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Membrane damage is repaired in autophagy- and PgE2-dependent manner.
Membrane damage is often identified as a major mechanism of this toxicity.
However, it is not known whether this membrane damage is the consequence of apoptotic degeneration or direct mechanical stress.
For production of short chain fatty acids, membrane damage is considered the primary mechanism of toxicity, particularly in regards to membrane integrity.
While it is generally accepted that membrane damage is the main mechanism of fatty acid toxicity, previous metabolic engineering efforts that increased membrane integrity did not enable increased carboxylic acid production.
We thus propose that the domain formation mechanism in which antimicrobial peptides exhibit activity solely by forming lipid domains without membrane damage is a major determinant of the antimicrobial activity of low amphipathic peptides.
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Ultrasound was rapidly microbicidal and cavitation-induced membrane damage was probably immediately lethal.
The results showed the membrane damage was synchronous with esterase inhibition during the exposure to sonication, leading to the immediate lethal effect.
The toxicity of individual mycotoxins on cell viability and cell membrane damage was determined using the MTT and lactate dehydrogenase (LDH) assays, respectively.
[NOTE: The treatment of cells with high-ionic-strength medium is a classical method for assaying for membrane damage after treating bacteria with heat.] Such membrane damage was not observed when cells were irradiated with far-UV radiation (254 nm) (A88).
The noise-induced membrane damage was assessed functionally, using membrane tracers with graded molecular sizes (propidium iodide and FITC-dextrans with molecular sizes of 3, 40, 500, and 2000 kDa), and morphologically, using DiO staining and semithin sections.
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