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This could, however, have a detrimental effect on preterm infants as exaggerated oxygen free radical formation may contribute to the development of such neonatal diseases as retinopathy of prematurity and broncho-pulmonary dysplasia, as well as to cardiovascular disease.
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In this scenario, the regenerative potential of the vessel wall would be preserved even when CPC start to get dysfunctional, as long as enough CPC are still available, able to home, and do not yet themselves contribute to endothelial dysfunction, e.g. through the exaggerated generation of oxygen radicals.
These impairments may stem from decreased NO synthesis and/or release, in combination with exaggerated consumption by reactive oxygen species (ROS) [ 16].
What's more, a study of their saliva showed an exaggerated response to the low oxygen conditions, including a proliferation of the enzymes that are associated with altitude headache.
At sites of tissue injury and inflammation, oxygen gradients become exaggerated – and it is within relatively oxygen-deplete tissue environments that myeloid cells are required to migrate and function.
PPAR α null mice develop more hypertrophy, production of more reactive oxygen species as well as an exaggerated production of extracellular matrix components [ 35, 36].
64 The primary causes of dyspnea and exercise limitation are reduced breathing reserve, dynamic hyperinflation, and an exaggerated ventilatory response to exercise because of limitation in oxygen transfer due to loss of alveolar capillary surface area.
The finding that epinephrine can produce exaggerated aerobic glycolysis within muscles, decrease splanchnic and hepatic blood flow, and may increase oxygen consumption, despite an increase in oxygen delivery to the tissues likely explains the increased arterial lactate and reduced pH [ 4, 7, 8].
Therefore, these data demonstrate that the exaggerated hypoxia response observed in basal-like tumors cannot be solely attributed to decreased oxygen levels.
Culture of aASCs under 3% oxygen resulted in reduced expression of NOX1 compared with aASCs that were grown under normoxic conditions, further indicating exaggerated activity of NOX1 as a probable cause for ROS accumulation in aASCs.
The mechanism behind this phenomenon involves increased levels of reactive oxygen species (ROS), as HKII knockdown increased ROS accumulation, and treatment with the antioxidant N-acetylcysteine (NAC) abrogated the exaggerated response.
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