https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34087 Wed 17 Nov 2021 16:20:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14924 Wed 11 Apr 2018 10:46:03 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19499 Wed 11 Apr 2018 09:49:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26496 ex vivo osteoclast formation of bone marrow cells from MTX-treated rats (p < 0.001). However, MTX-induced changes in bone volume, trabecular architecture, metaphyseal mRNA expression of pro-osteoclastogenic cytokines, and marrow adiposity were not significantly affected by the co-administration of genistein. This study suggests that genistein may suppress MTX-induced osteoclastogenesis; however, further studies are required to examine its potential in protecting against MTX chemotherapy-induced bone damage.]]> Wed 02 Oct 2019 10:14:51 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30512 Wed 02 Oct 2019 10:14:24 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46671 n = 4; 5,438 ± 783 pg/ml vs. control 193 ± 27 pg/ml, P < 0.05). Repeated hypoglycemia significantly reduced the plasma epinephrine response to subsequent hypoglycemia (n = 4; 2,179 ± 220 pg/ml vs. 5,438 ± 783 pg/ml, P < 0.05). Activation of medullary C1 (n = 4; 50 ± 5% vs. control 3 ± 1%, P < 0.05) and C3 (n = 4; 45 ± 5% vs. control 4 ± 1%, P < 0.05) neurons was significantly increased after a single episode of hypoglycemia. Activation of C1 (n = 4; 12 ± 3%, P < 0.05) and C3 (n = 4; 19 ± 5%, P < 0.05) neurons was significantly reduced in the HAAF groups. Hypoglycemia prevention or treatment with naloxone did not restore the plasma epinephrine response or C1 and C3 neuronal activation. Thus repeated hypoglycemia reduced the activation of C1 and C3 neurons mediating adrenal medullary responses to subsequent bouts of hypoglycemia.]]> Tue 29 Nov 2022 09:14:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32446 Thu 27 Jan 2022 15:57:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38163 Thu 24 Aug 2023 15:10:03 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34250 75% cure rate following chemotherapy; there is an increasing population of survivors who live with chronic bone defects. Studies suggest that these defects are the result of reduced bone from increased marrow fat formation and increased bone resorption following chemotherapy. These changes probably result from altered expression/activation of regulatory molecules or pathways regulating skeletal cell formation and activity. Treatment with methotrexate, an antimetabolite commonly used in childhood oncology, has been shown to increase levels of proinflammatory/pro-osteoclastogenic cytokines (e.g., enhanced NF-κB activation), leading to increased osteoclast formation and bone resorption, as well as to attenuate Wnt signaling, leading to both decreased bone and increased marrow fat formation. In recent years, understanding the mechanisms of action and potential health benefits of selected nutraceuticals, including resveratrol, genistein, icariin, and inflammatory fatty acids, has led to preclinical studies that, in some cases, indicate efficacy in reducing chemotherapy-induced bone defects. We summarize the supporting evidence.]]> Fri 22 Feb 2019 16:56:01 AEDT ]]>