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It has been postulated that activation of innate immune defences in pregnant women might contribute to the limitation of the occurrence and severity of congenital infection.
It has been postulated that activation of microglia and macrophages following brain injury aids survival of brain cells by removing cell debris [ 9, 10], and by promoting neuronal sprouting and growth as observed in vitro [ 11].
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It was postulated that activation of VEGFR2 on LECs might be needed to induce maximal lymphangiogenic signaling.
The mechanism of activation has not been precisely determined but it is postulated that activation might arise through the interaction of the homeodomain and C-terminal domain with general transcription factors such as TBP (TATA-box-binding protein) [ 30] as these regions of PRH bind to TBP in pulldown assays [ 16].
Moreover, it is postulated that needle proteins are involved in conducting an activation signal bidirectionally to coordinate the regulation of T3SS [61], [61].
It has been postulated that polyclonal activation of circulating, antigen specific memory B cells may account for the continuous generation of plasma cells and for the maintenance of humoral memory [28].
It has also been postulated that EGFR activation may be an important step in the progression to estrogen independence [ 51].
Tendons of the cervical multifidus muscles insert directly onto the capsular ligaments [ 13, 14] and it has been postulated that multifidus activation during the neuromuscular response to a rear-end automobile impact could increase the strain in the capsular ligaments above that imposed passively by the impact-induced head and neck dynamics [ 7, 13].
It has been postulated that sustained JNK activation is required to activate death-promoting downstream targets such as Bim and Bak [ 41].
Furthermore, it has been postulated that NLRP3 inflammasome activation can be mediated by pannexin-1 and P2X7 receptor, a member of the ATP-activated P2X purinergic receptors family [ 68].
Among other mechanisms it has been postulated that minocycline can inhibit microglial activation and develop beneficial effects by decreasing glutamate excitotoxicity.
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