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The Lived Experience of Being a Hundred Years and Over
The lived experience of being a hundred years and over By Ashwina Naiker-Ratan A thesis submitted to Victoria University of Wellington in fulfilment of the requirements for the Degree of Master of Health Research Victoria University of Wellington 2016 ABSTRACT The twentieth century has seen a decline in mortality after the age of eighty and an increase in survival rates of the oldest of the old. Centenarians (people over a hundred years of age) are the fastest growing group of this population in developed countries; however qualitative research on the oldest of the old is limited. The primary aim of this study was to gain an understanding of the essence of lived experiences and meanings of extended longevity as perceived by centenarians. It also aimed to explore the role of lifestyle characteristics, family, social, health and cultural factors in regards to their prolonged existence. The research was conducted with ten centenarians aged between 100 and 106 years living in the Lower North Island namely Wairarapa, Kapiti and Wellington of Aotearoa New Zealand. Biographical Narrative Interpretive Method of inquiry was used to guide the data collection through face-to-face interviews using unstructured open ended questions. Colazzi’s phenomenological framework was employed for data analysis. There were common patterns throughout the life stories related by the centenarians and resilience and acceptance of life was notable. The centenarians spoke nonchalantly about their experience of turning a hundred, describing their birthday as; “Just another day.” Positive personalities and resilient nature were prominent features of the participants who all expressed a sense of acceptance and satisfaction with life and contentment with living in the present. -
Disruptive Chemicals, Senescence and Immortality
Disruptive chemicals, senescence and immortality Carnero, A., Blanco-Aparicio, C., Kondoh, H., Lleonart, M. E., Martinez-Leal, J. F., Mondello, C., ... & Yasaei, H. (2015). Disruptive chemicals, senescence and immortality. Carcinogenesis, 36(Suppl 1), S19-S37. doi:10.1093/carcin/bgv029 10.1093/carcin/bgv029 Oxford University Press Version of Record http://cdss.library.oregonstate.edu/sa-termsofuse Carcinogenesis, 2015, Vol. 36, Supplement 1, S19–S37 doi:10.1093/carcin/bgv029 Review review Disruptive chemicals, senescence and immortality Amancio Carnero*, Carmen Blanco-Aparicio1, Hiroshi Kondoh2, Matilde E. Lleonart3, Juan Fernando Martinez-Leal4, Chiara Mondello5, A.Ivana Scovassi5, William H.Bisson6, Amedeo Amedei7, Rabindra Roy8, Jordan Woodrick8, Annamaria Colacci9, Monica Vaccari9, Jayadev Raju10, Fahd Al-Mulla11, Rabeah Al- Downloaded from Temaimi11, Hosni K. Salem12, Lorenzo Memeo13, Stefano Forte13, Neetu Singh14, Roslida A. Hamid15, Elizabeth P. Ryan16, Dustin G. Brown16, John Pierce Wise Sr17, Sandra S.Wise17 and Hemad Yasaei18 http://carcin.oxfordjournals.org/ Instituto de Biomedicina de Sevilla (IBIS/CSIC/HUVR/Univ. Sevilla), Oncohematology and Genetics Department, Avda Manuel siurot sn, 41013 Sevilla, Spain, 1Spanish National Cancer Research Center, Experimental Therapuetics Department, Melchor Fernandez Almagro, 3, 28029 Madrid, Spain, 2Department of Geriatric Medicine, Kyoto University Hospital, 54 Kawaharacho, Shogoin, Sakyo-ku Kyoto 606-8507, Japan, 3Institut De Recerca Hospital Vall D’Hebron, Passeig Vall d’Hebron, 119–129, -
The Emergence of Senescent Surface Biomarkers As Senotherapeutic Targets
cells Review The Emergence of Senescent Surface Biomarkers as Senotherapeutic Targets Martina Rossi and Kotb Abdelmohsen * Laboratory of Genetics and Genomics, RNA Regulation Section, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Blvd., Baltimore, MD 21224, USA; [email protected] * Correspondence: [email protected] Abstract: Senescence is linked to a wide range of age-associated diseases and physiological declines. Thus, senotherapeutics are emerging to suppress the detrimental effects of senescence either by senomorphics or senolytics. Senomorphics suppress the traits associated with senescence phenotypes, while senolytics aim to clear senescent cells by suppressing their survival and enhancing the apoptotic pathways. The main goal of these approaches is to suppress the proinflammatory senescence- associated secretory phenotype (SASP) and to promote the immune recognition and elimination of senescent cells. One increasingly attractive approach is the targeting of molecules or proteins specifically present on the surface of senescent cells. These proteins may play roles in the maintenance and survival of senescent cells and hence can be targeted for senolysis. In this review, we summarize the recent knowledge regarding senolysis with a focus on novel surface biomarkers of cellular senescence and discuss their emergence as senotherapeutic targets. Keywords: senescence; surface proteins; surfaceome; senolytics; senolysis; senostatic; senescent cell clearance; senotherapeutics; senotherapy Citation: Rossi, M.; Abdelmohsen, K. The Emergence of Senescent Surface Biomarkers as Senotherapeutic Targets. Cells 2021, 10, 1740. 1. Introduction https://doi.org/10.3390/cells Cellular senescence is a phenotype associated with limited replicative capacity and 10071740 irreversible growth arrest of primary cells first described by Leonard Hayflick in the early 1960s [1]. -
Does Senescence Promote Fitness in Caenorhabditis Elegans by Causing Death?
Institute of Healthy Ageing Preprint 1st Nov 2018 Essay Does senescence promote fitness in Caenorhabditis elegans by causing death? Jennifer N. Lohr1, Evgeniy R. Galimov1 and David Gems* Institute of Healthy Ageing, and Research Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, UK. 1These authors contributed equally. ∗ Corresponding author. E-mail address: [email protected] (D. Gems). 1 Institute of Healthy Ageing Preprint 1st Nov 2018 Abstract A widely appreciated conclusion from evolutionary theory is that senescence (aging) is of no adaptive value to the individual that it afflicts. Yet studies of C. elegans and S. cerevisiae are increasingly revealing the presence of processes which actively cause senescence and death, leading some biogerontologists to wonder about the established theory. Here we argue that programmed death that increases fitness could occur in C. elegans and S. cerevisiae, and that this is consistent with the classic evolutionary theory of aging. This is because of the special conditions under which these organisms have evolved, particularly the existence of clonal populations with limited dispersal and, in the case of C. elegans, the brevity of the reproductive period caused by protandry. Under these conditions, death-promoting mechanisms could promote worm fitness by enhancing inclusive fitness, or worm colony fitness through group selection. Such altruistic, adaptive death is not expected to evolve in organisms with outbred, dispersed populations. The plausibility of adaptive death in C. elegans is supported by computer modelling studies, and new knowledge about the ecology of this species. To support these arguments we also review the biology of adaptive death, and distinguish three forms: consumer sacrifice, biomass sacrifice and defensive sacrifice. -
Understanding the Molecular Interplay Between Senescence, Rejuvenation, and Healthy Ageing. Eleanor Tyler
Understanding the molecular interplay between senescence, rejuvenation, and healthy ageing. Eleanor Tyler A thesis presented for the degree of Doctor of Philosophy 2016 Supervisors: Dr Cleo L. Bishop Prof. Mike P. Philpott Centre for Cell Biology and Cutaneous Research The Blizard Institute Barts and the London School of Medicine and Dentistry Queen Mary University of London Statement of originality I, Eleanor Tyler, confirm that the research included within this thesis is my own work or that where it has been carried out in collaboration with, or supported by others, that this is duly acknowledged below and my contribution indicated. I attest that I have exercised reasonable care to ensure that the work is original, and does not to the best of my knowledge break any UK law, infringe any third party’s copyright or other Intellectual Property Right, or contain any confidential material. I accept that the College has the right to use plagiarism detection software to check the electronic version of the thesis. I confirm that this thesis has not been previously submitted for the award of a degree by this or any other university. The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without the prior written consent of the author. Signature: Eleanor Tyler Date: 19.12.16 1 Abstract Senescence is classically defined as an irreversible cell cycle arrest. There is now convincing evidence that senescent cells accumulate during human ageing, potentially driving age-related dysfunction through depletion of mitotically active cells and stimulation of chronic inflammation. -
Dissecting Aging and Senescence—Current Concepts and Open Lessons
cells Review Dissecting Aging and Senescence—Current Concepts and Open Lessons 1,2, , 1,2, 1 1,2 Christian Schmeer * y , Alexandra Kretz y, Diane Wengerodt , Milan Stojiljkovic and Otto W. Witte 1,2 1 Hans-Berger Department of Neurology, Jena University Hospital, 07747 Jena, Thuringia, Germany; [email protected] (A.K.); [email protected] (D.W.); [email protected] (M.S.); [email protected] (O.W.W.) 2 Jena Center for Healthy Ageing, Jena University Hospital, 07747 Jena, Thuringia, Germany * Correspondence: [email protected] These authors have contributed equally. y Received: 2 October 2019; Accepted: 13 November 2019; Published: 15 November 2019 Abstract: In contrast to the programmed nature of development, it is still a matter of debate whether aging is an adaptive and regulated process, or merely a consequence arising from a stochastic accumulation of harmful events that culminate in a global state of reduced fitness, risk for disease acquisition, and death. Similarly unanswered are the questions of whether aging is reversible and can be turned into rejuvenation as well as how aging is distinguishable from and influenced by cellular senescence. With the discovery of beneficial aspects of cellular senescence and evidence of senescence being not limited to replicative cellular states, a redefinition of our comprehension of aging and senescence appears scientifically overdue. Here, we provide a factor-based comparison of current knowledge on aging and senescence, which we converge on four suggested concepts, thereby implementing the newly emerging cellular and molecular aspects of geroconversion and amitosenescence, and the signatures of a genetic state termed genosenium. -
Chapter 9. Myths of Life Extension
Chapter 9. Myths of Life Extension Ever since humans became fully aware that they will get old and die, individuals must have wondered about the possibility of extending longevity, or achieving immortality on earth. This has resulted in innumerable myths relating to supposed examples of life-extension, one of the most notable being the 969 year lifespan of Methuselah, as recorded in the Bible. Christian fundamentalists are liable to say that in those days people lived much longer than they do today! These are many other claims, and far too many to list here. The Guiness Book of Records has stated that maximum lifespans of people and animals are some of the hardest records to document. Some of the claims of human longevity have occurred in the 20th century, and as in some cases they were initially accepted by scientists, and they provide good examples of how people are deceived. Many people living in the Caucasus region of the ex-Soviet Union claimed their ages were over 120 years, or even 160 years. There was even a touring troup of centenarian dancers, so it is not surprising the claims received wide publicity, and also wide acceptance. The oldest people were usually males which is intrinsically unlikely as human females live longer that males. Careful scrutiny of these cases, particularly by the gerontologist Zhores Medvedev, has shown that none are backed up by reliable records. In some cases, individuals took on the identity of their father, in others they exaggerated their age to escape military conscription, or they simply added on years, because the societies in which they lived respected the wisdom and experience of very old people. -
Aging, Life Span, and Senescence
Proc. Natl. Acad. Sci. USA Vol. 95, pp. 11034–11036, September 1998 From the Academy This paper is summary of a session presented at the Ninth Annual Frontiers of Science Symposium, held November 7–9, 1997, at the Arnold and Mabel Beckman Center of the National Academies of Sciences and Engineering in Irvine, CA. Aging, life span, and senescence LEONARD GUARENTE*, GARY RUVKUN†, AND RICHARD AMASINO‡ *Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139; †Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114; and ‡Department of Biochemistry, University of Wisconsin, Madison, WI 53706 Research in the field of aging recently has entered a new era. in old sgs1 mother cells were enlarged and fragmented, Model systems have begun to provide insight into cellular, changes that are also found in very old wild type cells. molecular, and organismal changes that are related intimately What is the molecular basis of this fragmentation and does to aging. One important approach has been the identification it cause aging? Examination of the rDNA in old cells revealed of genes that determine the life span of an organism. The very an accumulation of extrachromosomal rDNA circles (ERCs) existence of genes that when mutated can extend life span of discrete sizes representing oligomers of the rDNA unit (7). suggests that one or a few processes may be critical in aging and ERCs arise from recombination within the rDNA of chromo- that a slowing of these processes may slow aging itself. some XII in the early part of the life span (Fig. 1). Each subsequent cell cycle, the ERCs replicate via the replication Yeast sequence in the rDNA repeats and then segregate asymmetri- cally into mother cells. -
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Do You Still Need Aspirin? LifeExtension.com Stay Healthy, Live Better August 2019 Faster, Longer, More Restful SLEEP Enhance Male Sexual Health PQQ Refreshes Brain Energy Maintain Healthy Coagulation Balance Carotenoids to Protect Eye and Brain Function Omega-3 Intake Associated with Lower Mortality Risk REJUVENATE YOUR SKIN FROM WITHIN Restore Collagen AND Hyaluronic Acid WITH DELIGHTFUL GUMMIES Oral ingestion of collagen peptides and hyaluronic acid boosts these rejuvenating factors in normal, aging skin. Clinical results reveal improved skin elasticity, increased moisture, and a % reduction in the depth of eye wrinkles. The new Gummy Science™ Youthful Collagen formula provides clinically studied* doses with daily intake of tasty chewable gummies. For full product description and to order Gummy Science™ Youthful Collagen, call --- or visit www.LifeExtension.com Item # • gummies gummiess jar $. * Skin Pharmacol Physiol. ;():-. * Skin Pharmacol Physiol. ;():-. VERISOL® and Bioactive Collagen Peptides® are registered trademarks of GELITA AG. jars $ each These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Table of Contents Volume Twenty Five / Number Eight • August 2019 REPORTS 38 ENHANCE MALE SEXUAL HEALTH A ginger-like root was shown to improve sexual health in 61.5% of male participants in a published study. 46 PQQ REVITALIZES CELLULAR ENERGY A nutrient called PQQ helps grow new mitochondria in aging cells. The result is more energy in human studies and increased lifespan (in animal studies). 57 LUTEIN AND ZEAXANTHIN IMPROVE COGNITION Lutein and zeaxanthin are plant carotenoids known for protecting the eyes. New studies reveal they also increase brain processing speed, visual memory, cognitive 28 ON THE COVER flexibility, and brain blood flow. -
A Biomarker That Identifies Senescent Human Cells in Culture and in Aging Skin in Vivo (Replicative Senescence/Tumor Suppression/18-Galactosidase) GOBERDHAN P
Proc. Natl. Acad. Sci. USA Vol. 92, pp. 9363-9367, September 1995 Cell Bioiogy A biomarker that identifies senescent human cells in culture and in aging skin in vivo (replicative senescence/tumor suppression/18-galactosidase) GOBERDHAN P. DIMRI*, XINHUA LEEt, GEORGE BASILE*, MEILEEN ACOSTA*, GLYNIS SCOrrt, CALVIN ROSKELLEY*, ESTELA E. MEDRANO§, MAARTEN LINSKENSI, IVICA RUBELJII, OLIVIA PEREIRA-SMITHII, MONICA PEACOCKEt, AND JUDITH CAMPISI* ** *Department of Cell and Molecular Biology, Lawrence Berkeley Laboratory, University of California, Berkeley, CA 94720; tDepartment of Dermatology, New England Medical Center, Tufts University Medical School, Boston, MA 02111; iDepartment of Dermatology and Pathology, University of Rochester School of Medicine, Rochester, NY 14642; §Department of Cell Biology and IDivision of Molecular Virology, Huffington Center on Aging, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030; and IGeron Corporation, 200 Constitution Drive, Menlo Park, CA 94025 Communicated by Arthur B. Pardee, Dana-Farber Cancer Institute, Boston, MA, June 12, 1995 (received for review March 28, 1995) ABSTRACT Normal somatic cells invariably enter a state The idea that cellular senescence is tumor suppressive stems of irreversibly arrested growth and altered function after a from molecular, cellular, and in vivo data. Immortality greatly finite number of divisions. This process, termed replicative increases the susceptibility to malignant transformation, in senescence, is thought to be a tumor-suppressive mechanism culture and in vivo (5, 6). Indeed, many tumors contain and an underlying cause ofaging. There is ample evidence that immortal cells or cells with an extended replicative lifespan (7). escape from senescence, or immortality, is important for In addition, some oncogenes act primarily to immortalize or malignant transformation. -
Life Extension Pseudoscience and the SENS Plan
Life Extension Pseudoscience and the SENS Plan Preston W. Estep III, Ph.D. President and CEO, Longenity Inc. Matt Kaeberlein, Ph.D. Department of Pathology University of Washington Pankaj Kapahi, Ph.D. Buck Institute for Age Research Brian K. Kennedy, Ph.D. Department of Biochemistry University of Washington Gordon J. Lithgow Ph.D. Buck Institute for Age Research George M. Martin, M.D. Department of Pathology University of Washington Simon Melov, Ph.D. Buck Institute for Age Research R. Wilson Powers III Department of Genome Sciences University of Washington Heidi A. Tissenbaum, Ph.D. Program in Gene Function and Expression Program in Molecular Medicine University of Massachusetts Medical School Abstract Recent scientific advances have taken gerontological research to challenging and exciting new frontiers, and have given many scientists increased confidence that human aging is to some degree controllable. We have been on the front lines of some of these developments and the speculative discussions they have engendered, and we are proud to be part of the increasingly productive biomedical effort to reduce the pathologies of aging, and age-associated diseases, to the greatest degree possible—and to extend healthy human life span to the greatest degree possible. In contrast to clearly justifiable speculations regarding future advances in human longevity a few have made claims that biological immortality is within reach. One, Aubrey de Grey, claims to have developed a “detailed plan to cure human aging” called Strategies for Engineered Negligible Senescence (SENS) [1, 2]. This is an extraordinary claim, and we believe that extraordinary claims require extraordinary evidentiary support. In supplementary material posted on the Technology Review web site we evaluate SENS in detail. -
Get Connected: Linking Older Adults with Resources on Medication, Alcohol, and Mental Health
GET CONNECTED Linking Older Adults with Resources on Medication, Alcohol, and Mental Health 2019 EDITION Acknowledgments The Get Connected Toolkit curriculum was developed under contract No. 00M008406 with the Substance Abuse and Mental Health Services Administration (SAMHSA) by the National Council on Aging (NCOA). Hanley-Hazelden donated both a brochure and video to this Toolkit partnership. Expert advice and guidance were provided by Eileen Elias and Jennifer Solomon (SAMHSA); Alixe McNeil, Nancy Whitelaw, and Ron Schoeffler (NCOA); Dr. Frederic Blow (University of Michigan); Melanie Starns (Administration on Aging); David Turner (Health Promotion Institute); Carol Colleran (Hanley- Hazelden); and Willard Mays (National Coalition on Mental Health & Aging). Disclaimer The views and opinions expressed in this publication are those of the authors and do not necessarily reflect the policies or opinions of SAMHSA or the U.S. Department of Health and Human Services (HHS). Public Domain Notice With two exceptions, the materials contained in this Toolkit are in the public domain and may be reproduced at will. The video “It Can Happen to Anyone” was developed by Hanley-Hazelden and is subject to copyright law. Permission to SAMHSA to include both the video and brochure in this Toolkit was granted by the originators. Any reproduction of the video requires specific permission directly from Hanley-Hazelden. Citation of the source of materials in the public domain is appreciated. However, these federal products may not be reproduced or distributed for a fee without the specific, written authorization of the Office of Communications, SAMHSA, HHS. Electronic Access and Copies of Publication This publication may be downloaded or ordered at www.store.samhsa.gov, or call SAMHSA at 1–877–SAMHSA–7 (1–877–726–4727) (English and Español).