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Yet, we cannot ignore the fact that many students in the present study are struggling with the concept that novel traits in organisms initially arise through mutations, and not through some sort of centralized force.
By that they refer to the situation where many students are struggling with the concept that novel traits in organisms initially arise through mutations and not through some sort of a centralized force.
However, given the traditional focus of cancer biology on mutations, and not selection, the most frequently used tests for carcinogens (such as the Ames test; Mortelmans and Zeiger 2000) only determine whether a substance increases mutations, ignoring potential impacts on selection.
Direct comparison of mutation induction between mitotically active and quiescent embryonic fibroblasts indicated that only point mutations and not the larger genome rearrangements are replication-dependent.
It is worth re-emphasizing here that our present model only considers point mutations, and not the other more significant forms of genetic modifications including chromosomal instability, deletions etc.
Since the assay on demand primer and probe available from ABI for Smn exon 7 are too close or overlap the C-T and 2B mutations and could hinder interpretation of results, we designed and validated FL-Smn and Δ7Smn assays to specifically amplify Smn transcripts with similar efficiencies between the WT, C-T and 2B mutations and not cross react with human SMN.
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It would be important to consider the actual type of mutation (and not just which gene was mutated), since in a particular gene, one type of mutation may not be equivalent to another type.
You can have the mutation and not get the disease, or get it and not have the mutation.
This evidence shows that resistance arises due to receptor mutation and not due to JG068 lysogeny.
Although apoptosis is associated with mips1 mutation and not with mrp mutation, induction of the defense-related genes in 3mlpa may not be solely due to mips1 mutation.
In RCC the CA IX induction is associated with VHL-mutation and not with hypoxia as in brain tumours [ 52].
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