Fundamental analysis of the failure of polymer-based fiber reinforced composites

A mathematical model is described which will permit predictions of the strength of fiber reinforced composites containing known flaws to be made from the basic properties of their constituents. The approach was to embed a local heterogeneous region (LHR) surrounding the crack tip into an anisotropic elastic continuum. The model should (1) permit an explicit analysis of the micromechanical processes involved in the fracture process, and (2) remain simple enough to be useful in practical computations. Computations for arbitrary flaw size and orientation under arbitrary applied load combinations were performed from unidirectional composites with linear elastic-brittle constituent behavior. The mechanical properties were nominally those of graphite epoxy. With the rupture properties arbitrarily varied to test the capability of the model to reflect real fracture modes in fiber composites, it was shown that fiber breakage, matrix crazing, crack bridging, matrix-fiber debonding, and axial splitting can all occur during a period of (gradually) increasing load prior to catastrophic fracture. The computations reveal qualitatively the sequential nature of the stable crack process that precedes fracture

Fracturing highly disordered materials

We investigate the role of disorder on the fracturing process of heterogeneous materials by means of a two-dimensional fuse network model. Our results in the extreme disorder limit reveal that the backbone of the fracture at collapse, namely the subset of the largest fracture that effectively halts the global current, has a fractal dimension of $1.22 \pm 0.01$. This exponent value is compatible with the universality class of several other physical models, including optimal paths under strong disorder, disordered polymers, watersheds and optimal path cracks on uncorrelated substrates, hulls of explosive percolation clusters, and strands of invasion percolation fronts. Moreover, we find that the fractal dimension of the largest fracture under extreme disorder, $d_f=1.86 \pm 0.01$, is outside the statistical error bar of standard percolation. This discrepancy is due to the appearance of trapped regions or cavities of all sizes that remain intact till the entire collapse of the fuse network, but are always accessible in the case of standard percolation. Finally, we quantify the role of disorder on the structure of the largest cluster, as well as on the backbone of the fracture, in terms of a distinctive transition from weak to strong disorder characterized by a new crossover exponent.Comment: 5 pages, 4 figure

Financial attractiveness of wood production in smallholder plantations of Central Vietnam in the context of developing carbon markets

In Vietnam, fast-growing Acacia hybrid dominates commercial smallholdings and is largely managed in short rotations for pulpwood. However, increasing demand for logwood implies growing Acacia hybrid in longer rotations. One way of encouraging smallholders to prolong the rotation would be payments for aboveground carbon storage. Thus, this study evaluated the financial attractiveness of shifting from pulpwood to logwood production, with and without hypothetical carbon payments of $5,$10 and $20 tCO(2)e ha(-1). The data were drawn from smallholder interviews, a plantation inventory and a market study. The growth models for a 5-year pulpwood regime and various logwood regimes used for financial modelling were developed in CO2FIX simulation software. With a financially optimal rotation length of 9-10 years, the study finds that growing Acacia hybrid for logwood is much more profitable than growing it for pulpwood. However, due to thinning in logwood regime, a financially optimal logwood regime stores only 15-16% more carbon than a 5-year pulpwood regime. Consequently, carbon payments at any of the three price levels would not shift the financially optimal rotation length. The study concluded that carbon payments alone are unlikely to be an effective means to encourage smallholders in central Vietnam to prolong the rotation.Peer reviewe

Increased iron content in the heart of the Fmr1 knockout mouse

Peer reviewe

Systemic Inflammation Induced Changes in Protein Expression of ABC Transporters and Ionotropic Glutamate Receptor Subunit 1 in the Cerebral Cortex of Familial Alzheimer`s Disease Mouse Model

Alzheimer's disease (AD) is an incurable disease, with complex pathophysiology and a myriad of proteins involved in its development. In this study, we applied quantitative targeted absolute proteomic analysis for investigation of changes in potential AD drug targets, biomarkers, and transporters in cerebral cortices of lipopolysaccharide (LPS)-induced neuroinflammation mouse model, familial AD mice (APdE9) with and without LPS treatment as compared to age-matched wild type (WT) mice. The ABCB1, ABCG2 and GluN1 protein expression ratios between LPS treated APdE9 and WT control mice were 0.58 (95% CI 0.44-0.72), 0.65 (95% CI 0.53-0.77) and 0.61 (95% CI 0.52-0.69), respectively. The protein expression levels of other proteins such as MGLL, COX-2, CytC, ABCC1, ABCC4, SLC2A1 and SLC7A5 did not differ between the study groups. Overall, the study revealed that systemic inflammation can alter ABCB1 and ABCG2 protein expression in brain in AD, which can affect intra-brain drug distribution and play a role in AD development. Moreover, the inflammatory insult caused by peripheral infection in AD may be important factor triggering changes in GluN1 protein expression. However, more studies need to be performed in order to confirm these findings. The quantitative information about the expression of selected proteins provides important knowledge, which may help in the optimal use of the mouse models in AD drug development and better translation of preclinical data to humans. (c) 2021 American Pharmacists Association. Published by Elsevier Inc. All rights reserved.Peer reviewe

Regular Physical Exercise Modulates Iron Homeostasis in the 5xFAD Mouse Model of Alzheimer’s Disease

Dysregulation of brain iron metabolism is one of the pathological features of aging and Alzheimer’s disease (AD), a neurodegenerative disease characterized by progressive memory loss and cognitive impairment. While physical inactivity is one of the risk factors for AD and regular exercise improves cognitive function and reduces pathology associated with AD, the underlying mechanisms remain unclear. The purpose of the study is to explore the effect of regular physical exercise on modulation of iron homeostasis in the brain and periphery of the 5xFAD mouse model of AD. By using inductively coupled plasma mass spectrometry and a variety of biochemical techniques, we measured total iron content and level of proteins essential in iron homeostasis in the brain and skeletal muscles of sedentary and exercised mice. Long-term voluntary running induced redistribution of iron resulted in altered iron metabolism and trafficking in the brain and increased iron content in skeletal muscle. Exercise reduced levels of cortical hepcidin, a key regulator of iron homeostasis, coupled with interleukin-6 (IL-6) decrease in cortex and plasma. We propose that regular exercise induces a reduction of hepcidin in the brain, possibly via the IL-6/STAT3/JAK1 pathway. These findings indicate that regular exercise modulates iron homeostasis in both wild-type and AD mice

Increased Expression and Activity of Brain Cortical cPLA2 Due to Chronic Lipopolysaccharide Administration in Mouse Model of Familial Alzheimer’s Disease

Cytosolic phospholipase A2 (cPLA2) is an enzyme regulating membrane phospholipid homeostasis and the release of arachidonic acid utilized in inflammatory responses. It represents an attractive target for the treatment of Alzheimer’s disease (AD). Previously, we showed that lipopolysaccharide (LPS)-induced systemic inflammation caused abnormal lipid metabolism in the brain of a transgenic AD mouse model (APdE9), which might be associated with potential changes in cPLA2 activity. Here, we investigated changes in cPLA2 expression and activity, as well as the molecular mechanisms underlying these alterations due to chronic LPS administration in the cerebral cortex of female APdE9 mice as compared to saline- and LPS-treated female wild-type mice and saline-treated APdE9 mice. The study revealed the significant effects of genotype LPS treatment on cortical cPLA2 protein expression and activity in APdE9 mice. LPS treatment resulted in nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) activation in the cortex of APdE9 mice. The gene expressions of inflammation markers Il1b and Tnfa were significantly elevated in the cortex of both APdE9 groups compared to the wild-type groups. The study provides evidence of the elevated expression and activity of cPLA2 in the brain cortex of APdE9 mice after chronic LPS treatment, which could be associated with NFkB activation