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The latest break in the case is a pair of new studies showing that GPI has the means and opportunity to attack joints.
In previous observational studies a low use of GPI has already been documented [ 13].
GPI has been identified as a motility factor: autocrine motility factor (AMF) [ 5], neuroleukin [ 7, 8] or maturation factors [ 9].
Meanwhile, GPI has been found to function both as a cytokine and as a growth factor, to regulate cell migration, proliferation, apoptosis and cellular senescence.
GPI has been shown to regulate the proliferation and survival of tumor cells and prevent stress-induced apoptosis and oxidative stress-induced cellular senescence in tumor cells [ 24- 27].
A pathogenic role for IgG autoantibodies to glucose-6-phosphate isomerase (GPI) has been documented in the KRN/NOD model; it was found that infusions of these autoantibodies into otherwise healthy mice rapidly led to the development of synovitis [ 14].
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The final electrode position for the GPi had the tendency to go more laterally than medially.
The subthalamic nucleus (STN) and globus pallidus interna (GPi) have received much attention in the treatment of movement disorders because of their efficacious effects during surgical treatment [ 3].
Expression plasmids for RACE-mapped gL, the gL ORF and gL-GPI have been described [13].
In this respect, pathogenic human monoclonal antibodies that bind phospholipids in the absence of β2-GPI have been described [ 46, 47].
Numerous GP inhibitors (GPIs) have been synthesised targeting various substrate or cofactor binding sites, such as the AMP stimulatory, purine nucleoside and indole-binding sites (Hoover et al, 1998; Treadway et al, 2001).
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