Magnetisation processes in geometrically frustrated spin networks with self-assembled cliques

(c) 2020 by the authors. Functional design of nanostructured materials seeks to exploit potential of complex morphologies and disorder. In this context, the spin dynamics in disordered antiferromagnetic materials present a significant challenge due to induced geometric frustration. Here we analyse the processes of magnetisation reversal driven by an external field in generalised spin networks with higher-order connectivity and antiferromagnetic defects. Using the model in [Tadic´ et al. Arxiv:1912.4331v1], we grow nanonetworks with geometrical constraint self-assembly of simplexes (cliques) of a given size n; with probability p each simplex possesses a defect edge affecting its binding, leading to a tree-like pattern of defects. The Ising spins are attached to vertices and have ferromagnetic interactions, while antiferromagnetic couplings apply between pairs of spins along each defect edge. Thus, a defect edge induces n −2 frustrated triangles per n-clique participating in a larger-scale complex. We determine several topological, entropy, and graph-theoretic measures to characterise the structure of these assemblies. Further, we show how the size of simplexes building the aggregates with a given pattern of defects affects the magnetisation curves, the length of the domain walls, and the shape of the hysteresis loop. The hysteresis shows a sequence of plateaus of fractional magnetisation and multi-scale fluctuations in the passage between them. For fully antiferromagnetic interactions, the loop splits into two parts only in mono-disperse assemblies of cliques consisting of an odd number of vertices n. At the same time, remanent magnetisation occurs when n is even, as well as in poly-disperse assemblies of cliques in the range n 2 [2, 10]. These results shed light on spin dynamics in complex nano-magnetic assemblies in which geometric frustration arises in the interplay of higher-order connectivity and antiferromagnetic interactions.Slovenian Research Agency; Ministry of Education, Science and Technological Development of the Republic of Serbi

GSTM1 Modulates Expression of Endothelial Adhesion Molecules in Uremic Milieu

Deletion polymorphism of glutathione S-transferase M1 (GSTM1), a phase II detoxification and antioxidant enzyme, increases susceptibility to end-stage renal disease (ESRD) as well as the development of cardiovascular diseases (CVD) among ESRD patients and leads to their shorter cardiovascular survival. The mechanisms by which GSTM1 downregulation contributes to oxidative stress and inflammation in endothelial cells in uremic conditions have not been investigated so far. Therefore, the aim of the present study was to elucidate the effects of GSTM1 knockdown on oxidative stress and expression of a panel of inflammatory markers in human umbilical vein endothelial cells (HUVECs) exposed to uremic serum. Additionally, we aimed to discern whether GSTM1-null genotype is associated with serum levels of adhesion molecules in ESRD patients. HUVECs treated with uremic serum exhibited impaired redox balance characterized by enhanced lipid peroxidation and decreased antioxidant enzyme activities, independently of the GSTM1 knockdown. In response to uremic injury, HUVECs exhibited alteration in the expression of a series of inflammatory cytokines including retinol-binding protein 4 (RBP4), regulated on activation, normal T cell expressed and secreted (RANTES), C-reactive protein (CRP), angiogenin, dickkopf-1 (Dkk-1), and platelet factor 4 (PF4). GSTM1 knockdown in HUVECs showed upregulation of monocyte chemoattractant protein-1 (MCP-1), a cytokine involved in the regulation of monocyte migration and adhesion. These cells also have shown upregulated intracellular and vascular cell adhesion molecules (ICAM-1 and VCAM-1). In accordance with these findings, the levels of serum ICAM-1 and VCAM-1 (sICAM-1 and sVCAM-1) were increased in ESRD patients lacking GSTM1, in comparison with patients with the GSTM1-active genotype. Based on these results, it may be concluded that incubation of endothelial cells in uremic serum induces redox imbalance accompanied with altered expression of a series of cytokines involved in arteriosclerosis and atherosclerosis. The association of GSTM1 downregulation with the altered expression of adhesion molecules might be at least partly responsible for the increased susceptibility of ESRD patients to CVD

Role of A Novel Angiogenesis FKBPL-CD44 Pathway in Preeclampsia Risk Stratification and Mesenchymal Stem Cell Treatment.

ContextPreeclampsia is a leading cardiovascular complication in pregnancy lacking effective diagnostic and treatment strategies.ObjectiveTo investigate the diagnostic and therapeutic target potential of the angiogenesis proteins, FK506-binding protein like (FKBPL) and CD44.Design and interventionFKBPL and CD44 plasma concentration or placental expression were determined in women pre- or postdiagnosis of preeclampsia. Trophoblast and endothelial cell function was assessed following mesenchymal stem cell (MSC) treatment and in the context of FKBPL signaling.Settings and participantsHuman samples prediagnosis (15 and 20 weeks of gestation; n ≥ 57), or postdiagnosis (n = 18 for plasma; n = 4 for placenta) of preeclampsia were used to determine FKBPL and CD44 levels, compared to healthy controls. Trophoblast or endothelial cells were exposed to low/high oxygen, and treated with MSC-conditioned media (MSC-CM) or a FKBPL overexpression plasmid.Main outcome measuresPreeclampsia risk stratification and diagnostic potential of FKBPL and CD44 were investigated. MSC treatment effects and FKBPL-CD44 signaling in trophoblast and endothelial cells were assessed.ResultsThe CD44/FKBPL ratio was reduced in placenta and plasma following clinical diagnosis of preeclampsia. At 20 weeks of gestation, a high plasma CD44/FKBPL ratio was independently associated with the 2.3-fold increased risk of preeclampsia (odds ratio = 2.3, 95% confidence interval [CI] 1.03-5.23, P = 0.04). In combination with high mean arterial blood pressure (>82.5 mmHg), the risk further increased to 3.9-fold (95% CI 1.30-11.84, P = 0.016). Both hypoxia and MSC-based therapy inhibited FKBPL-CD44 signaling, enhancing cell angiogenesis.ConclusionsThe FKBPL-CD44 pathway appears to have a central role in the pathogenesis of preeclampsia, showing promising utilities for early diagnostic and therapeutic purposes

Size Dependence of Current-Voltage Properties in Coulomb Blockade Networks

We theoretically investigate the current-voltage (I-V) property of two-dimensional Coulomb blockade (CB) arrays by conducting Monte Carlo simulations. The I-V property can be divided into three regions and we report the dependence of the aspect ratio delta (namely, the lateral size N_{y} over the longitudinal one N_{x}). We show that the average CB threshold obeys a power-law decay as a function of delta. Its exponent gamma corresponds to a sensitivity of the threshold depending on delta, and is inversely proportional to N_{x} (i.e., delta at fixed N_{y}). Further, the power-law exponent zeta, characterizing the nonlinearity of the I-V property in the intermediate region, logarithmically increases as delta increases. Our simulations describe the experimental result zeta=2.25 obtained by Parthasarathy et al. [Phys. Rev. Lett. 87 (2001) 186807]. In addition, the asymptotic I-V property of one-dimensional arrays obtained by Bascones et al. [Phys. Rev. B. 77 (2008) 245422] is applied to two-dimensional arrays. The asymptotic equation converges to the Ohm's law at the large voltage limit, and the combined tunneling-resistance is inversely proportional to delta. The extended asymptotic equation with the first-order perturbation well describes the experimental result obtained by Kurdak et al. [Phys. Rev. B 57 (1998) R6842]. Based on our asymptotic equation, we can estimate physical values that it is hard to obtain experimentally.Comment: 21 pages, 10 figures, accepted for publication in Journal of the Physical Society of Japa

Large scale influence of defect bonds in geometrically constrained self-assembly

Slovenian Research Agency; Ministry of Education, Science and Technological Development of the Republic of Serbi

Monte Carlo simulation of non-conservative positron transport in pure argon

The main aim of this paper is to apply modern phenomenology and accurate Monte Carlo simulation techniques to obtain the same level of understanding of positron transport as has been achieved for electrons. To this end, a reasonably complete set of cross sections for low energy positron scattering in argon has been used to calculate transport coefficients of low energy positrons in pure argon gas subject to an electrostatic field. We have analyzed the main features of these coefficients and have compared the calculated values with those for electrons in the same gas. The particular focus is on the influence of the non-conservative nature of positronium formation. This effect is substantial, generally speaking much larger than any comparable effects in electron transport due to attachment and/or ionization. As a result several new phenomena have been observed, such as negative differential conductivity (NDC) in the bulk drift velocity, but with no indication of any NDC for the flux drift velocity. In addition, there is a drastic effect on the bulk longitudinal diffusion coefficient for positrons, which is reduced to almost zero, in contrast to the other components of the diffusion tensor, which have normal values. It is found that the best way of explaining these kinetic phenomena is by sampling real space distributions which reveal drastic modification of the usual Gaussian profile due to pronounced spatial differentiation of the positrons by energy