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Methodological considerations are a major concern when carrying out molecular epidemiological studies of diagnostic markers to avoid errors that increase the potential for bias.
However, we did not filter these markers to avoid removing potentially useful information, and also because a rigorous study of the behavior of the MI approach at different missing rates is merited.
To date, in tongue cancer, stage is the most common prognostic factor used, but prognosis varies considerably even among similar tumours; and hence, we need better prognostic markers to avoid unnecessary adjuvant treatment for those with a favourable prognosis (Bello et al, 2010a, 2010b).
In order to create an informative dataset of common autosomal markers, to avoid detection of false positive signals of association and to remove SNPs incorrectly genotyped, we excluded from 905,556 called markers, SNPs without map references, SNPs with call rate < 95%, MAF < 0.05 and out of Hardy-Weinberg Equilibrium (P<10−5).
Markers that meet any of the following conditions were excluded: low call rate (<98% subjects received values for the marker), G/C and A/T markers (to avoid strand issues), deviation from Hardy-Weinberg equilibrium at p <10 −8, significant cohort calling discrepancy and being monomorphic.
We conclude that (i) some studies on primate spermatogonia probably have to be re-evaluated to prevent misinterpretation of data and (ii) future studies should employ unequivocal combinations of technically and biologically well-established markers to avoid unjustified conclusions from cell culture experiments with the rare primate (and human) testis tissue.
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Consequently, Lily-All and Tulip-All assemblies were not used for markers development to avoid possible mistakes related to the assembly of these relatively distant genotypes.
Our results show that confirmation of second-line resistance with phenotypic DST should remain mainstay unless the sensitivity of molecular markers improves, to avoid unfavorable effects on infection control and patient outcomes.
Another alternative for developing codominant markers is to avoid SSRs entirely and to design PCR primers to conserved exons in protein-coding genes to screen for polymorphisms in the intervening intron (EPIC markers, for example as developed as an alternative to microsatellites for H. armigera, [ 49]).
We used also marker information to avoid building chimeric metacontigs from different LGs (see Text S1 for more details).
Moreover, they restricted the questions to a single marker (CD150) to avoid having too many different experimental arms.
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