Theory and simulation of electronic and optical properties of charged defects in two-dimensional semiconductors

Charged defects are frequently observed in quasi two-dimensional (2D) semiconductors such as monolayer transition-metal dichalcogenides (TMDCs) and few-layer black phosphorus (BP), and can have a significant effect on the performance of such materials in transport and optical applications. To aid the development of nanoscale devices fabricated using 2D materials, a detailed understanding of charged defects in these systems is needed. In this thesis, isolated charged defects are modelled in 2D semiconductors using the tight-binding approach which allows the use of large supercells which are required to capture the bound states that arise. The screened defect potential is described through an external potential determined via first-principles random-phase approximation. The binding energies and wavefunctions of bound states induced by charged defects in monolayer forms of MoS$_2$, WS$_2$, and BP as well as bilayer BP, were studied and the effect of varying the defect charge, defect height and the dielectric constant of possible substrates was investigated. It was found that for shallow defects in TMDCs, the binding energies of bound states can be mostly understood using effective mass theory. However, the presence of multiple low-energy valleys in the conduction and valence bands with different effective masses results in an interplay and competition between defect levels originating from different valleys. This results in resonant states that hybridise with the continuum bands, which has implications for transport, and results in the optical conductivity exhibiting excitonic resonances at energies below the optical band gap. Applying a similar analysis to monolayer BP, it was found that the substrate dielectric constant presents a promising means of control over both the donor and acceptor binding energies. In both monolayer and bilayer BP, it was found that the large difference between the armchair and zigzag effective masses of holes and electrons results in highly anisotropic wavefunctions of the defect states.Open Acces

Introductory Guide to the Common European Framework of Reference (CEFR) for English Language Teachers

The Common European Framework of Reference for Languages: Learning, Teaching, Assessment, abbreviated in English as CEFR or CEF or CEFRL, is a guideline used to describe achievements of learners of foreign languages across Europe and, increasingly, in other countries. The CEFR is also intended to make it easier for educational institutions and employers to evaluate the language qualifications of candidates for education admission or employment. Its main aim is to provide a method of learning, teaching, and assessing that applies to all languages in Europe. The Common European Framework of Reference (CEFR) guidelines describe language proficiency of learners on a scale of 6 levels. While the description of CEFR guidelines is generic across languages, the development of automated proficiency classification systems for different languages follows different approaches

Metabolism makes and mends the heart

Experiments in zebrafish have shed new light on the relationship between development and regeneration in the heart

Regulatory Logic Underlying Diversification of the Neural Crest

The neural crest is a transient, multipotent population of cells that arises at the border of the developing nervous system. After closure of the neural tube, these cells undergo an epithelial-to-mesenchymal transition (EMT) to delaminate and migrate, often to distant locations in the embryo. Neural crest cells give rise to a diverse array of derivatives including neurons and glia of the peripheral nervous system, melanocytes, and bone and cartilage of the face. A gene regulatory network (GRN) controls the specification, delamination, migration, and differentiation of this fascinating cell type. With increasing technological advances, direct linkages within the neural crest GRN are being uncovered. The underlying circuitry is useful for understanding important topics such as reprogramming, evolution, and disease

Optical Properties of Charged Defects in Monolayer MoS2_2

We present theoretical calculations of the optical spectrum of monolayer MoS$_2$ with a charged defect. In particular, we solve the Bethe-Salpeter equation based on an atomistic tight-binding model of the MoS$_2$ electronic structure which allows calculations for large supercells. The defect is modelled as a point charge whose potential is screened by the MoS$_2$ electrons. We find that the defect gives rise to new peaks in the optical spectrum approximately 100-200 meV below the first free exciton peak. These peaks arise from transitions involving in-gap bound states induced by the charged defect. Our findings are in good agreement with experimental measurements

Regulatory Logic Underlying Diversification of the Neural Crest

The neural crest is a transient, multipotent population of cells that arises at the border of the developing nervous system. After closure of the neural tube, these cells undergo an epithelial-to-mesenchymal transition (EMT) to delaminate and migrate, often to distant locations in the embryo. Neural crest cells give rise to a diverse array of derivatives including neurons and glia of the peripheral nervous system, melanocytes, and bone and cartilage of the face. A gene regulatory network (GRN) controls the specification, delamination, migration, and differentiation of this fascinating cell type. With increasing technological advances, direct linkages within the neural crest GRN are being uncovered. The underlying circuitry is useful for understanding important topics such as reprogramming, evolution, and disease

Uncoupling of complex regulatory patterning during evolution of larval development in echinoderms

<p>Abstract</p> <p>Background</p> <p>Conservation of orthologous regulatory gene expression domains, especially along the neuroectodermal anterior-posterior axis, in animals as disparate as flies and vertebrates suggests that common patterning mechanisms have been conserved since the base of Bilateria. The homology of axial patterning is far less clear for the many marine animals that undergo a radical transformation in body plan during metamorphosis. The embryos of these animals are microscopic, feeding within the plankton until they metamorphose into their adult forms.</p> <p>Results</p> <p>We describe here the localization of 14 transcription factors within the ectoderm during early embryogenesis in <it>Patiria miniata</it>, a sea star with an indirectly developing planktonic bipinnaria larva. We find that the animal-vegetal axis of this very simple embryo is surprisingly well patterned. Furthermore, the patterning that we observe throughout the ectoderm generally corresponds to that of "head/anterior brain" patterning known for hemichordates and vertebrates, which share a common ancestor with the sea star. While we suggest here that aspects of head/anterior brain patterning are generally conserved, we show that another suite of genes involved in retinal determination is absent from the ectoderm of these echinoderms and instead operates within the mesoderm.</p> <p>Conclusions</p> <p>Our findings therefore extend, for the first time, evidence of a conserved axial pattering to echinoderm embryos exhibiting maximal indirect development. The dissociation of head/anterior brain patterning from "retinal specification" in echinoderm blastulae might reflect modular changes to a developmental gene regulatory network within the ectoderm that facilitates the evolution of these microscopic larvae.</p

Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death.

The altered metabolism of cancer can render cells dependent on the availability of metabolic substrates for viability. Investigating the signaling mechanisms underlying cell death in cells dependent upon glucose for survival, we demonstrate that glucose withdrawal rapidly induces supra-physiological levels of phospho-tyrosine signaling, even in cells expressing constitutively active tyrosine kinases. Using unbiased mass spectrometry-based phospho-proteomics, we show that glucose withdrawal initiates a unique signature of phospho-tyrosine activation that is associated with focal adhesions. Building upon this observation, we demonstrate that glucose withdrawal activates a positive feedback loop involving generation of reactive oxygen species (ROS) by NADPH oxidase and mitochondria, inhibition of protein tyrosine phosphatases by oxidation, and increased tyrosine kinase signaling. In cells dependent on glucose for survival, glucose withdrawal-induced ROS generation and tyrosine kinase signaling synergize to amplify ROS levels, ultimately resulting in ROS-mediated cell death. Taken together, these findings illustrate the systems-level cross-talk between metabolism and signaling in the maintenance of cancer cell homeostasis

Cardiac neural crest contributes to cardiomyocytes in amniotes and heart regeneration in zebrafish

Cardiac neural crest cells contribute to important portions of the cardiovascular system including the aorticopulmonary septum and cardiac ganglion. Using replication incompetent avian retroviruses for precise high-resolution lineage analysis, we uncover a previously undescribed neural crest contribution to cardiomyocytes of the ventricles in Gallus gallus, supported by Wnt1-Cre lineage analysis in Mus musculus. To test the intriguing possibility that neural crest cells contribute to heart repair, we examined Danio rerio adult heart regeneration in the neural crest transgenic line, Tg(-4.9sox10:eGFP). Whereas the adult heart has few sox10+ cells in the apex, sox10 and other neural crest regulatory network genes are upregulated in the regenerating myocardium after resection. The results suggest that neural crest cells contribute to many cardiovascular structures including cardiomyocytes across vertebrates and to the regenerating heart of teleost fish. Thus, understanding molecular mechanisms that control the normal development of the neural crest into cardiomyocytes and reactivation of the neural crest program upon regeneration may open potential therapeutic approaches to repair heart damage in amniotes