Engineering the semiconductor/oxide interaction for stacking twin suppression in single crystalline epitaxial silicon(111)/insulator/Si(111) heterostructures

The integration of alternative semiconductor layers on the Si material platform via oxide heterostructures is of interest to increase the performance and/or functionality of future Si-based integrated circuits. The single crystalline quality of epitaxial (epi) semiconductor-insulator-Si heterostructures is however limited by too high defect densities, mainly due to a lack of knowledge about the fundamental physics of the heteroepitaxy mechanisms at work. To shed light on the physics of stacking twin formation as one of the major defect mechanisms in (111)-oriented fcc-related heterostructures on Si(111), we report a detailed experimental and theoretical study on the structure and defect properties of epi-Si(111)/Y2O 3/Pr2O3/Si(111) heterostructures. Synchrotron radiation-grazing incidence x-ray diffraction (SR-GIXRD) proves that the engineered Y2O3/Pr2O3 buffer dielectric heterostructure on Si(111) allows control of the stacking sequence of the overgrowing single crystalline epi-Si(111) layers. The epitaxy relationship of the epi-Si(111)/insulator/Si(111) heterostructure is characterized by a type A/B/A stacking configuration. Theoretical ab initio calculations show that this stacking sequence control of the heterostructure is mainly achieved by electrostatic interaction effects across the ionic oxide/covalent Si interface (IF). Transmission electron microscopy (TEM) studies detect only a small population of misaligned type B epi-Si(111) stacking twins whose location is limited to the oxide/epiSi IF region. Engineering the oxide/semiconductor IF physics by using tailored oxide systems opens thus a promising approach to grow heterostructures with well-controlled properties. © IOP Publishing Ltd and Deutsche Physikalische Gesellschaft

Gene and protein expression of glucose transporter 1 and glucose transporter 3 in human laryngeal cancer—the relationship with regulatory hypoxia-inducible factor-1α expression, tumor invasiveness, and patient prognosis

Increased glucose uptake mediated by glucose transporters and reliance on glycolysis are common features of malignant cells. Hypoxia-inducible factor-1α supports the adaptation of hypoxic cells by inducing genes related to glucose metabolism. The contribution of glucose transporter (GLUT) and hypoxia-inducible factor-1α (HIF-1α) activity to tumor behavior and their prognostic value in head and neck cancers remains unclear. The aim of this study was to examine the predictive value of GLUT1, GLUT3, and HIF-1α messenger RNA (mRNA)/protein expression as markers of tumor aggressiveness and prognosis in laryngeal cancer. The level of hypoxia/metabolic marker genes was determined in 106 squamous cell laryngeal cancer (SCC) and 73 noncancerous matched mucosa (NCM) controls using quantitative realtime PCR. The related protein levels were analyzed by Western blot. Positive expression of SLC2A1, SLC2A3, and HIF-1α genes was noted in 83.9, 82.1, and 71.7 % of SCC specimens and in 34.4, 59.4, and 62.5 % of laryngeal cancer samples. Higher levels of mRNA/protein for GLUT1 and HIF-1α were noted in SCC compared to NCM (p<0.05). SLC2A1 was found to have a positive relationship with grade, tumor front grading (TFG) score, and depth and mode of invasion (p<0.05). SLC2A3 was related to grade and invasion type (p<0.05). There were also relationships of HIF-1α with pTNM, TFG scale, invasion depth and mode, tumor recurrences, and overall survival (p<0.05). In addition, more advanced tumors were found to be more likely to demonstrate positive expression of these proteins. In conclusion, the hypoxia/metabolic markers studied could be used as molecular markers of tumor invasiveness in laryngeal cancer.This work was supported, in part, by the statutory fund of the Department of Cytobiochemistry, University of Łódź, Poland (506/811), and by grant fromtheNational Science Council, Poland (N403 043 32/2326)

Differential expression of the brassinosteroid receptor-encoding BRI1 gene in Arabidopsis

Abstract Brassinosteroid (BR)-regulated growth and development in Arabidopsis depends on BRASSINOSTEROID INSENSITIVE 1 (BRI1), the BR receptor that is responsible for initiating the events of BR signalling. We analysed the temporal and spatial regulation of BRI1 expression using stable transgenic lines that carried BRI1 promoter:reporter fusions. In both seedlings and mature plants the tissues undergoing elongation or differentiation showed elevated BRI1 gene activity, and it could be demonstrated that in the hypocotyl this was accompanied by accumulation of the BRI1 transcript and its receptor protein product. In seedlings the BRI1 promoter was also found to be under diurnal regulation, determined primarily by light repression and a superimposed circadian control. To determine the functional importance of transcriptional regulation we complemented the severely BR insensitive bri1-101 mutant with a BRI1-luciferase fusion construct that was driven by promoters with contrasting specificities. Whereas the BRI1 promoter-driven transgene fully restored the wild phenotype, expression from the photosynthesisassociated CAB3 and the vasculature-specific SUC2 and ATHB8 promoters resulted in plants with varying morphogenic defects. Our results reveal complex differential regulation of BRI1 expression, and suggest that by influencing the distribution and abundance of the receptor this regulation can enhance or attenuate BR signalling

The evolving place of incretin-based therapies in type 2 diabetes

Treatment options for type 2 diabetes based on the action of the incretin hormone glucagon-like peptide-1 (GLP-1) were first introduced in 2005. These comprise the injectable GLP-1 receptor agonists solely acting on the GLP-1 receptor on the one hand and orally active dipeptidyl-peptidase inhibitors (DPP-4 inhibitors) raising endogenous GLP-1 and other hormone levels by inhibiting the degrading enzyme DPP-4. In adult medicine, both treatment options are attractive and more commonly used because of their action and safety profile. The incretin-based therapies stimulate insulin secretion and inhibit glucagon secretion in a glucose-dependent manner and carry no intrinsic risk of hypoglycaemia. GLP-1 receptor agonists allow weight loss, whereas DPP-4 inhibitors are weight neutral. This review gives an overview of the mechanism of action and the substances and clinical data available