ABSTRACT
The original version of this Article contained an error in Equation 1. A factor of 'c' was included in the right-hand term. This has been corrected in the PDF and HTML versions of the Article.
ABSTRACT
Fermi level control by doping is established since decades in inorganic semiconductors and has been successfully introduced in organic semiconductors. Despite its commercial success in the multi-billion OLED display business, molecular doping is little understood, with its elementary steps controversially discussed and mostly-empirical-materials design. Particularly puzzling is the efficient carrier release, despite a presumably large Coulomb barrier. Here we quantitatively investigate doping as a two-step process, involving single-electron transfer from donor to acceptor molecules and subsequent dissociation of the ground-state integer-charge transfer complex (ICTC). We show that carrier release by ICTC dissociation has an activation energy of only a few tens of meV, despite a Coulomb binding of several 100 meV. We resolve this discrepancy by taking energetic disorder into account. The overall doping process is explained by an extended semiconductor model in which occupation of ICTCs causes the classically known reserve regime at device-relevant doping concentrations.
ABSTRACT
Scarring is an extensive problem in burn care, and treatment can be especially complicated in cases of hypertrophic scarring. Contraction is an important factor in scarring but the contribution of different cell types remains unclear. We have investigated the contractile behavior of keratinocytes, melanocytes and fibroblasts by using an in vitro collagen gel assay aimed at identifying a modulating role of melanocytes in keratinocyte-mediated contraction. Cells were seeded on a collagen type I gel substrate and the change in gel dimensions were measured over time. Hematoxylin & Eosin-staining and immunohistochemistry against pan-cytokeratin and microphthalmia-associated transcription factor showed that melanocytes integrated between keratinocytes and remained there throughout the experiments. Keratinocyte- and fibroblast-seeded gels contracted significantly over time, whereas melanocyte-seeded gels did not. Co-culture assays showed that melanocytes mitigate the keratinocyte-dependent contraction (significantly slower and 18-32% less). Fibroblasts augmented the contraction in most assays (approximately 6% more). Non-contact co-cultures showed some influence on the keratinocyte-dependent contraction. Results show that mechanisms attributable to melanocytes, but not fibroblasts, can mitigate keratinocyte contractile behavior. Contact-dependent mechanisms are stronger modulators than non-contact dependent mechanisms, but both modes carry significance to the contraction modulation of keratinocytes. Further investigations are required to determine the mechanisms involved and to determine the utility of melanocytes beyond hypopigmentation in improved clinical regimes of burn wounds and wound healing.
