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This book explores the methionine dependence of cancer and its effects on aging, a great story of science that is not widely known. The chapters in this book describe the discovery of methionine dependence of cancer; the molecular basis for the increased methionine demand of cancer cells and tumors; the clinical application of methionine dependence of cancer in PET imaging with [11C]methionine; the development of methioninases as cancer drugs; the anti-aging and anti-diabetes effects of methionine restriction; and the future of targeting methionine in the body for the elimination of cancer and for the extension of a healthy life-span. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Cutting-edge and thorough, Methionine Dependence of Cancer and Aging: Methods and Protocols is an important resource for researchers and scientists wishing to pursue this exciting and vital area of study."
This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.
Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
During the last 15 years the research on homocysteine and the vitamins involved in its metabolism has become very dynamic. About 1,500 publications on the subject are now published each year. The research has long mainly focused on the association between homocysteine and cardiovascular disease, but also pregnancy complications/ fetal malformations. There is, however, an increasing interest in the connection between the homocysteine metabolism and neuropsychiatric disease with a steeply increasing number of publications. In particular, the association between homocysteine metabolism and cognitive decline/dementia attracts much interest. If simple, non-toxic homocysteine-lowering treatment with vitamins can reduce the incidence of, or delay the onset of dementia, it would have an enormous impact in societies with a rapidly increasing number of elderly at risk for dementia. This book summarises the research within the neuropsychiatric field, but also gives an overview of the underlying biochemistry and of diagnostic aspects. About 1,000 references are given. Christina Bolander-Gouaille, a pharmacist, has for over 10 years specialised in writing reviews/monographs on homocysteine and related vitamins. This is her third book in a series edited by Springer Verlag. This book, however, is written in collaboration with Teodoro Bottiglieri, who is director of neuropharmacology and senior research scientist at Baylor University, Institute for Metabolic Diseases in Dallas, USA.
Recent studies have indicated that epigenetic processes may play a major role in both cellular and organismal aging. These epigenetic processes include not only DNA methylation and histone modifications, but also extend to many other epigenetic mediators such as the polycomb group proteins, chromosomal position effects, and noncoding RNA. The topics of this book range from fundamental changes in DNA methylation in aging to the most recent research on intervention into epigenetic modifications to modulate the aging process. The major topics of epigenetics and aging covered in this book are: 1) DNA methylation and histone modifications in aging; 2) Other epigenetic processes and aging; 3) Impact of epigenetics on aging; 4) Epigenetics of age-related diseases; 5) Epigenetic interventions and aging: and 6) Future directions in epigenetic aging research. The most studied of epigenetic processes, DNA methylation, has been associated with cellular aging and aging of organisms for many years. It is now apparent that both global and gene-specific alterations occur not only in DNA methylation during aging, but also in several histone alterations. Many epigenetic alterations can have an impact on aging processes such as stem cell aging, control of telomerase, modifications of telomeres, and epigenetic drift can impact the aging process as evident in the recent studies of aging monozygotic twins. Numerous age-related diseases are affected by epigenetic mechanisms. For example, recent studies have shown that DNA methylation is altered in Alzheimer’s disease and autoimmunity. Other prevalent diseases that have been associated with age-related epigenetic changes include cancer and diabetes. Paternal age and epigenetic changes appear to have an effect on schizophrenia and epigenetic silencing has been associated with several of the progeroid syndromes of premature aging. Moreover, the impact of dietary or drug intervention into epigenetic processes as they affect normal aging or age-related diseases is becoming increasingly feasible.
This authoritative overview on an emerging topic in the molecular life sciences covers all aspects of the aging of (long-lived) proteins. It describes the molecular mechanisms of aging on the protein level, in particular the most common side chain modifications and includes analytical methods to study protein half-life and the accumulation of modifications. Finally, the impact of protein aging on several age-related disases in humans is dissected, and their role in limiting human lifespan is discussed.
This book is intended as a comprehensive resource for clinicians and researchers seeking in-depth information on geriatric oncology. The coverage encompasses epidemiology, the biology and (patho)physiology of aging and cancer, geriatric assessment and management, hematologic malignancies, solid tumors, issues in patient care, and research methods. Since cancer is a disease of aging and people are living longer, most cancer patients are now aged 70 and older. Yet the more we age, the more diverse we become in terms of our health, biologic fitness, and cancer behavior. Typically, however, general oncology clinical trials address only a selected healthier and younger population of patients. Geriatric oncology is the area of oncology that addresses these issues but while a wealth of knowledge has been accumulated, information is often difficult to retrieve or insufficiently detailed. The SpringerReference program, in which this book is published, offers an ideal format for overcoming these limitations since it combines thorough coverage with access to living editions constantly updated chapter by chapter via a dynamic peer-review process, ensuring that information remains current and pertinent.
Nutrient Metabolism defines the molecular fate of nutrients and other dietary compounds in humans, as well as outlining the molecular basis of processes supporting nutrition, such as chemical sensing and appetite control. It focuses on the presentation of nutritional biochemistry; and the reader is given a clear and specific perspective on the events that control utilization of dietary compounds. Slightly over 100 self-contained chapters cover all essential and important nutrients as well as many other dietary compounds with relevance for human health. An essential read for healthcare professionals and researchers in all areas of health and nutrition who want to access the wealth of nutrition knowledge available today in one single source.Key Features* Highly illustrated with relevant chemical structures and metabolic pathways* Foreword by Steven Zeisel, Editor-in-chief of the Journal of Nutritional Biochemistry* First comprehensive work on the subject
This book describes the challenges involved in developing mTOR inhibitors for cancer treatment, starting with an in-depth examination of their molecular mechanism of action, with emphasis on the class side-effects, efficacy and mechanisms of resistance, as well as on promising novel directions for their development, including novel compounds and rational combinations with other anti-neoplastic drugs. Over the last 10 years, inhibitors of mTOR have emerged as a major class of anticancer drugs. Two rapamycin analogs are currently approved for the treatment of renal cell carcinoma, and it is estimated that a variety of other tumor types could benefit from mTOR inhibition, with numerous clinical trials (including pivotal registration trials) already underway. Second-generation small-molecule inhibitors of the pathway have also shown promise in terms of their superior tolerability and efficacy and are undergoing extensive clinical evaluation, with an estimated 30+ compounds currently under evaluation.
In his midtwenties, Dave Asprey was a successful Silicon Valley multimillionaire. He also weighed 300 pounds, despite the fact that he was doing what doctors recommended: eating 1,800 calories a day and working out 90 minutes a day, six times a week. When his excess fat started causing brain fog and food cravings sapped his energy and willpower, Asprey turned to the same hacking techniques that made his fortune to "hack" his own biology, investing more than $300,000 and 15 years to uncover what was hindering his energy, performance, appearance, and happiness. From private brain EEG facilities to remote monasteries in Tibet, through radioactive brain scans, blood chemistry work, nervous system testing, and more, he explored traditional and alternative technologies to reach his physical and mental prime. The result? The Bulletproof Diet, an anti-inflammatory program for hunger-free, rapid weight loss and peak performance. The Bulletproof Diet will challenge--and change--the way you think about weight loss and wellness. You will skip breakfast, stop counting calories, eat high levels of healthy saturated fat, work out and sleep less, and add smart supplements. In doing so, you'll gain energy, build lean muscle, and watch the pounds melt off. By ditching traditional "diet" thinking, Asprey went from being overweight and sick in his twenties to maintaining a 100-pound weight loss, increasing his IQ, and feeling better than ever in his forties. The Bulletproof Diet is your blueprint to a better life.