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The purpose of this study was to develop a novel isogenic rat model of impaired vasculogenesis of the regenerate mandible in order to determine quantifiable metrics of vascular injury and associated damage.
As the diabetic mouse is a recognised model of impaired healing, which may share some characteristics of human chronic wounds, the results of this in vivo study, taken together with those relating the positive effects of ORC/collagen in vitro, may predict the beneficial use of this device in the clinical setting.
From an autoimmune hypothesis to a model of impaired mitochondria, these provocative explanations challenge conventional wisdom, and may, in fact, open the door to a new way of thinking about ASDs.
We report here on the first mouse model of impaired Mcph1-function.
A mammalian model of impaired fecundity with abnormal lipoprotein metabolism also has been described, but different mechanisms are likely responsible for its reproductive dysfunction.
With this goal in mind, in our studies we use a well‐established model of impaired energy metabolism by incubating neuronal cells in a medium not containing glucose.
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Clinical importance of this signaling pathway is evidenced by the fact that animal models of impaired nitrergic neurotransmission reveal phenotypes resembling major human gastrointestinal motility disorders [3] [7].
Its retina is cone dominant and a number of disease models of impaired vision exist in larval zebrafish [4], [5], most of which were identified in large-scale mutagenesis screens.
Improving activity-dependent plasticity using PDE1 inhibitors should be seriously considered in other animal models of impaired cortical development, since orientation selectivity map formation is believed to share similarities to the development of other cortical areas [13], [83], [84], and because impairments in sensory function are present in many other neurodevelopmental disorders [85] [89].
Animal models of impaired bone healing are rare.
The use of animal models of impaired extinction has revealed an important prerequisite for the clinical use of HDAC inhibitors.
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