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Notes: We use single nanoparticle luminescence microscopy to determine a distribution of individual chromophores present in porous Si nanoparticles. From these distributions, we determine the average number of emitting chromophores in each nanoparticle and the fluorescence emission count rate of a single chromophore within the porous silicon nanoparticle. We also show that the same size nanoparticles prepared under two different electrochemical conditions have different fluorescence peak maxima, and exhibit different chromophore number distributions, consistent with the quantum confinement model for the luminescence in porous silicon. © 2001 American Institute of Physics.

Notes: Spatial hole burning near-field scanning optical microscopy (SHB–NSOM) is used to locally photopattern three species of organic thin films, poly(2-methoxy, 5-(2′-ethyl hexyloxy)–p-phenylene vinylene) (MEH–PPV), tris-8-hydroxyquinoline aluminum (Alq3) and dye-functionalized polyelectrolyte self-assembled layers, on a 100 nm length scale. In SHB–NSOM the film is illuminated with light from a stationary NSOM tip to induce photo-oxidation. The reduction in the fluorescence yield resulting from this exposure is then mapped using fluorescence NSOM (FL–NSOM). We have examined the localized photo-oxidation as a function of time, position, and environment free from the limits of far-field spatial averaging. In all of the thin film materials studied we find that the long-time diameter of the dark spot is much larger than the tip diameter and is a signature of energy migration. Characteristic lengths of the energy migration are extracted from this data by a simple diffusion model and are found to be of the order of a few hundred nanometers for each of the films studied. © 2000 American Institute of Physics.

Notes: [Auszug] Maxwell's equations successfully describe the statistical properties of fluorescence from an ensemble of atoms or semiconductors in one or more dimensions. But quantization of the radiation field is required to explain the correlations of light generated by a single two-level quantum ...

Notes: Experimentally induced wounds in animal models are useful in gaining a better understanding of the cellular and molecular processes of wound healing and in the initial evaluation of the safety and effectiveness of potential therapeutic agents. However, studying delayed healing has proven difficult in animals, whose wounds heal within a few days. In this report, we describe a novel method for establishing mouse wounds that require up to more than three weeks for complete closure, and we show the validity of this model in Smad3 null mice, which are known to display accelerated healing. Full-thickness wounds, measuring 0.3 by 1.0 cm, were made down to fascia on the dorsal aspect of the mouse tail in Smad3 KO mice and control littermates, approximately 1 cm distal to the body of the animal. The wounds were left to heal by secondary intention and were assessed histologically by computerized planimetry for wound closure at various times after wounding. These wounds in wild-type mice displayed delayed healing, with full closure occurring between 14 and 25 days after wounding. Complete closure of similar wounds in Smad3 null mice healed 30% faster (p 〈 0.01). By immunostaining with ki67, a marker for proliferation, Smad3 null animals also showed increased proliferation of dermal wound cells. Cultured dermal fibroblasts from Smad3 null mice showed increased baseline DNA synthesis and, interestingly, enhanced response to TGF-β1. By Western blot analysis, Smad3 null mice fibroblasts showed a compensatory increase in MAPK phosphorylation in response to TGF-β1, suggesting that MAPK overcompensation together with loss of Smad3 may be involved in the modulation of faster healing. We conclude that this novel tail wounding model can be useful for studying delayed or prolonged wound closure.Experimentally induced wounds in animal models can be useful in gaining a better understanding of the cellular and molecular processes of wound healing. Such models have also proven themselves valuable in the initial evaluation of the safety and effectiveness of potential therapeutic agents targeted for chronic non-healing wounds. (Gottrup, Agren et al. 2000). However, no ideal animal model exists which reliably reproduces delayed healing. In the mouse, a mammal whose genome has been completely cloned and which is easily manipulated genetically, wounds normally heal within a few days, and with a great deal of contraction. (Morris, Wu et al. 1997; Gottrup, Agren et al. 2000) There are models utilizing either genetically altered and inbred mice with certain characteristics that cause delayed healing. (Carmeliet 1995) However, it would be useful to have wound healing models that are applicable to most wild type mice used as controls and which would have a large enough window of observation before healing occurs. In this report, we describe a novel method for studying delayed healing in mice. This method utilizes full-thickness wounds made down to fascia on the dorsal and mostly hairless aspect of the mouse tail. The wounds are left to heal by secondary intention and assessed histologically by computerized planimetry for wound closure at various times after wounding. In this first report, the validity of the model was determined by studying control littermates and Smad3 null mice, which have been shown to display accelerated healing. The results shown here suggest that this is a useful model for studying delayed healing in mice.

Notes: There are only a few models for studying epidermal migration in vitro, and their interpretation is made difficult by reliance on cell monolayers and the choice of a specific substrate. In this study, the process of keratinocyte migration and epiboly were investigated by using a bilayered bioengineered skin construct, consisting of human neonatal foreskin keratinocytes and dermal fibroblasts (Apligraf, Organogenesis, Canton, MA). At baseline, 6-mm punch biopsies of the construct were placed in serum-free media (AIM-V) or DMEM with or without 10% FBS. At varying time points the bioengineered skin samples were processed and analyzed by histology and immunostaining. By 72 hours, in a time-dependent manner, the epidermis had migrated over and enveloped the entire dermis (full epiboly). Full epiboly was partially inhibited by serum and was maximal in serum-free medium. Epiboly was preserved 5 days after stated expiration date and was equivalent to that seen in unexpired construct when stored at room temperature. The process of epiboly was downregulated in a dose-dependent manner by neutralizing antibodies to EGF and TGF-beta 1. The migrating epithelium was characterized by decreased keratinocyte proliferation (as per Ki67 immunostaining) and increased expression of vitronectin (epibolin). Increasing concentrations of antibodies of vitronectin blocked the process of epiboly, as did antibodies to the alpha5-betaV integrin receptor, which mediates vitronectin-driven keratinocyte locomotion. Interesting, epiboly was also blocked by preseeding human dermal fibroblasts on the dermal side of the construct. We propose that the process of epiboly in this model can be used to better understand and assess the mechanisms involved in keratinocyte migration and may be used as an assay for establishing construct functional viability.