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It is currently known that the relationships between the different parts of the nervous system are mediated by neurotransmitters and that their disorders lead to unbalanced functioning of certain structures and to the development of well known diseases.
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In Figure 2(c), for unbalanced function based MDR, the TNs are not always higher than the TPs.
In contrast, we demonstrated that our proposed unbalanced function based MDR is suitable for an imbalanced data set.
The MDR method was briefly introduced and the unbalanced function based MDR method was explained in detail as follows.
The results show that unbalanced function based MDR can avoid the drawback of common MDR in an unbalanced real data set.
The effect of IFIT4 on monocyte differentiation into DCs was suggested to be partially responsible for this unbalanced function of monocytes and DCs in SLE [ 2].
Here we provide an example to show how the unbalanced function based MDR works (see Supplementary File in Supplementary Material available online at http://dx.doi.org/10.1155/2015/454091).org/10.1155/2015/454091
The unbalanced function based MDR model can explore the epistasis network of SNPs AGT, ACE, and AT1 R of RAS genes and identify strongly significant hypertension association.
Thus, the best unbalanced function based MDR model can correctly predict high order SNP-SNP interactions of hypertension susceptibility using real data sets.
Here, we introduce an unbalanced function based on multifactor dimensionality reduction (MDR) for multiloci genotypes to detect high order gene-gene (SNP-SNP) interaction in unbalanced cases and controls of HT data.
Surprisingly, a high (>2) FcopyA copy number was also associated with susceptibility to SLE (Table 2), suggesting that the unbalanced functions of FCGR3A (both a deficiency and an overload) play a role in the pathogenesis of SLE.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com