ABSTRACT
The aim of this work was a deep spectroscopical characterization of a thick 4H SiC epitaxial layer and a comparison of results between samples before and after a thermal oxidation process carried out at 1400 °C for 48 h. Through Raman and photoluminescence (PL) spectroscopies, the carrier lifetimes and the general status of the epilayer were evaluated. Time-resolved photoluminescence (TRPL) was used to estimate carrier lifetime over the entire 250 µm epilayer using different wavelengths to obtain information from different depths. Furthermore, an analysis of stacking fault defects was conducted through PL and Raman maps to evaluate how these defects could affect the carrier lifetime, in particular after the thermal oxidation process, in comparison with non-oxidated samples. This study shows that the oxidation process allows an improvement in the epitaxial layer performances in terms of carrier lifetime and diffusion length. These results were confirmed using deep level transient spectroscopy (DLTS) measurements evidencing a decrease in the Z1/2 centers, although the oxidation generated other types of defects, ON1 and ON2, which appeared to affect the carrier lifetime less than Z1/2 centers.
ABSTRACT
The purpose of this work is to study the 4H-SiC epitaxial layer properties for the fabrication of a device for neutron detection as an alternative material to diamond detectors used in this field. We have studied a high growth rate process to grow a thick epitaxial layer (250 µm) of 4H-SiC and, in order to estimate the quality of the epitaxial layer, an optical characterization was done through Photoluminescence (PL) spectroscopy for stacking fault defect evaluation. Micro Raman spectroscopy was used for simultaneous determination of both carrier lifetime and induced carriers in equilibrium. We have compared these results with other two samples with an epitaxial layer of 100 micron, obtained with two different growth rates, 60 and 90 µm/h, respectively. From Raman measurements it has been observed that both the growth rate and the grown epitaxial layer thickness have an effect on the measured carrier lifetime. A comparison between different kinds of stacking faults (SF) was done, evaluating the influence of these defects on the carrier lifetime as a function of the injection level and it was observed that only at a low injection is the effect on the carrier lifetime low.
ABSTRACT
The use of wide-band-gap solid-state neutron detectors is expanding in environments where a compact size and high radiation hardness are needed, such as spallation neutron sources and next-generation fusion machines. Silicon carbide is a very promising material for use as a neutron detector in these fields because of its high resistance to radiation, fast response time, stability and good energy resolution. In this paper, measurements were performed with neutrons from the ISIS spallation source with two different silicon carbide detectors together with stability measurements performed in a laboratory under alpha-particle irradiation for one week. Some consideration to the impact of the casing of the detector on the detector's counting rate is given. In addition, the detector response to Deuterium-Deuterium (D-D) fusion neutrons is described by comparing neutron measurements at the Frascati Neutron Generator with a GEANT4 simulation. The good stability measurements and the assessment of the detector response function indicate that such a detector can be used as both a neutron counter and spectrometer for 2-4 MeV neutrons. Furthermore, the absence of polarization effects during neutron and alpha irradiation makes silicon carbide an interesting alternative to diamond detectors for fast neutron detection.
ABSTRACT
Adipose tissue has been recognized as a complex organ with endocrine and metabolic roles. The excess of fat mass, as occurs during overweight and obesity states, alters the regulation of adipose tissue, contributing to the development of obesity-related disorders. In this regard, many epidemiological studies shown an association between obesity and numerous types of malignancies, comprising those linked to the endocrine system (e.g., breast, endometrial, ovarian, thyroid and prostate cancers). Multiple factors may contribute to this phenomenon, such as hyperinsulinemia, dyslipidemia, oxidative stress, inflammation, abnormal adipokines secretion and metabolism. Among adipokines, growing interest has been placed in recent years on adiponectin (APN) and on its role in carcinogenesis. APN is secreted by adipose tissue and exerts both anti-inflammatory and anti-proliferative actions. It has been demonstrated that APN is drastically decreased in obese individuals and that it can play a crucial role in tumor growth. Although literature data on the impact of APN on carcinogenesis are sometimes conflicting, the most accredited hypothesis is that it has a protective action, preventing cancer development and progression. The aim of the present review is to summarize the currently available evidence on the involvement of APN and its signaling in the etiology of cancer, focusing on endocrine malignancies.
Subject(s)
Adiponectin/metabolism , Adipose Tissue/metabolism , Endocrine Gland Neoplasms/etiology , Obesity/complications , Obesity/metabolism , Adiponectin/chemistry , Adiponectin/genetics , Animals , Biomarkers , Cell Transformation, Neoplastic/genetics , Cell Transformation, Neoplastic/metabolism , Endocrine Gland Neoplasms/diagnosis , Endocrine Gland Neoplasms/metabolism , Endocrine Gland Neoplasms/therapy , Humans , Insulin/metabolism , Models, Biological , Neoplasm Metastasis , Paracrine Communication , Protein Binding , Receptors, Adiponectin/genetics , Receptors, Adiponectin/metabolism , Risk , Risk Assessment , Structure-Activity RelationshipABSTRACT
In the last two decades, numerous in vitro studies demonstrated that insulin receptors and theirs downstream pathways are widely distributed throughout the brain. This evidence has proven that; at variance with previous believes; insulin/insulin-like-growth-factor (IGF) signalling plays a crucial role in the regulation of different central nervous system (CNS) tasks. The most important of these functions include: synaptic formation; neuronal plasticity; learning; memory; neuronal stem cell activation; neurite growth and repair. Therefore; dysfunction at different levels of insulin signalling and metabolism can contribute to the development of a number of brain disorders. Growing evidences demonstrate a close relationship between Type 2 Diabetes Mellitus (T2DM) and neurodegenerative disorders such as Alzheimer's disease. They, in fact, share many pathophysiological characteristics comprising impaired insulin sensitivity, amyloid ß accumulation, tau hyper-phosphorylation, brain vasculopathy, inflammation and oxidative stress. In this article, we will review the clinical and experimental evidences linking insulin resistance, T2DM and neurodegeneration, with the objective to specifically focus on insulin signalling-related mechanisms. We will also evaluate the pharmacological strategies targeting T2DM as potential therapeutic tools in patients with cognitive impairment.