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It has been hypothesized that abnormal regulation of neutrophil apoptosis, promoting longevity and necrotic death, may contribute to the ineffective resolution of inflammation in COPD.
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It is hypothesized that abnormal expression of these and related genes has a major impact on the pathophysiology of schizophrenia.
It is hypothesized that abnormal expression of genes involved in structural functions such as cytoskeleton stabilization has a major impact in the pathophysiology of schizophrenia.
Therefore, it was hypothesized that: H1.
It has been hypothesized that this abnormal pattern might favour the trigger and the repetition of migraine attacks [13], and therefore it could represent a possible target for migraine prophylaxis.
It has previously been hypothesized that an abnormal acetylation/deacetylation pattern and thereby an altered regulation of gene expression could play a role in the pathogenesis of type 2 diabetes [35].
Moreover, it has been hypothesized that the use of sperms with an abnormal P1/P2 ratio or defects of histone protamine may be responsible of imprinting diseases in the offspring conceived with ART [ 50].
First, it has been hypothesized that a high near-accommodation lag induces abnormal axial growth of the eye [ 16], though many studies have found no association between accommodative lag and myopic progression [ 17, 18].
It has therefore been hypothesized that, in some SSS patients, the disease may be caused by abnormal Popdc gene expression or function.
The presence of bacteria in the lower airways is, however, regarded as abnormal since these airways are sterile in healthy adults, and it has been hypothesized that the presence of bacteria in stable COPD represents a low-grade smouldering infection.
We thus hypothesized that abnormal responses of RA bone marrow CD34+ cells to TNF-α might result from abnormal expression of NFκB genes.
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