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Muscle and spinal cord tissue was collected from WT, AR100 and AR20 control male mice at different stages of disease progression: presymptomatic mice (3 months old), symptomatic (12 months).
We have previously determined the extent of organ atrophy [15] in 12 week old symptomatic R6/2 mice for the heart, liver, kidneys, testes and skeletal muscle.
The efficacy of SP resulted in similarly poor parasitologic clearance in 2 10 month old asymptomatic infants when compared with 6 59 month old symptomatic children.
To search for a potential association between α-Syn related pathologies and tumor growth, we next measured the effect of α-Syn expression on tumor growth in old, symptomatic A53T α-Syn+/+ and control mice.
An open label single arm (SP) standard 28 day in vivo WHO antimalarial efficacy protocol was used in 6 to 59 months old symptomatic children and a modified protocol used in 2 to 10 months old asymptomatic infants.
Importantly, catalase expression and activity were similarly affected in young, healthy, mice and in old, symptomatic, mice.
Similar(52)
TBS- and SDS-soluble brain fractions (30 µg) from 17 months-old non symptomatic and 17 25 months-old symptomatic mice were used for assaying α-synuclein and PS129-α-synuclein proteins (Figure 7).
Although hippocampal neurogenesis has been shown to decrease with age [18], [19], we have demonstrated here that in the oldest symptomatic HD animals tested (33 weeks) there was in fact a significant increase in precursor numbers in vitro to levels greater than those recorded in much younger WT animals (16 weeks).
The purpose of this study was to compare the effects of house mite (HM) atopy on lung function in subsamples of 12-year-old symptomatic and nonsymptomatic preadolescent children taken from the community sample.
A booster dose of PCV in older symptomatic HIV-infected children (median age 128 mo), 79% of whom were on ART, however, induced only a modest increase in GMCs, indicating either absence of having induced or failure to sustain an anamnestic response.
A recent study using a transgenic mouse model of synucleinopathy (TgM83), demonstrated that inoculation of young asymptomatic mice with brain homogenates prepared from older symptomatic mice accelerated the presence of both αsyn hyperphosphorylated at serine 129 and aggregated αsyn and significantly decreased survival time [ 45].
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