Approximation error of one finite-difference scheme for the problem of diffraction by a gradient layer

© 2017 Pushpa Publishing House, Allahabad, India.The finite-difference scheme, constructed by the method of approximating an integral identity, is considered for a boundary value problem involving the one-dimensional Lame equations, which describe the problem of diffraction by gradient isotropic and transversal-isotropic layers. We prove that the finite-difference scheme is second-order accurate and can be recommended for use in solving the Lame equations with continuous coefficients

Application of a second order accurate finite-difference method to problems of diffraction of elastic waves by gradient layers

© Published under licence by IOP Publishing Ltd.A generalized statement is formulated for the boundary-value problem describing diffraction of elastic waves by gradient isotropic and transversely isotropic layers. Numerical experiments are conducted for various types of materials filling the layer. A conclusion is drawn that the obtained finite-difference scheme is second-order accurate, when distributions of elastic parameters in the layer are described by smooth curves

The sharpeness of some cluster set results

We show that a recent cluster set theorem of Rung is sharp in a certain sense. This is accomplished through the construction of an interpolating sequence whose limit set is closed, totally disconnected and porous. The results also generalize some of Dolzenko's cluster set theorems

Second-Order Accurate Finite-Difference Scheme for Solving the Problem of Elastic Wave Diffraction by the Anisotropic Gradient Layer

© 2018, Pleiades Publishing, Ltd. The boundary value problem for the Lame equations for the problem of elastic wave diffraction by an anisotropic layer with continuously varying elastic parameters is considered. The original problem is reduced to the boundary value problem for a system of ordinary differential equations of the given form. The finite-difference scheme is obtained by the method of approximation of integral identities. The theorem is proved that the error of approximation of the solution has a second order of accuracy for sufficiently continuous values of the elements of the elasticity tensor. Numerical results confirming theoretical conclusions are given

Obesity-induced insulin resistance in human skeletal muscle is characterised by defective activation of p42/p44 MAP kinase

Insulin resistance (IR), an impaired cellular, tissue and whole body response to insulin, is a major pathophysiological defect of type 2 diabetes mellitus. Although IR is closely associated with obesity, the identity of the molecular defect(s) underlying obesity-induced IR in skeletal muscle remains controversial; reduced post-receptor signalling of the insulin receptor substrate 1 (IRS1) adaptor protein and downstream effectors such as protein kinase B (PKB) have previously been implicated. We examined expression and/or activation of a number of components of the insulin-signalling cascade in skeletal muscle of 22 healthy young men (with body mass index (BMI) range, 20–37 kg/m2). Whole body insulin sensitivity (M value) and body composition was determined by the hyperinsulinaemic (40 mU. min−1.m−2.), euglycaemic clamp and by dual energy X-ray absorptiometry (DEXA) respectively. Skeletal muscle (vastus lateralis) biopsies were taken before and after one hour of hyperinsulinaemia and the muscle insulin signalling proteins examined by western blot and immunoprecipitation assay. There was a strong inverse relationship between M-value and BMI. The most striking abnormality was significantly reduced insulin-induced activation of p42/44 MAP kinase, measured by specific assay, in the volunteers with poor insulin sensitivity. However, there was no relationship between individuals' BMI or M-value and protein expression/phosphorylation of IRS1, PKB, or p42/44 MAP kinase protein, under basal or hyperinsulinaemic conditions. In the few individuals with poor insulin sensitivity but preserved p42/44 MAP kinase activation, other signalling defects were evident. These findings implicate defective p42/44 MAP kinase signalling as a potential contributor to obesity-related IR in a non-diabetic population, although clearly multiple signalling defects underlie obesity associated IR

SUMOylation of the mitochondrial fission protein Drpl occurs at multiple nonconsensus sites within the B domain and is linked to its activity cycle

Dynamin‐related protein (Drp) 1 is a key regulator of mitochondrial fission and is composed of GTP‐binding, Middle, insert B, and C‐terminal GTPase effector (GED) domains. Drpl associates with mitochondrial fission sites and promotes membrane constriction through its intrinsic GTPase activity. The mechanisms that regulate Drpl activity remain poorly understood but are likely to involve reversible post‐translational modifications, such as conjugation of small ubiquitin‐like modifier (SUMO) proteins. Through a detailed analysis, we find that Drpl interacts with the SUMO‐conjugating enzyme Ubc9 via multiple regions and demonstrate that Drpl is a direct target of SUMO modification by all three SUMO isoforms. While Drpl does not harbor consensus SUMOylation sequences, our analysis identified2 clusters of lysine residues within the B domain that serve as noncanonical conjugation sites. Although initial analysis indicates that mitochondrial recruitment of ectopically expressed Drpl in response to staurosporine is unaffected by loss of SUMOylation, we find that Drpl SUMOylation is enhanced in the context of the K38A mutation. This dominant‐negative mutant, which is deficient in GTP binding and hydrolysis, does not associate with mitochondria and prevents normal mitochondrial fission. This finding suggests that SUMOylation of Drpl is linked to its activity cycle and is influenced by Drpl localization.—Figueroa‐Romero, C., Iniguez‐Lluhi, J. A., Stadler, J., Chang, C.‐R., Arnoult, D., Keller, P. J., Hong, Y., Blackstone, C., Feldman, E. L. SUMOylation of the mitochondrial fission protein Drpl occurs at multiple nonconsensus sites within the B domain and is linked to its activity cycle. FASEB J. 23, 3917–3927 (2009). www.fasebj.orgPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154272/1/fsb2fj09136630.pd

Band Edge Tailoring in Few-Layer Two-Dimensional Molybdenum Sulfide/Selenide Alloys

Chemical alloying is a powerful approach to tune the electronic structure of semiconductors and has led to the synthesis of ternary and quaternary two-dimensional (2D) dichalcogenide semiconductor alloys (e.g., MoSSe₂, WSSe₂, etc.). To date, most of the studies have been focused on determining the chemical composition by evaluating the optical properties, primarily via photoluminescence and reflection spectroscopy of these materials in the 2D monolayer limit. However, a comprehensive study of alloying in multilayer films with direct measurement of electronic structure, combined with first-principles theory, is required for a complete understanding of this promising class of semiconductors. We have combined first-principles density functional theory calculations with experimental characterization of MoS_(2(1-x))Se_(2x) (where x ranges from 0 to 1) alloys using X-ray photoelectron spectroscopy to evaluate the valence and conduction band edge positions in each alloy. Moreover, our observations reveal that the valence band edge energies for molybdenum sulfide/selenide alloys increase as a function of increasing selenium concentration. These experimental results agree well with the results of density functional theory calculations showing a similar trend in calculated valence band edges. Our studies suggest that alloying is an effective technique for tuning the band edges of transition-metal dichalcogenides, with implications for applications such as solar cells and photoelectrochemical devices

The association between green space and cause-specific mortality in urban New Zealand: an ecological analysis of green space utility

<b>Background:</b> There is mounting international evidence that exposure to green environments is associated with health benefits, including lower mortality rates. Consequently, it has been suggested that the uneven distribution of such environments may contribute to health inequalities. Possible causative mechanisms behind the green space and health relationship include the provision of physical activity opportunities, facilitation of social contact and the restorative effects of nature. In the New Zealand context we investigated whether there was a socioeconomic gradient in green space exposure and whether green space exposure was associated with cause-specific mortality (cardiovascular disease and lung cancer). We subsequently asked what is the mechanism(s) by which green space availability may influence mortality outcomes, by contrasting health associations for different types of green space. <b>Methods:</b> This was an observational study on a population of 1,546,405 living in 1009 small urban areas in New Zealand. A neighbourhood-level classification was developed to distinguish between usable (i.e., visitable) and non-usable green space (i.e., visible but not visitable) in the urban areas. Negative binomial regression models were fitted to examine the association between quartiles of area-level green space availability and risk of mortality from cardiovascular disease (n = 9,484; 1996 - 2005) and from lung cancer (n = 2,603; 1996 - 2005), after control for age, sex, socio-economic deprivation, smoking, air pollution and population density. <b>Results:</b> Deprived neighbourhoods were relatively disadvantaged in total green space availability (11% less total green space for a one standard deviation increase in NZDep2001 deprivation score, p < 0.001), but had marginally more usable green space (2% more for a one standard deviation increase in deprivation score, p = 0.002). No significant associations between usable or total green space and mortality were observed after adjustment for confounders. <b>Conclusion</b> Contrary to expectations we found no evidence that green space influenced cardiovascular disease mortality in New Zealand, suggesting that green space and health relationships may vary according to national, societal or environmental context. Hence we were unable to infer the mechanism in the relationship. Our inability to adjust for individual-level factors with a significant influence on cardiovascular disease and lung cancer mortality risk (e.g., diet and alcohol consumption) will have limited the ability of the analyses to detect green space effects, if present. Additionally, green space variation may have lesser relevance for health in New Zealand because green space is generally more abundant and there is less social and spatial variation in its availability than found in other contexts