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Sepsis is frequently complicated by acute kidney injury, which is associated with higher risk of in-hospital mortality [3, 4], and by disseminated intravascular coagulation (DIC) due to a massive activation of the coagulation system [5, 6].
Participants with acute motion sickness did not only show low endocannabinoid signaling, they also demonstrated a massive activation of the hypothalamic-pituitary-adrenal (HPA) axis.
In the mean time this dual subcellular compartmentation renders spatially feasible the massive activation of the strictosidine pool upon organelle reunion occurring during herbivore feeding.
The subsequent accumulation of p53 in the nucleus ultimately results in the massive activation of the downstream signaling, whereby a range of diverse antiproliferation and proapoptotic genes are actively transcribed by the p53 transcription factor.
At the moment, apart from an efficient physical separation of SGD from the vacuole-accumulated strictosidine which circumvents the potential deleterious effect of a massive activation of the strictosidine pool, the physiological reason for the intriguing SGD and RGD nuclear sequestration appears unclear.
The model also illustrates the possible mechanism of massive activation of the strictosidine vacuolar pool upon enzyme-substrate reunion occurring during potential herbivore feeding constituting a so-called "nuclear time bomb" in reference to the "mustard oil bomb" commonly used to describe the myrosinase-glucosinolate defence system in Brassicaceae.
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The water stress provoked by the massive invasion of xylem vessels by bacteria may be one of the causes of the massive activation of ABA-related genes during disease.
The high bicarbonate levels could be explained by the severe ECV depletion and the subsequent massive activation of renin angiotensin aldosterone system (RAAS), resulting in the override of the Tmax of proximal tubular bicarbonate reabsorption and the impossibility to excrete the bicarbonate excess [ 14].
One possible explanation for this could be that in the acute phase after HRG-β1 addition, there was a massive activation of Akt due to the already mutated PIK3CA in T47-DERβ cells, an activation that ERβ could not inhibit.
Thus, different pathogenetic mechanisms may funnel into similar disease pathway(s), leading to massive activation of Mφ and providing the rationale for targeted anti-Mφ therapy.
The most extensively studied category, apoptosis, is characterized by the massive activation of caspases, chromatin condensation, and a reduction in cell volume.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com