• IMMUNE NETWORK
• /
• 제1권2호
• /
• pp.104-108
• /
• 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.

• 한국재료학회지
• /
• 제28권12호
• /
• pp.702-708
• /
• 2018

This study deals with the effect of microstructure factors on the strain aging properties of API X70 pipeline steels with different microstructure fractions and grain sizes. The grain size and microstructure fraction of the API pipeline steels are analyzed by optical and scanning electron microscopy and electron backscatter diffraction analysis. Tensile tests before and after 1 % pre-strain and thermal aging treatment are conducted to simulate pipe forming and coating processes. All the steels are composed mostly of polygonal ferrite, acicular ferrite, granular bainite, and bainitic ferrite. After 1 % pre-strain and thermal aging treatment, the tensile test results reveal that yield strength, tensile strength and yield ratio increase, while uniform elongation decreases with an increasing thermal aging temperature. The increment of yield and tensile strengths are affected by the fraction of bainitic ferrite with high dislocation density because the mobility of dislocations is inhibited by interaction between interstitial atoms and dislocations in bainitic ferrite. On the other hand, the variation of yield ratio and uniform elongation is the smallest in the steel with the largest grain size because of the decrease in the grain boundary area for dislocation pile-ups and the presence of many dislocations inside large grains after 1 % pre-strain.

• The Korean Journal of Physiology and Pharmacology
• /
• 제1권2호
• /
• pp.117-125
• /
• 1997

The N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic neurotransmission is involved in synaptic plasticity, developmental processes, learning and memory and many neuropathological disorders including age-related diseases. In the present study, regulation of the NMDA receptor properties by various ligands was investigated using $[^3H]MK-801$ binding studies in the synaptic membranes of young and aged rat forebrains. The binding in the presence of glutamate and glycine increased dramatically with growth between 1 and 6 weeks old, and thereafter declined gradually with aging. Glutamate, glycine or spermine respectively increased the binding with growth. Glutamate maintained the binding during aging, while glycine or spermine significantly decreased the binding in the aged brain. The maximum stimulation by glycine varied depending on the ages of brains. Greater sensitivity to glycine was observed at 1 week and 3 months and the sensitivity was significantly reduced in the aged brain. In contrast, spermine showed similar stimulation patterns in young and aged rats. These results indicated that the functional properties of the NMDA receptor-ion channel complex in young and aged rat forebrains are differentially regulated by agonists, and the reduction of the receptor function with normal aging may be, in some degree, due to the reduction of the receptor sensitivity to glycine.

• Molecules and Cells
• /
• 제38권8호
• /
• pp.729-733
• /
• 2015

C. elegans has two functional peroxidasins (PXN), PXN-1 and PXN-2. PXN-2 is essential to consolidate the extracellular matrix during development and is suggested to interact with PXN-1 antagonistically. pxn-1 is involved in neuronal development and possibly maintenance; therefore, we investigated the relationship between pxn-1 and pxn-2 in neuronal development and in aging. During neuronal development, defects caused by pxn-1 overexpression were suppressed by overexpression of both pxn-1 and pxn-2. In neuronal aging process, pxn-1 mutants showed less age-related neuronal defects, such as neuronal outgrowth, neuronal wavy processes, and enhanced short-term memory performance. In addition, pxn-2 overexpressing animals retained an intact neuronal morphology when compared with age-matched controls. Consistent with these results, overexpression of both pxn-1 and pxn-2 restored the severe neuronal defects present with pxn-1 overexpression. These results implied that there is a negative relationship between pxn-1 and pxn-2 via pxn-1 regulating pxn-2. Therefore, pxn-1 may function in neuronal development and age-related neuronal maintenance through pxn-2.

• 생명과학회지
• /
• 제26권8호
• /
• pp.983-989
• /
• 2016

체내를 구성하는 모든 세포는 시간이 흐름에 따라 그들의 주위환경에 좌우되어 분화, 괴사, 세포자살, 세포노화와 같은 운명을 경험한다. 이러한 세포과정에서 발생하는 실수가 암, 염증, 노화 및 질병과 같은 표현형에서의 여러가지 이상을 발생시킨다. 천연물로부터 유래한 항 노화 화합물을 탐색하기 위해서는 새로운 전략과 접근방식이 요구된다. 그러므로, 여기서는 핵심적인 역할을 하는 타켓 단백질에 대하여 설명한다. 먼저 기질금속단백질분해효소(MMPs)는 노화마커로 암전이, 만성염증 및 피부노화에 관여한다. 특히 히스톤 탈아세틸화효소(HDACs)는 모델동물의 수명을 연장시키려고 노력하는 노화연구원들에게 큰 관심의 대상이다. 뿐만 아니라, 여기서 p53, IGF-1 및 SIRT1이 중요한 역할을 하는 세포노화와 관련된 신호경로에 대하여 기술한다. 더욱이, 자가포식과정이 노화와 관련한 신호경로에도 관여하고 있다. 세포노화의 신호경로를 조절할 수 있는 여러가지 새로운 화합물도 본 총설논문에서 소개된다. 여기서 우리는 노화기전에 대한 분자기반 및 노화마커 개발에 대한 새로운 통찰력을 제공하려고 한다. 뿐만 아니라 소개되는 화합물은 노화와 관련 있는 질병의 예방 및 치료를 위하여 의학적으로 응용이 가능하다.

• 융합정보논문지
• /
• 제9권12호
• /
• pp.286-293
• /
• 2019

본 연구에서는 식약청 고시 원료인 레티놀, 레티닐팔미테이트, 아데노신, 폴리에톡실레이티드레틴아마이드 4종류와 항 노화의 효능을 가진 천연 원료인 금송, 하고초, 맨드라미, 브라질린, 여뀌, 황기, 연교, 자근, 대황, 육종용에 대한 연구 동향을 살펴보았다. 현재까지의 항 노화 연구는 주로 콜라겐 생성과 엘라스타아제 합성 억제 기전을 중심으로 이루어지고 있는 것이 확인되었다. 하지만, 피부의 노화 과정은 여러 가지 원인에 의해서 발생하는 것으로 볼 때, 다양한 기전에 맞춰 피부 항노화에 도움을 줄 수 있는 안전하고 효과적인 천연 원료를 활용한 항노화 연구가 지속적으로 이루어져야할 것으로 사료되어 진다.

• Journal of Ginseng Research
• /
• 제45권1호
• /
• pp.183-190
• /
• 2021

Background: The circadian rhythm is the internal clock that controls sleep-wake cycles, metabolism, cognition, and several processes in the body, and its disruption has been associated with aging. The differentiated embryo chondrocyte (Dec) gene is related to circadian rhythm. To our knowledge, there are no reports of the relationship between dec gene expression and KRG effect. Therefore, we treated Dec gene knockout (KO) aging mice with KRG to study anti-aging related effects and possible mechanisms. Methods: We evaluated KRG and expression of Dec genes in an ototoxicity model. Dec genes expression in livers of aging mice was further analyzed. Then, we assessed the effects of DEC KO on hearing function in mice by ABR. Finally, we performed DNA microarray to identify KRG-related gene expression changes in mouse liver and assessed the results using KEGG analysis. Results: KRG decreased the expression of Dec genes in ototoxicity model, which may contribute to its anti-aging efficacy. Moreover, KRG suppressed Dec genes expression in liver of wild type indicating inhibition of senescence. ABR test indicated that KRG improved auditory function in aging mouse, demonstrating KRG efficacy on aging related diseases. Conclusion: Finally, in KEGG analysis of 238 genes that were activated and 158 that were inhibited by KRG in DEC KO mice, activated genes were involved in proliferation signaling, mineral absorption, and PPAR signaling whereas the inhibited genes were involved in arachidonic acid metabolism and peroxisomes. Our data indicate that inhibition of senescence-related Dec genes may explain the anti-aging efficacy of KRG.

• 대한간호학회지
• /
• 제38권6호
• /
• pp.831-842
• /
• 2008

Purpose: The purpose of this study was to develop a web-based senescence preparation education program to promote successful aging. Methods: This program was developed based on Network-Based Instructional System Design (NBISD) model, using the following 5 processes: analysis, design, development, implementation, and evaluation. The program was operated for 10 weeks from March 17 to May 25, 2008. Results: There were 4 menu bars, introduction, related data, lecture room, and communication on the main page. In the operation of this program, HTML, ASP, JAVA Script, Namo web editor, Edit Plus, Front Page and multimedia technology were applied. The program content consisted of understanding elderly people, physical health, activity & exercise, nutrition, medication use, psychological health, intellectual health, understanding death, welfare system and leisure activity. Conclusion: This program could be a useful means to provide senescence preparation information to middle-aged adults. Also, it is expected to offer individualized learning opportunities to many learners in various settings. Nurses should further develop and facilitate various learning strategies including web-based programs for elder care.

• 소성∙가공
• /
• 제30권2호
• /
• pp.61-68
• /
• 2021

As part of efforts to reduce the weight of automotive body-in-white, a hybrid center pillar with high strength 7075 aluminum alloy (AA7075) sheet and carbon fiber reinforced plastic (CFRP) has been recently studied. In the fabrication of the AA7075-CFRP hybrid center pillar, the AA7075 sheet might go through heating-forming-in-die quenching (HFQ), artificial aging, hybridizing, and then paint baking processes. In this study, we investigate the effects of the heat treatment history associated with each process on the tensile strength of the AA7075 sheet. Typical heat treatment conditions are HFQ for 20 minutes at 480℃ and then cooling down with die, artificial aging of T6 temper for 24 hours at 120℃, hybridizing for 10 minutes at 150℃, and paint baking for 20 minutes at 180℃. The tensile strength of the AA7075 sheet is continuously increased by a series of heat treatments of hybridizing and paint baking and is expected to have yield stress above 500MPa without artificial aging of T6 temper.

• BMB Reports
• /
• 제56권12호
• /
• pp.651-656
• /
• 2023

Senescence, a cellular process through which damaged or dysfunctional cells suppress the cell cycle, contributes to aging or age-related functional decline. Cell metabolism has been closely correlated with aging processes, and it has been widely recognized that metabolic changes underlie the cellular alterations that occur with aging. Here, we report that fatty acid oxidation (FAO) serves as a critical regulator of cellular senescence and uncover the underlying mechanism by which FAO inhibition induces senescence. Pharmacological or genetic ablation of FAO results in a p53-dependent induction of cellular senescence in human fibroblasts, whereas enhancing FAO suppresses replicative senescence. We found that FAO inhibition promotes cellular senescence through acetyl-CoA, independent of energy depletion. Mechanistically, increased formation of autophagosomes following FAO inhibition leads to a reduction in SIRT1 protein levels, thereby contributing to senescence induction. Finally, we found that inhibition of autophagy or enforced expression of SIRT1 can rescue the induction of senescence as a result of FAO inhibition. Collectively, our study reveals a distinctive role for the FAO-autophagy-SIRT1 axis in the regulation of cellular senescence.