However, similar characterization of cause-effect in multidomain ferroelectric single crystals is lacking.
By combining the removal of irrelevant variables with this new characterization of weak cause, we then obtain techniques for deciding and computing causes and explanations in the structural-model approach, which can be done in polynomial time under suitable restrictions.
Moreover it takes into account the uncertainties on the maintenance knowledge by giving a fuzzy characterization of each cause.
We then present a new characterization of weak cause for a certain class of causal models in which the causal graph over the endogenous variables has the form of a directed chain of causal subgraphs, called decomposable causal graph.
Finally, by extending the new characterization of weak cause, we obtain similar techniques for computing the degrees of responsibility and blame, and hence also novel tractability results for structure-based responsibility and blame.
Many research teams, brought together in international consortiums, are engaged in the characterization of mutations causing tumorigenesis.
Much of our understanding of GAS epidemiology has been based on the characterization of strains causing local outbreaks of invasive disease and large surveillance networks encompassing geographically expansive catchment regions.
To the best of our knowledge, this particular characterization of changes caused by long-term CIH has not been attempted previously, and new data would provide a better understanding of these phenomena.
Recently, there have been a number of international workshops and projects to establish standardization of terms for these attributes, most with reference to the characterization of hepatotoxicity caused by exposure to a marketed drug in non-study outpatients who are referred for evaluation [ 5– 7].
The genetic basis for disrupted mitochondrial integrity as a cause of neurodegeneration in PD was uncovered by the functional characterization of mutations that cause loss of Parkin or PINK1 function in autosomal recessive forms of the disease.
The involvement of homologous proteins in vertebrate lens development was subsequently elucidated by the characterization of mutations that cause congenital human or murine ocular disorders and their comparison to mutations in model organisms [1].
