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We developed Stress Transcription Factor Identification Algorithm (STFIA), which integrates these two kinds of high throughput genome-scale data (gene expression and TF-gene association data) to identify plausible stress TFs that regulate the target genes to confer stress protection.
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While it is biologically plausible that stress could play an etiological role in genetically susceptible individuals, there are no reported positive associations between stress and autoimmune induced hypothyroidism in the current literature [ 60– 60].
It is also plausible that stress, racism and overcrowding (and the other potential mediators discussed above) lead to lower SES which, in turn, has a detrimental impact on mental wellbeing.
As we had observed that stimulation of glucocorticoid receptors results in an increase in surface GluA1, it seemed plausible that stress-induced LTP is also triggered via CP-AMPARs.
An association between job strain and diabetes is biologically plausible (11) because stress response increases secretion of the fight-or-flight hormone cortisol, which stimulates glucose production in the liver and antagonizes the action of insulin in peripheral tissues (12– 12).
It is also plausible that the stress associated with medical need or food insufficiency may increase parental stress and depressive symptoms that adversely affect the quality of parenting behaviors that are relevant to child health.
We illustrate the complexity and subjective nature of the process used to generate a plausible house price stress test scenarios.
It is plausible that increased stress response gene expression restricts cotyledon development in SEs as a result of reallocation of resources away from cotyledonary reserves.
It is plausible that multiple stress kinases employ similar downstream mechanisms to mediate their functions, and perhaps do so in a context-dependent manner.
Plausible causes of stress in the wake of wildfires include loss of property, shelter, money, and other basic individual resources; physical incapacitation or injury; and disruption of sharing and support networks (Fowler 2003).
Thus, it is plausible that oxidative stress may modulate multiple mechanisms (e.g., p38 and CRM1) capable of inhibiting ERK oscillations, and the antioxidant status of the cell system may be an additional variable for consideration.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com