Muscle atrophy involves a massive catabolism of intracellular components leading to a significant reduction in cellular and tissue volume. In this regard, autophagy, an intracellular mechanism that degrades proteins and organelles, has been implicated with muscle breakdown. Recently, it has shown that polycystin-2 (PC2), a membrane protein that belongs to the transient receptor potential (TRP) family, is required for the maintenance of cellular proteostasis, by regulating autophagy in several cell types.
View Article and Find Full Text PDFObjectives: To evaluate the effect of addition of zinc oxide and copper nanoparticles (ZnO/CuNp) into universal adhesives, on antimicrobial activity (AMA), cytotoxicity (CTX), water sorption (WS) and solubility (SO), microhardness (MH) and in vitro degree of conversion (DC), as well as resin-dentin microtensile bond strength (μTBS), nanoleakage (NL) and in situ DC.
Methods: ZnO/CuNp (0% [control]; 5/0.1 and 5/0.
Background: Masseter muscle paralysis induced by botulinum toxin type A (BoNTA) evokes subchondral bone loss in mandibular heads of adult rats and growing mice after 4 weeks. However, the primary cellular and molecular events leading to altered bone remodeling remain unexplored. Thus, the aim of the current work has been to assess the molecular response that precedes the early microanatomical changes in the masseter muscle and subchondral bone of the mandibular head in adult mice after BoNTA intervention.
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