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Based on the observation that in RA the aggressive phenotype of fibroblasts is maintained in the absence of inflammatory stimuli [ 17], it has been hypothesized that activated fibroblasts are permanently imprinted or altered by the specific environment [ 25].
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The resultant damage to muscle cells can occur in various ways; it is hypothesized that extra calcium may activate proteases or lipases within the cell, which eventually leads to muscle fiber breakdown and an increase in calcium influx, initiating a "vicious cycle" of further muscle damage and calcium release [ 24].
Therefore, it was hypothesized that: H1.
While it was hypothesized that active Net1 translocates from the nucleus to activate RhoA in the cytosol, this has not been specifically demonstrated.
It is hypothesized that activation of extracellular signal-related kinase (ERK) is critical in activating matrix metalloproteinases (MMPs) during abdominal aortic aneurysm (AAA) formation.
In the case of PEG-albumin, the mechanism related to viscosity remains unclear and it has been hypothesized that it may activate endothelial pathways by direct physical interaction of the PEG with the glycocalyx on the endothelium surface [ 37].
Furthermore, it has been hypothesized that prolonged ER stress activates cell death pathways [ 17, 18].
16– 19 In a rat model, it has been hypothesized that, in principle, CSD activates both vasoconstriction and vasodilatation in a biphasic fashion, the ratio between the 2 being shifted toward vasoconstriction by ischemic/hypoxic tissue conditions.
It has been hypothesized that the physical stress of MV activates the sympathetic nervous system [ 19].
Potentially explaining these observations, it has been hypothesized that ESAs could bind and activate EpoR on tumor cells to promote their growth and/or survival [ 8, 9] or stimulate EpoR on endothelial cells to promote tumor angiogenesis [ 10].
It has been hypothesized that HN stimulates its receptor(s) and activates signaling cascade(s) to exert its effects [2], [4].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com