These data suggest that hMSCs together with bFGF in a skin defect model accelerate cutaneous wound healing as the hMSCs transdifferentiate into the epithelium.

These results demonstrated that the administration of B. breve to preterm infants can up-regulate TGF-beta1 signaling and may possibly be beneficial in attenuating inflammatory and allergic reactions in these infants.

Organic electroluminescent (EL) cells with azomethin-zinc complexes as an emitting layer showed bright blue emission. A cell structure of [indium-tin-oxide (ITO)/hole transport layer/emitting layer/MgIn] was employed. The color was blue, and emission peaks were 458∼470 nm. High luminance exceeding 1000 cd/m2 was obtained for the first time with an EL cell using a complex emitting material. The azomethin-zinc complexes exhibited good electron transport, as indicated by the high luminance obtained in two-layer EL cells.

Keloid is a dermal fibroproliferative tissue of unknown etiology. Protein tyrosine kinases (PTKs) play an important role in the regulation of cell growth and differentiation. Activation of PTK cascades in keloid fibroblasts is thought to be closely linked to abnormal cell proliferation and migration. We determined the expression profile of PTK genes in normal skin and keloid fibroblasts using the homology cloning method with a degenerated primer. Eight PTK genes were expressed among a total of 46 receptor-type clones. The most abundant type of PTK receptors was the platelet-derived growth factor receptor in both fibroblasts. However, insulin-like growth factor-I receptor (IGF-IR) was overexpressed only in keloid-derived fibroblasts (9 of 24). Immunohistochemical analysis confirmed the high expression of IGF-IR in keloid fibroblasts, but not in normal fibroblasts. To examine the functional properties of the IGF-I/IGF-IR pathway, we investigated cell proliferation and invasion activities of both types of fibroblasts. The mitogenic effect of IGF-I on both fibroblasts was very weak compared with serum stimulation. In contrast, the invasive activity of keloid fibroblasts was markedly increased in the presence of IGF-I, and inhibited by a neutralizing antibody against IGF-IR. Our results indicate the involvement of activated IGF-I/IGF-IR in the pathogenesis of keloid by enhancing the invasive activity of fibroblasts.

Organic electroluminescent (EL) devices with 8-hydroxy-quinoline derivative-metal complexes (Znq2, Beq2, Mgq2, ZnMq2, BeMq2 and AlPrq3) as the emitter have been developed. The emissions of these devices are green or yellow. These devices have a luminance of more than 3000 cd/m2. In particular, the EL device with Znq2 has a luminance of 16200 cd/m2.

No abstract

A volatile Eu complex, Eu(TTA)3(phen) (TTA=thenoyltrifluoroacetone, phen=1,10-phenanthroline), was synthesized and applied to an electroluminescent (EL) cell structure of [ITO(=indium-tin-oxide)/hole transporting layer/emitting layer (host material=azomethin zinc complex, and dopant= Eu(TTA)3(phen))/MgIn]. The emitting layers were formed by a codeposition technique. A red emission (EL peak wavelength 614 nm) with a very sharp spectral band was observed from the EL cell with 5 wt% Eu(TTA)3(phen), and a maximum luminance of 137 cd/m2 was achieved.

Keloids are benign dermal tumors, characterized by overgrowth of lesions, invasiveness beyond the original boundary of the insult, and recurrence of lesions. The exact etiology is unknown, however. Our hypothesis is that keloids are acquired as a result of an abnormal or prolonged wound healing process, with persistent proliferation and extracellular matrix production of fibroblasts that should otherwise discontinue in normal wound healing. In this study, we examined the response of keloid fibroblasts to proapoptotic signaling. Cell-permeable ceramide, N-acetyl-D-sphingosine, induced apoptosis of dermal fibroblasts in a dose- and time-dependent manner, which was detected by phase contrast microscopy, fluorescent microscopy, the TUNEL method, flow cytometric analysis, and WST-1 assay. In contrast, keloid fibroblasts resisted apoptosis induced by N-acetyl-D-sphingosine (percent survival with 40 mM ceramide treatment for 12 h, normal versus keloid: 9.6% +/- 6.6% vs 66.8% +/- 5.5%). Western blotting analysis showed insulin-like growth factor I receptor overexpression in keloid fibroblasts, but not in normal fibroblasts. Exogenously added insulin-like growth factor I enhanced the resistance of keloid fibroblasts to ceramide-induced apoptosis. Wort- mannin, a phosphatidylinositol 3 kinase inhibitor, suppressed the antiapoptotic action of insulin-like growth factor I in keloid fibroblasts. Our results suggest that keloid fibroblasts overexpressing insulin-like growth factor I receptor are resistant to apoptosis, thus allowing persistent proliferation and production of excessive extracellular matrix. J Invest Dermatol 115:1065-1071 2000