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Exact(13)
Given the role that Jak2 selectively regulates DC-mediated innate immune response, we next examined its implication in the pathogenesis of septic shock, in which excessive innate immune response is suggested to be responsible for the disease etiology [32] [34].
A charter of reflective response is suggested.
Our results indicate that Salmonella Enteritidis biofilms altered their structure and extracellular glycoconjugate composition in response to flow and this response is suggested to be significant in the survival of this pathogen as biofilms.
A role for PKAcα in the network of signaling events leading to the activation of HSF1 during the stress response is suggested.
In particular, a dominant role of TRBV11 and type-1/CTL effector cells in the T-cell mediated antiviral immune response is suggested.
A neuroinflammatory response is suggested to play an important role in delirium, a common complication in older hospitalized patients.
Similar(47)
However, these findings correspond to those in other conditions such as AKI, where reduced oxidative stress [29] and attenuated neutrophil granulocyte response were suggested as possible mechanisms of steroid pretreatment on NGAL levels [30].
A role for inositols in the stress response was suggested, as was control of proline metabolism.
This dilution response was suggested to be either due to salivation or acid secretion.
The pathogenic link between MP and malignant disease remained unclear and a possible paraneoplastic response was suggested [ 5, 21].
Exaggerating BP response was suggested to be a sign of dysregulated autonomic function and thus could be associated with recurrent transient cerebral hypoperfusion.
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