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Additionally, dysfunction of these molecules may also contribute to the etiology of several neurodegenerative conditions.
We conclude that dysfunction of these pathways may represent a point of convergence in the pathophysiology of several forms of inherited dystonia.
They are involved in apoptotic cell death and inflammation, and dysfunction of these enzymes is directly linked to a variety of diseases.
In conclusion, these studies strongly support an essential role for sweet taste receptors in maintaining an appropriate balance of glucose and insulin levels in the blood, and dysfunction of these proteins might hasten the development of type II diabetes.
The finding of severe pathological changes in some brainstem nuclei also raises the possibility that the dysfunction of these nuclei may contribute to the cognitive defects and increased rates of morbidity and mortality in patients with Alzheimer's disease.
The cumulative evidence makes a strong case implicating dysfunction of these systems in the pathogenesis of depression and leads us beyond the monoaminergic synapse in search of eagerly anticipated strategies to discover and develop better therapies for depression.
With the rapid change of urban area in Mashad city during the past decades, green spaces have been fragmented and dispersed causing impairment and dysfunction of these important urban elements.
Growing evidence suggests that dysfunction of these pathways contribute to the progressive loss of neurons in Alzheimer's disease (AD) and Parkinson's disease (PD), the two most frequent neurodegenerative disorders.
Dysfunction of these circuits leads to obesity, a growing health concern.
Dysfunction of these cells may be related to AD development through accumulation of amyloid β peptide.
Contraction and relaxation of airway smooth muscles is mediated, in part, by G protein-coupled receptors (GPCRs) and dysfunction of these receptors has been implicated in asthma.
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