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There is little evidence regarding long-term outcomes of locomotor dysfunction such as cardiovascular events, quality of life, and death.
We are conducting a prospective cohort study to evaluate risk of cardiovascular disease, quality of life, medical costs, and mortality attributable to locomotor dysfunction.
Taken together our results suggest that exogenous antioxidant cannabinoids can protect against and rescue from locomotor dysfunction in wild type (Canton-S) Drosophila exposed to stress stimuli.
Moreover, DMF ameliorated dopaminergic neurotoxicity in 6-OHDA-induced PD animal models as evidenced by amelioration of locomotor dysfunction, loss in striatal dopamine, and reductions in dopaminergic neurons in the substantia nigra and striatum.
BC4: Players who do not have cerebral palsy but have another disability with locomotor dysfunction in all four limbs and have similar functional ability to BC2 athletes.
Reduced lifespan in mutant LRRK2 (G2019S or R1441C) [128] N2; baIn20 [P dat-1 ::LRRK2 (G2019S) + P dat-1 ::GFP] UA118 Dopaminergic neuron Age-dependent degeneration of DAergic neurons, behavioural deficit, locomotor dysfunction and depletion of dopamine(~72 % loss).
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We further examined the effects of a reduction in neuronal PKA-R2 expression on Aβ42-induced locomotor dysfunctions.
In contrast, in the rutabaga mutant background (rut[1]), Aβ42 caused locomotor dysfunctions by 7 dae (Figure 4A, right).
These Aβ42 flies show late-onset, progressive short-term memory defects, locomotor dysfunctions, neurodegeneration, and premature death, accompanied by formation of Aβ42 deposits [13], [14].
Neuronal knockdown of milton by UAS-milton-RNAi driven by the pan-neuronal elav-GAL4 driver did not affect locomotor function up to 10 dae (Figure 7A, left), but caused locomotor dysfunctions after 17 dae (Figure 7A, left).
7, 8 Therefore, preventing these locomotor dysfunctions is considered essential to maintain quality of life.
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