22,005 research outputs found
sj-docx-1-tam-10.1177_17588359231221907 – Supplemental material for Major adverse cardiovascular events in advanced-stage lung cancer: a multicenter cohort study
No full textSupplemental material, sj-docx-1-tam-10.1177_17588359231221907 for Major adverse cardiovascular events in advanced-stage lung cancer: a multicenter cohort study by Chih-Hao Chang, Shih-Hao Huang, Hung-Yu Huang, Meng-Hung Lin, Chung-Shu Lee, Hsin-Fu Lee, Jason Chia-Hsun Hsieh and Chun-Yu Cheng in Therapeutic Advances in Medical Oncology</p
Developing Collaborative Applications with Mobile Cloud-A Case Study of Speech Recognition
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V2X: An Automated Tool for Building SystemC-Based Simulation Environments in Designing Multicore Systems-on-Chips
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Pipeline Schedule Synthesis for Real-Time Streaming Tasks with Inter/Intra-instance Precedence Constraints
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Epidemiological Studies on Multiple Risk Factors for Myopia in Taiwan: Gene-Environment Interaction
No full textAnalysis of EGF signaling in healthy aging promotion in caenorhabditis elegans
No full textThe increase in longevity expectancy has been a focused issue goal of much current aging research. Many genes have been noted to modulate longevity of simple model systems, acting through distinct mechanisms. However, in principle, promotion of healthy aging of individual tissues can be accomplished without a major impact on the longevity endpoint. As such, healthspan-only genes may have been missed by genetic screens for longevity. New screens for tissue–specific betterment of aging phenotypes were anticipated to reveal a class of genes that might be manipulated for tissue-specific anti-aging outcomes. We identified two novel healthspan regulators, called HPA-1 and HPA-2 (for the high performance in old age locomotory phenotypes that their disruption confers) that delay age-associated locomotory decline when they are knocked down by RNAi or by genetic deletion. Surprisingly, hpa-1 and hpa-2 do not regulate healthspan through canonical recognized longevity pathways. Instead, the structure of HPA proteins implicated a novel function of EGF signaling in anti–aging protection, and my genetic studies supported this mechanism. Activated EGF signaling confers a positive effect on multiple aging phenotypes, acting through the downstream branch of the EGF pathway involving PLCanalysis defined the temporal and spatial benefits from EGF signaling. EGF/lin-3 ligand is expressed into late life and acts throughout life to influence healthy aging. lin-3 alternative slice variants, lin-3S and lin-3XL show healthspan promotion. Muscle and neuron are the most potent tissue for EGFR signaling on healthspan enhancement. I also identified global and tissue-specific modulators of healthy aging in the EGF pathway and identified candidate calcium-sensitive transducers of the anti-aging function of EGF signaling. Recent data in vertebrates suggest that EGF signaling might contribute to long-term maintenance. Thus, EGF signaling may exert a conserved impact on healthy aging and might be a plausible reagent for anti-aging therapies.Ph. D.Includes bibliographical referencesIncludes vitaby Shih-Hung Y
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