It takes two to tango: NAD+ and sirtuins in aging/longevity control

AbstractThe coupling of nicotinamide adenine dinucleotide (NAD+) breakdown and protein deacylation is a unique feature of the family of proteins called ‘sirtuins.’ This intimate connection between NAD+ and sirtuins has an ancient origin and provides a mechanistic foundation that translates the regulation of energy metabolism into aging and longevity control in diverse organisms. Although the field of sirtuin research went through intensive controversies, an increasing number of recent studies have put those controversies to rest and fully established the significance of sirtuins as an evolutionarily conserved aging/longevity regulator. The tight connection between NAD+ and sirtuins is regulated at several different levels, adding further complexity to their coordination in metabolic and aging/longevity control. Interestingly, it has been demonstrated that NAD+ availability decreases over age, reducing sirtuin activities and affecting the communication between the nucleus and mitochondria at a cellular level and also between the hypothalamus and adipose tissue at a systemic level. These dynamic cellular and systemic processes likely contribute to the development of age-associated functional decline and the pathogenesis of diseases of aging. To mitigate these age-associated problems, supplementation of key NAD+ intermediates is currently drawing significant attention. In this review article, we will summarize these important aspects of the intimate connection between NAD+ and sirtuins in aging/longevity control.</jats:p

Non-compact simple Lie group E₇₍₋₂₅₎ of type E₇

Article信州大学理学部紀要 15(1): 1-18(1980)departmental bulletin pape

Another definitions of exceptional simple Lie groups of type E₇₍₋₂₅₎ and E₇₍₋₁₃₃₎

Article信州大学理学部紀要 15(2): 47-52(1981)departmental bulletin pape

Non-compact simple Lie group E₈₍₋₂₄₎ of type E₈

Article信州大学理学部紀要 15(2): 53-76(1981)departmental bulletin pape

X-ray Investigation of Low-Cycle Fatigue in Martensitic Steels

Specimens of 0.38%C steel and Fe-25%Ni alloy were put to test of their low-cycle fatigue, tensile and hardness properties, both in their tempered state. The maximum bending strain on their surfaces under which the fatigue was tested was controlled at between 1.0 and 1.6%. The X-ray diffraction and thin film electronmicroscopy methods and some other techniques were employed for the purpose. The results obtained may be summarized in two phenomena. One is similar to the contrast of annealed metals versus cold-worked metals, and the other is what is considered to characterize the tempered martensite. Both materials in tempered condition present a remarkable variation in microstructure, and the difference in microstructure is almost leveled out only in the low carbon 25%Ni alloy by the fatigue and this phenomenon is similar to the contrast of annealed metals versus cold-worked metals. But in the 0.38%C steel the difference is not leveled out even after the fatigue to failure. The results obtained are not yet adequate enough to explain the correlation between the microstructural variation and the damage fraction in a tempered martensite. The crack initiation and propagation in the 0.38%C steel and 25%Ni alloy are often related longitudinally to the edges of martensite leaves

It takes two to tango: NAD+ and sirtuins in aging/longevity control

The coupling of nicotinamide adenine dinucleotide (NAD⁺) breakdown and protein deacylation is a unique feature of the family of proteins called ‘sirtuins.’ This intimate connection between NAD⁺ and sirtuins has an ancient origin and provides a mechanistic foundation that translates the regulation of energy metabolism into aging and longevity control in diverse organisms. Although the field of sirtuin research went through intensive controversies, an increasing number of recent studies have put those controversies to rest and fully established the significance of sirtuins as an evolutionarily conserved aging/longevity regulator. The tight connection between NAD⁺ and sirtuins is regulated at several different levels, adding further complexity to their coordination in metabolic and aging/longevity control. Interestingly, it has been demonstrated that NAD⁺ availability decreases over age, reducing sirtuin activities and affecting the communication between the nucleus and mitochondria at a cellular level and also between the hypothalamus and adipose tissue at a systemic level. These dynamic cellular and systemic processes likely contribute to the development of age-associated functional decline and the pathogenesis of diseases of aging. To mitigate these age-associated problems, supplementation of key NAD⁺ intermediates is currently drawing significant attention. In this review article, we will summarize these important aspects of the intimate connection between NAD⁺ and sirtuins in aging/longevity control.National Institute on Aging (Grant AG037457)National Institute on Aging (Grant AG047902