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Commonly used screening techniques for biomaterial based cartilage regeneration in pre-clinical small animal studies include by inducing a defect into the medial femoral condyle or the trochlear groove.
RAGE has been shown to have a major mechanistic role in this maladaptive response by reducing VEGF mRNA and by inducing a defect in signal transduction resulting in fewer monocytes in the tissue to stimulate angiogenesis [10 12].
RAGE has been shown to have a major mechanistic role in this maladaptive response by reducing VEGF mRNA and by inducing a defect in signal transduction of VEGF in monocytes which reduces their response to chemotactic protein-1, resulting in fewer monocytes in the tissue to stimulate angiogenesis [11, 12, 17].
CNIs are diabetogenic by inducing a defect in insulin secretion by interfering with the nuclear factor of activated T-cell signaling in pancreatic β-cells.
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Thus, immunosuppressive drugs (CNIs, glucocorticoids, and m-TOR inhibitors), by inducing an insulin secretion defect and insulin resistance, probably act as triggers for glucose metabolism abnormalities in patients at risk.
Published data indicate that HDAC1 knockdown by siRNA induces a mitotic defect, cell growth inhibition, and an increased percentage of apoptotic cells in human tumor cells [ 38].
Since chemotherapy and irradiation act primarily by inducing apoptosis, defects in the apoptotic pathway make the therapy less efficient [ 7].
Accumulating evidence suggests that free radical mediated oxidative stress is implicated in the pathogenesis of diabetic neuropathy by inducing neurovascular defects that result in endoneurial hypoxia and subsequent nerve dysfunction.
In filamentous fungi, actin cytoskeleton organization is commonly linked with endo- or exocytic pathways [ 40]; thus, hypersecretion induced by a defect in NCU01161 might result from alteration of such pathways.
Furthermore, our in vivo results showed that inhibition of miR-29b by in utero electroporation induced a profound defect in corticogenesis during mouse development.
Taken together, these data provide evidence that (i) the S81L mutation mainly induces a functional defect, by reducing the AGT catalytic activity and strongly decreasing the coenzyme binding affinity and (ii) the heterodimer G170R-Mi/S81L-Ma shows kcat and KD PLP) values similar to or lower than, respectively, those derived by the average of the corresponding ones of the homodimeric counterparts.
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