pressure of 2.89 psia (Tsat=60 °C) using 1×1 cm2 polished copper surfaces as a boiling surface. The tested nanofluid contains alumina (Al2O3) nanoparticles dispersed in distilled and deionized water. Tested concentrations of nanoparticles range from 0 g/l to 0.05 g/l. The measured pool boiling curves of nanofluids saturated at 60 °C have demonstrated that the CHF increases dramatically (∼200% increase) compared to pure water case; however, the nucleate boiling heat transfer coefficients appear to be about the same.

Recent evidence shows that amniotic fluid (AF) contains multiple cell types derived from the developing fetus, and may represent a novel source of stem cells for cell therapy. In this study, we examined the paracrine factors released by human amniotic fluid-derived mesenchymal stem cells (AF-MSCs) and their ability to accelerate the wound-healing process by stimulating proliferation and migration of dermal fibroblasts. AF-MSCs expressed the typical MSC marker proteins CD13, CD29, and CD44 and differentiated into adipocytes, osteoblasts, and chondrocytes when exposed to the appropriate differentiation media. In addition, AF-MSC-conditioned media (AF-MSC-CM) significantly enhanced proliferation of dermal fibroblasts. Antibody-based protein array and enzyme-linked immunosorbent assay (ELISA) indicated that AF-MSC-CM contains various cytokines and chemokines that are known to be important in normal wound healing, including IL-8, IL-6, TGF-beta, TNFRI, VEGF, and EGF. Application of AF-MSC-CM significantly enhanced wound healing by dermal fibroblasts via the TGF-beta/SMAD2 pathway. Levels of p-SMAD2 were increased by AF-MSC-CM, and both the increase in p-SMAD2 and migration of dermal fibroblasts were blocked by inhibiting the TGF-beta/SMAD2 pathway. Moreover, in a mouse excisional wound model, AF-MSC-CM accelerated wound healing. These data provide the first evidence of the potential for AF-MSC-CM in the treatment of skin wounds.

In a previous study, we isolated human amniotic fluid (AF)-derived mesenchymal stem cells (AF-MSCs) and utilized normoxic conditioned medium (AF-MSC-norCM) which has been shown to accelerate cutaneous wound healing. Because hypoxia enhances the wound healing function of mesenchymal stem cell-conditioned medium (MSC-CM), it is interesting to explore the mechanism responsible for the enhancement of wound healing function. In this work, hypoxia not only increased the proliferation of AF-MSCs but also maintained their constitutive characteristics (surface marker expression and differentiation potentials). Notably, more paracrine factors, VEGF and TGF-β1, were secreted into hypoxic conditioned medium from AF-MSCs (AF-MSC-hypoCM) compared to AF-MSC-norCM. Moreover, AF-MSC-hypoCM enhanced the proliferation and migration of human dermal fibroblasts in vitro, and wound closure in a skin injury model, as compared to AF-MSC-norCM. However, the enhancement of migration of fibroblasts accelerated by AF-MSC-hypoCM was inhibited by SB505124 and LY294002, inhibitors of TGF-β/SMAD2 and PI3K/AKT, suggesting that AF-MSC-hypoCM-enhanced wound healing is mediated by the activation of TGF-β/SMAD2 and PI3K/AKT. Therefore, AF-MSC-hypoCM enhances wound healing through the increase of hypoxia-induced paracrine factors via activation of TGF-β/SMAD2 and PI3K/AKT pathways.

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