Life sciences
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It has long been demonstrated that epidermal growth factor (EGF) has catabolic effects on bone. Thus, we examined the role of EGF in regulating mechanically induced bone modeling in a rat model of orthodontic tooth movement. ⋯ Local delivery of EGF-liposome stimulates osteoclastogenesis and tooth movement.
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This study was performed to elucidate whether mitogen-activated protein kinases (MAPKs) are involved in the modulation of apoptosis and cell-cycle arrest by N'-(11H-indolo[3,2-c]quinolin-6-yl)-N,N-dimethylethane-1,2-diamine (IQDMA), in human lung adenocarcinoma A549 cells. ⋯ These findings indicate that JNK/p38 MAPK pathways play an important role in IQDMA-induced G(2)/M arrest and apoptosis of A549 cells.
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In this study, we investigated whether the opioid system and the nitric oxide pathway were involved in the peripheral antinociception induced by a cannabinoid receptor agonist anandamide. ⋯ This study provides evidence that the peripheral antinociceptive effect of the cannabinoid receptor agonist anandamide may result from l-arginine/NO/cGMP pathway activation and that the opioid system is also involved.
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To investigate whether ischemia/reperfusion (I/R)-induced apoptosis in the bile duct epithelium could be mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors in biliary epithelial cells, we examined the effects of hypoxia/reoxygenation (H/R) on TRAIL cytotoxicity. ⋯ H/R up-regulated the expression of DR4 and DR5, and enhanced TRAIL-mediated apoptosis in normal human intrahepatic biliary epithelial cells.
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This study aims to investigate the role of peripheral delta(2) opioid receptors in cardiac tolerance to ischemia/reperfusion injury and to examine the contribution of PKC, TK, K(ATP) channels and the autonomic nervous system in delta(2) cardioprotection. ⋯ The cardioprotective mechanism of deltorphin II is mediated via stimulation of peripheral delta(2) opioid receptors. PKC and NOS are involved in both its infarct-sparing and antiarrhythmic effects. Infarct-sparing is dependent upon mitochondrial K(ATP) channel activation while the antiarrhythmic effect is dependent upon TK activation. Endogenous catecholamine depletion reduced antiarrhythmic effects but did not alter the infarct-sparing effect of deltorphin II.