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Steel's proposed solution is that even in the absence of strong evidence as to what mechanism(s) operate in a target system compared to a model system, scientists can compare the two systems with respect to certain crucial nodes in the respective causal structures, namely those where the two systems are most likely to differ.
One main line of research toward the representation of explicit models is the study of causal qualitative models and the respective causal QR techniques.
Notably, many of the cited research articles investigated respective causal components as therapeutic targets for T1DM or T2DM.
Phenotype/genotype associations provide evidence for a role of affected gene products in respective causal mechanisms and extensive resources document medically relevant gene variants [ 2, 3].
For the treatment of lung cancers, which is a group of heterogeneous diseases, persistent effort in developing individual therapies based on the respective causal genes is important.
Identification of loci and the respective causal variants in individual populations will be necessary to provide better insights as to whether genetic risks contribute to T2D disparity among different populations.
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If, for example, there is a maximal possibility, otherwise indiscernible from actuality, where mass and charge swap their respective causal-nomic roles (e.g., where objects resist acceleration in virtue of their charge), this maximal possibility would differ quidditistically from actuality.
First, there are various causal properties.
He argues that two agents could be in identical internal physical conditions while thinking different thoughts expressed by "water", and thus realizing different mental properties, because their respective histories of causal interaction and acquisition of the relevant concepts are different.
Hence, if these other genes were causing the respective eQTL, all causal genes in Qrr1 would be affected in cis.
In the following, we denote respective genes as causal genes.
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