Cellular Aging: Theories and Technological Influence
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Cryonics Magazine, Q1 2001
SOURCE FEATURES PAGE Fred Chamberlain Glass Transitions: A Project Proposal 3 Mike Perry Interview with Dr. Jerry Lemler, M.D. 13 Austin Esfandiary A Tribute to FM-2030 16 Johnny Boston FM & I 18 Billy H. Seidel the ALCOR adventure 39 Natasha Vita-More Considering Aesthetics 45 Columns Book Review: Affective Computing..................................41 You Only Go Around Twice .................................................42 First Thoughts on Last Matters............................................48 TechNews.......................................................................51 Alcor update - 19 The Global Membership Challenge . 19 Letter from Steve Bridge . 26 President’s Report . 22 “Last-Minute” Calls . 27 Transitions and New Developments . 24 Alcor Membership Status . 37 1st Qtr. 2001 • Cryonics 1 Alcor: the need for a rescue team or even for ingly evident that the leadership of The Origin of Our Name cryonics itself. Symbolically then, Alcor CSC would not support or even would be a “test” of vision as regards life tolerate a rescue team concept. Less In September of 1970 Fred and extension. than one year after the 1970 dinner Linda Chamberlain (the founders of As an acronym, Alcor is a close if meeting, the Chamberlains severed all Alcor) were asked to come up with a not perfect fit with Allopathic Cryogenic ties with CSC and incorporated the name for a rescue team for the now- Rescue. The Chamberlains could have “Rocky Mountain Cryonics Society” defunct Cryonics Society of California forced a five-word string, but these three in the State of Washington. The articles (CSC). In view of our logical destiny seemed sufficient. Allopathy (as opposed and bylaws of this organization (the stars), they searched through star to Homeopathy) is a medical perspective specifically provided for “Alcor catalogs and books on astronomy, wherein any treatment that improves the Members,” who were to be the core of hoping to find a star that could serve as prognosis is valid. -
Markers of T Cell Senescence in Humans
International Journal of Molecular Sciences Review Markers of T Cell Senescence in Humans Weili Xu 1,2 and Anis Larbi 1,2,3,4,5,* 1 Biology of Aging Program and Immunomonitoring Platform, Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Immunos Building, Biopolis, Singapore 138648, Singapore; [email protected] 2 School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore 3 Department of Microbiology, National University of Singapore, Singapore 117597, Singapore 4 Department of Geriatrics, Faculty of Medicine, University of Sherbrooke, Sherbrooke, QC J1K 2R1, Canada 5 Faculty of Sciences, University ElManar, Tunis 1068, Tunisia * Correspondence: [email protected]; Tel.: +65-6407-0412 Received: 31 May 2017; Accepted: 26 July 2017; Published: 10 August 2017 Abstract: Many countries are facing the aging of their population, and many more will face a similar obstacle in the near future, which could be a burden to many healthcare systems. Increased susceptibility to infections, cardiovascular and neurodegenerative disease, cancer as well as reduced efficacy of vaccination are important matters for researchers in the field of aging. As older adults show higher prevalence for a variety of diseases, this also implies higher risk of complications, including nosocomial infections, slower recovery and sequels that may reduce the autonomy and overall quality of life of older adults. The age-related effects on the immune system termed as “immunosenescence” can be exemplified by the reported hypo-responsiveness to influenza vaccination of the elderly. T cells, which belong to the adaptive arm of the immune system, have been extensively studied and the knowledge gathered enables a better understanding of how the immune system may be affected after acute/chronic infections and how this matters in the long run. -
Moderate Stem Cell Telomere Shortening Rate Postpones Cancer Onset in Stochastic Model
Moderate stem cell telomere shortening rate postpones cancer onset in stochastic model. Simon Holbek, Kristian Moss Bendtsen, Jeppe Juul University of Copenhagen, Niels Bohr Institute, Blegdamsvej 17, DK-2100 Copenhagen, Denmark (Dated: November 3, 2018) Mammalian cells are restricted from proliferating indefinitely. Telomeres at the end of each chromosome are shortened at cell division and, when they reach a critical length, the cell will enter permanent cell cycle arrest - a state known as senescence. This mechanism is thought to be tumor suppressing, as it helps prevent precancerous cells from dividing uncontrollably. Stem cells express the enzyme telomerase, which elongates the telomeres, thereby postponing senescence. However, unlike germ cells and most types of cancer cells, stem cells only express telomerase at levels insufficient to fully maintain the length of their telomeres leading to a slow decline in proliferation potential. It is not yet fully understood how this decline influences the risk of cancer and the longevity of the organism. We here develop a stochastic model to explore the role of telomere dynamics in relation to both senescence and cancer. The model describes the accumulation of cancerous mutations in a multicel- lular organism and creates a coherent theoretical framework for interpreting the results of several recent experiments on telomerase regulation. We demonstrate that the longest average cancer free life span before cancer onset is obtained when stem cells start with relatively long telomeres that are shortened at a steady rate at cell division. Furthermore, the risk of cancer early in life can be reduced by having a short initial telomere length. Finally, our model suggests that evolution will favour a shorter than optimal average cancer free life span in order to postpone cancer onset until late in life. -
Human Cell and Organism Aging: Are There Limits? Interrupted Case Study on Cell Aging
Human Cell and Organism Aging: Are there Limits? Interrupted Case study on Cell Aging Teresa Gonya Department of Biological Sciences University of Wisconsin-Fox Valley Menasha, WI The search for the fountain of youth persists in advertising, and individuals are constantly bombarded with messages about diet, exercise, vitamins and minerals that can help prolong one’s life. The biological basis of aging is often not mentioned in the anti-aging promotions. Is it possible that a diet rich in protein, or fruits and vegetables can add years to your life? Is it possible that a vitamin or mineral ‘tonic’ can promote tissue repair and extend life? Is it possible that a vitamin drink can extend your normal life expectancy? Even clinical medicine focuses on developing new treatments that are based on preventing aging and maintaining organ longevity. We are told to exercise to keep our heart healthy and to stop smoking to prevent damage to body tissues, especially the lungs and blood vessels. The new field of regenerative medicine is based on the premise that stem cells may one day be able to repair tissue and return function to damaged organs. There are real limits to longevity that are based on genetics, lifestyle, medical history and sociology. (1) At the foundation of organism longevity is cell longevity. All organisms are composed of cells. Four different types of tissue cells form the basis of all organs that are found in any animal organism. Each type of tissue cell has a different ability to undergo mitosis and replace itself, should it become damaged or injured. -
Hayflick, His Limit, and Cellular Ageing Clearly a Next Step Is Automation
PERSPECTIVES Finally, the most apparent drawback is the Whether or not nucleic acid computers 175–179 (2000). 3. Faulhammer, D., Cukras, A., Lipton, R. J. & Landweber, L. time required for each computation. ultimately prove feasible, they have already F. Molecular computation: RNA solutions to chess Whereas a simple desktop computer can contributed to multi-disciplinary science by problems. Proc. Natl Acad. Sci. USA 97, 1385–1389 (2000). solve the seven-city instance of the Travelling causing us to question the nature of comput- 4. Ouyang, Q., Kaplan, P. D., Liu, S. & Libchaber, A. DNA Salesman Problem in less than a second, ing and to forge new links between the biolog- solution of the maximal clique problem. Science 278, 1 446–449 (1997). Adleman took seven days . The use of DNA ical and computational sciences. For example, 5. Henegariu, O., Heerema, N. A., Dlouhy, S. R., Vance, G. H. chips2 or other approaches may eventually it has led us to focus on the nature of biologi- & Vogt, P. H. Multiplex PCR: Critical parameters and step- by-step protocol. Biotechniques 23, 504–511 (1997). lead to automation, which would save con- cal DNA computations, such as the assembly 6. Karp, G. Cell and Molecular Biology: Concepts and siderable amounts of time, but fundamental of modern genes from encrypted building- Experiments 2nd edn (John Wiley & Sons, New York, 1999). DNA computing technology needs to blocks in the genomes of some single-celled 7. Seife, C. RNA works out knight moves. Science 287, advance far beyond its current bounds before ciliates (FIG. 5)14. -
Muller's Ratchet As a Mechanism of Frailty and Multimorbidity
bioRxivMuller’s preprint ratchetdoi: https://doi.org/10.1101/439877 and frailty ; this version posted[Type Octoberhere] 10, 2018. The copyright holder Govindarajufor this preprint and (which Innan was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Muller’s ratchet as a mechanism of frailty and multimorbidity 2 3 Diddahally R. Govindarajua,b,1, 2, and Hideki Innanc,1,2 4 5 aDepartment of Human Evolutionary Biology, Harvard University, Cambridge, MA 02138; 6 and bThe Institute of Aging Research, Albert Einstein College of Medicine, Bronx, 7 NY 1046, and cGraduate University for Advanced Studies, Hayama, Kanagawa, 8 240-0193, Japan 9 10 11 12 Authors contributions: D.R.G., H.I designed study, performed research, contributed new 13 analytical tools, analyzed data and wrote the paper 14 15 The authors declare no conflict of interest 16 1D.R.G., and H.I. contributed equally to this work and listed alphabetically 17 2 Correspondence: Email: [email protected]; [email protected] 18 19 Senescence | mutation accumulation | asexual reproduction | somatic cell-lineages| 20 organs and organ systems |Muller’s ratchet | fitness decay| frailty and multimorbidity 21 22 23 24 25 26 27 28 29 30 31 32 1 bioRxivMuller’s preprint ratchetdoi: https://doi.org/10.1101/439877 and frailty ; this version posted[Type Octoberhere] 10, 2018. The copyright holder Govindarajufor this preprint and (which Innan was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 33 Mutation accumulation has been proposed as a cause of senescence. -
Etergen Whitepaper.Pages
ETERGEN WHITE PAPER Executive Summary I. Brief History II. The problem III. Solution – business model IV. Token offer V. Our Accountability with Your investments VI. Timeline VII. Our Team Disclamer The ETERGEN Foundation – Live longer. Executive Summary At Eternity foundation we believe that human life is precious. And we want you and your loved ones to live longer. In fact, we are doing everything we can for it, through supporting scientific research in the field of human life extension. With technology and knowledge our society has now, we all can live a longer, healthier life, only if the needed attention was paid to the financing of the research in the field of life extension. We support international medical and scientific research, aimed at human life extension, with system of grants and investments for the best projects. We believe that significant human life extension can be reached within our lifetime. To finance this research, we offer our own cryptocurrency, THE ETER. THE ETER is state of the art cryptocurrency giving you the lowest cost per transaction and true anonymous security . Not only will the ETER help the mankind to solve the most important question we face, but it will also create great value for all the currency holders, since every project, financed by us, will have a contract obligation to share the profits with all the holders. This will be guaranteed through use of smart contracts utilizing the blockchain technology. "1 ETERGEN WHITE PAPER We will build up the industry of human life extension through introducing cutting edge technology. Our key advantages are: A global project A growing multibillion industry with huge growth potential Real value behind the currency Experienced team with high qualifications Unique idea - there is no other project like this. -
Telomeres and Telomerase
Oncogene (2010) 29, 1561–1565 & 2010 Macmillan Publishers Limited All rights reserved 0950-9232/10 $32.00 www.nature.com/onc GUEST EDITORIAL 2009 Nobel Prize in Physiology or Medicine: telomeres and telomerase Oncogene (2010) 29, 1561–1565; doi:10.1038/onc.2010.15 sate for the chromosomal shortening produced asso- ciated with cell division, suggesting that progressive telomere shortening may be a key factor to limit the Elizabeth H Blackburn, Carol W Greider and Jack W number of cell divisions. James D Watson (Nobel Prize Szostak were acknowledged with this year’s Nobel Prize 1962) also recognized that the unidirectional nature of in Physiology or Medicine for their discoveries on how DNA replication was a problem for the complete copy chromosomes are protected by telomeres and the of chromosomal ends (Watson, 1972). This was called enzyme telomerase. the ‘end-replication problem’. In this manner, during In the first half of the twentieth century, classic studies each cycle of cell division, a small fragment of telomeric by Hermann Mu¨ller (Nobel Prize 1945) working with DNA is lost from the end. After several rounds of the fruit fly (Drosophila melanogaster) and by Barbara division, telomeres eventually reach a critically short McClintock (Nobel Prize 1983) studying maize (Zea length, which activates the pathways for senescence and Mays) proposed the existence of a special structure at cell death (Hermann et al., 2001; Samper et al., 2001). the chromosome ends (Mu¨ller, 1938; McClintock, 1939). Uncovering the solution to the end-replication pro- This structure would have the essential role of protect- blem took several years of intense research. -
Intercellular Competition and the Inevitability of Multicellular Aging
Intercellular competition and the inevitability of multicellular aging Paul Nelsona,1 and Joanna Masela aDepartment of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721 Edited by Raghavendra Gadagkar, Indian Institute of Science, Bangalore, India, and approved October 6, 2017 (received for review November 14, 2016) Current theories attribute aging to a failure of selection, due to Aging in multicellular organisms occurs at both the cellular either pleiotropic constraints or declining strength of selection and intercellular levels (17). Multicellular organisms, by definition, after the onset of reproduction. These theories implicitly leave require a high degree of intercellular cooperation to maintain open the possibility that if senescence-causing alleles could be homeostasis. Often, cellular traits required for producing a viable identified, or if antagonistic pleiotropy could be broken, the multicellular phenotype come at a steep cost to individual cells effects of aging might be ameliorated or delayed indefinitely. (14, 18, 19). Conversely, many mutant cells that do not invest in These theories are built on models of selection between multicel- holistic organismal fitness have a selective advantage over cells lular organisms, but a full understanding of aging also requires that do. If intercellular competition occurs, such “cheater” or examining the role of somatic selection within an organism. “defector” cells may proliferate and displace “cooperating” cells, Selection between somatic cells (i.e., intercellular competition) with detrimental consequences for the multicellular organism can delay aging by purging nonfunctioning cells. However, the (20, 21). Cancer, a leading cause of death in humans at rates that fitness of a multicellular organism depends not just on how increase with age, is one obvious manifestation of cheater pro- functional its individual cells are but also on how well cells work liferation (22–24). -
Anti-Aging 2018
Anti-Aging 2018 Altern verstehen Altern messen Altern behandeln Prof. Dr. Bernd Kleine-Gunk Präsident der Deutschen Gesellschaft für Präventions- und Anti-Aging Medizin (GSAAM) www. kleine-gunk.de Metropol Medical Center Nürnberg Ist Altern eine Krankheit? www. kleine-gunk.de Metropol Medical Center Nürnberg Risikofaktor biologisches Lebensalter ESC Score – Kardiovaskuläre Erkrankungen ¹ DeBacker G et al. European guidelines on cardiovascular disease prevention in clinical practice. The Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of eight societies and by invited experts) executive summary. Eur Heart J 2003; 24: 1601–10. www. kleine-gunk.de Metropol Medical Center Nürnberg Risikofaktor biologisches Lebensalter AGLA Score – Kardiovaskuläre Erkrankungen Eur J Clin Invest. 2007; 37:925-32 www. kleine-gunk.de Metropol Medical Center Nürnberg www. kleine-gunk.de www. Heft 39,2006: 2542-2548 Häusler,Gothe, Göl, Glaeske,Pientka, Felsenberg,Dtsch. Ärzteblatt 103, Jg [%] Anteil der Patienten mit Osteoporose Risikofaktor Lebensalter biologisches 7% 7% 7% 7% 1,3 Mio1,3 Männer 1,3 Mio1,3 Männer Osteoporose in Deutschland in Osteoporose > 75> Jahre 65–74Jahre 50–64Jahre > 75> Jahre 65–74Jahre 50–64Jahre 11% 11% 11% 11% 16% 16% 16% 16% 23% 23% 23% 23% 6,5 Mio Frauen 6,5 Mio Frauen 47% 47% 47% 47% 59% 59% 59% 59% Nürnberg Center Medical Metropol Risikofaktor biologisches Lebensalter Altersabhängige Häufigkeit der Demenz http://www.alzheimerinfo.de/alzheimer/zahlen/index.jsp www. kleine-gunk.de Metropol Medical Center Nürnberg Risikofaktor biologisches Lebensalter Bösartige Neuerkrankungen nach Alter 1989 bis 1998 im Saarland Frauen Quelle der Statistik: Arbeitsgemeinschaft Bevölkerungsbezogener Krebsregister in Deutschland. -
Controversy 2
Controversy 2 WHY DO OUR BODIES GROW OLD? liver Wendell Holmes (1858/1891), in his poem “The Wonderful One-Hoss Shay,” invokes a memorable image of longevity and mortality, the example of a wooden Ohorse cart or shay that was designed to be long-lasting: Have you heard of the wonderful one-hoss shay, That was built in such a logical way, It ran a hundred years to a day . ? This wonderful “one-hoss shay,” we learn, was carefully built so that every part of it “aged” at the same rate and didn’t wear out until the whole thing fell apart all at once. Exactly a century after the carriage was produced, the village parson was driving this marvelous machine down the street, when What do you think the parson found, When he got up and stared around? The poor old chaise in a heap or mound, As if it had been to the mill and ground! You see, of course, if you’re not a dunce, How it went to pieces all at once, All at once, and nothing first, Just as bubbles do when they burst. The wonderful one-horse shay is the perfect image of an optimistic hope about aging: a long, healthy existence followed by an abrupt end of life, with no decline. The one-horse shay image also suggests that life has a built-in “warranty expiration” date. But where does this limit on longevity come from? Is it possible to extend life beyond what we know? The living organism with the longest individual life span is the bristlecone pine tree found in California, more than 4,500 years old, with no end in sight. -
Ray Kurzweil Reader Pdf 6-20-03
Acknowledgements The essays in this collection were published on KurzweilAI.net during 2001-2003, and have benefited from the devoted efforts of the KurzweilAI.net editorial team. Our team includes Amara D. Angelica, editor; Nanda Barker-Hook, editorial projects manager; Sarah Black, associate editor; Emily Brown, editorial assistant; and Celia Black-Brooks, graphics design manager and vice president of business development. Also providing technical and administrative support to KurzweilAI.net are Ken Linde, systems manager; Matt Bridges, lead software developer; Aaron Kleiner, chief operating and financial officer; Zoux, sound engineer and music consultant; Toshi Hoo, video engineering and videography consultant; Denise Scutellaro, accounting manager; Joan Walsh, accounting supervisor; Maria Ellis, accounting assistant; and Don Gonson, strategic advisor. —Ray Kurzweil, Editor-in-Chief TABLE OF CONTENTS LIVING FOREVER 1 Is immortality coming in your lifetime? Medical Advances, genetic engineering, cell and tissue engineering, rational drug design and other advances offer tantalizing promises. This section will look at the possibilities. Human Body Version 2.0 3 In the coming decades, a radical upgrading of our body's physical and mental systems, already underway, will use nanobots to augment and ultimately replace our organs. We already know how to prevent most degenerative disease through nutrition and supplementation; this will be a bridge to the emerging biotechnology revolution, which in turn will be a bridge to the nanotechnology revolution. By 2030, reverse-engineering of the human brain will have been completed and nonbiological intelligence will merge with our biological brains. Human Cloning is the Least Interesting Application of Cloning Technology 14 Cloning is an extremely important technology—not for cloning humans but for life extension: therapeutic cloning of one's own organs, creating new tissues to replace defective tissues or organs, or replacing one's organs and tissues with their "young" telomere-extended replacements without surgery.