Conductance of a spin-1 quantum dot: the two-stage Kondo effect

We discuss the physics of a of a spin-1 quantum dot, coupled to two metallic leads and develop a simple model for the temperature dependence of its conductance. Such quantum dots are described by a two-channel Kondo model with asymmetric coupling constants and the spin screening of the dot by the leads is expected to proceed via a two-stage process. When the Kondo temperatures of each channel are widely separated, on cooling, the dot passes through a broad cross-over regime dominated by underscreened Kondo physics. A singular, or non-fermi liquid correction to the conductance develops in this regime. At the lowest temperatures, destructive interference between resonant scattering in both channels leads to the eventual suppression of the conductance of the dot. We develop a model to describe the growth, and ultimate suppression of the conductance in the two channel Kondo model as it is screened successively by its two channels. Our model is based upon large-N approximation in which the localized spin degrees of freedom are described using the Schwinger boson formalism.Comment: 16 pages, 10 figure

Spatial considerations in the resolution of inflammation

Understanding the mechanisms that control the body's response to inflammation is of key importance, due to its involvement in myriad medical conditions, including cancer, arthritis, Alzheimer's disease and asthma. While resolving inflammation has historically been considered a passive process, since the turn of the century the hunt for novel therapeutic interventions has begun to focus upon active manipulation of constituent mechanisms, particularly involving interactions between immune cells and pro- and anti-inflammatory mediators. We here address the specific question of how inflammatory damage can spread spatially due to the motility of these cells and mediators using mathematical and agent-based modelling. We firstly extend the existing homogeneous models of Dunster et al. (2014) to incorporate spatial behaviours. Through bifurcation analysis and numerical simulation of the resulting partial differential equation (PDE) models, we show that spatially-inhomogeneous outcomes can present close to the switch from bistability to guaranteed resolution in the corresponding homogeneous models, but that this behaviour is tightly controlled by the dynamics of anti-inflammatory mediators. We then move to a hybrid PDE-Agent Based Model (ABM) approach, capable of simulating individual cells and a more diverse range of cell behaviours. In particular, we address the questions of whether initially localised damage can invade neighbouring healthy tissue, and the extent to which sub-optimal directed cell motility (such as that associated inflammatory conditions such as chronic obstructive pulmonary disease) can impact upon the long-term outcome. We illustrate that changes to the values of physiologically-relevant parameters can act as a switch between healthy and pathological scenarios; with careful parameterisation, our approach exhibits scope for elucidating how these key mechanisms could be actively manipulated to potentially identify new therapeutic interventions

Mechanisms and points of control in the spread of inflammation: a mathematical investigation

Understanding the mechanisms that control the body’s response to inflammation is of key importance, due to its involvement in myriad medical conditions, including cancer, arthritis, Alzheimer’s disease and asthma. While resolving inflammation has historically been considered a passive process, since the turn of the century the hunt for novel therapeutic interventions has begun to focus upon active manipulation of constituent mechanisms, particularly involving the roles of apoptosing neutrophils, phagocytosing macrophages and anti-inflammatory mediators. Moreover, there is growing interest in how inflammatory damage can spread spatially due to the motility of inflammatory mediators and immune cells. For example, impaired neutrophil chemotaxis is implicated in causing chronic inflammation under trauma and in ageing, while neutrophil migration is an attractive therapeutic target in ailments such as chronic obstructive pulmonary disease. We extend an existing homogeneous model that captures interactions between inflammatory mediators, neutrophils and macrophages to incorporate spatial behaviour. Through bifurcation analysis and numerical simulation, we show that spatially inhomogeneous outcomes can present close to the switch from bistability to guaranteed resolution in the corresponding homogeneous model. Finally, we show how aberrant spatial mechanisms can play a role in the failure of inflammation to resolve and discuss our results within the broader context of seeking novel inflammatory treatments

Correlation between anthropometric indexes and risk factors of cardiovascular diseases among the elderly population in Amirkola

Background: The ageing of population is an increasing phenomenon worldwide. Cardiovascular diseases are one of the most important chronic disease in ageing. The aim of this study was to investigate the correlation between the anthropometric indexes and risk factors of cardiovascular diseases among the elderly population in Amirkola (Mazandaran, Iran). Materials and Methods: This descriptive-analytical cross-sectional study was a part of the Amirkola Health and Ageing Cohort Project (AHAP). Demographic information was collected using a standard questionnaire. Fasting blood samples were collected from all participants to measure the serum level of lipids. Measurement of systolic and diastolic blood pressure and anthropometric indexes e.g. body mass index (BMI), waist circumference (WC), waist to hip ratio (WHR) and waist to height ratio (WHR) were done for all participants. Results: One thousand five hundred and six elderly people of Amirkola (age> 60 years) were participated in this study. There was a positive and significant correlation between the BMI and systolic and diastolic blood pressures, total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C) and triglyceride. The WC had a positive and significant correlation with systolic and diastolic blood pressures, HDL-C and triglyceride. The correlation between WHR and systolic and diastolic blood pressures, HDL-C and triglyceride was positive and significant; however the correlation between the anthropometric indexes and TC and low density lipoprotein-cholesterol (LDL-C) was negative and significant. The WHR had a significant positive correlation with all studied risk factors. Conclusion: According to the findings of present study, WHR index had stronger correlation with risk factors for cardiovascular disease in the elderly

Quality improvement of liver ultrasound images using fuzzy techniques

Background: Liver ultrasound images are so common and are applied so often to diagnose diffuse liver diseases like fatty liver. However, the low quality of such images makes it difficult to analyze them and diagnose diseases. The purpose of this study, therefore, is to improve the contrast and quality of liver ultrasound images. Methods: In this study, a number of image contrast enhancement algorithms which are based on fuzzy logic were applied to liver ultrasound images - in which the view of kidney is observable - using Matlab2013b to improve the image contrast and quality which has a fuzzy definition; just like image contrast improvement algorithms using a fuzzy intensification operator, contrast improvement algorithms applying fuzzy image histogram hyperbolization, and contrast improvement algorithms by fuzzy IF-THEN rules. Results: With the measurement of Mean Squared Error and Peak Signal to Noise Ratio obtained from different images, fuzzy methods provided better results, and their implementation - compared with histogram equalization method - led both to the improvement of contrast and visual quality of images and to the improvement of liver segmentation algorithms results in images. Conclusion: Comparison of the four algorithms revealed the power of fuzzy logic in improving image contrast compared with traditional image processing algorithms. Moreover, contrast improvement algorithm based on a fuzzy intensification operator was selected as the strongest algorithm considering the measured indicators. This method can also be used in future studies on other ultrasound images for quality improvement and other image processing and analysis applications. © 2016 Azadeh Bayani, Leila Shahmoradi, Mostafa Langarizadeh, Amir Reza Radmard, and Ahmadreza Farzaneh Nejad

Haptoglobin frequencies in Jewish communities *

Haptoglobin and transferrin types have been determined by starch gel electrophoresis on blood from 929 subjects belonging to various Jewish communities. The frequency of the Hp 1 gene in 499 Ashkenazic Jews is 0.29 and does not differ significantly from the value of 0–26 found in 345 Jews of Oriental origin. The Hp 1 frequency of Ashkenazic Jews is significantly lower than that reported for the autochthonous populations of Central and Western Europe. Two small samples collected among Sephardic Jews and among the offspring of intercommunity marriages exhibit somewhat higher frequencies of the Hp 1 gene. The modified 2-1 phenotype was found in a single subject from Baghdad. There were three cases of ahaptoglobinaemia among Ashkenazic Jews and three among the Oriental groups. No ahaptoglobinaemia was discovered in a family sample of ninety-two Jews from Kurdistan among whom thalassaemia minor was common and the majority of whom were affeeted with G-6-P-D deficiency. All transferrins were of type C.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66130/1/j.1469-1809.1962.tb01307.x.pd

Spatial considerations in the resolution of inflammation: elucidating leukocyte interactions via an experimentally-calibrated agent-based model

Many common medical conditions (such as cancer, arthritis, chronic obstructive pulmonary disease (COPD), and others) are associated with inflammation, and even more so when combined with the effects of ageing and multimorbidity. While the inflammatory response varies in different tissue types, under disease and in response to therapeutic interventions, it has common interactions that occur between immune cells and inflammatory mediators. Understanding these underlying inflammatory mechanisms is key in progressing treatments and therapies for numerous inflammatory conditions. It is now considered that constituent mechanisms of the inflammatory response can be actively manipulated in order to drive resolution of inflammatory damage; particularly, those mechanisms related to the pro-inflammatory role of neutrophils and the anti-inflammatory role of macrophages. In this article, we describe the assembly of a hybrid mathematical model in which the spatial spread of inflammatory mediators is described through partial differential equations, and immune cells (neutrophils and macrophages) are described individually via an agent-based modelling approach. We pay close attention to how immune cells chemotax toward pro-inflammatory mediators, presenting a model for cell chemotaxis that is calibrated against experimentally observed cell trajectories in healthy and COPD-affected scenarios. We illustrate how variations in key model parameters can drive the switch from resolution of inflammation to chronic outcomes, and show that aberrant neutrophil chemotaxis can move an otherwise healthy outcome to one of chronicity. Finally, we reflect on our results in the context of the on-going hunt for new therapeutic interventions

Association of plasma total testosterone level and metabolic syndrome in adult males

Introduction: Low testosterone level has strongly been correlated with body fat accumulation and abdominal obesity in men. Objectives: This study aimed to evaluate testosterone level in men with and without metabolic syndrome to determine the relationship between testosterone and metabolic syndrome. Patients and Methods: This case-control study was conducted on 172 cases of metabolic syndrome and 172 participants as a control group in Rasoul Akram hospital, Tehran, Iran. Demographic characteristics, fasting blood sugar (FBS), high-density lipoprotein (HDL), low-density lipoprotein (LDL), cholesterol, triglyceride (TG), and testosterone levels were recorded. SPSS version 21.0 and SAS version 9.1 were used for statistical analysis. Level of significance was considered 0.05. Results: The mean age of the two groups were 45.1 ± 9.3 years and 41.5 ± 11.2 years, respectively. There was a significant difference in serum testosterone levels between both groups and low testosterone levels were associated with metabolic syndrome (P < 0.001). Serum testosterone levels showed a significant negative correlation with age in the metabolic syndrome group (r =-0.16, P = 0.02). The relationship between metabolic syndrome and total plasma testosterone level using logistic regression model showed that, by increasing the total plasma testosterone level, the odds ratio for metabolic syndrome was 0.076 (95 CI: 0.027-0.216; P < 0.001). Conclusion: According to the results, low level of testosterone was related to the presence of metabolic syndrome in adult males. Future studies can investigate diagnostic value of testosterone level in this syndrome. © 2020 The Author(s)

Modulation by decitabine of gene expression and growth of osteosarcoma U2OS cells in vitro and in xenografts: Identification of apoptotic genes as targets for demethylation

<p>Abstract</p> <p>Background</p> <p>Methylation-mediated silencing of genes is one epigenetic mechanism implicated in cancer. Studies regarding the role of modulation of gene expression utilizing inhibitors of DNA methylation, such as decitabine, in osteosarcoma (OS) have been limited. A biological understanding of the overall effects of decitabine in OS is important because this particular agent is currently undergoing clinical trials. The objective of this study was to measure the response of the OS cell line, U2OS, to decitabine treatment both <it>in vitro </it>and <it>in vivo</it>.</p> <p>Results</p> <p>Microarray expression profiling was used to distinguish decitabine-dependent changes in gene expression in U2OS cells, and to identify responsive loci with demethylated CpG promoter regions. U2OS xenografts were established under the sub-renal capsule of immune-deficient mice to study the effect of decitabine <it>in vivo </it>on tumor growth and differentiation. Reduced nuclear methylation levels could be detected in xenografts derived from treated mice by immunohistochemistry utilizing a 5-methylcytidine antibody. Decitabine treatment reduced tumor xenograft size significantly (p < 0.05). Histological analysis of treated U2OS xenograft sections revealed a lower mitotic activity (p < 0.0001), increased bone matrix production (p < 0.0001), and a higher number of apoptotic cells (p = 0.0329). Microarray expression profiling of U2OS cultured cells showed that decitabine treatment caused a significant induction (p < 0.0025) in the expression of 88 genes. Thirteen had a ≥2-fold change, 11 of which had CpG-island-associated promoters. Interestingly, 6 of these 11 were pro-apoptotic genes and decitabine resulted in a significant induction of cell death in U2OS cells <it>in vitro </it>(p < 0.05). The 6 pro-apoptotic genes (<it>GADD45A</it>, <it>HSPA9B</it>, <it>PAWR</it>, <it>PDCD5</it>, <it>NFKBIA</it>, and <it>TNFAIP3</it>) were also induced to ≥2-fold <it>in vivo</it>. Quantitative methylation pyrosequencing confirmed that the tested pro-apoptotic genes had CpG-island DNA demethylationas a result of U2OS decitabine treatment both <it>in vitro </it>and in xenografts</p> <p>Conclusion</p> <p>These data provide new insights regarding the use of epigenetic modifiers in OS, and have important implications for therapeutic trials involving demethylation drugs. Collectively, these data have provided biological evidence that one mode of action of decitabine may be the induction of apoptosis utilizing promoter-CpG demethylation of specific effectors in cell death pathways in OS.</p