• Title, Summary, Keyword: Aging Mechanism

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The Study on Aging Process Research (노화(老化)의 연구동향(硏究動向)에 관한 고찰(考察))

  • Lee, Hong-Min;Seo, Jung-Chul;Kim, Yong-Suk
    • Journal of Acupuncture Research
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    • v.18 no.1
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    • pp.146-156
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    • 2001
  • Objectrve : To research the trends of the study related to aging process, and to establish the direction of the study on aging process. Method : We reviewed the journal and essay about the aging process which are published as well in Korea as in foreign country. Results : 1. The study on the Oriental Medicine field can be classfied with the fourth. first, the study of single herb medication's effect on the aging process. second, the study of multiple herb medication's effect on the aging process. third, the study of herb-acupuncture solution's effect on the aging process. fourth, journal review. We find the fact that the study on the Oriental Medicine is concerned with pathology of deficiency syndrome of the kidneys, retention of phlegm and fluid, blood stasis. 2. On the Western Medicine field, mechanism and pathology of aging pracess primarily has been studied. The mechanism of aging process is classified with 'Wear and tear theory' and 'Genome-based theory'. Among the mechanism of aging process, 'Free radical theory' is the most important. Additionally 'Senescence-Accelerated Mouse' has been studied. 3. We review the journal published in foreign country and its subject was the following: first, moxibustion combined with acu-area skin allograft therapy for the aging was effective, second, the traditional chinese medicine bu-zhong-yi-qi-tang in mice have anti-aging effect. third, the overview Preventive geriatrics of Traditional chinese medicine. 4. We researched anti-aging effect study in the journal of the Korean Acupuncture and Moxibustion, and we found a few journal of Herb-acupuncture solution's anti-aging effect. Hereafter, it is necessory that we will study about relationship between acupuncture-moxibustion therpy and anti-aging effect using Senescence-Accelerated Mouse.

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A Comparison of the Failure Mechanism for High Power Converted White LEDs(3W) (고 출력 백색 변환용 LED(3W용)의 고장메커니즘 비교)

  • Yun, Yang-Gi;Jang, Jung-Sun
    • Journal of Applied Reliability
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    • v.12 no.3
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    • pp.177-186
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    • 2012
  • This paper presents a comparison of the failure mechanism for high power converted white LEDs(3W) with the commercially available YAG:Ce and silicate phosphor. We carry out the normal aging life test for 10,000 hours, the high temperature aging test for 8,000 hours, the high temperature and humidity aging test for 8,000 hours and the current aging testing for 5,000 hours. The optical and electrical parameters of LEDs were monitored, such as lumen, correlated color temperature (CCT), chromaticity coordinates(x, y), thermal resistance, I -V curve and spectrum intensity. The stress induced a luminous flux decay on LED in all experiments and causes a failure. So we try to find out what's a main failure mechanism for a high power LED.

Target Proteins Involved in Aging Mechanism as an Aging Molecular Marker (노화 분자마커로서 노화기전에 관여하는 타켓 단백질)

  • Kim, Moon-Moo
    • Journal of Life Science
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    • v.26 no.8
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    • pp.983-989
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    • 2016
  • All cells composing of our body undergo their destiny such as proliferation, differentiation, necrosis, apoptosis and senescence depending on their circumstance with time. The errors occurring in these processes develop several aberrations in phenotypes including cancer, inflammation, aging and diseases. New strategy and approach are required to screen anti-aging compounds derived from natural products. Therefore, here we explain the target proteins to play a key role in aging mechanism. In the first place, matrix metalloproteinases (MMPs) are involved in metastasis, chronic inflammation and skin aging as an aging marker. In particular, histone deacetylases (HDACs) give a great attention to aging researchers who try to extend the life span of animal model. In addition, we describe the signaling pathway related to senescence which p53, IGF-1 and SIRT1 play an important role in. Furthermore, autophagy is involved in the signaling pathway associated with aging. Several new compounds modulating the signaling pathway of senescence are introduced in this review. Here, we try to provide a new insight in the molecular basis for the aging mechanism and development of aging marker. In addition, the compounds introduced here could be available for pharmaceutical applications for the prevention and the treatment of diseases related to aging.

Development of a Safety Assessment System on Aging Management in Existing CANDU Steam Generators (가압중수로 증기발생기의 경년열화 관리를 위한 안전성 평가 시스템 개발)

  • Shin, So Eun;Lee, Jeong Hun;Park, Tong Kyu;Jung, Jong Yeob
    • Journal of the Korea Society of Systems Engineering
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    • v.10 no.1
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    • pp.49-56
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    • 2014
  • Since steam generator (SG) tubes are located in the boundary between the primary and secondary systems of nuclear power plant (NPP), the SG is one of the most important components in the aspects of the safety of NPP. The magnetite ($Fe_30_4$) deposition, so-called fouling, is generally known as a major aging mechanism of CANDU SGs, and this aging mechanism makes the heat transfer efficiency between the primary and secondary systems of NPP reduced. Therefore, the development of SG safety assessment system which can evaluate the effect of the SG aging degradation mechanism should be needed for safety of NPP. In this study, through the suggestion of the guideline for SG safety assessment, it is possible to strengthen the basic of establishing the effective SG aging management technique. The SG safety assessment is carried out by CATHENA(Canadian Algorithm for THErmalhydraulic Network Analysis). It is possible to determine the integrity of SGs by identifying the main safety parameters which can be changed by the aging degradation of CANDU SGs.

Mechanism of aging and prevention (노화의 기전과 예방)

  • Kim, Jay Sik
    • IMMUNE NETWORK
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    • v.1 no.2
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    • pp.104-108
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    • 2001
  • Aging is a senescence and defined as a normal physiologic and structural alterations in almost all organ systems with age. As Leonard Hayflick, one of the first gerontologists to propose a theory of biologic aging, indicated that a theory of aging or longevity satisfies the changes of above conditions to be universal, progressive, intrinsic and deleterious. Although a number of theories have been proposed, it is now clear that cell aging (cell senescence) is multifactorial. No single mechanism can account for the many varied manifestations of biological aging. Many theories have been proposed in attempt to understand and explain the process of aging. Aging is effected in individual by genetic factors, diet, social conditions, and the occurrence of age-related diseases as diabetes, hypertension, and arthritis. It involves an endogenous molecular program of cellular senescence as well as continuous exposure throughout life to adverse exogenous influences, leading to progressive infringement on the cell's survivability so called wear and tear. So we could say the basic mechanism of aging depends on the irreversible and universal processes at cellular and molecular level. The immediate cause of these changes is probably an interference in the function of cell's macromolecules-DNA, RNA, and cell proteins-and in the flow of information between these macromolecules. The crucial questions, unanswered at present, concerns what causes these changes in truth. Common theories of aging are able to classify as followings for the easy comprehension. 1. Biological, 1) molecular theories - a. error theory, b. programmed aging theory, c. somatic mutation theory, d. transcription theory, e. run-out-of program theory, 2) cellular theories - a. wear and tear theory, b. cross-link theory, c. clinker theory, d. free radical theory, e. waste product theory, 3) system level theory-a. immunologic/autoimmune theory, 4) others - a. telomere theory, b. rate of living theory, c. stress theory, etc. Prevention of aging is theoretically depending on the cause or theory of aging. However no single theory is available and no definite method of delaying the aging process is possible by this moment. The most popular action is anti-oxidant therapy using vitamin E and C, melatonin and DHEA, etc. Another proposal for the reverse of life-span is TCP-17 and IL-16 administration from the mouse bone marrow B cell line study for the immunoglobulin VDJ rearrangement with RAG-1 and RAG-2. Recently conclusional suggestion for the extending of maximum life-span thought to be the calory restriction.

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Analysis of Insulation Aging Mechanism in Generator Stator Windings (발전기 고정자 권선의 절연열화 메카니즘 분석)

  • 김희동
    • Journal of the Korean Institute of Electrical and Electronic Material Engineers
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    • v.15 no.2
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    • pp.119-126
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    • 2002
  • The mica/epoxy composite used in generator(rated 22 kV and 500 MW) stator windings was aged at 180$\^{C}$ for up to 1000 hours in air and hydrogen. The degradation mechanism was investigated through the defect of evolution and microstructural analysis by performing SEM(Scanning Electron Microscope). As the thermal aging time increases, the number of voids per unit volume increases at the mica/epoxy interface of generator stator windings. The aged specimens in hydrogen showed retarded generation and growth of voids. Accelerated aging tests were conducted using the combination of thermal and electrical aging in air and hydrogen. The aging was carried out at a combined stress such as thermal aging at 110$\^{C}$, electrical aging at 5.5 kV/mm and frequencies 420 Hz in air, and electrical aging at 5.5 kV/mm and frequencies 420 Hz in hydrogen (pressure 4 kg/㎠). Thermal and electrical aging generates large voids at the mica/epoxy interface in air. Electrical aging in hydrogen also generates small voids, delaminations and cracks in mica tapes.

Sarcopenia targeting with autophagy mechanism by exercise

  • Park, Sung Sup;Seo, Young-Kyo;Kwon, Ki-Sun
    • BMB Reports
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    • v.52 no.1
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    • pp.64-69
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    • 2019
  • The loss of skeletal muscle, called sarcopenia, is an inevitable event during the aging process, and significantly impacts quality of life. Autophagy is known to reduce muscle atrophy caused by dysfunctional organelles, even though the molecular mechanism remains unclear. Here, we have discuss the current understanding of exercise-induced autophagy activation in skeletal muscle regeneration and remodeling, leading to sarcopenia intervention. With aging, dysregulation of autophagy flux inhibits lysosomal storage processes involved in muscle biogenesis. AMPK-ULK1 and the $FoxO/PGC-1{\alpha}$ signaling pathways play a critical role in the induction of autophagy machinery in skeletal muscle, thus these pathways could be targets for therapeutics development. Autophagy has been also shown to be a critical regulator of stem cell fate, which determines satellite cell differentiation into muscle fiber, thereby increasing muscle mass. This review aims to provide a comprehensive understanding of the physiological role of autophagy in skeletal muscle aging and sarcopenia.

Alleviation of Senescence via ATM Inhibition in Accelerated Aging Models

  • Kuk, Myeong Uk;Kim, Jae Won;Lee, Young-Sam;Cho, Kyung A;Park, Joon Tae;Park, Sang Chul
    • Molecules and Cells
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    • v.42 no.3
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    • pp.210-217
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    • 2019
  • The maintenance of mitochondrial function is closely linked to the control of senescence. In our previous study, we uncovered a novel mechanism in which senescence amelioration in normal aging cells is mediated by the recovered mitochondrial function upon Ataxia telangiectasia mutated (ATM) inhibition. However, it remains elusive whether this mechanism is also applicable to senescence amelioration in accelerated aging cells. In this study, we examined the role of ATM inhibition on mitochondrial function in Hutchinson-Gilford progeria syndrome (HGPS) and Werner syndrome (WS) cells. We found that ATM inhibition induced mitochondrial functional recovery accompanied by metabolic reprogramming, which has been known to be a prerequisite for senescence alleviation in normal aging cells. Indeed, the induced mitochondrial metabolic reprogramming was coupled with senescence amelioration in accelerated aging cells. Furthermore, the therapeutic effect via ATM inhibition was observed in HGPS as evidenced by reduced progerin accumulation with concomitant decrease of abnormal nuclear morphology. Taken together, our data indicate that the mitochondrial functional recovery by ATM inhibition might represent a promising strategy to ameliorate the accelerated aging phenotypes and to treat age-related disease.

Survive or thrive: tradeoff strategy for cellular senescence

  • Park, Sang Chul
    • Experimental and Molecular Medicine
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    • v.49 no.6
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    • pp.6.1-6.7
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    • 2017
  • Aging-dependent cellular behaviors toward extrinsic stress are characterized by the confined localization of certain molecules to either nuclear or perinuclear regions. Although most growth factors can activate downstream signaling in aging cells, they do not in fact have any impact on the cells because the signals cannot reach their genetic targets in the nucleus. For the same reason, varying apoptotic stress factors cannot stimulate the apoptotic pathway in senescent cells. Thus, the operation of a functional nuclear barrier in an aging-dependent manner has been investigated. To elucidate the mechanism for this process, the housekeeping transcription factor Sp1 was identified as a general regulator of nucleocytoplasmic trafficking (NCT) genes, including various nucleoporins, importins, exportins and Ran GTPase cycle-related genes. Interestingly, the posttranslational modification of Sp1 is readily influenced by extrinsic stress, including oxidative and metabolic stress. The decrease in SP1 O-GlcNAcylation under oxidative stress or during replicative senescence makes it susceptible to proteosomal degradation, resulting in defective NCT functions and leading to nuclear barrier formation. The operation of the nuclear barrier in aging provides a fundamental mechanism for cellular protection against stress and promotes survival at the expense of growth via stress-sensitive transcriptional control.