Monte Carlo Calculations of Secondary Electron Emission

Monte Carlo calculations of secondary electron (SE) generation have been performed using a hybrid model of the exponential decay law and cascade multiplication process. The contributions of both valence and core electron excitations, and the production of secondaries by the volume plasmon decay, have been included. The calculation has been extended to include SE\u27s with energies up to half the incident beam energy. The SE yield δSE1 component due to excitation by primary electrons, the SE yield δSE2 due to excitation by backscattered electrons, and the β coefficient are estimated using this model. Calculated SE yields, energy distributions, and β coefficients are in good agreement with the experimental data . The influence of elastic and inelastic scattering for angular distribution of the SE\u27s is discussed

Monte Carlo Calculations of Secondary Electron Emission

Monte Carlo calculations of slow secondary electron (SE) generation have been performed. Construction of a model for SE production involves three distinct steps, determining the trajectory of the incident electron, computing the rate of secondary electron generation along the trajectory of both primary and backscattered electrons, and finally calculating the secondary electron emission by using a hybrid model of the exponential decay law and cascade process. The incident electron trajectory is computed using a plural scattering Monte Carlo model. For secondary electron generation our models take into account all possible creation processes of SE resulting from the interaction of primary and backscattered electrons with free as well as bound (core) electrons and from the volume plasmon decay. Calculated SE yields, energy distributions, angular and depth distributions for Au, Ag Cu and Al are in good agreement with the experimental data available in the literature

Comparative genomics and transcriptomics of Escherichia coli isolates carrying virulence factors of both enteropathogenic and enterotoxigenic E. coli

AbstractEscherichia coli that are capable of causing human disease are often classified into pathogenic variants (pathovars) based on their virulence gene content. However, disease-associated hybrid E. coli, containing unique combinations of multiple canonical virulence factors have also been described. Such was the case of the E. coli O104:H4 outbreak in 2011, which caused significant morbidity and mortality. Among the pathovars of diarrheagenic E. coli that cause significant human disease are the enteropathogenic E. coli (EPEC) and enterotoxigenic E. coli (ETEC). In the current study we use comparative genomics, transcriptomics, and functional studies to characterize isolates that contain virulence factors of both EPEC and ETEC. Based on phylogenomic analysis, these hybrid isolates are more genomically-related to EPEC, but appear to have acquired ETEC virulence genes. Global transcriptional analysis using RNA sequencing, demonstrated that the EPEC and ETEC virulence genes of these hybrid isolates were differentially-expressed under virulence-inducing laboratory conditions, similar to reference isolates. Immunoblot assays further verified that the virulence gene products were produced and that the T3SS effector EspB of EPEC, and heat-labile toxin of ETEC were secreted. These findings document the existence and virulence potential of an E. coli pathovar hybrid that blurs the distinction between E. coli pathovars.</jats:p

Autophagic activity in neuronal cell death.

As post-mitotic cells with great energy demands, neurons depend upon the homeostatic and waste-recycling functions provided by autophagy. In addition, autophagy also promotes survival during periods of harsh stress and targets aggregate-prone proteins associated with neurodegeneration for degradation. Despite this, autophagy has also been controversially described as a mechanism of programmed cell death. Instances of autophagic cell death are typically associated with elevated numbers of cytoplasmic autophagosomes, which have been assumed to lead to excessive degradation of cellular components. Due to the high activity and reliance on autophagy in neurons, these cells may be particularly susceptible to autophagic death. In this review, we summarize and assess current evidence in support of autophagic cell death in neurons, as well as how the dysregulation of autophagy commonly seen in neurodegeneration can contribute to neuron loss. From here, we discuss potential treatment strategies relevant to such cell-death pathways.DCR is funded by a Wellcome Trust Principal Research Fellowship and the NIHR Biomedical Research Unit in Dementia at Addenbrooke’s Hospital. This review is supported by Plymouth University and Northcott Medical Foundation.This is the author accepted manuscript. The final version is available from Springer via http://dx.doi.org/10.1007/s12264-015-1528-

Experimental Measurements of Electron Stopping Power at Low Energies

The electron stopping power has been measured for twelve elements and fifteen compounds, over the energy range from 1 eV to 10 keV, by the analysis of electron energy loss spectra, optical data, and photon mass absorption data. Values of the effective mean ionization potential Jeff and the effective number of participating electrons Neff have also been determined in each case. The results obtained have been compared with other experimental data, with first-principles theoretical calculations, and with a number of proposed analytical models

Gordian Adjacency for Positive Braid Knots

A knot $K_1$ is said to be Gordian adjacent to a knot $K_2$ if $K_1$ is an intermediate knot on an unknotting sequence of $K_2$. We extend previous results on Gordian adjacency by showing sufficient conditions for Gordian adjacency between classes of positive braid knots through manipulations of braid words. In addition, we explore unknotting sequences of positive braid knots and give a proof that there are only finitely many positive braid knots for a given unknotting number

Cdk5 phosphorylation of huntingtin reduces its cleavage by caspases: implications for mutant huntingtin toxicity

Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded polyglutamine (polyQ) tract in the huntingtin (htt) protein. Mutant htt toxicity is exposed after htt cleavage by caspases and other proteases release NH2-terminal fragments containing the polyQ expansion. Here, we show htt interacts and colocalizes with cdk5 in cellular membrane fractions. Cdk5 phosphorylates htt at Ser434, and this phosphorylation reduces caspase-mediated htt cleavage at residue 513. Reduced mutant htt cleavage resulting from cdk5 phosphorylation attenuated aggregate formation and toxicity in cells expressing the NH2-terminal 588 amino acids (htt588) of mutant htt. Cdk5 activity is reduced in the brains of HD transgenic mice compared with controls. This result can be accounted for by the polyQ-expanded htt fragments reducing the interaction between cdk5 and its activator p35. These data predict that the ability of cdk5 phosphorylation to protect against htt cleavage, aggregation, and toxicity is compromised in cells expressing toxic fragments of htt

Spin Waves in Detwinned BaFe2_2As2_2

Understanding magnetic interactions in the parent compounds of high-temperature superconductors forms the basis for determining their role for the mechanism of superconductivity. For parent compounds of iron pnictide superconductors such as $A$Fe$_2$As$_2$ ($A=$ Ba, Ca, Sr), although spin excitations have been mapped out throughout the entire Brillouin zone (BZ), measurements were carried out on twinned samples and did not allow for a conclusive determination of the spin dynamics. Here we use inelastic neutron scattering to completely map out spin excitations of $\sim$100\% detwinned BaFe$_2$As$_2$. By comparing observed spectra with theoretical calculations, we conclude that the spin excitations can be well described by an itinerant model with important contributions from electronic correlations.Comment: 6 pages, 4 figures, with supplemental materia