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Consequently, surfactant alterations are attributed to several pathological mechanisms, which have not been fully explored by human studies.
These alterations are attributed to the loss of thymic function, with an increase of peripheral proliferation of naive T cells.
These alterations are attributed to changes in vascular permeability due to the inflammatory process and the damage of epithelial cells that are responsible for the synthesis of milk components as well as changes in the enzymatic action of somatic cells or microorganisms in the infected mammary gland [ 6].
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Early and recent studies done in the ED and the intensive care unit (ICU) have reported significant delays in the diagnosis of NCSE, especially when subtle alterations were attributed to other etiologies [10 12].
When identified, the causes of these alterations were attributed to almost all the regulatory steps controlling AS [ 23– 25].
In all cases, the chief complaint and the metabolic alterations were attributed to DKA and all alternative diagnoses were ruled out.
The risk of cardiovascular mortality increases dramatically in women after menopause [ 22] because of lipid-metabolism alterations that are attributed to estrogen deprivation.
The post-shock mechanical response is significantly affected, with shock hardening exceeding the expected hardening due to the transient shock strain ϵs = (43) ln(VV0); this enhanced hardening, and other alterations in response, are attributed to the barriers presented to plastic deformation by the deformation twins.
Since paclitaxel was given intravenously, alterations in plasma pharmacokinetics are attributed entirely to alterations in paclitaxel distribution and/or systemic elimination.
Hyaluronan is the main component of the endothelial glycocalyx, and alterations in its concentration are attributed to glycocalyx volume loss.
We present a novel computational model for maladaptive cardiac growth in which kinematic changes of the cardiac chambers are attributed to alterations in cytoskeletal architecture and in cellular morphology.
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