Data-based detection and quantification of causation in complex, nonlinear dynamical systems is of paramount importance to science, engineering, and beyond. Inspired by the widely used methodology in recent years, the cross-map-based techniques, we develop a general framework to advance towards a comprehensive understanding of dynamical causal mechanisms, which is consistent with the natural interpretation of causality. In particular, instead of measuring the smoothness of the cross-map as conventionally implemented, we define causation through measuring the scaling law for the continuity of the investigated dynamical system directly. The uncovered scaling law enables accurate, reliable, and efficient detection of causation and assessment of its strength in general complex dynamical systems, outperforming those existing representative methods. The continuity scaling-based framework is rigorously established and demonstrated using datasets from model complex systems and the real world.

We establish by exact, nonperturbative methods a universality for the correlation functions in Kraichnan's``rapid-change''model of a passively advected scalar field. We show that the solutions for separated points in the convective range of scales are unique and independent of the particular mechanism of the scalar dissipation. Any non-universal dependences therefore must arise from the large length-scale features. The main step in the proof is to show that solutions of the model equations are unique even in the idealized case of zero diffusivity, under a very modest regularity requirement (square-integrability). Within this regularity class the only zero-modes of the global many-body operators are shown to be trivial ones (ie constants). In a bounded domain of size L , with physical boundary conditions, the``ground-state energy''is strictly positive and scales as L with an exponent L .

Gene expression data from microarrays are being applied to predict preclinical and clinical endpoints, but the reliability of these predictions has not been established. In the MAQC-II project, 36 independent teams analyzed six microarray data sets to generate predictive models for classifying a sample with respect to one of 13 endpoints indicative of lung or liver toxicity in rodents, or of breast cancer, multiple myeloma or neuroblastoma in humans. In total,> 30,000 models were built using many combinations of analytical methods. The teams generated predictive models without knowing the biological meaning of some of the endpoints and, to mimic clinical reality, tested the models on data that had not been used for training. We found that model performance depended largely on the endpoint and team proficiency and that different approaches generated models of similar performance. The conclusions and