Correlation between the results of charge deep-level transient spectroscopy and ESR techniques for undoped hydrogenated amorphous silicon

金沢大学大学院自然科学研究科電子物性デバイス金沢大学工学部Results of charge deep-level transient spectroscopy (DLTS) and electron spin resonance (ESR) measurements on undoped hydrogenated amorphous silicon (a-Si:H) clearly demonstrate that a group of gap states with a mean energy of 0.82 eV as observed in charge DLTS experiments for a-Si:H based metal/oxide/semiconductor structure is the same as the g=2.0055 ESR defect (the Dz component). This correlation provides a distinct marker for charge DLTS technique. We obtained a very good fit to spectra obtained on undoped a-Si:H in the annealed state whilst there is some discrepancy between the experimental and simulated spectra for the light-soaked state. The first quantitative comparison of defect pool model with gap states directly observed by charge DLTS offers not only additional data for more accurate identification of all the intrinsic and light-induced defects. This also renders distinct counter-evidence to recently published conjectures about the creation of another charged defect during early stage of Staebler-Wronski effect. By contrast, our presented results clearly argue for opposite process, i.e., decay of positively charged defect states Dh

Syndecan-1 and FGF-2, but Not FGF Receptor-1, Share a Common Transport Route and Co-Localize with Heparanase in the Nuclei of Mesenchymal Tumor Cells

Syndecan-1 forms complexes with growth factors and their cognate receptors in the cell membrane. We have previously reported a tubulin-mediated translocation of syndecan-1 to the nucleus. The transport route and functional significance of nuclear syndecan-1 is still incompletely understood. Here we investigate the sub-cellular distribution of syndecan-1, FGF-2, FGFR-1 and heparanase in malignant mesenchymal tumor cells, and explore the possibility of their coordinated translocation to the nucleus. To elucidate a structural requirement for this nuclear transport, we have transfected cells with a syndecan-1/EGFP construct or with a short truncated version containing only the tubulin binding RMKKK sequence. The sub-cellular distribution of the EGFP fusion proteins was monitored by fluorescence microscopy. Our data indicate that syndecan-1, FGF-2 and heparanase co-localize in the nucleus, whereas FGFR-1 is enriched mainly in the perinuclear area. Overexpression of syndecan-1 results in increased nuclear accumulation of FGF-2, demonstrating the functional importance of syndecan-1 for this nuclear transport. Interestingly, exogenously added FGF-2 does not follow the route taken by endogenous FGF-2. Furthermore, we prove that the RMKKK sequence of syndecan-1 is necessary and sufficient for nuclear translocation, acting as a nuclear localization signal, and the Arginine residue is vital for this localization. We conclude that syndecan-1 and FGF-2, but not FGFR-1 share a common transport route and co-localize with heparanase in the nucleus, and this transport is mediated by the RMKKK motif in syndecan-1. Our study opens a new perspective in the proteoglycan field and provides more evidence of nuclear interactions of syndecan-1

Specific Syndecan-1 Domains Regulate Mesenchymal Tumor Cell Adhesion, Motility and Migration

Malignant mesothelioma is an asbestos induced cancer that is difficult to diagnose. Several studies have combined biomarkers to improve mesothelioma diagnosis, but with moderate success, and there is a need for new mesothelioma biomarkers. The tumour is often resistant to treatment and most patients will survive less than a year. An indicator of patient survival is the tumours growth pattern, which in turn is influenced by expressed proteoglycans. In this thesis work, we aim to improve the possibilities to diagnose malignant mesothelioma by combining biomarkers and by identifying new ones. We also investigate tumour driving mechanisms with focus on one of these suggested biomarkers, the cell-bound proteoglycan syndecan-1. We were able to construct a diagnostic two-step model based on biomarkers in patient material. By implementing a cut-off level and thereafter focusing on unresolved patients we combined hyaluronan and N-ERC/mesothelin (paper I), which significantly increased the diagnostic accuracy for malignant mesothelioma. To further improve diagnosis, we used mass spectrometry to find new biomarkers. We identified and validated galectin-1, which was excellent in discriminating mesotheliomas from adenocarcinomas (paper II). In the same study, we were also the first to describe aldo-keto reductase 1B10 as a novel prognostic mesothelioma biomarker. Syndecan-1 has been indicated as a marker for carcinomas. In paper I we describe how higher levels of syndecan-1 indicate the presence of a carcinoma over a mesothelioma. This was verified in paper II when syndecan-1 was identified as downregulated in fluids from mesothelioma patients compared to lung cancer patients. Paper III and paper IV focus on this proteoglycan. Malignant cell lines transfected with syndecan-1 and various truncated forms of syndecan-1 affected adhesion and migration, which are key features of cancer invasion (paper III). The results showed a domain- and cell type specific effect on the cells’ motility. Regulating syndecan-1 levels and analysing the global gene expression of mesothelioma cells made it evident that this proteoglycan has a strong influence on transforming growth factor β signalling and several growth factor pathways (paper IV). Links to cell migration and proliferation were furthermore identified, along with glycosaminoglycan modifying enzymes. These results can shed light on the complex role of syndecan-1 in invasion and growth of malignant mesenchymal cells. Taken together, this thesis work describes a complement to conventional mesothelioma diagnosis and identifies novel biomarkers. Furthermore, the potential biomarker syndecan-1 was shown to have an effect on cell motility and proliferation. These results increase our understanding of this aggressive malignancy

Experimental study of passivating ion-beam-induced distributed energy levels in n-GaAs by hydrogen species from boiling water

Moderately doped n-GaAs substrates were etched by a 250 eV Ar+-ion beam and subsequently immersed up to 80 min in boiling distilled water, to remove the radiation damage. Comparative studies of the remaining damage to the GaAs surface region, benefiting from both alternating current (capacitance DLTS, high-frequency C-V) and time-domain (charge DLTS, feedback-charge C-V) techniques, were conducted. Prior to the passivation in water, there was a spectrum of deep levels distributed in energy, responsible for a large capacitance dispersion in Al GaAs Schottky junctions at ambient temperatures. Apart from significant differences between the responses to pulsed excitation in the frequency and time domains, the damage due to the ion beam is effectively reduced by hydrogenation. In contrast to the case of a discrete energy level, efficiency of passivating distributed levels is difficult to assess as a scalar quantity. Long-term stability of the deep-level neutralization over a period of 16 months has been confirmed. © 1995