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| 1 | Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease显示文摘AIM To determine if manipulation of dietary advanced glycation end product(AGE), intake affects nonalcoholic fatty liver disease(NAFLD) progression and whether these effects are mediated via RAGE. METHODS Male C57Bl6 mice were fed a high fat, high fructose, high cholesterol(HFHC) diet for 33 wk and compared with animals on normal chow. A third group were given a HFHC diet that was high in AGEs. Another group was given a HFHC diet that was marinated in vinegar to prevent the formation of AGEs. In a second experiment, RAGE KO animals were fed a HFHC diet or a high AGE HFHC diet and compared with wildtype controls. Hepatic biochemistry, histology, picrosirius red morphometry and hepatic mR NA were determined. RESULTS Long-term consumption of the HFHC diet generated significant steatohepatitis and fibrosis after 33 wk. In this model, hepatic 4-hydroxynonenal content(a marker of chronic oxidative stress), hepatocyte ballooning, picrosirius red staining, α-smooth muscle actin and collagen type 1A gene expression were all significantly increased. Increasing the AGE content of the HFHC diet by baking further increased these markers of liver damage, but this was abrogated by pre-marination in acetic acid. In response to the HFHC diet, RAGE-/-animals developed NASH of similar severity to RAGE+/+ animals but were protected from the additional harmful effects of the high AGE containing diet. Studies in isolated Kupffer cells showed that AGEs increase cell proliferation and oxidative stress, providing a likely mechanism through which these compounds contribute to liver injury. CONCLUSION In the HFHC model of NAFLD, manipulation of dietary AGEs modulates liver injury, inflammation, and liver fibrosis via a RAGE dependent pathway. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD. | Christopher Leung Chandana B Herath Zhiyuan Jia Sof Andrikopoulos Bronwyn E Brown Michael J Davies Leni R Rivera John B Furness Josephine M Forbes Peter W Angus | 2016 | World Journal of Gastroenterology2016，22，35： | 7 |
| 2 | A Cognitive Behavioral Coaching Intervention for the Treatment of Perfectionism and Self-Handicapping in a Nonclinical Population显示文摘 | Hugh Kearns Angus Forbes Maria Gardiner | 2007 | Behavior Change2007，24，3： | 1 |
| 3 | 心理韧性导向的青少年1型糖尿病患者结构化治疗与教育课程的开发及初步实践显示文摘背景我国青少年1型糖尿病患者疾病控制不佳,给家庭和社会带来沉重负担。目前国内糖尿病教育主要面向2型糖尿病患者,缺乏针对青少年1型糖尿病患者的自我管理支持项目。目的开发心理韧性导向的青少年1型糖尿病患者结构化治疗与教育课程,并验证其在我国青少年1型糖尿病群体中的适用性和可行性。方法2020年1—5月,以心理韧性模型为切入点,通过文献分析和访谈对青少年1型糖尿病患者进行需求分析,借鉴现有1型糖尿病结构化教育模式,开发心理韧性导向的结构化治疗与教育课程,并通过专家会议进一步修订和完善心理韧性导向的青少年1型糖尿病患者结构化治疗与教育课程。采用门诊张贴海报和打电话的方式招募潜在参与者,在南京医科大学第一附属医院进行预试验,从招募应答率、真实性和可接受性3个方面评价课程可行性。结果心理韧性导向的青少年1型糖尿病患者结构化治疗与教育课程终稿涵盖认知、动作技能和情感3个领域,12项认知领域目标、14项动作技能领域目标及17项情感领域目标,共43项教学目标。课程采用小组式教学法,每组5~8名患者,1名医生和1名护士,6次课为1个课程周期。共招募8例1型糖尿病患者进行心理韧性导向的青少年1型糖尿病患者结构化治疗与教育课程的可行性评价,其中6例患者完成了所有课程。患者表示该课程内容全面、贴近生活、氛围轻松,参与后自我管理能力增强、对疾病接受度提高、情绪调节能力改善。结论心理韧性导向的青少年1型糖尿病患者结构化治疗与教育课程内容系统可行性高,值得进一步临床验证。 | 罗丹 徐晶晶 王玉冰 李明子 Forbes Angus | 2023 | 中国全科医学2023，26，27： | 1 |
| 4 | Advanced glycation end products augment experimental hepatic fibrosis显示文摘 | Michelle Goodwin Chandana Herath Zhiyuan Jia Chris Leung Melinda T Coughlan Josephine Forbes Peter Angus | 2013 | J Gastroenterol Hepatol2013，，2： | 1 |
| 5 | Informal carer activities,carer burden and health status in multiple sclerosis显示文摘 | Angus Forbes Alison While Lucia Mathes | 2007 | Clinical Rehabilitation2007，21，6： | 1 |
| 6 | Clinical intervention research in nursing显示文摘 | Angus Forbes | 2009 | International Journal of Nursing Studies2009，46，： | 1 |
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