• Preventive Nutrition and Food Science
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• v.22 no.2
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• pp.81-89
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• 2017

Healthy aging has become a major goal of public health. Many studies have provided evidence and theories to explain molecular mechanisms of the aging process. Recent studies suggest that epigenetic mechanisms are responsible for life span and the progression of aging. Epigenetics is a fascinating field of molecular biology, which studies heritable modifications of DNA and histones that regulate gene expression without altering the DNA sequence. DNA methylation is a major epigenetic mark that shows progressive changes during aging. Recent studies have investigated aging-related DNA methylation as a biomarker that predicts cellular age. Interestingly, growing evidence proposes that nutrients play a crucial role in the regulation of epigenetic modifiers. Because various nutrients and their metabolites function as substrates or cofactors for epigenetic modifiers, nutrition can modulate or reverse epigenetic marks in the genome as well as expression patterns. Here, we will review the results on aging-associated epigenetic modifications and the possible mechanisms by which nutrition, including nutrient availability and bioactive compounds, regulate epigenetic changes and affect aging physiology.

• Osteoporosis and Sarcopenia
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• v.3 no.3
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• pp.117-122
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• 2017

Sarcopenia is the degenerative loss of muscle mass and function with aging. Recently sarcopenia was recognized as a clinical disease by the International Classification of Disease, 10th revision, Clinical Modification. An imbalance between protein synthesis and degradation causes a gradual loss of muscle mass, resulting in a decline of muscle function as a progress of sarcopenia. Many mechanisms involved in the onset of sarcopenia include age-related factors as well as activity-, disease-, and nutrition-related factors. The stage of sarcopenia reflecting the severity of conditions assists clinical management of sarcopenia. It is important that systemic descriptions of the disease conditions include age, sex, and other environmental risk factors as well as levels of physical function. To develop a new therapeutic intervention needed is the detailed understanding of molecular and cellular mechanisms by which apoptosis, autophagy, atrophy, and hypertrophy occur in the muscle stem cells, myotubes, and/or neuromuscular junction. The new strategy to managing sarcopenia will be signal-modulating small molecules, natural compounds, repurposing of old drugs, and muscle-specific microRNAs.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.25 no.1
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• pp.24-26
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• 2014

Aging causes a variety of changes in the structure of the vocal fold (VF), resulting in aging-induced dysphonia (presbyphonia). Several studies have investigated the structure of the VF of elderly people from autopsy as well as animal studies. There is an increasing evidence on correlation of structural changes of VF with deteriorated voice in elderly. Although the cellular mechanisms of aging VF have only partially been elucidated, there are many recent advances in biological treatment on aging VF using bioactive molecules such as growth factors. In this study, I'd like to address aging-related structural, biological, and physiological changes in previous literature about human and rodent aging VFs, to provide further insight into the mechanisms responsible for presbyphonia and to translate the basic researches for future clinical trials.

• BMB Reports
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• v.54 no.5
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• pp.253-259
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• 2021

Aging is characterized by a functional decline in most physiological processes, including alterations in cellular metabolism and defense mechanisms. Increasing evidence suggests that caloric restriction extends longevity and retards age-related diseases at least in part by reducing metabolic rate and oxidative stress in a variety of species, including yeast, worms, flies, and mice. Moreover, recent studies in invertebrates - worms and flies, highlight the intricate interrelation between reproductive longevity and somatic aging (known as disposable soma theory of aging), which appears to be conserved in vertebrates. This review is specifically focused on how the reproductive system modulates somatic aging and vice versa in genetic model systems. Since many signaling pathways governing the aging process are evolutionarily conserved, similar mechanisms may be involved in controlling soma and reproductive aging in vertebrates.

• Proceedings of the Korean Society for Technology of Plasticity Conference
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• 2009.05a
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• pp.382-384
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• 2009

Strengthening mechanisms of metastable austenitic stainless steel, containing $\alpha'$-martensite phase, during strain aging was investigated. The variations of volume fraction of $\alpha'$-martensite phase, hardness of $\alpha'$-martensite phase, hardness of austenite were examined.

• BMB Reports
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• v.44 no.5
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• pp.291-297
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• 2011

Aging is one of the most complicated biological processes in all species. A number of different model organisms from yeast to monkeys have been studied to understand the aging process. Until recently, many different age-related genes and age-regulating cellular pathways, such as insulin/IGF-1-like signal, mitochondrial dysfunction, Sir2 pathway, have been identified through classical genetic studies. Parallel to genetic approaches, genome-wide approaches have provided valuable insights for the understanding of molecular mechanisms occurring during aging. Gene expression profiling analysis can measure the transcriptional alteration of multiple genes in a genome simultaneously and is widely used to elucidate the mechanisms of complex biological pathways. Here, current global gene expression profiling studies on normal aging and age-related genetic/environmental interventions in widely-used model organisms are briefly reviewed.

• Proceedings of the Korean Society for Food Science of Animal Resources Conference
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• 1996.06a
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• pp.6-6
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• 1996

• Molecules and Cells
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• v.42 no.12
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• pp.821-827
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• 2019

Aging is the most important single risk factor for many chronic diseases such as cancer, metabolic syndrome, and neurodegenerative disorders. Targeting aging itself might, therefore, be a better strategy than targeting each chronic disease individually for enhancing human health. Although much should be achieved for completely understanding the biological basis of aging, cellular senescence is now believed to mainly contribute to organismal aging via two independent, yet not mutually exclusive mechanisms: on the one hand, senescence of stem cells leads to exhaustion of stem cells and thus decreases tissue regeneration. On the other hand, senescent cells secrete many proinflammatory cytokines, chemokines, growth factors, and proteases, collectively termed as the senescence-associated secretory phenotype (SASP), which causes chronic inflammation and tissue dysfunction. Much effort has been recently made to therapeutically target detrimental effects of cellular senescence including selectively eliminating senescent cells (senolytics) and modulating a proinflammatory senescent secretome (senostatics). Here, we discuss current progress and limitations in understanding molecular mechanisms of senolytics and senostatics and therapeutic strategies for applying them. Furthermore, we propose how these novel interventions for aging treatment could be improved, based on lessons learned from cancer treatment.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.2
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• pp.187-196
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• 1991

Aging is the progressive accumulation of changes with time associated with responsible for the ever-increasing susceptibility to disease and death which accompanies advancing age. Lipid peroxides easily produced in the membrane system by the chain reaction of free radicals which occurred from various environmental factors. The amount of lipid peroxides produced in biological system increased with aging process, and lipid peroxidation damages involved in aging process and pathological disorders. Although lipid peroxides have such deleterious effects on the organisms, there are numerous substances and mechanisms which prevent the reaction of peroxide formation and protect the subject from its toxicity. This review provides an overview of how does lipid peroxidation of unsaturated lipids take place by free radical, and what is the intervention of lipid peroxides in pathogenesis of some human diseases, and also how does food restriction influences the aging process and various pathological disorders. The major focus of this paper is to review the evidence indicating that food restriction retards the aging process, and possible mechanisms of its actions. Therefore, it discussed the effects of age and food restriction on life-span, membrane yield, lipid peroxidation, fatty acid composition and peroxidizability, cholesterol and triglyceride levels, prostaglasndin and thromboxane synthesis, which may be concerned with blood flow, membrane fluidity, homeostasis and glomerular filtration rate in living body.

• Proceedings of the Korea Concrete Institute Conference
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• 1996.04a
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• pp.1-6
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• 1996

Cellulose fiber reinforced cement composites manufactured by the slurry-dewatering process have found broad applications in thin cement products as replacement for asbestos cement. This paper focuses on the durability characteristics of these composites under different aging conditions. The effects of wetting-drying and freezing-thaw cycles, carbonation, and exposure to hot and humid environments on the structure and properties of cellulose fiber-cement composites were investigated. The predominant mechanisms of aging in the composites were identified through investigation of structure-property relationships. Measures to control these aging mechanisms were diversed and evaluated. Refined cellulose fiber-cement composites are shown to possess excellent durability characteristics under the effects of various aging processes.