La Trobe University

About: La Trobe University is a education organization based out in Melbourne, Victoria, Australia. It is known for research contribution in the topics: Population & Health care. The organization has 13370 authors who have published 41291 publications receiving 1138269 citations. The organization is also known as: LaTrobe University & LTU.

Interaction, growth, and ordering of epitaxial graphene on SiC{0001} surfaces: A comparative photoelectron spectroscopy study

Abstract: Thermally induced growth of graphene on the two polar surfaces of $6H\text{\ensuremath{-}}\mathrm{Si}\mathrm{C}$ is investigated with emphasis on the initial stages of growth and interface structure. The experimental methods employed are angle-resolved valence band photoelectron spectroscopy, soft x-ray induced core-level spectroscopy, and low-energy electron diffraction. On the Si-terminated (0001) surface, the $(6\sqrt{3}\ifmmode\times\else\texttimes\fi{}6\sqrt{3})R30\ifmmode^\circ\else\textdegree\fi{}$ reconstruction is the precursor of the growth of graphene and it persists at the interface upon the growth of few layer graphene (FLG). The $(6\sqrt{3}\ifmmode\times\else\texttimes\fi{}6\sqrt{3})R30\ifmmode^\circ\else\textdegree\fi{}$ structure is a carbon layer with graphene-like atomic arrangement covalently bonded to the substrate where it is responsible for the azimuthal ordering of FLG on SiC(0001). In contrast, the interaction between graphene and the C-terminated $(000\overline{1})$ surface is much weaker, which accounts for the low degree of order of FLG on this surface. A model for the growth of FLG on SiC{0001} is developed, wherein each new graphene layer is formed at the bottom of the existing stack rather than on its top. This model yields, in conjunction with the differences in the interfacial bonding strength, a natural explanation for the different degrees of azimuthal order observed for FLG on the two surfaces.

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Abstract: Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.

Associations between corporate characteristics and disclosure levels in annual reports: a meta-analysis

Abstract: Accounting researchers have investigated associations between corporate characteristics and disclosures in corporate annual reports since 1961. Findings have consistently shown corporate size and listing status to be significantly associated with disclosure levels, while mixed results have been reported for leverage, profitability, and audit firm size. The purpose of the present paper is to integrate prior disclosure studies and to identify the underlying factors that moderate the apparent variation in results. A meta-analysis of 29 studies confirms significant and positive relationships between disclosure levels and corporate size, listing status and leverage. No significant association is found between corporate profitability or size of audit firm, with aggregate disclosure levels. This study also found that in addition to sampling error, the results are moderated by differences in disclosure index construction, differences in definition of the explanatory variables, and differences in research settings.

Linear ubiquitination prevents inflammation and regulates immune signalling

Abstract: Members of the tumour necrosis factor (TNF) receptor superfamily have important functions in immunity and inflammation Recently linear ubiquitin chains assembled by a complex containing HOIL-1 and HOIP (also known as RBCK1 and RNF31, respectively) were implicated in TNF signalling, yet their relevance in vivo remained uncertain Here we identify SHARPIN as a third component of the linear ubiquitin chain assembly complex, recruited to the CD40 and TNF receptor signalling complexes together with its other constituents, HOIL-1 and HOIP Mass spectrometry of TNF signalling complexes revealed RIP1 (also known as RIPK1) and NEMO (also known as IKKγ or IKBKG) to be linearly ubiquitinated Mutation of the Sharpin gene (Sharpin(cpdm/cpdm)) causes chronic proliferative dermatitis (cpdm) characterized by inflammatory skin lesions and defective lymphoid organogenesis Gene induction by TNF, CD40 ligand and interleukin-1β was attenuated in cpdm-derived cells which were rendered sensitive to TNF-induced death Importantly, Tnf gene deficiency prevented skin lesions in cpdm mice We conclude that by enabling linear ubiquitination in the TNF receptor signalling complex, SHARPIN interferes with TNF-induced cell death and, thereby, prevents inflammation Our results provide evidence for the relevance of linear ubiquitination in vivo in preventing inflammation and regulating immune signalling