Equation of state of the neutron star matter, and the nuclear symmetry energy

The nuclear mean-field potentials obtained in the Hartree-Fock method with different choices of the in-medium nucleon-nucleon (NN) interaction have been used to study the equation of state (EOS) of the neutron star (NS) matter. The EOS of the uniform NS core has been calculated for the np$e\mu$ composition in the $\beta$-equilibrium at zero temperature, using version Sly4 of the Skyrme interaction as well as two density-dependent versions of the finite-range M3Y interaction (CDM3Y$n$ and M3Y-P$n$), and versions D1S and D1N of the Gogny interaction. Although the considered effective NN interactions were proven to be quite realistic in numerous nuclear structure and/or reaction studies, they give quite different behaviors of the symmetry energy of nuclear matter at supranuclear densities that lead to the \emph{soft} and \emph{stiff} scenarios discussed recently in the literature. Different EOS's of the NS core and the EOS of the NS crust given by the compressible liquid drop model have been used as input of the Tolman-Oppenheimer-Volkov equations to study how the nuclear symmetry energy affects the model prediction of different NS properties, like the cooling process as well as the gravitational mass, radius, and moment of inertia.Comment: To be published in Physical Review

WNT5A regulates adipose tissue angiogenesis via antiangiogenic VEGF-A165b in obese humans

Experimental studies have suggested that Wingless-related integration site 5A (WNT5A) is a proinflammatory secreted protein that is associated with metabolic dysfunction in obesity. Impaired angiogenesis in fat depots has been implicated in the development of adipose tissue capillary rarefaction, hypoxia, inflammation, and metabolic dysfunction. We have recently demonstrated that impaired adipose tissue angiogenesis is associated with overexpression of antiangiogenic factor VEGF-A165b in human fat and the systemic circulation. In the present study, we postulated that upregulation of WNT5A is associated with angiogenic dysfunction and examined its role in regulating VEGF-A165b expression in human obesity. We biopsied subcutaneous and visceral adipose tissue from 38 obese individuals (body mass index: 44 ± 7 kg/m2, age: 37 ± 11 yr) during planned bariatric surgery and characterized depot-specific protein expression of VEGF-A165b and WNT5A using Western blot analysis. In both subcutaneous and visceral fat, VEGF-A165b expression correlated strongly with WNT5A protein (r = 0.9, P \u3c 0.001). In subcutaneous adipose tissue where angiogenic capacity is greater than in the visceral depot, exogenous human recombinant WNT5A increased VEGF-A165b expression in both whole adipose tissue and isolated vascular endothelial cell fractions (P \u3c 0.01 and P \u3c 0.05, respectively). This was associated with markedly blunted angiogenic capillary sprout formation in human fat pad explants. Moreover, recombinant WNT5A increased secretion of soluble fms-like tyrosine kinase-1, a negative regulator of angiogenesis, in the sprout media (P \u3c 0.01). Both VEGF-A165b-neutralizing antibody and secreted frizzled-related protein 5, which acts as a decoy receptor for WNT5A, significantly improved capillary sprout formation and reduced soluble fms-like tyrosine kinase-1 production (P \u3c 0.05). We demonstrated a significant regulatory nexus between WNT5A and antiangiogenic VEGF-A165b in the adipose tissue of obese subjects that was linked to angiogenic dysfunction. Elevated WNT5A expression in obesity may function as a negative regulator of angiogenesis

Adipose tissue-derived cytokines and their correlations with clinical characteristics in Vietnamese patients with type 2 diabetes mellitus

Adipokines are involved in the pathogenesis of metabolic disorders including obesity and type 2 diabetes mellitus (T2DM). This study investigates the levels of leptin, resistin, visfatin, secreted frizzled-related protein 5 (SFRP5), monocyte chemoattractant protein-1 (MCP-1) and retinol-binding protein 4 (RBP4) and their correlations with clinical parameters of overweight and T2DM. Methods: We recruited overweight 50 patients with T2DM, 88 non-overweight patients with T2DM, 29 overweight and 100 non-overweight individuals devoid of T2DM for this study. The levels of studied adipokines were measured by enzyme-linked immunosorbent assay and correlated with clinical parameters. Results: The levels of MCP-1 and SFRP5 were decreased while visfatin and RBP4 levels were increased in patients with T2DM compared to those in the control individuals (P<0.01). Among patients with T2DM, leptin and resistin levels were higher while RBP4 levels were lower in patients with overweight T2DM compared to those in patients with non overweight T2DM (P<0.0001, 0.019 and 0.05, respectively). Leptin and MCP-1 levels were correlated with HOMA-IR, QUICKI and HOMA-β. Leptin/MCP-1 ratio was correlated with insulin levels, HOMA-IR and HOMA-β indexes. Resistin/ RBP4, visfatin/MCP-1 and MCP-1/RBP4 ratios were strongly correlated with the levels of fasting glucose, HbA1c and HOMA-β. In addition, ROC curve analyses indicated a diagnostic potential of resistin/RBP4 and MCP-1/RBP4 indexes for T2DM (AUC=0.81 and 0.83, respectively) and β-cell function (AUC=0.76 and 0.74, respectively). Conclusions: Adipokines (leptin, resistin, visfatin, SFRP5, MCP-1, and RBP4) are associated with overweight and T2DM and may serve as a potential prognostic marker and therapeutic intervention for overweight-related T2DM

Cardiovascular outcomes of cancer patients in rural Australia

BackgroundCancer and heart disease are the two most common health conditions in the world, associated with high morbidity and mortality, with even worse outcomes in regional areas. Cardiovascular disease is the leading cause of death in cancer survivors. We aimed to evaluate the cardiovascular outcomes of patients receiving cancer treatment (CT) in a regional hospital.MethodsThis was an observational retrospective cohort study in a single rural hospital over a ten-year period (17th February 2010 to 19th March 2019). Outcomes of all patients receiving CT during this period were compared to those who were admitted to the hospital without a cancer diagnosis.Results268 patients received CT during the study period. High rates of cardiovascular risk factors: hypertension (52.2%), smoking (54.9%), and dyslipidaemia (38.4%) were observed in the CT group. Patients who had CT were more likely to be readmitted with ACS (5.9% vs. 2.8% p = 0.005) and AF (8.2% vs. 4.5% p = 0.006) when compared to the general admission cohort. There was a statistically significant difference observed for all cause cardiac readmission, with a higher rate observed in the CT group (17.1% vs. 13.2% p = 0.042). Patients undergoing CT had a higher rate of mortality (49.5% vs. 10.2%, p ≤ 0.001) and shorter time (days) from first admission to death (401.06 vs. 994.91, p ≤ 0.001) when compared to the general admission cohort, acknowledging this reduction in survival may be driven at least in part by the cancer itself.ConclusionThere is an increased incidence of adverse cardiovascular outcomes, including higher readmission rate, higher mortality rate and shorter survival in people undergoing cancer treatment in rural environments. Rural cancer patients demonstrated a high burden of cardiovascular risk factors

A Conceptual Design and Numerical Analysis for a Small-Scale and Low-Cost Plastic Recycling Machine

A new conceptual design for a small-scale and low-cost plastic recycling machine is generated by combining melting part and compression process. Starting with one of the outstanding requirements is in terms of an affordable-priced machine that can perform two processes with high accuracy and capacity, some issues related to balancing among quality, capacity and cost of machine occurred during a discussion. After implementing various designing methods such as Quality Function Deployment, Reverse Engineering, Morphological Matrix and Pugh Method, an idea of final concept about using an electric oven and hydraulic system to melt down and compress plastic tile which has a dimension of 300x300x9 mm was created. The design of concept is divided into two parts which are mechanical and electrical systems. In a mechanical section, the technical drawing and simulation are made to see how machine performs under operation. Besides, we examined the forces that applied in the moulds to evaluate the strength of the system. In heating and electricity section, we chose electrical components, designed oven parameters and conducted the heating simulation on the mould. In addition, the heating and cooling time was calculated based on the principles of thermodynamics and heat transfer. Furthermore, the manufacturing plan is created to estimate the essential resources producing a certain number of heat-forming machines. In general, the machine needs to be prototyped for controlling its main function and finding practical issues. After that, some improvements could be made to enhance efficiency and increase capacity by designing an optimal mould to more heat absorb and reduce post process, calculate and design more efficient oven, create faster lock mechanism and other improvements for an automatizing machine

The Role of Pathological Aging in Cardiac and Pulmonary Fibrosis

Aging promotes a range of degenerative pathologies characterized by progressive losses of tissue and/or cellular function. Fibrosis is the hardening, overgrowth and scarring of various tissues characterized by the accumulation of extracellular matrix components. Aging is an important predisposing factor common for fibrotic heart and respiratory disease. Age-related processes such as senescence, inflammaging, autophagy and mitochondrial dysfunction are interconnected biological processes that diminish the regenerative capacity of the aged heart and lung and have been shown to play a crucial role in cardiac fibrosis and idiopathic pulmonary fibrosis. This review focuses on these four processes of aging in relation to their role in fibrosis. It has long been established that the heart and lung are linked both functionally and anatomically when it comes to health and disease, with an ever-expanding aging population, the incidence of fibrotic disease and therefore the number of fibrosis-related deaths will continue to rise. There are currently no feasible therapies to treat the effects of chronic fibrosis therefore highlighting the importance of exploring the processes of aging and its role in inducing and exacerbating fibrosis of each organ. The focus of this review may help to highlight potential avenues of therapeutic exploration</p

Fibulin-3 is necessary to prevent cardiac rupture following myocardial infarction

Despite the high prevalence of heart failure in the western world, there are few effective treatments. Fibulin-3 is a protein involved in extracellular matrix (ECM) structural integrity, however its role in the heart is unknown. We have demonstrated, using single cell RNA-seq, that fibulin-3 was highly expressed in quiescent murine cardiac fibroblasts, with expression highest prior to injury and late post-infarct (from ~ day-28 to week-8). In humans, fibulin-3 was upregulated in left ventricular tissue and plasma of heart failure patients. Fibulin-3 knockout (Efemp1−/−) and wildtype mice were subjected to experimental myocardial infarction. Fibulin-3 deletion resulted in significantly higher rate of cardiac rupture days 3–6 post-infarct, indicating a weak and poorly formed scar, with severe ventricular remodelling in surviving mice at day-28 post-infarct. Fibulin-3 knockout mice demonstrated less collagen deposition at day-3 post-infarct, with abnormal collagen fibre-alignment. RNA-seq on day-3 infarct tissue revealed upregulation of ECM degradation and inflammatory genes, but downregulation of ECM assembly/structure/organisation genes in fibulin-3 knockout mice. GSEA pathway analysis showed enrichment of inflammatory pathways and a depletion of ECM organisation pathways. Fibulin-3 originates from cardiac fibroblasts, is upregulated in human heart failure, and is necessary for correct ECM organisation/structural integrity of fibrotic tissue to prevent cardiac rupture post-infarct