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We believe there are several broad implications arising from the patterns of coverage described: for individuals as both citizens assessing the appropriateness of government foreign policy toward LMICs and as potential private donors; and for domestic non-government organisations (NGOs) concerned with international development.
Clinical and pathological examinations of affected animals showed striking similarities to findings described for individuals suffering from zinc deficiency in cattle [ 4, 6, 18] and humans [ 19].
Despite PPVs of 96% and above for most races, significant limitations of the data quality were described for individuals of AIAN origin.
Although chromosomal deletions encompassing GRIA2 had been described for individuals with mental and developmental retardation (see ref. 12 for review), only recent studies have identified specific mutations in GRIA2 in the context of ID,, suggesting that GRIA2 haploinsufficiency might cause ID.
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A strong increase in mRNA levels has been described for individual genes using the same gene-optimization approach [10], [16], [17], [19], [31].
This can be observed in general, as risk evaluations and acceptable exposure doses are consistently only described for individual compounds (Table 3) without considering additive or synergistic effects among multiple compounds [ 16, 90].
We selected the fixed effects influencing FCR in the same step-wise manner as previously described for individual feeding traits except that the lamb random effect was not included in the model.
Interestingly, we observed that the body mass of the RasGrf1-Pttg1 DKO mice was significantly reduced (about 60-70%) in both males and females at 3 and 10 months of age as compared with their WT controls, but this reduction was quantitatively similar, and not stronger than that already previously described for individual RasGrf1 and Pttg1 KO mice [ 17, 86].
Irrespective of EBV, CD4+CD28- T cells were more expanded in CMV seropositive AS patients, as was described for healthy individuals and seropositive patients with RA [ 38].
Until the present time, a total of ∼122 germline variations in POLI gene have been described for human individuals in dbSNP (http://www.ncbi.nlm.nih.gov/projects/SNP), but the functional impacts of these genetic variations have not been biochemically evaluated yet.
Over 25 different individual genes are now known to produce muscular dystrophy, and many different "private" mutations have been described for each individual muscular dystrophy gene.
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