47 research outputs found
Accelerate Microstructure Evolution Simulation Using Graph Neural Networks with Adaptive Spatiotemporal Resolution
Surrogate models driven by sizeable datasets and scientific machine-learning
methods have emerged as an attractive microstructure simulation tool with the
potential to deliver predictive microstructure evolution dynamics with huge
savings in computational costs. Taking 2D and 3D grain growth simulations as an
example, we present a completely overhauled computational framework based on
graph neural networks with not only excellent agreement to both the ground
truth phase-field methods and theoretical predictions, but enhanced accuracy
and efficiency compared to previous works based on convolutional neural
networks. These improvements can be attributed to the graph representation,
both improved predictive power and a more flexible data structure amenable to
adaptive mesh refinement. As the simulated microstructures coarsen, our method
can adaptively adopt remeshed grids and larger timesteps to achieve further
speedup. The data-to-model pipeline with training procedures together with the
source codes are provided.Comment: 28 pages, 11 figure
A conceptual framework for implementation fidelity
<p>Abstract</p> <p>Background</p> <p>Implementation fidelity refers to the degree to which an intervention or programme is delivered as intended. Only by understanding and measuring whether an intervention has been implemented with fidelity can researchers and practitioners gain a better understanding of how and why an intervention works, and the extent to which outcomes can be improved.</p> <p>Discussion</p> <p>The authors undertook a critical review of existing conceptualisations of implementation fidelity and developed a new conceptual framework for understanding and measuring the process. The resulting theoretical framework requires testing by empirical research.</p> <p>Summary</p> <p>Implementation fidelity is an important source of variation affecting the credibility and utility of research. The conceptual framework presented here offers a means for measuring this variable and understanding its place in the process of intervention implementation.</p
Heterogeneity and Strategic Choices: The Case of Stock Repurchases
Strategic decisions are fundamentally tough choices. Theory suggests that managers are likely to display bounded rationality. Empirics on the other hand assume rationality in choice behavior. Recognizing this inherent disconnect between theory and empirics, we try to account for behavioral biases using a theoretically consistent choice model. The traditional approach to modeling strategic choice has been to use discrete choice models and make inference on the conditional mean effects. We argue that the conditional mean effect does not capture behavioral biases. The focus should be on the conditional variance. Explicitly modeling the conditional variance (in the discrete choice framework) provides us with valuable information on individual level variation in decision-making. We demonstrate the effect of ignoring the role of variance in choice modeling in the context of firm’s decisions to conduct open market repurchases. We show that when taking into account the heterogeneity in choices, manager’s choices of conducting open market repurchases displays considerable heterogeneity and that not accounting for such heterogeneity might lead to wrong conclusions on the mean effects
Genetic Signatures of Exceptional Longevity in Humans
Like most complex phenotypes, exceptional longevity is thought to reflect a combined influence of environmental (e.g., lifestyle choices, where we live) and genetic factors. To explore the genetic contribution, we undertook a genome-wide association study of exceptional longevity in 801 centenarians (median age at death 104 years) and 914 genetically matched healthy controls. Using these data, we built a genetic model that includes 281 single nucleotide polymorphisms (SNPs) and discriminated between cases and controls of the discovery set with 89% sensitivity and specificity, and with 58% specificity and 60% sensitivity in an independent cohort of 341 controls and 253 genetically matched nonagenarians and centenarians (median age 100 years). Consistent with the hypothesis that the genetic contribution is largest with the oldest ages, the sensitivity of the model increased in the independent cohort with older and older ages (71% to classify subjects with an age at death>102 and 85% to classify subjects with an age at death>105). For further validation, we applied the model to an additional, unmatched 60 centenarians (median age 107 years) resulting in 78% sensitivity, and 2863 unmatched controls with 61% specificity. The 281 SNPs include the SNP rs2075650 in TOMM40/APOE that reached irrefutable genome wide significance (posterior probability of association = 1) and replicated in the independent cohort. Removal of this SNP from the model reduced the accuracy by only 1%. Further in-silico analysis suggests that 90% of centenarians can be grouped into clusters characterized by different “genetic signatures” of varying predictive values for exceptional longevity. The correlation between 3 signatures and 3 different life spans was replicated in the combined replication sets. The different signatures may help dissect this complex phenotype into sub-phenotypes of exceptional longevity
Building Dynamic Capabilities: Innovation Driven By Individual, Firm, and Network Level Effects
Following the dynamic capabilities perspective, we suggest that antecedents to innovation can be found at the individual,
firm, and network level. Thus, we challenge two assumptions common in prior research: (1) that significant variance exists
at the focal level of analysis, while other levels of analysis are assumed to be homogeneous, and (2) that the focal level of
analysis is independent from other levels of analysis. Accordingly, we advance a set of hypotheses to simultaneously assess the
direct effects of antecedents at the individual, firm, and network level on innovation output. We then investigate whether a
firm’s antecedents to innovation lie across different levels. To accomplish this, we propose two competing interaction
hypotheses. We juxtapose the hypothesis that the individual, firm, and network level antecedents to innovation are
substitutes versus the proposition that these innovation mechanisms are complements. We test our multi-level theoretical
model using an unusually comprehensive and detailed panel dataset that documents the innovation attempts of global
pharmaceutical companies within biotechnology over a 22-year time period (1980-2001). We combine these data with
direct field observations conducted prior to, during, and after the completion of the study. We find evidence that the
antecedents to innovation lie across different levels of analysis and can have compensating or reinforcing effects on firm-level
innovative output
A Genome-Wide Association Study of Diabetic Kidney Disease in Subjects With Type 2 Diabetes
dentification of sequence variants robustly associated with predisposition to diabetic kidney disease (DKD) has the potential to provide insights into the pathophysiological mechanisms responsible. We conducted a genome-wide association study (GWAS) of DKD in type 2 diabetes (T2D) using eight complementary dichotomous and quantitative DKD phenotypes: the principal dichotomous analysis involved 5,717 T2D subjects, 3,345 with DKD. Promising association signals were evaluated in up to 26,827 subjects with T2D (12,710 with DKD). A combined T1D+T2D GWAS was performed using complementary data available for subjects with T1D, which, with replication samples, involved up to 40,340 subjects with diabetes (18,582 with DKD). Analysis of specific DKD phenotypes identified a novel signal near GABRR1 (rs9942471, P = 4.5 x 10(-8)) associated with microalbuminuria in European T2D case subjects. However, no replication of this signal was observed in Asian subjects with T2D or in the equivalent T1D analysis. There was only limited support, in this substantially enlarged analysis, for association at previously reported DKD signals, except for those at UMOD and PRKAG2, both associated with estimated glomerular filtration rate. We conclude that, despite challenges in addressing phenotypic heterogeneity, access to increased sample sizes will continue to provide more robust inference regarding risk variant discovery for DKD.Peer reviewe