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It has been hypothesized that activation of VEGFA may induce pathologic angiogenesis beneath the RPE layer.
First, it has been hypothesized that activation of the innate immune system through mobilization of monocytes to tissue macrophages develops an inflammatory state associated with increased risk of cancer and mortality [ 19– 219.
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It is hypothesized that activation of extracellular signal-related kinase (ERK) is critical in activating matrix metalloproteinases (MMPs) during abdominal aortic aneurysm (AAA) formation.
Based on these data it may be hypothesized that activation of both clusters by chromosomal rearrangements might be not restricted to thyroid tumors.
Since activation of ER-α can promote cell proliferation through cross-talk with other receptors such as the IGF1-R, it was hypothesized that activation of IGF1-R may be involved in the 17β-ED induction of SCD-1.
Since it is known that thermogenesis can be induced by diet, it could be hypothesized that activation of leptin receptors in the ARC could be involved in diet-induced BAT activity.
It has been hypothesized that repetitive activation of trigeminovascular neurons and consequently repetitive activation of modulatory pain pathways may lead to impairment of function or partial neuronal cell damage in these areas through the liberation of free radicals [1].
In addition to the roles of VEGFR1 activation in tumor endothelial cells, it has been hypothesized that VEGFR1 activation mediates the mobilization of bone marrow-derived cells (BMDCs) into blood circulation [4].
Both HB22.7 and rituximab activate the p38 signaling pathway, and it has been hypothesized that p38 activation may mediate cytotoxic effects.
It has been hypothesized that microglial activation and the subsequent increase of pro-inflammatory cytokines play an important role in the pathogenesis of PD.
In this context, it has been hypothesized that the activation of STAT-3 may be due to kinases that cannot be suppressed by SOCS-3 or that tumor cells may develop strategies to bypass the negative regulation mediated by SOCS-3 [ 40].
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