FIGHT AGING! NEWSLETTER
September 3rd 2012
The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!
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CONTENT
- A Perspective on Progress in Longevity Science
- What’s Really Delaying the Defeat of Aging?
- Absent Optimism
- Everyone Has a Plan to Save Medicare
- Discussion
- Latest Headlines from Fight Aging!
- SIRT6 Overexpression Reverses DNA Repair Decline in Aging Mice
- A Good Lifestyle Makes a Difference Even Late in Life
- Impact of Mid-Life Fitness on Later Risk of Age-Related Disease
- No Extension of Average Lifespan in Primate Study of Calorie Restriction
- A View of Diet and Aging
- Work on Blocking Damage in Brain Injury
- More on DNA Methylation and Human Longevity
- Cytomegalovirus and Type 2 Diabetes Risk
- How Long Do You Want to Live?
- Wiring Up Engineered Tissue
A PERSPECTIVE ON PROGRESS IN LONGEVITY SCIENCE
Here is an overview of some of what I see when looking out on the world of research and development relating to engineered longevity, spurred by someone who asked whether it was plausible for aging to be defeated by 2029:
http://www.fightaging.org/archives/2012/08/an-outline-of-progress-in-longevity-science.php
“The bottom line is that the research community and state of the field today is very different from that of even a mere ten years ago. This is a time of rapid change and progress: far more is known and far more impressive feats of medicine can be performed in the lab and the clinic. There is every reason to believe that ten years from now we’ll be able to say the same thing. Costs in biotechnology and life science research are falling rapidly, and with that trend more research can be accomplished in each new year.
“That said, however, the only way that we’ll see significant inroads into the defeat of aging by 2029 is for the SENS Foundation and its attendant research community to undergo the same sort of growth over the next decade as has been exhibited in recent years by regenerative medicine, calorie restriction research, or study of the genetics of longevity. A growth to billions in funding and thousands of researchers, in other words. It will require at least that and a decade of time in order to have a 50/50 shot at reversing aging in old mice in the lab – which is to say something that can make them live at least twice as long as they otherwise would have done.
“Of all the items covered in this post, only SENS provides a path towards achieving this end. Even regenerative medicine and complete control over stem cells can’t offer the possibility of reversing aging in and of itself – it is only the way to reverse one component of aging, the decline of tissue maintenance and frailty that results from stem cells shutting down. You will still get nailed by your own mitochondria and the build up of metabolic byproducts even if your stem cells are perfectly restored.
“[So], no, there is no plausible road to the defeat of aging by 2029. But there is a plausible road to the first laboratory demonstrations of real, meaningful, but partial age reversal by then, ways to actually repair the root biological causes of aging rather than just slow it down. Whether that happens or not depends absolutely on funding – there are more than enough scientists and research groups out there who would work on the SENS vision for rejuvenation biotechnology if given a budget, but as of yet not enough funding sources to make it a reality.”
WHAT’S REALLY DELAYING THE DEFEAT OF AGING?
Aubrey de Grey of the SENS Foundation answers this question in an open access editorial from the Rejuvenation Research journal:
http://www.fightaging.org/archives/2012/08/whats-really-delaying-the-defeat-of-aging.php
“In the mid-1990s, when I decided to switch from computer science to gerontology, I recognized that the creation of a credible assault on aging would require solving three basic problems: (1) Creating a credible plan; (2) getting the people best placed to implement it to be interested in doing so; and (3) giving them the financial resources to get on with the job.
“I broke the back of the first problem in mid-2000, when I realized that regenerative medicine – repairing the accumulating damage of aging – will probably be far simpler and easier to implement than the alternative followed by most biogerontologists, namely slowing the creation of that damage. By that time, I had also done most of the heavy lifting of item 2 (as I continued to do thereafter), by connecting with leading researchers worldwide, mostly face to face at conferences, and improving their understanding of how their expertise could be productively applied to aging. By way of illustration, quite a few of the most prestigious such people are named on the front cover of this journal as associate editors, and they accepted such a position for that reason. But what about item 3?
“Unfortunately, I cannot tell so positive a story with respect to financial resources. Nearly a decade ago, I began to make public predictions of how soon we would achieve success in our crusade. I did so, as I still do, in the manner that (for better or worse) preoccupies the general public, namely in terms of longevity, but I have always been careful to incorporate two key caveats: (1) The level of uncertainty of the time frames, even if only scientific uncertainty is considered, and (2) the reliance of such estimates on adequate funding.
“The first of these caveats is often elided, but it is simple: I estimate that we have a 50% chance of achieving the milestone of “robust human rejuvenation” (essentially, the rejuvenation of 60 year olds comprehensively enough that they won’t be biologically 60 again until they’re chronologically 90) within 25 years, but I also estimate that we have at least a 10% chance of not getting there in 100 years. But…that is all subject to the second caveat, namely funding.
“Tragically, the level of funding that has been forthcoming during the past decade is only a few percent (at most) of what is necessary. The rate of progress in research to defeat aging has been quite amazing in view of that, but nonetheless, I estimate that it has been only about one-third of what could have been achieved with 10-20 times more money.”
ABSENT OPTIMISM
Our culture is far too short-sighted, focused on what is, and pessimistic, and that harms the prospects for progress:
http://www.fightaging.org/archives/2012/08/absent-optimism.php
“For a society in the midst of accelerating, rapid, and evident technological progress, public discussion and attitudes show a surprising lack of optimism for the future. Optimism of course exists, but nowhere near as widely as it should. It seems self-evident at this point that a golden era lies ahead in which we defeat disease and aging, colonize the solar system, and expand the limits of what it means to be human. We and our descendants will discard pain and suffering along the way, just as we have already discarded so much of the pain and suffering that our ancestors bore. … The upward ramp of the necessary underlying technology is within our grasp. But you wouldn’t think this from listening to the public. Much of the world seems convinced that nothing but collapse and catastrophe lies ahead: their view of the future is the ever-mistaken Malthusian collection of beliefs revolving around static resources that are exhausted. They fail to see the dynamism of resource generation and progress that proved past Mathusians just as wrong as the present crop.”
EVERYONE HAS A PLAN TO SAVE MEDICARE
There are any number of people out there putting forward their proposals:
http://www.fightaging.org/archives/2012/08/everyone-has-a-plan-to-save-medicare.php
“Having a plan to save Medicare is somewhat like wearing a tie or cufflinks, in that it is somewhat de reigueur in some parts of society – but ultimately a cultural signal of belonging, of little value otherwise. The economic future of the US is somewhat grim; the decline of an empire is inevitable as its increasingly unaccountable elite class debauch the currency, centralize power, and regulate all aspects of a citizen’s life. They tax and waste ever more of the flow of resources whilst destroying the freedom and competition needed for the creation of those resources – in much the same way as a cancer is parasitic to its host but ultimately destroys both host and itself. This is an inexorable progression of society, built upon the foundation of human nature and the individual actions and interactions of millions of people. It has happened over and again and is just about as likely as the tide to be turned aside.
“So having a plan to save Medicare is rather like having a plan to save a part of your cancer. That portion in the lower left, perhaps. Medicare is but one part of the network of regulation, perverse incentives, and regulatory capture that causes medicine in the US to be ever more expensive, wasteful, and poor in quality. It’s large enough to be considered in the context of the more general economic decline across the board, which occurs for roughly the same set of reasons, and is just as hard to turn back. Medicine is in a more advanced state of socialist decrepitude than most other US industries, but the same process operates throughout society.
“From there let me segue into a discussion of responses to shortage. Regulation inevitably creates shortage and rationing: we see this in the provision of medicine in countries like Canada and the UK, where regulators set up waiting systems or simply forbid treatment, especially to the old. Much of the public discussion that results from this state of affairs looks at what to do about the shortages – though of course without a great deal of reflection on how they came to exist in the first place, sad to say. There are two broad lines of thinking here: firstly, use less of whatever is rationed; secondly try to create more of whatever is in short supply.
“One of the defining and frankly rather sorry aspects of our age is that public debates veer towards cutting back on use far more often than towards creating abundance. See the bulk of the environmentalist or other Malthusian movements for example – they have little to say about building more of whatever it is they think is in short supply.
“When it comes to Medicare, and given that very few people are calling to get rid of the whole system and let freedom and free markets rule the day, the two sides of the coin look much like (a) a call for increased rationing of services to ensure that people use less in the way of medicine, and (b) a call for ways to create greater health such that people use less in the way of medicine. There are of course many different approaches to either of these paths, but both ultimately sidestep the real issue, the real cause of the problem – and this again is absolutely characteristic of debate over societal organization and politics in our age.”
DISCUSSION
The highlights and headlines from the past week follow below. Remember – if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!
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LATEST HEADLINES FROM FIGHT AGING!
SIRT6 OVEREXPRESSION REVERSES DNA REPAIR DECLINE IN AGING MICE
Friday, August 31, 2012
http://www.fightaging.org/archives/2012/08/sirt6-overexpression-reverses-dna-repair-decline-in-aging-mice.php
This interesting research result adds a little more to the debate over whether nuclear DNA damage is relevant to aging beyond its effects on cancer risk – though I think it’s still a bit early to point to differences in DNA repair as the definitive cause of SIRT6-related longevity in mice: researchers “found that the decline in a cell’s ability to repair DNA during aging coincided with a global reduction in the levels of proteins involved in the repair process. [They] tried to reverse the age-related decline in DNA repair efficiency by restoring the proteins to their original levels and found only one protein, SIRT6, did the trick. … [Other research results have shown] that overexpressing the SIRT6 protein extended the lifespans of mice. Our research looked at DNA repair and found a reason for the increased longevity, and that is SIRT6′s role in promoting more efficient DNA repair. … The next step [is] to study the factors that regulate SIRT6, in an effort to learn more about the early stages of the DNA repair process. … multiple groups are trying to develop drugs that activate SIRT6, and [researchers hope] that this research will one day lead to therapies that help extend a person’s lifespan and treat cancer. … SIRT6 plays a critical role in repairing the most dangerous type of DNA damage: double-strand breaks. DNA is a two-stranded molecule, and breaks can occur to one strand of the molecule or to both. In the case of single-strand breaks, the unbroken strand guides the repair process and the DNA molecule is typically restored to its original state. However, double-strand breaks, in which both strands are severed, are particularly hazardous because they are more difficult to repair and can lead to a rearrangement of the cell’s genetic material.”
A GOOD LIFESTYLE MAKES A DIFFERENCE EVEN LATE IN LIFE
Friday, August 31, 2012
http://www.fightaging.org/archives/2012/08/a-good-lifestyle-makes-a-difference-even-late-in-life.php
Keeping up on the health basics makes a difference even in the last years of life: “It is well known that lifestyle factors, like being overweight, smoking and heavy drinking, predict death among elderly people. But is it uncertain whether these associations are applicable to people aged 75 years or more. So a team of researchers based in Sweden measured the differences in survival among adults aged 75 and older based on modifiable factors such as lifestyle behaviours, leisure activities, and social networks. The study involved just over 1,800 individuals who were followed for 18 years (1987-2005). Data on age, sex, occupation, education, lifestyle behaviours, social network and leisure activities were recorded. During the follow-up period 92% of participants died. Half of the participants lived longer than 90 years. Survivors were more likely to be women, be highly educated, have healthy lifestyle behaviours, have a better social network, and participate in more leisure activities than non-survivors. The results show that smokers died one year earlier than non-smokers. Former smokers had a similar pattern of survival to never smokers, suggesting that quitting smoking in middle age reduces the effect on mortality. Of the leisure activities, physical activity was most strongly associated with survival. The average age at death of participants who regularly swam, walked or did gymnastics was two years greater than those who did not. Overall, the average survival of people with a low risk profile (healthy lifestyle behaviours, participation in at least one leisure activity, and a rich or moderate social network) was 5.4 years longer than those with a high risk profile (unhealthy lifestyle behaviours, no participation in leisure activities, and a limited or poor social network). Even among those aged 85 years or older and people with chronic conditions, the average age at death was four years higher for those with a low risk profile compared with those with a high risk profile. In summary, the associations between leisure activity, not smoking, and increased survival still existed in those aged 75 years or more, with women’s lives prolonged by five years and men’s by six years, say the authors. These associations, although attenuated, were still present among people aged 85 or more and in those with chronic conditions.”
IMPACT OF MID-LIFE FITNESS ON LATER RISK OF AGE-RELATED DISEASE
Thursday, August 30, 2012
http://www.fightaging.org/archives/2012/08/impact-of-mid-life-fitness-on-later-risk-of-age-related-disease.php
How you manage your health in earlier parts of your life will have an effect further down the line: “To examine the association between midlife fitness and chronic disease outcomes in later life, participant data from the Cooper Center Longitudinal Study were linked with Medicare claims. We studied 18,670 healthy participants (21.1% women; median age, 49 years) who survived to receive Medicare coverage from January 1, 1999, to December 31, 2009. Fitness estimated by Balke treadmill time was analyzed [according] to age- and sex-specific quintiles. Eight common chronic conditions were defined [and] associations between midlife fitness and the number of conditions were assessed. … After 120,780 person-years of Medicare exposure with a median follow-up of 26 years, the highest quintile of fitness [was] associated with a lower incidence of chronic conditions [in men and women]. After multivariate adjustment, higher fitness [was] associated with a lower risk of developing chronic conditions in [men and women]. … In this cohort of healthy middle-aged adults, fitness was significantly associated with a lower risk of developing chronic disease outcomes during 26 years of follow-up. These findings suggest that higher midlife fitness may be associated with the compression of morbidity in older age.”
NO EXTENSION OF AVERAGE LIFESPAN IN PRIMATE STUDY OF CALORIE RESTRICTION
Thursday, August 30, 2012
http://www.fightaging.org/archives/2012/08/no-extension-of-average-lifespan-in-primate-study-of-calorie-restriction.php
A discussion on published results from this primate study suggest that both it and a comparison study are different in ways that make it harder to pull rigorous conclusions from the data – beyond the fact that diet clearly has influence, and the effects of calorie restriction on life span (average and maximum) are expected to be smaller in longer-lived species versus shorter-lived speces: “Scientists have found that calorie restriction – a diet composed of approximately 30 percent fewer calories but with the same nutrients of a standard diet – does not extend years of life or reduce age-related deaths in a 23-year study of rhesus monkeys. However, calorie restriction did extend certain aspects of health. … The survival results in the study reported [by] NIA researchers differ from those published in 2009 by NIA-supported investigators at the University of Wisconsin-Madison. The Wisconsin study followed two groups of rhesus monkeys for 20 years and found that monkeys on a calorie-restricted diet lived longer than those on a standard diet. Beyond longevity, the parallel NIA and Wisconsin studies have reported similar beneficial health effects of calorie-restriction. Both studies found that certain age-related diseases – including diabetes, arthritis, diverticulosis and cardiovascular problems – occurred at an earlier age in monkeys on the standard diet compared to those on calorie restriction. However, this observation was not statistically significant in the NIA study. NIA researchers did find that monkeys started on calorie restriction at an early age had a statistically significant reduction in cancer incidence. NIA researchers also found that while calorie restriction had a beneficial effect on several measures of metabolic health and function in monkeys who were started on the special diet regimen during old age (at 16 to 23 years), it did not have the same positive outcome for monkeys started on calorie restriction at a young age (less than 14 years). In the Wisconsin study, all the monkeys were 7 to 14 years when started on calorie restriction. … Differences in the monkeys’ meal and other nutritional factors were cited as possible explanations for NIA’s and Wisconsin’s different outcomes. Both studies used a similar percentage of calorie restriction with their intervention groups; however, the Wisconsin monkeys in both the calorie restricted and control groups were eating more and weighed more than the matched NIA monkeys. … NIA researchers cited genetics as another possible reason for their differing results. NIA monkeys had a greater genetic diversity, originating from China and India. Wisconsin’s monkeys came only from an Indian colony.”
A VIEW OF DIET AND AGING
Wednesday, August 29, 2012
http://www.fightaging.org/archives/2012/08/a-view-of-diet-and-aging.php
A review paper: “Nutrition has important long-term consequences for health that are not only limited to the individual but can be passed on to the next generation. It can contribute to the development and progression of chronic diseases thus effecting life span. Caloric restriction (CR) can extend the average and maximum life span and delay the onset of age-associated changes in many organisms. CR elicits coordinated and adaptive stress responses at the cellular and whole-organism level by modulating epigenetic mechanisms (e.g., DNA methylation, posttranslational histone modifications), signaling pathways that regulate cell growth and aging (e.g., TOR, AMPK, p53, and FOXO), and cell-to-cell signaling molecules (e.g., adiponectin). The overall effect of these adaptive stress responses is an increased resistance to subsequent stress, thus delaying age-related changes and promoting longevity. In human, CR could delay many diseases associated with aging including cancer, diabetes, atherosclerosis, cardiovascular disease, and neurodegenerative diseases.”
WORK ON BLOCKING DAMAGE IN BRAIN INJURY
Wednesday, August 29, 2012
http://www.fightaging.org/archives/2012/08/work-on-blocking-damage-in-brain-injury.php
Some of the damage that occurs in brain injury is secondary to the initial trauma and takes place at the level of cellular components. Researchers here demonstrate a possible way to stop that from happening: “Treatment with an agent that blocks the oxidation of an important component of the mitochondrial membrane prevented the secondary damage of severe traumatic brain injury (TBI) and preserved function that would otherwise have been impaired. … For the study, the research team conducted a global assessment of all the phospholipids in rat brain cells. This revealed that damage from TBI was nonrandom and mostly involved cardiolipin, a phospholipid that is found in the membranes that form mitochondria, the cell’s powerhouse. They noted that in the healthy animal, only 10 of the 190 cardiolipin species were modified by oxygen, but after a brain injury, the number of oxidized species rose many-fold. The researchers then developed an agent, called XJB-5-131, which can cross the blood-brain barrier and prevent the oxidation of cardiolipin. Using an established research model of severe TBI, the agent or a placebo was injected into the bloodstream of rats five minutes and again 24 hours after head injury. In the weeks that followed, treated animals performed akin to normal on tests of balance, agility and motor coordination, learning, and object recognition, while placebo-treated animals showed significant impairment. The results indicate that blocking cardiolipin oxidation by XJB-5-131 protected the brain from cell death. … a targeted oxidation-blocker might also be beneficial in the treatment of other neurological disorders, such as Parkinson’s disease, amyotrophic lateral sclerosis, or ALS, and stroke.”
MORE ON DNA METHYLATION AND HUMAN LONGEVITY
Tuesday, August 28, 2012
http://www.fightaging.org/archives/2012/08/more-on-dna-methylation-and-human-longevity.php
A great deal of data is being generated on patterns of DNA methylation, aging, and variations in human longevity: “(1) we evaluated the DNA methylation from peripheral leukocytes of 21 female centenarians, their 21 female offspring, 21 offspring of both non-long-lived parents, and 21 young women … (2) we compared the DNA methylation profiles of these populations … We observed an age-related decrease in global DNA methylation and a delay of this process in centenarians’ offspring. Interestingly, literature data suggest a link between the loss of DNA methylation observed during aging and the development of age-associated diseases. Genome-wide methylation analysis evidenced DNA methylation profiles specific for aging and longevity: (1) aging-associated DNA hypermethylation occurs predominantly in genes involved in the development of anatomical structures, organs, and multicellular organisms and in the regulation of transcription; (2) genes involved in nucleotide biosynthesis, metabolism, and control of signal transmission are differently methylated between centenarians’ offspring and offspring of both non-long-lived parents, hypothesizing a role for these genes in human longevity. Our results suggest that a better preservation of DNA methylation status, a slower cell growing/metabolism, and a better control in signal transmission through epigenetic mechanisms may be involved in the process of human longevity. These data fit well with the observations related to the beneficial effects of mild hypothyroidism and insulin-like growth factor I system impairment on the modulation of human lifespan.”
CYTOMEGALOVIRUS AND TYPE 2 DIABETES RISK
Tuesday, August 28, 2012
http://www.fightaging.org/archives/2012/08/cytomegalovirus-and-type-2-diabetes-risk.php
Cytomegalovirus (CMV) is a persistent and very common herpesvirus that is thought to be a major contributor to the age-related decline of the immune system, due to an ever increasing portion of its limited number of cells becoming specialized to CMV and thus unavailable for other duties. Various past studies have linked CMV with forms of age-related frailty, but here the researchers find an association with type 2 diabetes – which is interesting and perhaps somewhat unexpected, given that type 2 diabetes is essentially a lifestyle disease: “Cytomegalovirus (CMV) infection has been reported to contribute to the pathogenesis of type 1 diabetes and post-transplantation diabetes. However, CMV infection has not been evaluated as a possible risk factor for type 2 diabetes. Our aim was to investigate potential associations between CMV seropositivity, CMV IgG antibody level and glucose regulation in the oldest old. … CMV seropositive subjects were more likely to have type 2 diabetes (17.2% vs 7.9%), had a higher level of HbA1c and higher non-fasting glucose in the oldest olds. These associations remained significant after adjustment for possible confounders. CMV IgG antibody level was not significantly associated with glucose regulation … In the oldest old, CMV seropositivity is significantly associated with various indicators of glucose regulation. This finding suggests that CMV infection might be a risk factor for the development of type 2 diabetes in the elderly.”
HOW LONG DO YOU WANT TO LIVE?
Monday, August 27, 2012
http://www.fightaging.org/archives/2012/08/how-long-do-you-want-to-live.php
Here is an example to show that the urge to conform is somewhat stronger than the urge to live, and never mind the urge to think critically. People will tend to say that they want to be in the majority position now, no matter what that might be, and depending on how you phrase the question, the vast majority will tell you that they want to age to death and have a life that is no longer than that of their parents. Yet if longer lives were already common, those very same people would answer that they wanted to live those longer lives. It is frustrating, to say the least, the degree to which people live in the moment and blind themselves to what might be created: “How many years might be added to a life? A few longevity enthusiasts suggest a possible increase of decades. Most others believe in more modest gains. And when will they come? Are we a decade away? Twenty years? Fifty years? Even without a new high-tech ‘fix’ for aging, the United Nations estimates that life expectancy over the next century will approach 100 years for women in the developed world and over 90 years for women in the developing world. (Men lag behind by three or four years.) Whatever actually happens, this seems like a good time to ask a very basic question: How long do you want to live? Over the past three years I have posed this query to nearly 30,000 people at the start of talks and lectures on future trends in bioscience, taking an informal poll as a show of hands. To make it easier to tabulate responses I provided four possible answers: 80 years, currently the average life span in the West; 120 years, close to the maximum anyone has lived; 150 years, which would require a biotech breakthrough; and forever, which rejects the idea that life span has to have any limit at all. I made it clear that participants should not assume that science will come up with dramatic new anti-aging technologies, though people were free to imagine that breakthroughs might occur – or not. The results: some 60 percent opted for a life span of 80 years. Another 30 percent chose 120 years, and almost 10 percent chose 150 years. Less than 1 percent embraced the idea that people might avoid death altogether. These percentages have held up as I’ve spoken to people from many walks of life in libraries and bookstores; teenagers in high schools; physicians in medical centers; and investors and entrepreneurs at business conferences. I’ve popped the question at meetings of futurists and techno-optimists and gotten perhaps a doubling of people who want to live to 150 – less than I would have thought for these groups. Rarely, however, does anyone want to live forever, although abolishing disease and death from biological causes is a fervent hope for a small scattering of would-be immortals.”
WIRING UP ENGINEERED TISSUE
Monday, August 27, 2012
http://www.fightaging.org/archives/2012/08/wiring-up-engineered-tissue.php
This is interesting, the early stirrings of something that may change the tenor of future tissue engineering if carried through to its logical conclusions. Why build a plain heart if you can build a sensor-laden heart with its own embedded network for monitoring and medical intervention? From the release: “A multi-institutional research team has developed a method for embedding networks of biocompatible nanoscale wires within engineered tissues. These networks – which mark the first time that electronics and tissue have been truly merged in 3D – allow direct tissue sensing and potentially stimulation, a potential boon for development of engineered tissues that incorporate capabilities for monitoring and stimulation, and of devices for screening new drugs. … One of the major challenges in developing bioengineered tissues is creating systems to sense what is going on (e.g., chemically, electrically) within a tissue after it has been grown and/or implanted. Similarly, researchers have struggled to develop methods to directly stimulate engineered tissues and measure cellular reactions. … In the body, the autonomic nervous system keeps track of pH, chemistry, oxygen and other factors, and triggers responses as needed. We need to be able to mimic the kind of intrinsic feedback loops the body has evolved in order to maintain fine control at the cellular and tissue level. … With the autonomic nervous system as inspiration, [scientists] built mesh-like networks of nanoscale silicon wires – about 80 nm in diameter – shaped like flat planes or in a ‘cotton-candy’-like reticular conformation. The networks were porous enough to allow the team to seed them with cells and encourage those cells to grow in 3D cultures. … Previous efforts to create bioengineered sensing networks have focused on 2D layouts, where culture cells grow on top of electronic components, or on conformal layouts where probes are placed on tissue surfaces. It is desirable to have an accurate picture of cellular behavior within the 3D structure of a tissue, and it is also important to have nanoscale probes to avoid disruption of either cellular or tissue architecture.”
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