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・ Jan Wolthuis
・ Jan Woltjer
・ Jan Woltjer (astronomer)
・ Jan Wong
・ Jan Wong controversy
・ Jan Versleijen
・ Jan Verstraeten
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・ Jan Veselý (cyclist)
・ Jan Vetešník
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Jan Vijg
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・ Jan Villerius
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・ Jan Vincent
・ Jan Vincents Johannessen
・ Jan Vincentsz van der Vinne
・ Jan Vis
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・ Jan Viviani
・ Jan Vladimír Hráský
・ Jan Vodička
・ Jan Vogler
・ Jan Voigt
・ Jan Voje


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Jan Vijg : ウィキペディア英語版
Jan Vijg
Jan Vijg is the Lola and Saul Kramer Chair-person in Molecular Genetics at the Department of Genetics at the Albert Einstein College of Medicine, Yeshiva University, USA . Prior to this appointment, he was a Professor at the Buck Institute for Research on Aging, Novato , California , USA . He helps serve on the Advisory Board at the Lifeboat Foundation.

His research interests include studying genomic instability in aging. In 1989, he created the first transgenic mouse models for the study of in vivo mutagenesis. He discusses his genomic/epigenomic drift hypothesis as a cause of aging in his book Aging of the Genome.〔(An Anti-Aging Scientist Shines a Light on His Foe )〕
In his second book, The American Technological Challenge, Stagnation and Decline in the 21st Century, he argues that technological innovation has decelerated ever since 1970.〔(Did We Hit Our Innovation Peak in 1970? )〕
Professional Interests
==Genome Instability in Aging and Disease==
Genome instability, i.e., the tendency of the genome to acquire mutations and epimutations, underlies human genetic disease, causally contributes to cancer and has also been implicated in aging and age-related, degenerative conditions other than cancer. Little is known about the mechanisms that give rise to spontaneous changes in the genome or epigenome and how this may lead, in somatic cells, to increased cancer risk and loss of organ and tissue function with age. We study genome and epigenome instability as a function of age in various model organisms, including mouse and fruit fly, and its consequences in terms of alterations in tissue-specific patterns of gene regulation.
We developed transgenic reporter systems in mouse and fruit fly, which allow us to determine tissue-specific frequencies of various forms of genome instability, e.g., point mutations, deletions, translocations. By crossing the mutational reporter animals with mutants harboring specific defects in various genome maintenance pathways, the relevance of these pathways for the accumulation of specific forms of genome instability is assessed, in relation to the pathophysiology of aging. Similarly, by using knockdown approaches we assess the effect of specific genes implicated in longevity and healthy aging, e.g., SOD, FOXO, SIR2, on genome integrity.
More recently, we have begun to assess global gene mutation and epimutation loads in normal and disease tissues of both animal models and humans using massively parallel sequencing approaches.
〔http://www.einstein.yu.edu/faculty/11318/jan-vijg/〕

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