Covering Dimension of C*-Algebras and 2-Coloured Classification

Research partially supported by EPSRC (grant no. I019227/1-2), by NSF (grant no. DMS-1201385), by JSPS (the Grant-in-Aid for Research Activity Start-up 25887031), by NSERC (PDF, held by AT), by an Alexander von Humboldt foundation fellowship (held by SW) and by the DFG (SFB 878).Postprin

On variations of the brightness of type Ia supernovae with the age of the host stellar population

Recent observational studies of type Ia supernovae (SNeIa) suggest correlations between the peak brightness of an event and the age of the progenitor stellar population. This trend likely follows from properties of the progenitor white dwarf (WD), such as central density, that follow from properties of the host stellar population. We present a statistically well-controlled, systematic study utilizing a suite of multi-dimensional SNeIa simulations investigating the influence of central density of the progenitor WD on the production of Fe-group material, particularly radioactive Ni-56, which powers the light curve. We find that on average, as the progenitor's central density increases, production of Fe-group material does not change but production of Ni-56 decreases. We attribute this result to a higher rate of neutronization at higher density. The central density of the progenitor is determined by the mass of the WD and the cooling time prior to the onset of mass transfer from the companion, as well as the subsequent accretion heating and neutrino losses. The dependence of this density on cooling time, combined with the result of our central density study, offers an explanation for the observed age-luminosity correlation: a longer cooling time raises the central density at ignition thereby producing less Ni-56 and thus a dimmer event. While our ensemble of results demonstrates a significant trend, we find considerable variation between realizations, indicating the necessity for averaging over an ensemble of simulations to demonstrate a statistically significant result.Comment: 5 pages, 4 figures, 1 table, accepted to ApJ

Large-scale Spatiotemporal Spike Patterning Consistent with Wave Propagation in Motor Cortex

Aggregate signals in cortex are known to be spatiotemporally organized as propagating waves across the cortical surface, but it remains unclear whether the same is true for spiking activity in individual neurons. Furthermore, the functional interactions between cortical neurons are well documented but their spatial arrangement on the cortical surface has been largely ignored. Here we use a functional network analysis to demonstrate that a subset of motor cortical neurons in non-human primates spatially coordinate their spiking activity in a manner that closely matches wave propagation measured in the beta oscillatory band of the local field potential. We also demonstrate that sequential spiking of pairs of neuron contains task-relevant information that peaks when the neurons are spatially oriented along the wave axis. We hypothesize that the spatial anisotropy of spike patterning may reflect the underlying organization of motor cortex and may be a general property shared by other cortical areas

Interventional Radiology Readiness Assessment Tool for Global Health

The Interventional Radiology Readiness Assessment Tool for Global Health is a new tool to methodically evaluate the environment of a medical institution for interventional radiology services given the existing infrastructure. Global health provides an exciting opportunity for interventional radiology to impact health outcomes in developing countries. A systematic and thoughtful approach to integrating interventional radiology services in the health care institutions of resource poor countries is needed in order to maximize global health efforts and outcomes. The IR Readiness Assessment Tool is available as on online form and in PDF format under Additional Files below

Testing the transferability of a coarse-grained model to intrinsically disordered proteins

The intermediate-resolution coarse-grained protein model PLUM [T. Bereau and M. Deserno, J. Chem. Phys., 2009, 130, 235106] is used to simulate small systems of intrinsically disordered proteins involved in biomineralisation. With minor adjustments to reduce bias toward stable secondary structure, the model generates conformational ensembles conforming to structural predictions from atomistic simulation. Without additional structural information as input, the model distinguishes regions of the chain by predicted degree of disorder, manifestation of structure, and involvement in chain dimerisation. The model is also able to distinguish dimerisation behaviour between one intrinsically disordered peptide and a closely related mutant. We contrast this against the poor ability of PLUM to model the S1 quartz-binding peptide

A Model of Fluid-Structure and Biochemical Interactions for Applications to Subclinical Leaflet Thrombosis

Subclinical leaflet thrombosis (SLT) is a potentially serious complication of aortic valve replacement with a bioprosthetic valve in which blood clots form on the replacement valve. SLT is associated with increased risk of transient ischemic attacks and strokes and can progress to clinical leaflet thrombosis. SLT following aortic valve replacement also may be related to subsequent structural valve deterioration, which can impair the durability of the valve replacement. Because of the difficulty in clinical imaging of SLT, models are needed to determine the mechanisms of SLT and could eventually predict which patients will develop SLT. To this end, we develop methods to simulate leaflet thrombosis that combine fluid-structure interaction and a simplified thrombosis model that allows for deposition along the moving leaflets. Additionally, this model can be adapted to model deposition or absorption along other moving boundaries. We present convergence results and quantify the model's ability to realize changes in valve opening and pressures. These new approaches are an important advancement in our tools for modeling thrombosis in which they incorporate both adhesion to the surface of the moving leaflets and feedback to the fluid-structure interaction.Comment: 29 pages, 11 figure

G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle

Granulocyte-colony stimulating factor (G-CSF) increases recovery of rodent skeletal muscles after injury, and increases muscle function in rodent models of neuromuscular disease. However, the mechanisms by which G-CSF mediates these effects are poorly understood. G-CSF acts by binding to the membrane spanning G-CSFR and activating multiple intracellular signaling pathways. Expression of the G-CSFR within the haematopoietic system is well known, but more recently it has been demonstrated to be expressed in other tissues. However, comprehensive characterization of G-CSFR expression in healthy and diseased skeletal muscle, imperative before implementing G-CSF as a therapeutic agent for skeletal muscle conditions, has been lacking. Here we show that the G-CSFR is expressed in proliferating C2C12 myoblasts, differentiated C2C12 myotubes, human primary skeletal muscle cell cultures and in mouse and human skeletal muscle. In mdx mice, a model of human Duchenne muscular dystrophy (DMD), G-CSF mRNA and protein was down-regulated in limb and diaphragm muscle, but circulating G-CSF ligand levels were elevated. G-CSFR mRNA in the muscles of mdx mice was up-regulated however steady-state levels of the protein were down-regulated. We show that G-CSF does not influence C2C12 myoblast proliferation, differentiation or phosphorylation of Akt, STAT3, and Erk1/2. Media change alone was sufficient to elicit increases in Akt, STAT3, and Erk1/2 phosphorylation in C2C12 muscle cells and suggest previous observations showing a G-CSF increase in phosphoprotein signaling be viewed with caution. These results suggest that the actions of G-CSF may require the interaction with other cytokines and growth factors in vivo, however these data provides preliminary evidence supporting the investigation of G-CSF for the management of muscular dystrophy