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In oral and esophageal cancers, the p53 mutation load has been shown to be proportional to the extent of tobacco consumption, with an almost fourfold increase in mutation prevalence in heavy smokers as compared to nonsmokers (Brennan et al., 1995).
This mutation load has the potential to shape patterns of adaptive evolution via genetic linkage to beneficial mutations.
Once the deleterious mutation load has largely been shed, the reassortant virus would quickly rise and cause an antigenic cluster transition.
The process of outbreeding will indeed reduce the initial frequency at which recessive mutations are found on both copies of a gene, but this advantage will only last for a while, until the mutation load has increased to levels where the decrease in fertility due to mutations once again compensates for the rate at which they appear.
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Such a high mutation load had not been reported before and had originally been considered incompatible with life because COX-activities were extremely low in cultured myotubes with homoplasmy for the mutation [8].
It is likely that the mutational load has to be optimized depending on the vector size; an average mutation frequency of 1.25 mutations per 1 kb prove to be efficient to increase enzyme production and all three sequenced vector backbones contained five to six mutations.
There are of course a number of competing selective pressures acting on human populations (as well as a bottle neck in population size that can contribute to fixation of slightly deleterious mutations), and while pathogen load has been proposed as the most dominant driver of adaptation in the human lineage [ 70], cancer selection has a distinct possibility as a contributing factor [ 69, 73].
There are multiple mechanisms that could cause disease: a single point mutation that is clonally expanded throughout the cell, or a build up of random mutations (mutational load) that, having reached a threshold, causes the onset of disease.
In this report, both durum and bread wheat mutation lines and their wild-type siblings had reduced seed weights compared to their parental un-mutagenized lines indicating that the background mutation load is likely having an effect on this phenotype.
To test this hypothesis, we performed a dilution series of FFPE DNA samples for which the oncogene mutations, mutational load, and QFI had been well characterized.
In other words, females can show a strong preference based on male age-specific gamete mutation load even if they have no way of actually measuring gamete mutation load.
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