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The binding of autologous IgG and exposure of recognition molecules, possibly including phosphatidylserine (PS), ultimately lead to recognition of senescent erythrocytes by macrophages of the reticulo-endothelial system.
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Recognition is activated by exposure of the recognition region which is covered with a part of the photoresponsive region that is modified by azobenzene [ 3].
As in vivo it is progressively degraded by proteinases, it can result in the exposure of new recognition sites with potent bioactivity [ 29].
The diagnosis is therefore based on a history of exposure, recognition of the cholinergic toxidrome, and improvement or resolution of symptoms after appropriate treatment [4, 9, 10].
Industrial suppression of toxicity data impaired accurate risk assessment, as did imprecise estimates of exposure, delayed recognition of low-dose effects, and use of adult data only.
The paucity of exposure prevents recognition of the channels as products of multiple channel anastomosed systems or single channel high-constructive systems.
A long incubation period (from 2 to 7 days) and lengthy diagnostic procedures cause an estimated lag time of approximately 2 weeks between time of exposure and recognition of the waterborne transmission [ 8].
There is some kind of tender but also scary exposure, some kind of recognition that passes between subject and object.
We show that in type VI secretion, contraction leads to exposure of the ClpV recognition motif, which is embedded in the type VI-specific four-helix-bundle N-domain of VipB.
Upon activation, α2m proteins undergo a conformational change that traps the pathogen protease within the protein, leading to the exposure of the TEP C-terminal recognition domain, which binds phagocytic cells and promotes endocytotic clearance.
There is, as so often when looking at the Romans, a feeling of double exposure: a simultaneous sense of recognition, that they were somehow "just like us" – alongside an opposite sense, of alienation and confusion.
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