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It can be postulated that failure of signals through these receptors could affect the antigen-dependent pathway of B cell maturation during which CSR and SHM take place.
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Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
It could be postulated that in these cases failure of SOX2 to repress β-catenin activity may not be sufficient to sustain the growth of the pituitary mass and other factors (including other members of the SOX family) may be compensating for the impaired SOX2 function.
Therefore, it could be postulated that physiologic mucosal thickening does not contribute to implant failure.
It can be postulated that exogenously administered ALR provides beneficial effect reported in experimental fulminant hepatic failure [ 71] and cirrhosis [ 72] via mechanisms involving its actions on non-parenchymal cells or even on hepatocytes.
It has been postulated that the failure of angiogenesis in SSc may be due to a nonphysiological, overriding influence of antiangiogenic factors, which are present in high concentrations in the sera of patients with SSc [ 13- 15].
Previously, it was postulated that the failure of current treatments such as cyclodextrin (CYCLO) to correct the pathology of tissues such as the lung was due to the inability of CYCLO to reach lung macrophages (27, 34).
It has been postulated that this failure may originate from lowered BP in the candesartan treatment group because tissue hypoperfusion might accelerate ischemic damage in the acute phase after stroke.
The nursing home elderly are a group that are at high risk of infection, vaccine failure and mortality, and it is postulated that immunosenescence is associated with this increased risk [ 10].
Furthermore, it is postulated that the reduced sympathoadrenal response (the concept of hypoglycemia-associated autonomic failure) is induced by recent antecedent hypoglycemia, resulting in defective glucose counter-regulation and hypoglycemia unawareness that presents as recurrent cycles of hypoglycemia.
It is postulated that some of the germ cells within the gonadoblastoma, may have postponement or failure of the onset of meiosis and these cells could continue to divide mitotically [ 122].
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