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| 1 | High salt diet accelerates the progression of murine lupus through dendritic cells via the p38 MAPK and STAT1 signaling pathways显示文摘The increased incidence of systemic lupus erythematosus(SLE)in recent decades might be related to changes in modern dietary habits.Since sodium chloride(NaCl)promotes pathogenic T cell responses,we hypothesize that excessive salt intake contributes to the increased incidence of autoimmune diseases,including SLE.Given the importance of dendritic cells(DCs)in the pathogenesis of SLE,we explored the influence of an excessive sodium chloride diet on DCs in a murine SLE model.We used an induced lupus model in which bone marrow-derived dendritic cells(BMDCs)were incubated with activated lymphocyte-derived DNA(ALD-DNA)and transferred into C57BL/6 recipient mice.We observed that a high-salt diet(HSD)markedly exacerbated lupus progression,which was accompanied by increased DC activation.NaCl treatment also stimulated the maturation,activation and antigenpresenting ability of DCs in vitro.Pretreatment of BMDCs with NaCl also exacerbated BMDC-ALD-DNA-induced lupus.These mice had increased production of autoantibodies and proinflammatory cytokines,more pronounced splenomegaly and lymphadenopathy,and enhanced pathological renal lesions.The p38 MAPK–STAT1 pathway played an important role in NaClinduced DC immune activities.Taken together,our results demonstrate that HSD intake promotes immune activation of DCs through the p38 MAPK–STAT1 signaling pathway and exacerbates the features of SLE.Thus,changes in diet may provide a novel strategy for the prevention or amelioration of lupus or other autoimmune diseases. | Ze Xiu Xiao Xiaojiang Hu Ximei Zhang Zhigang Chen Julie Wang Ke Jin Feng Lin Cao Baoqing Sun Joseph A.Bellanti Nancy Olsen Song Guo Zheng | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 6 |
| 2 | Outcomes of systemic to pulmonary artery shunts in patients weighing less than 3 kg: Analysis of shunt type, size, and surgical approach显示文摘 | John W. Myers Nancy S. Ghanayem Yumei Cao Pippa Simpson Katie Trapp Michael E. Mitchell James S. Tweddell Ronald K. Woods | 2013 | The Journal of Thoracic and Cardiovascular Surgery2013，，： | 1 |
| 3 | Biomarkers for Primary Sjgren's Syndrome显示文摘Primary Sjo¨gren's syndrome(p SS) is a systemic autoimmune disease with exocrine gland dysfunction and multi-organ involvement. Recent progress in understanding the pathogenesis of p SS offers an opportunity to find new biomarkers for the diagnosis and assessment of disease activity. Screening noninvasive biomarkers from the saliva and tears has significant potential. The need for specific and sensitive biomarker candidates in p SS is significant. This review aims to summarize recent advances in the identification of biomarkers of Sjo¨gren syndrome, trying to identify reliable, sensitive, and specific biomarkers that can be used to guide treatment decisions. | Weiqian Chen Heng Cao Jin Lin Nancy Olsen Song Guo Zheng | 2015 | Genomics, Proteomics & Bioinformatics2015，13，4： | 1 |
| 4 | 模拟教学理论框架在心力衰竭高仿真模拟课程中的应用效果研究显示文摘目的探讨基于美国国家护理联盟(National League for Nursing)杰弗里斯(NLN Jeffries)仿真框架的心力衰竭护理高保真仿真教育对职前护理教育的影响。方法在美国萨克拉门托卡林顿学院进行心力衰竭高仿真模拟教学试点项目。23名学生参加了这项研究。本研究采用类实验设计,在教学前后测量学生的自我效能感、满意度和心力衰竭临床知识。结果结果显示,在高仿真模拟教学实施后,学生的自我效能感平均得分(45.39±7.88比38.91±8.35)、满意度(18.70±3.38比15.57±3.38)及心力衰竭临床知识得分(64.09±10.86比54.48±11.19)均明显提高(P<0.001)。该模拟教学设计中包含护士质量安全教育内容、以患者为中心的护理以及急性心力衰竭患者照护的团队合作,对教学效果产生了积极影响。结论基于NLN Jeffries理论框架的心力衰竭高仿真模拟教学提高了学生的知识、满意度、自我效能感及以患者为中心的护理、安全和团队合作意识。护理教育工作者在进行模拟教学计划时应考虑包含5个特性,即目标、解决问题、为学生提供支持、保真度和总结报告,同时结合安全、以患者为中心和团队合作教育,以保障教学效果。 | Tricia Nwokocha Nancy Cowan Pinio Yan Cao Holly Wei Satish Mahajan | 2023 | International Journal of Nursing Sciences2023，10，4： | 0 |
| 5 | Cell-autonomous effect of cardiomyocyte branched-chain amino acid catabolism in heart failure in mice显示文摘Parallel to major changes in fatty acid and glucose metabolism,defect in branched-chain amino acid(BCAA)catabolism has also been recognized as a metabolic hallmark and potential therapeutic target for heart failure.However,BCAA catabolic enzymes are ubiquitously expressed in all cell types and a systemic BCAA catabolic defect is also manifested in metabolic disorder associated with obesity and diabetes.Therefore,it remains to be determined the cell-autonomous impact of BCAA catabolic defect in cardiomyocytes in intact hearts independent from its potential global effects.In this study,we developed two mouse models.One is cardiomyocyte and temporal-specific inactivation of the E1αsubunit(BCKDHA-cKO)of the branched-chainα-ketoacid dehydrogenase(BCKDH)complex,which blocks BCAA catabolism.Another model is cardiomyocyte specific inactivation of the BCKDH kinase(BCKDK-cKO),which promotes BCAA catabolism by constitutively activating BCKDH activity in adult cardiomyocytes.Functional and molecular characterizations showed E1αinactivation in cardiomyocytes was sufficient to induce loss of cardiac function,systolic chamber dilation and pathological transcriptome reprogramming.On the other hand,inactivation of BCKDK in intact heart does not have an impact on baseline cardiac function or cardiac dysfunction under pressure overload.Our results for the first time established the cardiomyocyte cell autonomous role of BCAA catabolism in cardiac physiology.These mouse lines will serve as valuable model systems to investigate the underlying mechanisms of BCAA catabolic defect induced heart failure and to provide potential insights for BCAA targeted therapy. | Jia-yu Yu Nancy Cao Christoph DRau Ro-Po Lee Jieping Yang Rachel JRoth Flach Lauren Petersen Cansheng Zhu Yea-Lyn Pak Russell AMiller Yunxia Liu Yibin Wang Zhaoping Li Haipeng Sun Chen Gao | 2023 | Acta Pharmacologica Sinica2023，44，7： | 0 |
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