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This means that under mild exposure to organic plasma, the enzyme does not become seriously dysfunctional.
Intriguingly, there exists a protective phenomenon, termed hypoxic preconditioning (hPC), that occurs when brief or mild exposure to hypoxia protects against a subsequent more severe hypoxia exposure.
Absence of oxygen indicated that the Fe NPs had not undergone oxidation even though mild exposure to air during the synthesis process.
Furthermore, activation of caspase 3 was highly increased in Ctns −/− mouse fibroblasts following mild exposure to H2O2 (Fig 9C), further confirming increased susceptibility to oxidative stress-induced apoptotic cell death in these cells.
This latter phenomenon is also known as hormesis, where a mild exposure to a stressor induces beneficial effects but is toxic at higher exposure levels (Morse 1998; Costantini et al. 2010).
These results indicate that mild exposure to proteotoxic stress conditions counteract the formation of age-associated protein deposits and demonstrate that cells with an age-associated deposit prior to encountering the stress predominantly reverted back to this state.
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Cross-resistance to multiple stresses and the lifespan-extending effects associated with mild exposures to these stresses is the basis for the "hormesis hypothesis" of aging [33].
This causes tumor cell death due to necrosis, incase of high dose of temperature time [8, 9, 10] or apoptosis due to mild exposure and cell sensitization to chemotherapy and radiotherapy incase sublethal dose of temperature time [11, 12].
Therefore, symptoms of mild exposure are anticipated to resemble T-cell mediated recall responses, similar T-cell mediatedin test.
In contrast to mild heat stress treatment, exposure to mild acid, salt and oxidative stress resulted in significantly increased transcription of catA and cellular catalase activity.
Mild exposure may cause mild oxidative stress that ignites cellular antioxidant defense systems; exposure to moderate to higher concentrations may gradually overwhelm antioxidant defense systems to induce apoptosis, while exposure to even higher concentrations for long periods may quickly overwhelm antioxidant defenses to stimulate prooxidative effects leading to cellular damage via necrosis.
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