• 한국정밀공학회:학술대회논문집
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• 한국정밀공학회 2008년도 춘계학술대회 논문집
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• pp.173-174
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• 2008

• Journal of Acupuncture Research
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• 제18권1호
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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.

• 한국신뢰성학회지:신뢰성응용연구
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• 제12권3호
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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.

• 시스템엔지니어링학술지
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• 제10권1호
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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.

• IMMUNE NETWORK
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• 제1권2호
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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.

• 한국전기전자재료학회논문지
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• 제15권2호
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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.

• BMB Reports
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• 제52권1호
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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.

• Journal of Korean Biological Nursing Science
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• 제26권2호
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• pp.99-110
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• 2024

Purpose: This study reviewed the pathophysiological mechanisms of cellular aging caused by psychological stress and aimed to establish a biobehavioral theoretical framework for nursing interventions to promote autonomic balance based on these mechanisms. Methods: A comprehensive literature review was conducted. Results: A review of the literature showed that the stress response increases the secretion of catecholamines and glucocorticoids, resulting in a greater allostatic load. This load induces inflammatory reactions and oxidative stress, shortening telomere length and damaging mitochondrial DNA, which can lead to cellular aging. Based on this mechanism, a biobehavioral theoretical framework for nursing interventions was established. This framework focuses on delaying or inhibiting the cellular aging process by acting on the stress response stage and improving autonomic balance. Conclusion: According to the proposed biobehavioral theoretical framework, stress-relieving nursing interventions may act on the mechanism of cellular aging caused by stress responses. We believe that this framework could expand our understanding of the biobehavioral aspects of stress and would facilitate efforts to use biomarkers to evaluate the effectiveness of stress-related nursing interventions at the cellular level.

• Molecules and Cells
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• 제42권3호
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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.

• Biomolecules & Therapeutics
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• 제30권6호
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• pp.490-500
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• 2022

Aging is defined as physiological dysfunction of the body and a key risk factor for human diseases. During the aging process, cellular senescence occurs in response to various extrinsic and intrinsic factors such as radiation-induced DNA damage, the activation of oncogenes, and oxidative stress. These senescent cells accumulate in many tissues and exhibit diverse phenotypes, such as resistance to apoptosis, production of senescence-associated secretory phenotype, cellular flattening, and cellular hypertrophy. They also induce abnormal dysfunction of the microenvironment and damage neighboring cells, eventually causing harmful effects in the development of various chronic diseases such as diabetes, cancer, and neurodegenerative diseases. Thus, pharmacological interventions targeting senescent cells, called senotherapeutics, have been extensively studied. These senotherapeutics provide a novel strategy for extending the health span and improving age-related diseases. In this review, we discuss the current progress in understanding the molecular mechanisms of senotherapeutics and provide insights for developing senotherapeutics.