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Aging occurs at the level of individual cells, a complex interplay between intrinsic "programming" and exogenous "wear and tear", with genetically-determined cellular capacity to repair environmentally-induced DNA damage playing a central role in the rate of aging and its specific manifestations. In 12 chapters, "The Role of DNA Damage and Repair in Cell Aging" provides an intellectual framework for aging of mitotic and post-mitotic cells, describes a variety of model systems for further studies, and reviews current concepts of DNA responses and their relationship to the phenomenon of aging. As part of a series entitled "Advances in Cell Aging and Gerontology," this volume also summarizes seminal recent discoveries such as the molecular basis for Werner syndrome (a mutant DNA helicase), the complementary roles of telomere shortening and telomerase activity in cell senescence versus immortalization, the role of apoptosis in the homeostasis of aging tissue, and the existence of an inducible SOS-like response in mammalian cells that minimizes DNA damage from repeatedly encountered injurious environmental agents. Insights into the relationship between cellular aging and age-associated diseases, particularly malignancies, are also provided in several chapters. This book is an excellent single source of information for anyone interested in DNA repair, mechanisms of aging, or certainly their intersection. Students will gain a general appreciation of these fields, but even the most senior investigators will benefit from the detailed coverage of rapidly advancing areas.
Why organisms age and why sexual reproduction exists are major unsolved problems in biology. This book provides an integrated explanation of aging and sex based on current knowledge of DNA damage and repair. Discusses the universality of the problem of DNA damage Describes aging as a consequence of accumulated DNA damage Considers meiosis as an adaptation for DNA repair Discusses mating in eukaryotes as an adaptation for masking mutation
Cutting edge reviews by leading researchers illuminate key aspects of DNA repair in mammalian systems and its relationship to human genetic disease and cancer. Major topics include UV and X-Ray repair, repair of chemical damage, recombinational repair, mismatch repair, transcription-repair coupling, and the role of DNA repair in disease prevention. Extensive up-to-date references and rigorous peer-review of each chapter make this volume definitive and bring it to the active frontiers of research.
"How long can humans live? Is immortality possible? Just what is the aging process? The aging and inevitable death of the human body have inspired more myths and outrageous quackery than anything else subject to scientific inquiry. . . . Now comes a most fascinating book, insightful and scholarly, to provide what answers have emerged so far." --San Francisco Chronicle Here, at last, preeminent cell biologist Leonard Hayflick presents the truth about human aging. Based on more than thirty years of pioneering research in the field, How and Why We Age explores not only how our major biological systems change as we grow older, but also examines the intangible alterations in our modes of thinking and feeling, our moods and sexual desires, our personality traits and our memories. With the immediacy of the latest scientific discoveries, Dr. Hayflick explains how aging affects every part of the body, and dispels many of the most persistent aging myths, to show that: * Hearts do not naturally get weaker with age. * Regular exercise and a low-fat diet won't slow aging. * Curing cancer would only add two years to the average sixty-five-year-old American life. Curing heart disease, however would add fourteen years. * Only five percent of people over the age of sixty-five are in nursing homes * No human has lived--or probably can live--past 120 years. Gracefully written, clearly organized, and packed with essential facts and statistics, How and Why We Age is a landmark study of the aging process for readers of all ages. "Written in clear, nontechnical language, it is an excellent introduction to the scientific and demographic literature on this multifacetedsubject." --Nature
This book investigates the various processes that are affected by the age of an organism. Several new tools for the analysis of biological aging have been introduced recently, and this volume provides methods and protocols for these new techniques in addition to its coverage of established procedures. Researchers seeking new technology and techniques will find this volume of tremendous benefit as they move towards new directions.
The preservation of expected life span and longevity, as well as the assurance of life succession among all species requires the integrity and faithful transcription of DNA. A dedicated machinery of DNA repair factors is responsible for reversing DNA damage across the genome. Efficient response to various effectors of DNA damage is also dependent on a complex network of sensors and mediators of stress signals which are upstream of DNA repair activation and together constitute components of the DNA damage response (DDR). This book reviews research on cell cycle checkpoints as essential mechanisms for safeguarding genome stability; nucleotide excision repair (NER) which recognises and removes bulky DNA damage that leads to DNA double-helix distortion and others.
The ?eld of cellular responses to DNA damage has attained widespread recognition and interest in recent years commensurate with its fundamental role in the ma- tenance of genomic stability. These responses, which are essential to preventing cellular death or malignant transformation, are organized into a sophisticated s- tem designated the “DNA damage response”. This system operates in all living organisms to maintain genomic stability in the face of constant attacks on the DNA from a variety of endogenous by-products of normal metabolism, as well as exogenous agents such as radiation and toxic chemicals in the environment. The response repairs DNA damage via an intricate cellular signal transduction network that coordinates with various processes such as regulation of DNA replication, tr- scriptional responses, and temporary cell cycle arrest to allow the repair to take place. Defects in this system result in severe genetic disorders involving tissue degeneration, sensitivity to speci?c damaging agents, immunode?ciency, genomic instability, cancer predisposition and premature aging. The ?nding that many of the crucial players involved in DNA damage response are structurally and functionally conserved in different species spurred discoveries of new players through similar analyses in yeast and mammals. We now understand the chain of events that leads to instantaneous activation of the massive cellular responses to DNA lesions. This book summarizes several new concepts in this rapidly evolving ?eld, and the advances in our understanding of the complex network of processes that respond to DNA damage.
The First International Congress on DNA Damage and Repair was held in Rome, Italy, July 12-17, 1987. It was organized by the Italian Com mission for Nuclear Alternative Energy Sources. The subject of DNA damage and repair involves almost all the fields ofbidogical sciences. Some of the more prominent ones include carcino genesis, photobiology, radiation biology, aging, enzymology, genetics, and molecular biology. These individual fields have their own interna tional meetings and although the meetings often have sessions devoted to DNA repair, they do not bring together a wide diversity of international workers in the field to exchange ideas. The purpose of the Congress was to facilitate such an exchange among scientists representing many fields of endeavor and many countries. The 37 manuscripts in this volume, presented by the invited spea kers during the four and half days of the Congress, encompass the field of DNA damage and repair. They cover biological systems ranging from mo lecules to humans and deal with damages and repair after treatment of cells with various types of radiations, chemicals, and exogenous and en dogenous oxidative damages. The Congress and its Proceedings are dedicated to two international leaders in the field of DNA damage and repair, Alexander Hollaender of the United States and Adriano Buzzati Traverso of Italy. Hollaender, who died in December 1986, was one of the first investigators to recognize the damage to DNA was important in cell killing and mutagenesis. His early work indicated that cells could recover from radiation injury.
Jac A. Nickoloff and Merl F. Hoekstra update and expand their two earlier acclaimed volumes (Vol. I: DNA Repair in Prokaryotes and Lower Eukaryotes and Vol. II: DNA Repair in Higher Eurkaryotes) with cutting-edge reviews by leading authorities of primary experimental findings about DNA repair processes in cancer biology. The reviews cover a wide range of topics from viruses and prokaryotes to higher eukaryotes, and include several new topics, among them the role of recombination in replication of damaged DNA, X-ray crystallographic analysis of DNA repair protein structures, DNA repair proteins and teleomere function, and the roles of BRCA1 and BRCA2 in DNA repair. Authoritative and up-to-date, DNA Damage and Repair, Vol. III: Advances from Phage to Humans surveys the rapidly moving research in DNA damage and repair, and explains the important functional relationships among different DNA repair pathways and the relationship between DNA repair pathways, cancer etiology, and cancer therapies.
Aging represents a physiological and per se non-pathological and multifactorial process involving a set of key genes and mechanisms being triggered by different endogenous and exogenous factors. Since aging is a major risk factor in connection with a variety of human disorders, it is increasingly becoming a central topic in biochemical and medical research. The plethora of theories on aging – some of which have been discussed for decades – are neither isolated nor contradictory but instead can be connected in a network of pathways and processes at the cellular and molecular levels. This book summarizes the most prominent and important approaches, focusing on telomeres, DNA damage and oxidative stress as well as on the possible role of nutrition, the interplay between genes and environment (epigenetics) and intracellular protein homeostasis and introduces some genes that have actually extended life spans in animal models. Linking these different determinants of aging with disease, this volume aims to reveal their multiple interdependencies. We see that there is no single “perfect” theory of aging and that instead it is possible to define what the authors call the molecular aging matrix of the cell. A better knowledge of its key mechanisms and the mutual connections between its components will lead to a better understanding of age-associated disorders such as Alzheimer’s disease.