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Complete mitochondrial (mt) genome sequencing is becoming increasingly common for phylogenetic reconstruction and as a model for genome evolution.
We study a model for genome evolution that incorporates both beneficial and detrimental effects of HGT.
It might appear at first glance that such a stop-and-go model for genome scanning would be insufficiently effective.
An explicit population-genetic analysis of this discrepancy would be interesting but one needs a good model for genome rearrangements, of course.
Because yeast cells have served as the model for genome stability research for years, the wealth of knowledge in this field has been gathered for this organism.
Next, using the assumption that the scaling laws are time invariant, we derive a 'null model' for genome evolution that accounts for the observed scaling laws.
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The objectives of this work were to (1) present a multivariate model for genome-wide and region-wise association studies, (2) perform simultaneous estimation of genomic effects (allele substitution effects) for mastitis resistance using more than one trait, and (3) estimate covariances between traits across the chromosomes and across regions of various sizes.
A genetic stochastic process model for genome-wide joint analysis of biomarker dynamics and disease susceptibility with longitudinal data.
To provide a more comprehensive model for genome-wide Tup1 recruitment, we used ChIP-chip assays to identify the genome-wide distributions of Tup1 and Ssn6.
Lymphoblastoid cell lines (LCLs) constitute a well-established pharmacogenomic model for genome-wide expression profiling [ 18, 19].
To address this shortcoming, we included computationally predicted transcriptional regulatory interactions based on an improved version of a previously developed statistical model for genome-wide TF binding site enrichment [ 22] (see Methods).
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