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Research has shown that 90% of all cancer deaths are due to cancer metastasis. Cancer can only spread in the body when we have an environment of excess free radicals or oxidative stress. An ultra-high, universal, antioxidant like Carbon 60 hydrated fullerenes neutralize free radicals and prevent cancer metastasis.
Factsheet #6 Link between Oxidative Stress, Free Radicals and Cancer v4
Time Magazine and National Geographic both recently ran cover stories with a baby on the cover. The tagline reads: This baby could live to be 142 years old. So the question that immediately comes to mind is: Is this possible and can everyone age gracefully without chronic human diseases? And can we do it with today’s technology ?
To explore this question we first need to compare the mortality in 1900 versus today. In 1900, half of the deaths were caused by pneumonia, influenza, tuberculosis, gastrointestinal infections. These diseases were cured largely with antibiotics and antivirals after world war two. Cancer, diabetes, coronary heart disease, and Alzheimer’s were present but not near the rates we see today. Now, the top causes of death today, according to US statistics are heart disease, lung cancer, lung disease (asthma) , stroke, Alzheimer’s, diabetes and hypertension. An interesting question to ask would be: Do all these new, twenty first century diseases all have something in common, just like the top causes of death in 1900 where from bacterial or viral sources? A review of the medical literature shows two primary causes. In turns out that most chronic human diseases are 1) triggered by excess free radicals or oxidative stress and 2) are the result of a lack of essential minerals and trace minerals and cofactors in our diets.
Free radicals or oxidative stress is the result of our cells metabolizing or breathing oxygen. Free radical are the “waste” products of life, and they are very destructive to cell membranes, proteins and DNA. Our body has a natural protective system-antioxidant enzymes that neutralize excess free radicals. If this delicate balance is disrupted, this then leads to an inflammation response in the body and eventually, chronic diseases could ensue. As we age, our natural antioxidant protective systems decline and we are told to supplement with natural botanical antioxidants, such as blueberries , green tea or cinnamon or antioxidant supplements such as Vitamin E or coenzyme Q10. But then we run into the “antioxidant paradox”. All these food antioxidants work great as antioxidants in a test tube in the lab, but in human clinical trials, the beneficial effects are either inconclusive or negative. This is because saliva and gut bacteria metabolise many these botanical antioxidants, before they have a chance to act beneficially.
Ukrainian scientists discovered the world’s highest antioxidant called Carbon 60 hydrated fullerenes, which is stable and inert and not metabolised by bacteria. Carbon 60, a natural product, was discovered in 1985 and a Nobel prize in Chemistry was awarded for this discovery in 1996. Scientists and doctors were calling it the panacea or silver bullet in medicine, but because it’s not naturally water soluble, just like diamonds, charcoal or activated charcoal, this frustrated scientists. Ukrainian scientist in Kharkiv the first to discovered how to dissolve Carbon 60 in water in 1994. After 20 years of preclinical, safety and clinical studies, Carbon 60 hydrated fullerenes were approved as a “dietary supplement” by the Ukrainian Ministry of Health and has been on the Ukrainian market since 2010. There is now a US patent pending. Scientists are now claiming that most chronic human diseases are triggered by excess free radicals. Just do a search on PUBMED with the key words “oxidative stress” and your own disease and you will find a link. (http://www.ncbi.nlm.nih.gov/pubmed ). Reduce excess free radicals and reduce your disease symptoms. A study at the University of Paris in 2010 showed that rats feed a diet supplemented with Carbon 60 in olive oil, increased the lifespan of rats by 90% from an average of 25-30 months to over 55 months.
Essential minerals and trace minerals.
The National Post ran a story on May 1- “Obese Canadians should be granted legal protection from discrimination, professor says.” The obesity debate is totally missing the point. Most Doctors are ignoring their own medical research. The cause of the 400% increase in obesity in last 3 decades in Canada and sharp rise in most other chronic human diseases since the 1930’ is due to a chronic lack of essential minerals and trace minerals in our diet (plants, fruits and vegetables) that are needed as co-factors in the body for our biochemical pathways to work efficiently.
The soil minerals concentrations have been dropping worldwide for the last 100 years, so less and less minerals are absorbed in fruits, vegetables and other plants. This is due primarily to the fact that we no longer cook and heat our homes with wood and throw away the ashes (95% minerals) back into the garden to replenish the soil with the 60 essential and trace minerals that our bodies need. Fertilizer only has 3 minerals. Even the nutritional supplements commonly found in most health food stores don't carry the full complement of 90 essential nutrients, which should include 60 essential minerals, 15 essential vitamins, 12 essential amino acids and 3 fatty acids and the right doses of each and the correct easily absorbable mineral salts.
How do we know that we need 90 essential nutrients? Just talk to any veterinarian. Vets have cured over 600 chronic human diseases in farm animals and in zoo animals by supplementing their food with nutritional pellets. When was the last time you saw a cow with arthritis and a pig with Alzheimer’s? Vets have to cure an animal after the first time otherwise beef would cost over $500 a pound or eggs $50 a dozen. Why? Because animals don’t have health insurance. Doctors are quite content to treat your disease symptoms for the rest of your life, billing health insurance and not curing your disease after a few visits. Human clinical studies in the past 40 years have shown that most chronic human diseases are also caused by essential mineral deficiencies and can be controlled with the proper essential and trace minerals. Diabetes has been controlled with the right amount of chromium and vanadium and other essential cofactors. Arthritis is a lack of proper calcium absorption and cofactors such as Vitamin D and magnesium. Greying hair is a copper deficiency in the diet.
So can we live to be 100 or over without chronic human diseases? Yes by reducing excess oxidative stress or free radicals in our body and ensuring that we get the right daily balance of 90 essential nutrients including 60 minerals and trace minerals.
If you would like more information on the above or a copy of my presentation on Aging Gracefully without Chronic Human Diseases that I gave at Ukrainian Canadian Social Services last week, send me an email email@example.com or call (416) 819-9667 or download it from this link http://bit.ly/1KzZvm8 For Ukrainian listeners, catch my Ukrainian radio interview on Radio KONTAKT archives from Saturday April 25, 2015 http://www.kontaktglobal.com/radio-saturday.html
Walter Derzko is the president of the startup C60 Water North America
I’m adding a link to a presentation I gave last week to a group of seniors at the Ukrainian Canadian Social Services –Toronto Branch on Aging Gracefully without Chronic Human Diseases. It’s designed for a non-technical, layperson audience. You can download it from the link below.
Research carried out by the Copenhagen Centre for Team Sport and Health in Denmark shows that untrained elderly men get markedly fitter and healthier as a result of playing football (soccer). After only 4 months of twice-weekly 1-hour training sessions, the men achieved marked improvements in maximum oxygen uptake, muscle function and bone mineralization.
It is never too late to start playing football. Football boosts physical capacity and heart health, and minimizes the risk of falls and fractures in elderly men, who have never played football before or have not played for decades. Photo: Mikal Schlosser. Download free press photo.
Later today, three scientific articles will be published in the Scandinavian Journal of Medicine & Science in Sports describing the fitness and health effects of football (soccer) training for 63‒75-year-old untrained men.
The Copenhagen researchers, led by Professor Peter Krustrup of the Copenhagen Centre for Team Sport and Health, University of Copenhagen, have a compelling case. Football is a fun, social and effective form of high-intensity interval training that is open to all.
Untrained elderly men can also play
“Our previous studies have shown that 70-year-old men with lifelong participation in football possess a postural balance and rapid muscle force that is comparable to that of 30-year-old untrained men,” says Krustrup. “This time we have gone one step further by evaluating the intensity of football training as well as the health and fitness effects of football for untrained elderly men with little experience of football.”
“The study revealed that inactive elderly men improved their maximum oxygen uptake by 15% and their performance during interval exercise by as much as 50% by playing football for 1 hour two times per week over 4 months. Moreover, muscle function was improved by 30% and bone mineralization in the femoral neck increased by 2%,” says Krustrup.
“The results provide strong evidence that football is an intense, versatile and effective form of training, including for untrained elderly men. It is definitely never too late to start playing football. Football boosts physical capacity and heart health, and minimizes the risk of falls and fractures in elderly, men who have never played football before or have not played for decades,” says Krustrup.
“The players had heart rates that were sky high and corresponded to the values obtained during elite football games,” says Associate Professor Eva Wulff Helge of the Department of Nutrition, Exercise and Sports, University of Copenhagen.
“GPS measurements and video analyses also showed that there are many fast runs, stops, turns, dribbles, passes and shots, providing strong stimuli for muscle and bone adaptations. The fast runs, intense actions and unorthodox movements may well be the cause of a large increase in bone mineralization in the femur bone and femoral neck after only 4 months and of the further 3% improvement from 4 to 12 months of training,” says Helge.
An active everyday life and better health
“Our study shows that intense training such as football can change the lives of elderly men,” says Krustrup.
“The remarkable improvements in aerobic fitness and muscle strength make it easier for the players to live an active life and overcome the physical challenges of everyday life such as climbing stairs, shopping, cycling and gardening. This benefits not only the players themselves, but also their families and friends,” says Krustrup.
The scientific study
The researchers at the Copenhagen Centre for Team Sport and Health have conducted numerous randomized controlled training studies involving football and other team sports.
In the present study, a total of 27 untrained men aged 63 to 75 were recruited, tested and randomized into a football group, a strength training group and an inactive control group. The two training groups exercised for 1 hour twice a week for a year. A comprehensive testing battery was used at baseline, after 4 months and after 12 months. The research team, comprising 20 researchers from the Copenhagen Centre for Team Sport and Health, the University of Southern Denmark, Gentofte University Hospital and the National Research Centre for the Working Environment, was led by Professor Peter Krustrup, who has studied fitness and health effects for more than 10 years and published 55 articles in the area over the last 5 years.
On 19 June, the Copenhagen Centre for Team Sport and Health will be publishing a special issue of the Scandinavian Journal of Medicine & Science in Sports on the topic of football for health in collaboration with the FIFA Medical Assessment and Research Centre (F-MARC). Professors Peter Krustrup, Jens Bangsbo and Jiri Dvorak are the guest editors of this special issue, which will contain 16 original scientific articles based on the work of 63 researchers from eight countries.
Peter Krustrup, Professor, Copenhagen Centre for Team Sport and Health, Department of Nutrition, Exercise and Sports, University of Copenhagen and University of Exeter, United Kingdom. e-mail: firstname.lastname@example.org – tel.: +45 21 16 15 30
Bo Kousgaard, Head of Communication, Copenhagen Centre for Team Sport and Health, University of Copenhagen. e-mail: email@example.com – tel.: +45 23 23 86 24
Study gives new insight into similarity of complex brain networks in monkeys, humans
Monkeys that ate a diet rich in omega-3 fatty acids had brains with highly connected and well organized neural networks — in some ways akin to the neural networks in healthy humans — while monkeys that ate a diet deficient in the fatty acids had much more limited brain networking, according to an Oregon Health & Science University study.
The study, published today in the Journal of Neuroscience, provides further evidence for the importance of omega-3 fatty acids in healthy brain development. It also represents the first time scientists have been able to use functional brain imaging in live animals to see the large-scale interaction of multiple brain networks in a monkey. These patterns are remarkably similar to the networks found in humans using the same imaging techniques.
"The data shows the benefits in how the monkeys' brains organize over their lifetime if in the setting of a diet high in omega-3 fatty acids," said Damien Fair, PA-C, Ph.D., assistant professor of behavioral neuroscience and assistant professor of psychiatry in the OHSU School of Medicine and senior author on the paper. "The data also shows in detail how similar the networks in a monkey brain are to networks in a human brain, but only in the context of a diet rich in omega-3-fatty acids."
Omega-3 fatty acids are considered essential fatty acids for the human body. But while they are needed for human health, the body can't make them — it has to get them through food.
The study measured a kind of omega-3 fatty acid called docosahexaenoic acid, or DHA, which is a primary component of the human brain and important in development of the brain and vision. DHA is especially found in fatty fish and oils from those fish — including salmon, mackerel and tuna. Research by a co-author on the paper, Martha Neuringer, Ph.D., an associate scientist in the Division of Neuroscience at OHSU’s Oregon National Primate Research Center, previously showed the importance of DHA for infants’ visual development — a finding that led to the addition of DHA to infant formulas.
The scientists studied a group of older rhesus macaque monkeys — 17 to 19 years of age — from ONPRC that had been fed all of their lives either a diet low or high in omega-3 fatty acids, including DHA. The study found that the monkeys that had the high-DHA diet had strong connectivity of early visual pathways in their brains. It also found that monkeys with the high-DHA diet showed greater connections within various brain networks similar to the human brain — including networks for higher-level processing and cognition, said David Grayson, a former research assistant in Fair's lab and first author on the paper. Grayson is now studying at the Center for Neuroscience, University of California-Davis.
"For example, we could see activity and connections within areas of the macaque brain that are important in the human brain for attention," said Fair.
Now that those measurements and monitoring are possible, Fair said, the next step will be to analyze whether the monkeys with deficits in certain networks have behavioral patterns that are similar to behavioral patterns in humans with certain neurological or psychiatric conditions — including Attention Deficit Hyperactivity Disorder and autism.
Fair, who was among the 102 people given the 2013 Presidential Early Career Award for Scientists and Engineers by President Barack Obama, is a leader in using the same kind of brain imaging to explore brain networks in children with ADHD and autism. He said he hopes to use these non-invasive brain imaging techniques to provide an important link between research in humans and animals in order to better characterize, treat, and prevent these types of developmental mental health issues.
Fair added that another longer-term goal would be to study brain development in the monkeys fed various diets from birth into maturity.
"It would be important to see how a diet high in omega-3s might affect brain development early on in their lives, and across their lifespan," Fair said.
The study was funded by the Oregon Clinical and Translational Research Institute (through National Institutes of Health grant UL1TR000128), several other NIH grants (grants UL1 RR024140, P510D011092, K99/R00 MH091238, R01 MH096773, EY13199, and DK29930) and the Foundation Fighting Blindness.
About OHSU Brain Institute
The Oregon Health & Science University Brain Institute is a national neuroscience leader in patient care, research and education. With more than 1,000 brain scientists and specialists, OHSU is home to one of the largest communities of brain and central nervous system experts in the nation. OHSU Brain Institute scientists have won national recognition for breaking new ground in understanding Alzheimer’s disease and for discoveries that have led to new treatments for Parkinson’s disease, multiple sclerosis, stroke and other brain disorders and diseases.
Oregon Health & Science University is a nationally prominent research university and Oregon’s only public academic health center. It serves patients throughout the region with a Level 1 trauma center and nationally recognized Doernbecher Children’s Hospital. OHSU operates dental, medical, nursing and pharmacy schools that rank high both in research funding and in meeting the university’s social mission. OHSU’s Knight Cancer Institute helped pioneer personalized medicine through a discovery that identified how to shut down cells that enable cancer to grow without harming healthy ones. OHSU Brain Institute scientists are nationally recognized for discoveries that have led to a better understanding of Alzheimer’s disease and new treatments for Parkinson’s disease, multiple sclerosis and stroke. OHSU’s Casey Eye Institute is a global leader in ophthalmic imaging, and in clinical trials related to eye disease.
Do you believe in your own ability to succeed, or do you believe life events are largely beyond your control?
Think carefully about your answer — it could affect your risk of mortality.
People who feel in control and believe they can achieve goals despite hardships are more likely to live longer and healthier lives, especially among those with less education, according to a new study by Brandeis University and the University of Rochester. The study was published online in the journal of Health Psychology.
Previous studies have shown that people with a high school diploma or less education tend to die younger than those with a college degree or graduate training. Yet, that’s not a hard and fast rule. Why?
In this study, less educated people with higher perceived control in their life had a mortality rate three times lower than those with a lower sense of control. In fact, a high sense of control seemed to negate the mortality risks of lower education, says Margie Lachman, the Minnie and Harold Fierman Professor of Psychology, and an author on the paper.
“A high sense of control all but wipes out educational differences when it comes to mortality,” Lachman says. “A person with less education but a high sense of control is practically indistinguishable from a person of high education.”
Researchers determined attitudes about perceived control by asking participants to rank agreement to a set of statements. For example, participants were given the statement, “Sometimes I feel I am being pushed around in my life,” and asked to rank their agreement from one (strongly disagree) to seven (strongly agree).
The study’s public health implications are exciting, says Lachman.
“There are methods and strategies for improving one’s sense of control, and educational experiences are one of them,” Lachman says. “We could implement those approaches in educational and public health programs aimed at increasing health-promoting attitudes and behaviors and ultimately lowering mortality risks.”
The study’s authors include Nicolas Turiano and Benjamin Chapman of the University of Rochester Medical Center, Frank Infurna of the German Institute for Economic Research, and Stefan Agrigoroaei of Brandeis.
The research was supported by the National Institute on Aging and used data from Midlife in the United States (MIDUS), a national survey of more than 6,000 people.
According to new study of normal-weight and overweight or obese individuals published in the Journal of the Academy of Nutrition and Dietetics
Philadelphia, PA, December 30, 2013 – Obesity rates in the United States increased from 14.5% of the population in 1971-1974 to 35.9% of the population in 2009-2010. It's believed that one contributing factor to expanding waistlines is the reported increase in energy intake. Research suggests that the ability to control energy intake may be affected by the speed at which we eat, and a high eating rate may impair the relationship between the sensory signals and processes that regulate how much we eat.
In order to learn more about the relationship between eating speed and energy intake, a team of researchers in the Department of Kinesiology at Texas Christian University took a look at how eating speed affects calories consumed during a meal in both normal weight subjects as well as overweight or obese subjects. The investigators also collected data on feelings of hunger and fullness before and after the fast-paced and slow-paced meals and water consumption during the meals. Their results are published in the Journal of the Academy of Nutrition and Dietetics.
While previous studies have reviewed the relationship between eating speed and body weight, most of those studies were conducted with normal-weight individuals. In this new study, investigators asked a group of normal-weight subjects and a group of overweight or obese subjects to consume two meals in a controlled environment. All subjects ate one meal at a slow speed, for which they were instructed to imagine that they had no time constraints, take small bites, chew thoroughly, and pause and put the spoon down between bites, and a second meal at a fast speed, for which they were instructed to imagine that they had a time constraint, take large bites, chew quickly, and not pause and put the spoon down.
At the conclusion of the study, researchers found that only normal-weight subjects had a statistically significant reduction in caloric consumption during the slow compared to the fast meal: 88 kcal less for the normal weight group, versus only 58 kcal less for the overweight or obese group.
"Slowing the speed of eating led to a significant reduction in energy intake in the normal-weight group, but not in the overweight or obese group. A lack of statistical significance in the overweight and obese group may be partly due to the fact that they consumed less food during both eating conditions compared to the normal-weight subjects," explained lead author Meena Shah, PhD, professor in the Department of Kinesiology at Texas Christian University. "It is possible that the overweight and obese subjects felt more self-conscious, and thus ate less during the study."
Despite the differences in caloric consumption between the normal-weight and overweight and obese subjects, the study found some similarities. Both groups felt less hungry later on after the slow meal than after the fast meal. "In both groups, ratings of hunger were significantly lower at 60 minutes from when the meal began during the slow compared to the fast eating condition," added Dr. Shah. "These results indicate that greater hunger suppression among both groups could be expected from a meal that is consumed more slowly."
Also, both the normal weight and overweight or obese groups consumed more water during the slow meal. During the fast condition, participants across the study only consumed 9 ounces of water, but during the slow condition, that amount rose to 12 ounces. "Water consumption was higher during the slow compared to the fast eating condition by 27% in the normal weight and 33% in the overweight or obese group. The higher water intake during the slow eating condition probably caused stomach distention and may have affected food consumption," said Dr. Shah.
With obesity rates continuing to rise among the adult population in the United States, information about how different weight groups approach and consume food will be helpful in crafting strategies to lower energy intake, but for now, Dr. Shah suggested, "Slowing the speed of eating may help to lower energy intake and suppress hunger levels and may even enhance the enjoyment of a meal."
For centuries, humans have been exploring, researching, and, in some cases, discovering how to stave off life-threatening diseases, increase life spans, and obtain immortality. Biologists, doctors, spiritual gurus, and even explorers have pursued these quests—one of the most well-known examples being the legendary search by Ponce de León for the "Fountain of Youth." Yet the key to longevity may not lie in a miraculous essence of water, but rather in the structure and function of cells within a plant—and not a special, mysterious, rare plant, but one that we may think of as being quite commonplace, even ordinary: the palm.
As an honors botany student at the University of Leeds, P. Barry Tomlinson wrote a prize-winning essay during his final year titled, "The Span of Life." Fifty years later, Tomlinson (now a Distinguished Professor at The Kampong Garden of the National Tropical Botanical Garden, Miami, FL) teamed up with graduate student Brett Huggett (Harvard University, MA) to write a review paper exploring the idea that palms may be the longest-lived tree, and whether this might be due to genetic underpinnings. Having retained his essay in his personal files, Tomlinson found that it provided an excellent literature background for working on the question of cell longevity in relation to palms. Together, Tomlinson and Huggett published their review in the December issue of the American Journal of Botany (http://www.amjbot.org/content/99/12/1891.full.pdf+html).
A component of an organism's life span that biologists have been particularly interested in is whether longevity is genetically determined and adaptive. For botanists, discovering genetic links to increasing crop production and the reproductive lifespan of plants, especially long-lived ones such as trees, would be invaluable.
In their paper, Tomlinson and Huggett emphasize that in many respects, an organisms' life span, or longevity, is determined by the period of time in which its cells remain functionally metabolically active. In this respect, plants and animals differ drastically, and it has to do with how they are organized—plants are able to continually develop new organs and tissues, whereas animals have a fixed body plan and are not able to regenerate senescing organs. Thus, plants can potentially live longer than animals.
"The difference in potential cell longevity in plants versus animals is a significant point," states Tomlinson. "It is important to recognize that plants, which are so often neglected in modern biological research, can be informative of basic cell biological features in a way that impacts human concern at a fundamental level."
The authors focused their review on palm trees because palms have living cells that may be sustained throughout an individual palm's lifetime, and thus, they argue, may have some of the longest living cells in an organism. As a comparison, in most long-lived trees, or lignophytes, the main part, or trunk, of the tree is almost entirely composed of dead, woody, xylem tissues, and in a sense is essentially a supportive skeleton of the tree with only an inner ring of actively dividing cells. For example, the skeleton of Pinus longaeva may be up to 3000 years old, but the active living tissues can only live less than a century.
In contrast, the trunks of palms consist of cells that individually live for a long time, indeed for the entire life of an individual.
Which brings up the question of just how long can a palm tree live? The authors point out that palm age is difficult to determine, primarily because palms do not have secondary growth and therefore do not put down annual or seasonal growth rings that can easily be measured. However, age can be quite accurately assessed based on rate of leaf production and/or visible scars on the trunk from fallen leaves. Accordingly, the authors found that several species of palm have been estimated to live as long as 100 and even up to 740 years. The important connection here is that while the "skeleton" of the palm may not be as old as a pine, the individual cells in its trunk lived, or were metabolically active, as long as, or longer than those of the pine's.
Most plants, in addition to increasing in height as they age, also increase in girth, putting down secondary vascular tissue in layers both on the inner and outer sides of the cambium as they grow. However, palms do not have secondary growth, and there is no addition of secondary vascular tissue. Instead, stem tissues are laid down in a series of interconnected vascular bundles—thus, not only is the base of the palm the oldest and the top the youngest, but these tissues from old to young, from base to top, must also remain active in order to provide support and transport water and nutrients throughout the tree.
IMAGE:This shows Sabal causiarum, native to Puerto Rico, planted in 1932 at the Montgomery Botanical Center, Coral Gables Florida and in the prime of its long life (estimated height, 20...
Indeed, the authors illustrate this by reviewing evidence of sustained primary growth in two types of palms, the coconut and the sago palm. These species represent the spectrum in tissue organization from one where cells are relatively uniform and provide both hydraulic and mechanical functions (the coconut) to one where these functions are sharply divided with the inner cells functioning mainly for transporting water and nutrients and the outer ones for mechanical support (the sago palm). This represents a progression in specialization of the vascular tissues.
Moreover, there is evidence of continued metabolic activity in several types of tissues present in the stems of palms, including vascular tissue, fibers, ground tissue, and starch storage. Since the vascular tissues in palms are nonrenewable, they must function indefinitely, and Tomlinson and Huggett point out that sieve tubes and their companion cells are remarkable examples of cell longevity as they maintain a long-distance transport function without replacement throughout the life of the stem, which could be for centuries.
Despite several unique characteristics of palms, including the ability to sustain metabolically active cells in the absence of secondary tissues, seemingly indefinitely, unlike conventional trees, in which metabolically active cells are relatively short-lived, the authors do not conclude that the extended life span of palms is genetically determined.
"We are not saying that palms have the secret of eternal youth, and indeed claim no special chemical features which allows cells in certain organisms to retain fully differentiated cells with an indefinite lifespan," states Tomlinson. "Rather, we emphasize the distinctive developmental features of palm stems compared with those in conventional trees."
Tomlinson indicates that this reflects the neglect of the teaching of palm structure in modern biology courses. "This paper raises incompletely understood aspects of the structure and development of palms, emphasizing great diversity in these features," he concludes. "This approach needs elaborating in much greater detail, difficult though the subject is in terms of conventional approaches to plant anatomy."
Tomlinson, P. Barry and Brett A. Huggett. 2012. Cell longevity and sustained primary growth in palm stems. American Journal of Botany 99(12): 1891-1902. DOI: 10.3732/ajb.1200089
The Botanical Society of America (www.botany.org) is a non-profit membership society with a mission to promote botany, the field of basic science dealing with the study and inquiry into the form, function, development, diversity, reproduction, evolution, and uses of plants and their interactions within the biosphere. It has published the American Journal of Botany (www.amjbot.org) for nearly 100 years. In 2009, the Special Libraries Association named the American Journal of Botany one of the Top 10 Most Influential Journals of the Century in the field of Biology and Medicine.
For further information, please contact the AJB staff at firstname.lastname@example.org.
Studies bring unprecedented clarity to aging process and provide paradigm for studying how genes and environment -- including calorie restriction -- may influence lifespan
SEATTLE – For the first time, scientists at Fred Hutchinson Cancer Research Center have defined key events that take place early in the process of cellular aging.
Together the discoveries, made through a series of experiments in yeast, bring unprecedented clarity to the complex cascade of events that comprise the aging process and pave the way to understanding how genetics and environmental factors like diet interact to influence lifespan, aging and age-related diseases such as cancer and neurodegenerative disorders.
The findings, including unexpected results that link aspects of aging and lifespan to a mechanism cells use to store nutrients, are described in the Nov. 21 issue of Nature by co-authors Daniel Gottschling, Ph.D., a member of the Hutchinson Center's Basic Sciences Division, and Adam Hughes, Ph.D., a postdoctoral fellow in the Gottschling Lab.
The researchers found the acidity of a structure in yeast cells known as the vacuole is critical to aging and the functioning of mitochondria – the power plants of the cell. They also describe a novel mechanism, which may have parallels in human cells, by which calorie restriction extends lifespan.
The work began with Hughes and Gottschling searching for the source of age-related damage in mitochondria.
"Normally, mitochondria are beautiful, long tubes, but as cells get older, the mitochondria become fragmented and chunky," said Gottschling, also an affiliate professor in the Department of Genome Sciences at the University of Washington. "The changes in shape seen in aging yeast cells are also observed in certain human cells, such as neurons and pancreatic cells, and those changes have been associated with a number of age-related diseases in humans."
What causes mitochondria to become distorted and dysfunctional as cells age had long been a mystery, but Gottschling and Hughes have discovered that specific changes in the vacuole lead directly to its malfunctioning.
The vacuole – and its counterpart in humans and other organisms, the lysosome – has two main jobs: degrading proteins and storing molecular building blocks for the cell. To perform those jobs, the interior of the vacuole must be highly acidic.
Hughes and Gottschling found that the vacuole becomes less acidic relatively early in the yeast cell's lifespan and, critically, that the drop in acidity hinders the vacuole's ability to store certain nutrients. This, in turn, disrupts the mitochondria's energy source, causing them to break down. Conversely, when Hughes prevented the drop in vacuolar acidity, the mitochondria's function and shape were preserved and the yeast cells lived longer.
"Until now, the vacuole's role in breaking down proteins was thought to be of primary importance. We were surprised to learn it was the storage function, not protein degradation, that appears to cause mitochondrial dysfunction in aging yeast cells," Hughes said.
The unexpected discovery prompted Hughes and Gottschling to investigate the effects of calorie restriction, which is known to extend the lifespan of yeast, worms, flies and mammals, on vacuolar acidity. They found that calorie restriction – that is, limiting the raw material cells need – delays aging at least in part by boosting the acidity of the vacuole.
"Now that we have preliminary evidence in yeast of how calorie restriction extends lifespan, our hope is that it can be translated to higher organisms like humans," Hughes said. Given the similarities in the fundamental biology of yeast and human cells, the researchers' newly defined link between what cells "eat" and how they age could shed valuable light on the events that lead to age-related disorders in humans.
"There has been a lot in the scientific literature and the general media lately about how what you eat affects the aging process, but it has been incredibly confusing. Now we have a new paradigm for understanding how genetics and environment interact to influence lifespan, aging and age-related diseases. That's what I'm really excited about," Gottschling said.
Gottschling and Hughes speculate that if the vacuole's declining acidity limits its ability to store certain nutrients and metabolites, they may build up in the cell, flooding the mitochondria. Overwhelmed, the mitochondria use up all their energy – essentially burning out their motors – taking in the surplus. With no power left to import the proteins they need to maintain their elegant shape and execute their regular duties, the mitochondria literally break down. Gottschling and his colleagues are now investigating this hypothesis in detail. They are also exploring what triggers the initial drop in the vacuole's acidity.
The latter research question is of particular interest because the researchers found that even though vacuolar acidity drops as mother yeast cells age, the acidity in the vacuoles of their newborn daughter cells is normal. This corresponds to previous findings in the field that all daughter yeast cells have the same potential lifespan, regardless of the age of their mothers. The resetting of the daughter's vacuolar acidity is the earliest event yet observed in cellular rejuvenation, a phenomenon in which age-related defects are seemingly erased in an organism's offspring. This could help explain how the act of cell division itself contributes to aging.
These results are just the newest chapter in a "decade-old interest," according to Gottschling. He and his colleagues have made several landmark discoveries in the past 10 years, including finding that aging yeast cells exhibit the same genomic instability seen in human cancer cells and proving that mitochondrial dysfunction causes that instability. Gottschling's team also has developed innovative tools to leverage the power of yeast as a model organism, including a technique called the Mother Enrichment Program that makes experiments more efficient by enabling researchers to generate large populations of aging yeast cells.
"It's worth using yeast to study complex things like aging because a lot of person-years of research have gone into understanding the fundamentals. The genetic and cell-biology tools available for studying yeast are unparalleled," Gottschling said. "Having the proper tools is like having new glasses; you can see things you never could before, and once you start to see new things, you can dissect them to understand how they work."
In addition to the latest eye-popping technology, the researchers relied on sheer tenacity – with a little help from motion-sickness pills – in pursuit of their discoveries. Some of the painstaking experiments required Hughes to delicately manipulate individual yeast cells as they divided every two hours for days at a time. For another series of experiments that lasted several months, Hughes took Dramamine to ward off the queasiness that came with inspecting brightly colored yeast cells as they streaked across his microscope's field of view.
"There were definitely tough points, but it was worth it when we knew the story as a whole. Showing that the change in vacuolar acidity was real and that it mattered – that it affected lifespan – made the grueling experiments worthwhile," Hughes said. Gottschling is an elected member of the National Academy of Sciences, the American Academy of Arts & Sciences, the Washington State Academy of Sciences and the American Academy of Microbiology.
This research was funded by grants from the National Institutes of Health, the Helen Hay Whitney Foundation, a University of Washington's Genetic Approaches to Aging Training Grant and the Glenn Foundation for Medical Research. Preliminary support, including for the development of technologies used in this research, was provided by the Hutchinson Center's Hartwell Innovation Fund.
Editor's note: To obtain an embargoed copy of the Nature paper, "An early-age increase in vacuolar pH limits mitochondrial function and lifespan in yeast," please contact email@example.com. Once the paper is published electronically, the abstract (available to everyone) and full text (available only to subscribers) can be retrieved by visiting http://dx.doi.org/10.1038/nature11654
Image available upon request: A color image showing vacuolar acidity in a population of cells is available upon request
Public release date: 21-Nov-2012
Contact: Kristen Woodward
Fred Hutchinson Cancer Research Center
[N.B....Fullerenes (Hydrated Fullerenes Hy-C60) likely regulate/prevent protein aggregation and protein mis-folding--WD]
New discoveries in cell aging
A group of researchers led by the Institute of Biotechnology and Biomedicine (IBB) and Universitat Autònoma de Barcelona (UAB) have achieved to quantify with precision the effect of protein aggregation on cell aging processes using as models the Escherichia coli bacteria and the molecule which triggers Alzheimer's disease. Scientists demonstrated that the effect can be predicted before it occurs. Protein aggregation is related to several diseases, including neurodegenerative diseases.
The research, published recently in the Journal of Molecular Biology, provides an extremely reliable system with which to model and quantify the effect of protein aggregation on the viability, division and aging of cells. It also aids in further understanding the natural evolution of proteins. According to Salvador Ventura, researcher at IBB and director of the research project, "it will serve to develop computer approximations to predict the effects aggregation has on cell aging, as well as to search for molecules that act as natural chaperones, highly conserved proteins which are present also in humans and which have the ability to reduce this effect in the bacteria".
Although it is widely accepted that bad folding and aggregation of proteins reduces the cell's ability to survive and reproduce, the damage caused had not been previously measured experimentally as precisely as it was in this research.
In previous studies scientists had verified that the expression of the Alzheimer's AB42 peptide in bacteria induces the process of protein aggregation. Now they have demonstrated that this effect is coded in the protein aggregation sequence and that it depends on intrinsic properties, not on a direct response from within the cell. This makes it possible to predict the effect. Scientists also demonstrated that damage caused to the bacteria is controlled by molecular chaperones, which reduce the tendency of proteins to aggregate and favour cell survival.
In addition to researchers from IBB and the UAB Department of Biochemistry and Molecular Biology, participating in the project were scientists from the Biophysics Unit at CSIC-UPV, the University of the Basque Country, the Institute for Bioengineering of Catalonia and the Barcelona Centre for International Health Research.