<p><strong> https://drive.google.com/file/d/1l7_lD9bc5rsSOHafjovPCkntTliAEKWV/view?usp=sharing</strong></p>
<p><strong>3.Report Genomic View on aging</strong></p> <p><strong>https://drive.google.com/file/d/14MUlWejOZR3jW-YOw2501_w8C6G4QSXz/view?usp=sharing</strong></p> <p><strong>4.Report om Epigenomics: Principles and challenges of genome-wide DNA methylation analysis</strong></p> <p><strong>https://drive.google.com/file/d/1QbyxnEVI3N4v0o2IwPvmO17D5i37uU3g/view?usp=sharing</strong></p> <p><strong>5.Type2_Diabetes_and GWAS lt;ppt></strong></p> <p><strong>https://drive.google.com/file/d/1dbtvtFmcW5xlQZNa7rUpTaUnEDgTQtmq/view?usp=sharing</strong></p>
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<p>29) Allelic richness- demonstrate the average number of alleles per locus. Decrease in allelic richness can be interpreted as the reduction in the population's potential to adapt to different circumstances. Genetic diversity is important because it allows to adapt to sudden and unexpected situations. That's why, many ~ecologists worry about purebred animals.</p>
<p><strong>B.Report: Genomic View on aging</strong></p>
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<p><strong>1. Introduction</strong></p>
<p> Every creature is born to die and for the immediate time between the two Silence, they are surviving and producing offspring( or cloning themselves). In view of bioinformatics, All organism is in the flow of genetic information. So It is absolutely right to eliminate the old generation, not to perfectly repair their damaging on the cells, but enough to survive for certain time. But there is an organism, Homo sapiens, recognizing self-consciousness and trying to get over the natural tendency of physical decline by the time. This paper finds out the going-on study on aging and In a minor way cancer, too. </p>
<p><strong>2.Biochemical View of aging</strong></p>
<p> Before DNA sequence was observed, there was already a well-known symptom that genetic substance in the cell is protected from some damage. The natural ends were somehow protected from the frequent rearrangements that occur at broken ends. As McClintock wrote in a 1931 research report that described the frequent joining of broken chromosome ends, “no case was found of the attachment of a piece of one chromosome to the end of another [intact chromosome](2). Nowadays what you'd actually find is a single sequence –TTAGGG – repeated over and over again, hundreds or even thousands of times. it is clear that the specific DNA sequence, Telomeres, synthesized by telomerase act as a conservation barrier, that protects information on the chromatin structure from the physical and chemical losing during DNA is being copied.</p>
<p> Aging occurs once organismal growth ceases in the mature animal. The continuous action of the growth program appears to drive aging and with it malignancy (and indeed, cancer risk increases with increasing age). Interestingly, many cancer cells have shortened telomeres, and telomerase is active in these cells. the links between growth, cancer, and aging (normal versus malignant growth/cancer) are apparent(1). </p>
<p> telomeres and telomerase are the main cores relating to aging. there are some Mechanistic theories of aging attempt to elucidate processes</p>
<p>involved in the aging process, and all implicate somatic deterioration with age. Proximate theories include the telomere length theory, the rate of living theory, and a number of offshoots including the oxidative damage theory, the advanced glycation end product theory, and the membrane pacemaker theory(3).</p>
<p> Genome maintenance and its impact on aging and disease could be the main steam to explain aging, An intricate genome maintenance machinery has evolved to counteract the consequences of DNA damage, affecting the function of our genes. Nucleotide excision repair (NER) is one of the most versatile repair systems removing a wide range of helix-distorting lesions, mostly from exogenous sources (ultraviolet [UV], bulky adducts), but also of endogenous origin (oxidative damage, e.g., cyclosporine). It does so in a multistep “cut-and-patch”- a type of reaction involving more than 30 proteins. Two NER subpathways exist. Global genome NER operates genome-wide removing lesions, which otherwise would give rise to mutations during replication and hence is critical for preventing mutations. Transcription-coupled repair removes damage that obstructs transcription, primarily counteracting cytotoxic effects of DNA injury(4).</p>
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<p><strong>3. The Naked Mole-Rat, A Long-Living Model for Human Aging Research</strong></p>
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<p> Calico Labs, the mysterious life-extension research & development company backed by Google and pharmaceutical giant AbbVie, is harnessing a colony of walking, toothy scrotums known as naked mole rats to unlock the secrets of aging. Calico has an impressive budget for tackling these questions: $1.5 billion.</p>
<p> Naked Mole-Rat(NMR) is a new animal model for aging, they live in hard living condition; Hot and rack of oxygen, underground. These conditions make them safe from predator and other natural hazards, In that sense, this species is preserved by another strategy, conservation.</p>
<p> Humans and NMRs have telomeres of a similar size that are shorter than those of shorter-lived laboratory mice. Although telomerase activity can compensate for short telomeres, in both these long-lived species, young healthy adults have very low telomerase activity(5). There is some reason that why Calico Labs select NMR for Human aging research. but it is clear that it is more efficient and economical to get practical data comparing with human, rather selecting other animal models.</p>
<p> A striking correlation is found between severity and type of defective repair and rate of onset, severity, and type of aging symptoms, providing strong experimental support for the DNA damage theory of aging. Conditional tissue-specific repair mutants target accelerated aging to specific organs, e.g., dramatic neurodegeneration occurring only in the cerebellum, revealing organ-specific accelerated aging.</p>
<p> What we need to know to solve aging is related to genomic information, NMR has some secret for almost perfectly recovering DNA damage. following the NMR genomic research, The predicted NMR gene set included 22,561 genes, which is comparable to other mammals (22,389 in human, 23,317 in mouse, and 22,841 in rat). Of these, 21,394 (94.8%) genes were transcribed. More than 98% of NMR genes could be functionally annotated using homology approaches and the quality of predicted genes was comparable to that of well-annotated mammalian genomes. Most of the NMR genome (93%) showed synteny to human, mouse or rat genomes (Supplementary Table 9), and pairwise comparisons suggested a relatively low rate of NMR genome rearrangements after the split from the murid common ancestor(6). This study also shows common and unique NMR gene families. Among these gene families, TOP2A, along with TEP1 and TERF1 from the set of positively selected genes, are part of a five-protein complex of alternative lengthening of telomere pathway(7). Overall, these analyses point to altered telomerase function in the NMR, which may be related to its evolution of extended lifespan and cancer resistance.</p>
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<p><strong>4. Conclusion </strong></p>
<p> Mortality is a destination of all living beings. Richard Dawkins said</p>
<p> "the main agent of biological evolution is genes, and all living things are mechanical beings created in their own replication. "</p>
<p> Here, a living thing that recognizes that they are mechanical beings for genes. Human gets the high consciousness as a revolution result and the consciousness leads us to the inside of the living things. are we programmed to find out the code? or It also is a mistake? whatever the origin of motivation is, Refusing Imminent and silent death by the time is one of the supreme inherent, and somehow that inherent lead the mechanical beings to another dimension of beings.</p>
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<p><strong>Reference</strong></p>
<p>(1)Systems Biology and Bioinformatics in Aging Research: A Workshop Report. Jörn Dengjel, Andreas Hoeflich, Jan Hoeijemakers, Hans A. Kestler, Axel Kowald, Steffen Priebe /Rejuvenation ResearchVol. 15, No. 6 Meeting Report</p>
<p>(2)McClintock, B. Cytological observations of deficiencies involving known genes, translocations and an inversion in Zea mays. Missouri Agr. Exp. Sta. Res. Bull. 163, 1–48 (1931).</p>
<p>(3)The Naked Mole-Rat: A New Long-Living Model for Human Aging Research. Rochelle Buffenstein</p>
<p>(4)Systems Biology and Bioinformatics in Aging Research: A Workshop Report. Jan Hoeijmakers/ Rejuvenation ResearchVol. 15, No. 6 Meeting Report</p>
<p>(5) Yang and Buffenstein, unpublished data, 2005</p>
<p>(6)Genome sequencing reveals insights into physiology and longevity of the naked mole rat Eun Bae Kim, Xiaodong Fang[…]Vadim N. Gladyshev</p>
<p>Nature volume 479, pages 223–227 (10 November 2011)</p>
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<p>(7)Bhattacharyya, S. et al. Telomerase-associated protein 1, HSP90, and topoisomerase IIA associate directly with the BLM helicase in immortalized cells using ALT and modulate its helicase activity using telomeric DNA substrates. J. Biol. Chem. 284, 14966–14977 (2009)</p>
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