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Because a mild mouse model of SMA presented with EMG abnormalities [49], we also examined 6 month old control and Actb-MNsKO mice for spontaneous muscle depolarization consistent with motor neuron degeneration.
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To confirm involvement of mature BDNF and CREB activation in neuroprotection of PMC-12, we performed in vivo study using a mild ischemic mouse model [ 22, 23].
The hepatic accumulation of PPL was observed as an early response to cholestasis; it was detectable as early as 2 days post-BDL and even in a milder cholestatic mouse model lacking the hallmarks of severe obstructive injury (i.e., dietary CA administration).
Our detailed characterization of the mild myopathy and tendinopathy in the mouse model of mild PSACH may also help in the management and early diagnosis of some forms of PSACH-MED, specifically in those children that present with tiredness and muscle weakness prior to the diagnosis of an underlying skeletal dysplasia.
The present study was designed to test the anti-depressant effects of EOPF and the possible mechanisms in an chronic, unpredictable, mild stress (CUMS -induced mouse model.
These factors drove clear effects in cell models [ 46, 47], but rather mild effects in R6/2 mouse model [ 14, 15].
In that study, LMP2 and LMP7 were detected in a mouse model of mild transient ischemia (30 min).
In this study, we present a detailed study of skeletal muscle, tendon and ligament from a mouse model of mild PSACH harbouring a COMP mutation.
By using a mouse model of mild chronic cerebral hypoperfusion, we show that ABCB1 protein levels in brain capillaries were significantly decreased 24 hours after 1 VO.
Here we report a detailed study of the phenotypic and morphological effect of a C-terminal COMP mutation on skeletal muscle, Achilles tendon and spinal ligament in a mouse model of mild PSACH-MED (20).
Our previous study has shown that there is a correlation between the TLR4-Traf6 signandng and the severity of pancreatic inflammation in a mouse model with mild AP induced by caerulein.
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