Voronoi cells, fractal dimensions and fibre composites.

The use of fibre-reinforced polymer matrix composite materials is growing at a faster rate than the gross domestic product (GDP) in many countries. An improved understanding of their processing and mechanical behaviour would extend the potential applications of these materials. For unidirectional composites, it is predicted that localized absence of fibres is related to longitudinal compression failure. The use of woven reinforcements permits more effective manufacture than for unidirectional fibres. It has been demonstrated experimentally that compression strengths of woven composites are reduced when fibres are clustered. Summerscales predicted that clustering of fibres would increase the permeability of the reinforcement and hence expedite the processing of these materials. Commercial fabrics are available which employ this concept using flow-enhancing bound tows. The net effect of clustering fibres is to enhance processability whilst reducing the mechanical properties. The effects reported above were qualitative correlations. To improve the design tools for reinforcement fabrics we have sought to quantify the changes in the micro/meso-structure of woven reinforcement fabrics. Gross differences in the appearance of laminate sections are apparent for different weave styles. The use of automated image analysis is essential for the quantification of subtle changes in fabric architecture. This paper considers Voronoi tessellation and fractal dimensions for the quantification of the microstructures of woven fibre-reinforced composites. It reviews our studies in the last decade of the process-property-structure relationships for commercial and experimental fabric reinforcements in an attempt to resolve the processing vs. properties dilemma. A new flow-enhancement concept has been developed which has a reduced impact on laminate mechanical properties

The influence of Antarctic subglacial volcanism on the global iron cycle during the Last Glacial Maximum

Marine sediment records suggest that episodes of major atmospheric CO₂ drawdown during the last glacial period were linked to iron (Fe) fertilization of subantarctic surface waters. The principal source of this Fe is thought to be dust transported from southern mid-latitude deserts. However, uncertainty exists over contributions to CO₂ sequestration from complementary Fe sources, such as the Antarctic ice sheet, due to the difficulty of locating and interrogating suitable archives that have the potential to preserve such information. Here we present petrographic, geochemical and microbial DNA evidence preserved in precisely dated subglacial calcites from close to the East Antarctic Ice-Sheet margin, which together suggest that volcanically-induced drainage of Fe-rich waters during the Last Glacial Maximum could have reached the Southern Ocean. Our results support a significant contribution of Antarctic volcanism to subglacial transport and delivery of nutrients with implications on ocean productivity at peak glacial conditions

Investigating the history of volatiles in the solar system using synchrotron infrared micro-spectroscopy

keywords: Synchrotron infrared micro-spectroscopy, CM chondrite meteorite, Murchison, Aqueous alteration, Asteroids adsurl: https://ui.adsabs.harvard.edu/abs/2018InPhT..94..244K adsnote: Provided by the SAO/NASA Astrophysics Data Syste

Cannabinoid receptor type 2 activation induces a microglial anti-inflammatory phenotype and reduces migration via MKP induction and ERK dephosphorylation

<p>Abstract</p> <p>Background</p> <p>Cannabinoid receptor type 2 (CBR2) inhibits microglial reactivity through a molecular mechanism yet to be elucidated. We hypothesized that CBR2 activation induces an anti-inflammatory phenotype in microglia by inhibiting extracellular signal-regulated kinase (ERK) pathway, via mitogen-activated protein kinase-phosphatase (MKP) induction. MKPs regulate mitogen activated protein kinases, but their role in the modulation of microglial phenotype is not fully understood.</p> <p>Results</p> <p>JWH015 (a CBR2 agonist) increased MKP-1 and MKP-3 expression, which in turn reduced p-ERK1/2 in LPS-stimulated primary microglia. These effects resulted in a significant reduction of tumor necrosis factor-α (TNF) expression and microglial migration. We confirmed the causative link of these findings by using MKP inhibitors. We found that the selective inhibition of MKP-1 by Ro-31-8220 and PSI2106, did not affect p-ERK expression in LPS+JWH015-treated microglia. However, the inhibition of both MKP-1 and MKP-3 by triptolide induced an increase in p-ERK expression and in microglial migration using LPS+JWH015-treated microglia.</p> <p>Conclusion</p> <p>Our results uncover a cellular microglial pathway triggered by CBR2 activation. These data suggest that the reduction of pro-inflammatory factors and microglial migration via MKP-3 induction is part of the mechanism of action of CBR2 agonists. These findings may have clinical implications for further drug development.</p

A Quantum Scattering Interferometer

The collision of two ultra-cold atoms results in a quantum-mechanical superposition of two outcomes: each atom continues without scattering and each atom scatters as a spherically outgoing wave with an s-wave phase shift. The magnitude of the s-wave phase shift depends very sensitively on the interaction between the atoms. Quantum scattering and the underlying phase shifts are vitally important in many areas of contemporary atomic physics, including Bose-Einstein condensates, degenerate Fermi gases, frequency shifts in atomic clocks, and magnetically-tuned Feshbach resonances. Precise measurements of quantum scattering phase shifts have not been possible until now because, in scattering experiments, the number of scattered atoms depends on the s-wave phase shifts as well as the atomic density, which cannot be measured precisely. Here we demonstrate a fundamentally new type of scattering experiment that interferometrically detects the quantum scattering phase shifts of individual atoms. By performing an atomic clock measurement using only the scattered part of each atom, we directly and precisely measure the difference of the s-wave phase shifts for the two clock states in a density independent manner. Our method will give the most direct and precise measurements of ultracold atom-atom interactions and will place stringent limits on the time variations of fundamental constants.Comment: Corrected formatting and typo

Accurate Material Parameter Extraction from Broadband Terahertz Spectroscopy

We demonstrate how a transfer function model based parameter extraction method, combined with total variance analysis, allows the extraction of both the complex refractive index and the thickness of a sample over a bandwidth of > 6 THz from THz time-domain spectroscopy measurements. We discuss how the techniques developed have been applied to absorbent powders measured at variable low temperatures

Virtuous and right action: A relaxed view

In this chapter I consider two questions about action evaluation: (1) Is it the central task of normative ethics to concern itself with action evaluation?, and (2) When it does concern itself with action evaluation, should its focus be on developing an account of right and wrong action, as opposed to, say, good and bad (or virtuous and vicious) action? I argue that for virtue ethicists, the task of providing an account of right action is not of central importance, and that the strength of virtue ethics lies in the fact that it allows us to evaluate actions in terms of a rich aretaic vocabulary. In the second half of the chapter I propose a “relaxed” virtue-ethical account of right action, which denies that rightness is a particular quality shared by all actions appropriately referred to as “right,” and acknowledges that the meaning of “right action” differs from one context to another

A transient homotypic interaction model for the influenza A virus NS1 protein effector domain

Influenza A virus NS1 protein is a multifunctional virulence factor consisting of an RNA binding domain (RBD), a short linker, an effector domain (ED), and a C-terminal 'tail'. Although poorly understood, NS1 multimerization may autoregulate its actions. While RBD dimerization seems functionally conserved, two possible apo ED dimers have been proposed (helix-helix and strand-strand). Here, we analyze all available RBD, ED, and full-length NS1 structures, including four novel crystal structures obtained using EDs from divergent human and avian viruses, as well as two forms of a monomeric ED mutant. The data reveal the helix-helix interface as the only strictly conserved ED homodimeric contact. Furthermore, a mutant NS1 unable to form the helix-helix dimer is compromised in its ability to bind dsRNA efficiently, implying that ED multimerization influences RBD activity. Our bioinformatical work also suggests that the helix-helix interface is variable and transient, thereby allowing two ED monomers to twist relative to one another and possibly separate. In this regard, we found a mAb that recognizes NS1 via a residue completely buried within the ED helix-helix interface, and which may help highlight potential different conformational populations of NS1 (putatively termed 'helix-closed' and 'helix-open') in virus-infected cells. 'Helix-closed' conformations appear to enhance dsRNA binding, and 'helix-open' conformations allow otherwise inaccessible interactions with host factors. Our data support a new model of NS1 regulation in which the RBD remains dimeric throughout infection, while the ED switches between several quaternary states in order to expand its functional space. Such a concept may be applicable to other small multifunctional proteins

A behavioral comparison of male and female adults with high functioning autism spectrum conditions

Autism spectrum conditions (ASC) affect more males than females in the general population. However, within ASC it is unclear if there are phenotypic sex differences. Testing for similarities and differences between the sexes is important not only for clinical assessment but also has implications for theories of typical sex differences and of autism. Using cognitive and behavioral measures, we investigated similarities and differences between the sexes in age- and IQ-matched adults with ASC (high-functioning autism or Asperger syndrome). Of the 83 (45 males and 38 females) participants, 62 (33 males and 29 females) met Autism Diagnostic Interview-Revised (ADI-R) cut-off criteria for autism in childhood and were included in all subsequent analyses. The severity of childhood core autism symptoms did not differ between the sexes. Males and females also did not differ in self-reported empathy, systemizing, anxiety, depression, and obsessive-compulsive traits/symptoms or mentalizing performance. However, adult females with ASC showed more lifetime sensory symptoms (p = 0.036), fewer current socio-communication difficulties (p = 0.001), and more self-reported autistic traits (p = 0.012) than males. In addition, females with ASC who also had developmental language delay had lower current performance IQ than those without developmental language delay (p<0.001), a pattern not seen in males. The absence of typical sex differences in empathizing-systemizing profiles within the autism spectrum confirms a prediction from the extreme male brain theory. Behavioral sex differences within ASC may also reflect different developmental mechanisms between males and females with ASC. We discuss the importance of the superficially better socio-communication ability in adult females with ASC in terms of why females with ASC may more often go under-recognized, and receive their diagnosis later, than males

Autism as a disorder of neural information processing: directions for research and targets for therapy

The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients. Identification of these factors, and the common developmental path into which theyfeed, is hampered bythe large degrees of convergence from causal factors to altered brain development, and divergence from abnormal brain development into altered cognition and behaviour. Genetic, neurochemical, neuroimaging and behavioural findings on autism, as well as studies of normal development and of genetic syndromes that share symptoms with autism, offer hypotheses as to the nature of causal factors and their possible effects on the structure and dynamics of neural systems. Such alterations in neural properties may in turn perturb activity-dependent development, giving rise to a complex behavioural syndrome many steps removed from the root causes. Animal models based on genetic, neurochemical, neurophysiological, and behavioural manipulations offer the possibility of exploring these developmental processes in detail, as do human studies addressing endophenotypes beyond the diagnosis itself