RESUMO
Single-layer tungsten disulfide (WS2) is among the most widely investigated two-dimensional materials. Synthesizing it over large areas would enable the exploitation of its appealing optical and electronic properties in industrial applications. However, defects of different nature, concentration and distribution profoundly affect the optical as well as the electronic properties of this crystal. Controlling the defect density distribution can be an effective way to tailor the local dielectric environment and therefore the electronic properties of the system. In this work we investigate the defects in single-layer WS2, grown in different shapes by liquid phase chemical vapor deposition, where the concentration of certain defect species can be controlled by the growth conditions. The properties of the material are surveyed by means of optical spectroscopy, photoelectron spectroscopy and Kelvin probe force microscopy. We determine the chemical nature of the defects and study their influence on the optical and electronic properties of WS2. This work contributes to the understanding of the microscopic nature of the intrinsic defects in WS2, helping the development of defect-based technologies which rely on the control and engineering of defects in dielectric 2D crystals.
Assuntos
Fêmur , Úlcera da Perna/diagnóstico , Úlcera da Perna/etiologia , Lúpus Vulgar/diagnóstico , Cicatrização , Adulto , Biópsia , Doença Crônica , Diagnóstico Diferencial , Progressão da Doença , Feminino , Seguimentos , Humanos , Úlcera da Perna/patologia , Lúpus Vulgar/patologia , Gravidez , Complicações Infecciosas na Gravidez/diagnóstico , Pele/patologia , Tuberculose Pleural/diagnósticoRESUMO
Graphene was shown to reveal intriguing properties of its relativistic two-dimensional electron gas; however, its implementation to microelectronic applications is missing to date. In this work, we present a comprehensive study of epitaxial graphene on technologically relevant and in a standard CMOS process achievable Ge(100) epilayers grown on Si(100) substrates. Crystalline graphene monolayer structures were grown by means of chemical vapor deposition (CVD). Using angle-resolved photoemission spectroscopy and in situ surface transport measurements, we demonstrate their metallic character both in momentum and real space. Despite numerous crystalline imperfections, e.g., grain boundaries and strong corrugation, as compared to epitaxial graphene on SiC(0001), charge carrier mobilities of 1 × 104 cm2/Vs were obtained at room temperature, which is a result of the quasi-charge neutrality within the graphene monolayers on germanium and not dependent on the presence of an interface oxide. The interface roughness due to the facet structure of the Ge(100) epilayer, formed during the CVD growth of graphene, can be reduced via subsequent in situ annealing up to 850 °C coming along with an increase in the mobility by 30%. The formation of a Ge(100)-(2 × 1) structure demonstrates the weak interaction and effective delamination of graphene from the Ge/Si(100) substrate.
RESUMO
Loss of the coxsackie and adenovirus receptor (CAR) has been found in various human cancers. Underlying mechanisms, however, are still poorly understood. Therefore, the objective of this study was to investigate the function of hypoxia, a ubiquitous phenomenon in carcinomas, in CAR regulation. In our approach, hypoxia and treatment with cobalt-(II)-chloride (CoCl(2)) induced a downregulation of CAR protein and mRNA expression, as well as a suppression of CAR gene promoter activity in AGS (gastric), SW480 (colon) and PC3 (prostate) cancer cells. In line with these findings we noted a decreased adenoviral uptake under hypoxic conditions. Aiming to further elucidate the molecular basis of this observation, a full-length hypoxia-inducible factor-1alpha (HIF-1alpha) cDNA was ectopically overexpressed in the AGS cell line diminishing CAR expression and CAR gene promoter activity. In line with these findings, exposure of HIF-1alpha-deficient AGS cells to hypoxia did not alter CAR mRNA expression level. On the basis of these data, it may be suggested that loss of CAR in human cancer cell lines under hypoxic conditions occurs in an HIF-1alpha-dependent manner.
Assuntos
Hipóxia Celular/fisiologia , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Receptores Virais/metabolismo , Animais , Antimutagênicos/farmacologia , Western Blotting , Células CHO , Linhagem Celular Tumoral , Cobalto/farmacologia , Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus , Cricetinae , Cricetulus , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Regiões Promotoras Genéticas/genética , Receptores Virais/genéticaRESUMO
Cell surface presence of the coxsackie and adenovirus receptor (CAR) is considered a crucial prerequisite for the uptake of attenuated adenovirus. In cancers, however, a frequent loss of CAR has been noted potentially hampering the success of adenovirus-based therapy. In esophageal Barrett's carcinomas and its precursor lesions CAR presence has not been systematically determined yet. Immunohistochemical assessment in tissue specimens of 111 patients revealed CAR-positivity in all cases of Barrett's esophagus, including various degrees of intraepithelial neoplasia. In contrast, no considerable CAR presence was seen in squamous esophageal epithelium. Among Barrett's carcinomas, 93% displayed CAR presence, whereas CAR-negativity was observed preferentially in advanced cancers. Aiming to evaluate whether this loss of CAR impacts tumor-biologic properties of esophageal adenocarcinomas we studied cell lines OE19 and OE33 and observed an increased proliferation, migration and invasion upon siRNA-mediated functional CAR knock down. In conclusion, our results indicate that CAR may provide a valuable target for adenovirus-based therapy of Barrett's carcinomas and its precursor lesions. These data do also suggest that CAR does not contribute substantially to carcinogenesis in Barrett's esophagus, however, it may be speculated that loss of CAR promotes tumor progression in advanced stages of Barrett's carcinomas.