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Summary form only given, as follows. Since 1990 processing of materials using microwave heating is under development, with only few industrial applications till today in the high temperature range, e.g., with process temperatures T>1000/spl deg/C. Among the most promising technologies sintering of PM-products (cemented carbides, ceramic, metals) and melting of glass using microwaves of 2.45 GHz frequency should be mentioned. The peculiarities for industrial use of microwave materials processing technology are mainly of economical origin but there are also some basic technological problems, which need to be solved in order to promote microwave heating as a widely used materials processing technology.

A number of investigators have tried to facilitate engraftment with limited numbers of available HSPCs by enhancing responsiveness of HSPCs to CXCL12. Recently, granulocyte derived cationic peptide, LL-37, has been suggested as a useful pre-conditioning component to overcome the shortage of available HSPCs. In this study, we first evaluated the character of LL-37 pre-conditioned HSPCs and found that LL-37 pre-conditioning effects are specific only to the clonogenic stem cells which are considered relatively dormant. This raised our concern regarding the fate of LL-37 pre-conditioned cells after transplantation and led us to evaluate their repopulation capacity as HSPCs. Not betraying our expectations, hematopoietic recovery of LL-37 pre-conditioned cells gradually decreased from 4 weeks after transplantation in competitive repopulation experiments. Further, in vitro studies revealed that LL-37 lead HSPCs to be more vulnerable to extracellular stimuli such as extracellular glucose followed by increased calcium influx from extracellular sources, which dampen self-renewal capacity by activating mammalian target of rapamycin and its downstream signaling. These results suggest that a future strategy must focus on maintaining HSPCs in dormant and protecting them from various stimuli during their long journey to the bone marrow niches rather than activating them before transplantation for successful transplantation outcome.

It has been reported that activated granulocytes derived cationic peptide LL-37 positively prime responsiveness of hematopoietic progenitor cells (HPCs) to CXCL12 gradient through an ambiguous pathway. The goal of this study was to elucidate the mechanism of enhanced migration of LL-37 primed HPCs to CXCL12 gradient. We performed in vitro migration assay and found out that LL-37 pretreatment enhanced migration of HPCs to CXCL12 only in the presence of D-glucose, but not in the absence of glucose or in the presence of glucose uptake inhibitor, 2-deoxy-D-glucose (2-DG). This signifies that LL-37 may affect intracellular energy production machinery. So we tested if the priming effect of LL-37 is related to mTOR signaling since mTOR is a central regulator of nutrient sensing and glycolysis promoting glucose uptake and ATP production to match energy demands for cell migration. As we expected, LL-37 induced glucose uptake in mTOR signaling dependent manner. Also, LL-37 induced the activation of nutrient sensing AMPK and its downstream substrates. In line with this, pretreatment of AMPK activator AICAR promoted migration of HSPCs as well. These findings demonstrate that the priming mechanism of LL-37 is closely associated with increasing ATP production and the optimization of glucose uptake and ATP production for HPCs prior to transplantation would be particularly important in HPCs transplantation where the number of cells available for transplantation is usually limited.

Background: Skeletal muscle is the most important tissue contributing to insulin resistance. Several studies have shown that accumulation of intramyocellular lipid is associated with the development of insulin resistance. Thus, proteins involved in lipid transport, storage and metabolism might also be involved in insulin action in skeletal muscle. Adipose differentiation-related protein (ADRP), which is localized at the surface of lipid droplets, is known to be regulated by peroxisome proliferator activated receptor γ (PPARγ). However, it is not known whether ADRP plays a role in regulating glucose uptake and insulin action in skeletal muscle. Methods: ADRP expression in skeletal muscle was measured by RT-PCR and western blot in db/db mice with and without PPARγ agonist. The effect of PPARγ agonist or high lipid concent ration (0.4% intralipos) on ADRP expression was also obtained in cultured human skeletal mu scle cells. Glucose uptake was measured when ADRP was down-regulated with siRNA or when ADRP was overexpressed with adenovirus. Results: ADRP expression increased in the skeletal muscle of db/db mice in comparison with normal controls and tended to increase with the treatment of PPARγ agonist. In cultured human skeletal muscle cells, the treatment of PPARγ agonist or high lipid concentration increased ADRP expression. siADRP treatment decreased both basal and insulin-stimulated glucose uptake whereas ADRP overexpression increased glucose uptake in cultured human skeletal muscle cells. Conclusion: ADRP expression in skeletal muscle is increased by PPARγ agonist or exposure to high lipid concentration. In these conditions, increased ADRP contributed to increase glucose uptake. These results suggest that insulin-sensitizing effects of PPARγ are at least partially achieved by the increase of ADRP expression, and ADRP has a protective effect against intramyoce llular lipid-induced insulin resistance. (Korean Diabetes J 33:206-214, 2009)

Various investigators have attempted to overcome the shortage of available hematopoietic stem/progenitor cells (HSPCs) by facilitating their engraftment after transplantation. Preconditioning of HSPCs with the granulocyte-derived cationic peptide LL-37 has been suggested as a useful strategy to facilitate engraftment of transplanted cells by enhancing their responsiveness to CXCL12. In this study, we evaluated whether LL-37 preconditioning is acceptable for clinical application. We found that the effect of LL-37 preconditioning was specific to clonogenic cells and was mediated specifically by increased calcium influx with the activation of downstream signaling through mammalian target of rapamycin complex 1 (mTORC1). Because hyperactivation of mTORC1 and the disruption of 5′ adenosine monophosphate-activated protein kinase (AMPK) are known to deplete HSPC pools, we compared the repopulation capacity of HSPCs preconditioned with LL-37 and those preconditioned with AMPK activator (AICAR). In vivo competitive repopulation experiments revealed that LL-37 preconditioning impairs long-term repopulation of transplanted HSPCs, suggesting that this strategy might not acceptable for clinical applications in which long-term repopulation capacity is a prerequisite. AICAR preconditioning dramatically enhanced the long-term repopulation of transplanted HSPCs, however. Taken together, these results suggest that future strategies to ensure successful transplantation outcomes should focus on protecting HSPCs from various stimuli during their homing to the bone marrow niches rather than activating them before transplantation.