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The release profile of IL-1ra from these microspheres was described previously, and is characterized by an initial burst release, decreasing to an approximately linear and sustained release over the initial 10 days.
The IL-1ra release profile was characterized by an initial burst release, decreasing to an approximately linear and sustained release over the initial 10 days.
RGC acts by decreasing inflammation (inhibition of IL-8 and TNF release), decreasing degranulation of mast cells (inhibition of histamine release), and limiting the angiogenesis process (inhibition of VEGF production and neovessel formation).
The Goα, GOA-1 and the DAG kinase, DGK-1, inhibit acetylcholine release, decreasing DAG levels at nerve terminals: GOA-1 by decreasing DAG production and DGK-1 by converting DAG to phosphatidic acid [ 28].
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The drug release decreased as the drug content increased in the micelles.
The lag time increased when the quantity of top layer increased, whereas drug release decreased.
Overall, the rate of release decreased and the duration increased with increasing microsphere size.
Drug release decreased as the NIPAA content increased and correlated to hydrogel elasticity.
The rate of SA release decreased with increasing polymer and CaCl2 concentrations, but polymer concentration was more effective.
The rate of glucose release decreased from 0.47 to 0.43 mM/min when the extrusion temperature decreased.
Percentage chlorhexidine diacetate release decreased upon reducing A or B block length and drug concentration or particle size.
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