Microforces and the Theory of Solute Transport

A generalized continuum framework for the theory of solute transport in fluids is proposed and systematically developed. This framework rests on the introduction of a generic force balance for the solute, a balance distinct from the macroscopic momentum balance associated with the mixture. Special forms of such a force balance have been proposed and used going back at least as far as Nernst's 1888 theory of diffusion. Under certain circumstances, this force balance yields a Fickian constitutive relation for the diffusive solute flux, and, in conjunction with the solute mass balance, provides a generalized Smoluchowski equation for the mass fraction. Our format furnishes a systematic procedure for generalizing convection-diffusion models of solute transport, allowing for constitutive nonlinearities, external forces acting on the diffusing constituents, and coupling between convection and diffusion.Comment: 17 page

Theory for atomic diffusion on fixed and deformable crystal lattices

We develop a theoretical framework for the diffusion of a single unconstrained species of atoms on a crystal lattice that provides a generalization of the classical theories of atomic diffusion and diffusion-induced phase separation to account for constitutive nonlinearities, external forces, and the deformation of the lattice. In this framework, we regard atomic diffusion as a microscopic process described by two independent kinematic variables: (i) the atomic flux, which reckons the local motion of atoms relative to the motion of the underlying lattice, and (ii) the time-rate of the atomic density, which encompasses nonlocal interactions between migrating atoms and characterizes the kinematics of phase separation. We introduce generalized forces power-conjugate to each of these rates and require that these forces satisfy ancillary microbalances distinct from the conventional balance involving the forces that expend power over the rate at which the lattice deforms. A mechanical version of the second law, which takes the form of an energy imbalance accounting for all power expenditures (including those due to the atomic diffusion and phase separation), is used to derive restrictions on the constitutive equations. With these restrictions, the microbalance involving the forces conjugate to the atomic flux provides a generalization of the usual constitutive relation between the atomic flux and the gradient of the diffusion potential, a relation that in conjunction with the atomic balance yields a generalized Cahn-Hilliard equation.Comment: To appear in Journal of Elasticity, 18 pages, requires kluwer macr

Capital Sequestration: Degrowth through Investing in Community-Led Transformations of Provisioning Systems

Investing in different futures is an existential challenge that much research within and adjacent to Ecological Economics engages with, yet organizations that recognize this social ecological imperative have few options for funding and implementing radical transformations to the needs and well-being provisioning systems that currently exist. Ecological macroeconomic ideas and EE principles of long term well being and justice on a livable planet will be explored in the context of the housing crisis in Canada, and a rural Ontario community organization attempting to find transformative solutions to the lived, local experience of this crisis. Provisioning systems for housing, when tied to real estate markets, debt money creation, land enclosures, and financialized supply chains, contribute to capital accumulation cycles; it is hardly possible to meet our housing needs, in aggregate, without also perpetuating the form of this provisioning system. The idea presented here, that of Capital Sequestration, proposes to remove capital from markets and `invests' this capital in land trusts as an intentional transformation of financial capital into social and ecological values. Through land and housing trusts as well as non-market funding pathways, Capital Sequestration is a method of investing in the transformation of provisioning systems through the sustained and collective boundary management of financial markets and incommensurable values. This practice offers significant promise as it applies ecological macroeconomic theory work, is grounded in the normative goals of and emerges from empirical research of EE, and meets a pressing need within society for imagining alternative economies

From the Anthropocene to mutual thriving: An Agenda for higher education in the Ecozoic

Higher education in the global North, and exported elsewhere, is complicit in driving the planet\u27s socio-ecological crises by teaching how to most effectively marginalize and plunder Earth and human communities. As students and activists within the academic system, we take a firm stand to arrest this cycle, and to redirect education toward teaching how to create conditions for all life to thrive. In this paper, we articulate a research and education agenda for co-constructing knowledge and wisdom, and propose shifts in the \u27ologies from the current, destructive modes to intended regenerative counterparts. We offer to shift from an ontology of separation to that of interconnectedness; from an epistemology of domination to that of egalitarian relationship; and from an axiology of development to that of plural values for world- and meaning-making. Such paradigm shifts reflect the foundational aspirations of the consilient transdiscipline of ecological economics. We analyze several introductory university textbooks in economics, law, and natural sciences, to demonstrate how destructive \u27ologies are taught in North American universities, and how such teaching implicitly undermines critical inquiry and effective challenge. Our strategy for change is to provide a new theoretical framework for education: the regenerative \u27ologies of the Ecozoic\u27, based on biophysicality, embedded relationality, pluralism, and the sustainable well-being of all members in the community of life

Multi-Phase Equilibrium of Crystalline Solids

A continuum model of crystalline solid equilibrium is presented in which the underlying periodic lattice structure is taken explicitly into account. This model also allows for both point and line defects in the bulk of the lattice and at interfaces, and the kinematics of such defects is discussed in some detail. A Gibbsian variational argument is used to derive the necessary bulk and interfacial conditions for multi-phase equilibrium (crystal-crystal and crystal-melt) where the allowed lattice variations involve the creation and transport of defects in the bulk and at the phase interface. An interfacial energy, assumed to depend on the interfacial dislocation density and the orientation of the interface with respect to the lattices of both phases, is also included in the analysis. Previous equilibrium results based on nonlinear elastic models for incoherent and coherent interfaces are recovered as special cases for when the lattice distortion is constrained to coincide with the macroscopic deformation gradient, thereby excluding bulk dislocations. The formulation is purely spatial and needs no recourse to a fixed reference configuration or an elastic-plastic decomposition of the strain. Such a decomposition can be introduced however through an incremental elastic deformation superposed onto an already dislocated state, but leads to additional equilibrium conditions. The presentation emphasizes the role of {configurational forces} as they provide a natural framework for the description and interpretation of singularities and phase transitions.Comment: 32 pages, to appear in Journal of the Mechanics and Physics of Solid

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe

Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation

Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa

Soft elasticity is not necessary for striping in nematic elastomers

The occurrence of striped domains in stretched nematic elastomers has been suggested as evidence for soft elasticity. Conversely, the neo-classical model of Bladon, Terentjev and Warner, which displays soft elasticity, predicts striping. Here we show that the postulated director rotations and shears in the domain regions are also predicted by more general constitutive models that do not involve any notion of softness. Striping in nematic elastomers may therefore be a more general phenomena that is not necessarily an indication of soft elasticity. Furthermore, constitutive models more general than the neo-classical model may also explain the behavior of some nematic elastomers that do not appear to exhibit striping.published or submitted for publicationis peer reviewe