It isn't only rodent species that have a wide enough range of longevity to intrigue researchers. Amongst the rodents, naked mole rats can live nine times longer than shorter-lived and similarly sized cousin species, but amongst birds it is the case that parrots on average live more than five times as long as quail. The hope is that by comparing in detail the biochemistry of similar species with very different life spans, the research community will gain important new knowledge of aging - such as which of the mechanisms known to be associated with aging are more important determinants of life span. That understanding could help to steer research priorities in rejuvenation biotechnology by knowing which issues in the aging body will lead to greater benefits if repaired.

But back to the parrots and the quails: here is an example of the sort of research taking place in which researchers compare two species with different life spans. The context you should consider leading into the article is that there is some basis for thinking that levels of naturally produced antioxidants should partially determine life span in a species: oxidative damage can be tied to aging via a number of theories and their supporting evidence, and there are points in the biology of the cell where targeted antioxidants appear to be beneficial. So it is an interesting puzzle that this really doesn't seem to be the case in a direct and straightforward manner when comparing species. Mole-rats, for example, have high indicators of levels of oxidative compounds while being perfectly healthy and long-lived.

The oxidative damage hypothesis of ageing posits that the accumulation of oxidative damage is a determinant of an animal species' maximum lifespan potential (MLSP). Recent findings in extremely long-living mammal species such as naked mole-rats challenge this proposition. Among birds, parrots are exceptionally long-living with an average MLSP of 25 years, and with some species living more than 70 years. By contrast, quail are among the shortest living bird species, averaging about 5-fold lower MLSP than parrots.

To test if parrots have correspondingly (i) superior antioxidant protection and (ii) lower levels of oxidative damage compared to similar-sized quail, we measured [total antioxidant capacity and indicators of oxidative damage] in three species of long-living parrots and compared these results to corresponding measures in two species of short-living quails (average MLSP = 5.5 years). All birds were fed the same diet to exclude differences in dietary antioxidant levels.

...

Only glutathione peroxidase was consistently higher in tissues of the long-living parrots and suggests higher protection against the harmful effects of hydroperoxides, which might be important for parrot longevity. The levels of oxidative damage were mostly statistically indistinguishable between parrots and quails. ... Despite indications of higher protection against some aspects of oxidative stress in the parrots, the pronounced longevity of parrots appears to be independent of their antioxidant mechanisms and their accumulation of oxidative damage.

This is largely a null result - a lot of science is that way, as much a matter of eliminating leads or adding to a pile of data that may later, as a whole, contribute to a full understanding. For more on oxidative damage, birds, and mammals, you might look back into the archives:

• Of Rats, Pigeons, and Cell Membranes
• Why Avian Longevity?
• Bats and Birds: High Metabolic Rates, Great Longevity

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The latest in a series of articles on immunotherapies aimed at clearing out the build up of cellular aggregates involved in Alzheimer's disease: "Immunotherapy targeting the age-related accumulation of extracellular aggregates, in the form of ß-amyloid, is the first rejuvenation biotechnology to reach Phase III human clinical trials. The promise of this therapy for the treatment and prevention of Alzheimer's disease (and ultimately, of so-called 'normal' brain aging) has sparked an interest in utilizing the same approach for other forms of aging damage, including the clearance of aggregated intracellular proteinaceous aging damage. Notably, as we have reviewed in a series of four previous posts, recent years have seen the appearance of a rising number preclinical studies of therapeutic vaccines targeting pathological tau species accumulating in the brains and spinal cords of transgenic rodent models of tauopathic neurodegeneration. These studies have reported -- somewhat surprisingly -- the antibody-mediated clearance of these primarily intracellular aging lesions, accompanied by functional improvements in treated animals. These two forms of structural damage are major contributors to the age-related degeneration of the brain, whether it leads to frank dementia or to the diagnostic euphemism of 'normal' age-related cognitive decline, and novel therapeutics to effect the removal of both from aging neurons will be key elements of a comprehensive panel of rejuvenation biotechnologies."

Link: http://sens.org/node/2577

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via the IEET: "Suppose you had a chance to question an ancient Greek or Roman - or any of our distant ancestors, for that matter. Let's say you asked them to list the qualities of a deity. It's a pretty good bet that many of the 'god-like' traits he or she described might seem trivial nowadays. After all, we think little of flying through the air. We fill pitch-dark areas with sudden lavish light, by exerting a mere twitch of a finger. Average folks routinely send messages or observe events taking place far across the globe. Copious and detailed information about the universe is readily available through crystal tubes many of us keep on our desks and command like genies. Some modern citizens can even hurl lightning, if we choose to annoy our neighbors and the electric company. Few of us deem these powers to be miraculous, because they've been acquired by nearly everyone in prosperous nations. After all, nobody respects a gift if everybody has it. And yet, these are some of the very traits that earlier generations associated with divine beings. Even so, we remain mortal. Our obsession with that fate is as intense as it was in the time of Gilgamesh. Perhaps more, since we overcame so many other obstacles that thwarted our ancestors. Will our descendants conquer the last barriers standing between humanity and Olympian glory? Or may we encounter hurdles too daunting even for our brilliant, arrogant, ingenious and ever-persevering species? ... Here's the safest prediction for the next 100 years - that mortality will be a major theme. Assuming we don't blow up the world, or fall into some other catastrophic failure mode, human beings will inevitably focus on using advanced technology to cheat death."

Link: http://ieet.org/index.php/IEET/more/5068

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Telomeres are the protective caps of repeated DNA sequences stuck onto the end of chromosomes, cut short with each cell division, but maintained by an enzyme called telomerase whose job, amongst others, is to extend telomeres by adding extra repeats. As you can imagine, this lays the groundwork for complex feedback loops, influenced by many genes, and different in different species and cell types. Telomere biology is associated with aging, and telomeres tend to shorten in some species and some tissues with both advancing age and ill health - but it's still an open field for the development of a full explanation as to exactly how and why that is the case. Of great interest is whether the erosion of telomeres is one of the few primary causes of aging, or whether it is only a secondary consequence - for example, do telomeres erode because of mitochondrial damage?

At the moment, the best possible outcome would be that telomeres turn out to be a primary cause of aging and the various groups working on telomerase-based therapies wind up producing a useful tool for the rejuvenation toolkit. A more plausible outcome would be that telomeres are a useful biomarker of health and remaining life expectancy but don't actually require any specific medical intervention - other forms of rejuvenation biotechnology will address the primary causes of aging, and telomeres will lengthen as a result. But we shall see where it all ends up.

There has been a fair amount of back and forth as to just how well telomere length can serve as a biomarker: lots of different outcomes in different studies. To some degree this was expected due to the differing behavior of telomerase in different tissues, but even so there is much to debate given the results to date. Here, a study in birds provides further food for thought by showing that telomere length varies in usefulness as a measure at different periods in life:

The birds with the longest telomeres - the protective caps at the ends of chromosomes - live the longest, according to a new study. "It is the first time this has been shown for any species," ... The scientists measured telomere length in red blood cells of 99 captive zebra finches (Taeniopygia guttata). The birds resemble long-lived animals in that there is little restoration of telomeres in body cells as they age. The first measurement was taken at 25 days; the researchers then followed the birds over their natural life span, ranging from less than a year to nearly 9 years, and measured telomeres again at various time points. They found a highly significant correlation between telomere length at 25 days and life span; birds with longer telomeres lived longer. Length measured at 1 year also predicted life span, but the relationship was weaker, whereas at later time points (after 3, 4, 6, and 7 years) there was no correlation ... This might explain why previous results in humans and animals have not been consistent. "So far studies just looked at individuals that were already quite old," Monaghan says. "But if you look at telomeres in old age, then those individuals with the shortest telomeres will have already died."

And birds, by the way, are not necessarily the best model for thinking about telomeres in mammals - they are quite different, possibly as a result of the metabolic demands of flight given that bats exhibit many of the same tropes. It has to be said that the general theme in biology is that the situation inside a living organism is always more complex than was thought a few years ago, and definitely more complex than we'd like. The foundations of medical technology would be easier if we were simpler.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Algebra Tutor in Baltimore Maryland

The two essential traits any algebra tutor MUST have are 1) knowledge of the subject and 2) the ability to explain it in simple, easy to understand English.

I have them both.

I’m a honors graduate of both the University of Maryland and The Johns Hopkins University, majoring in biologic sciences and biochemistry, with 30+ years of professional experience.

I have a passion for teaching.

Here are just a few of the comments I’ve received:

- He was able to convey the biomedical info in an easily understandable way.

- Able to make potentially complicated information understandable to the lay person.

- Amazing info – the nonscientist in me was somewhat challenged, but I learned a lot.

- Makes the science easy. I wish I would have had him for a science teacher!

- Awesome. Loved how Dr. Ron made the “science” understandable for us.

To me Science is a verb; it is active and on-going. Rather than make students memorize what Scientists have learned, I prefer to teach them how they learned it, and hopefully in that way they can begin to truly understand and think for themselves.

Contact me for algebra tutoring

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http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

Chemistry Tutor in Baltimore Maryland

I have a PhD in Chemistry with over 5 years experience as a chemistry tutor. I have had a lot of successes in tutoring.

For example I was hired by the mother of a high school student, who failed his final Grade 12 chemistry exams to prepare him for a retake of the exam. After meeting with the student for 2 hours he retook the exam and passed. I also tutored an undergraduate student (in general chemistry, organic chemistry, and DAT chemistry preparation), who had no background in science but was interested in going to dental school. He had a minimum of B's in his classes and he is now in dental school. My tutoring methods involves bringing chemistry to the level of the student and approaching the problems from their perspective whether middle school, high school, or college students.

Contact me

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http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

Uncoupling proteins (UCPs) govern the process of mitochondrial uncoupling, which changes the operation of the mitochondria in our cells to generate more heat and less of the cellular fuel chemical ATP. It's one of the mechanisms by which mammals regulate their body temperature. As for many processes that alter the behavior of mitochondria, uncoupling has an effect on life span, with more uncoupling usually leading to longer life spans:

Mitochondria are the power plants of your cells: they toil to turn food into ATP, used as fuel by the cell. In recent years, the eye of the research community has turned towards the process of mitochondrial uncoupling, whereby the processing of food is uncoupled from the generation of ATP. The result is less ATP and more energy in the form of heat - this is a part of the temperature regulation process in mammals, for example. It also appears to be important in calorie restriction, and therefore possibly important to longevity and aging.

The mitochondria are clearly very important in any consideration of aging, given that there are so very many ways to manipulate them to either shorten or lengthen life in laboratory animals. This is one of the reasons that any serious program of rejuvenation biotechnology has to include efforts to repair accumulated, age-related mitochondrial damage: there is an enormous weight of evidence telling us that mitochondria are a lynchpin in aging.

But back to uncoupling: there are compounds that promote uncoupling in mammals, such as DNP, but you can't just load up on an uncoupler and wait for the benefits to roll in. If your mitochondria produce too much heat for too long, you will simply roll over and die from something that looks a lot like heat stroke. Metabolism is a finely balanced machine, and taking it beyond its limits is easy to do once you bring this sort of process manipulation into the picture.

There exists a sizable amount of published work on uncoupling and longevity, and this field is, I think, helped by the fact that it borders on the study of calorie restriction, which is a heated area of research these days. A group that has published previously on human uncoupling protein variations and longevity in the past recently put out an open access paper on their research, which goes into more detail as to the findings.

Further Support to the Uncoupling-to-Survive Theory: The Genetic Variation of Human UCP Genes Is Associated with Longevity:

In humans Uncoupling Proteins (UCPs) are a group of five mitochondrial inner membrane transporters with variable tissue expression, which seem to function as regulators of energy homeostasis and antioxidants. In particular, these proteins uncouple respiration from ATP production, allowing stored energy to be released as heat. Data from experimental models have previously suggested that UCPs may play an important role on aging rate and lifespan. We analyzed the genetic variability of human UCPs in cohorts of subjects ranging between 64 and 105 years of age (for a total of 598 subjects), to determine whether specific UCP variability affects human longevity. Indeed, we found that the genetic variability of UCP2, UCP3 and UCP4 do affect the individual's chances of surviving up to a very old age.

...

Substantial evidence suggests that the ability of UCPs to reduce ROS and regulate energy utilization underpins the ability of UCPs to promote lifespan in various experimental models. In the present study we found that variants in UCP2, UCP3, and UCP4 significantly affect an individual's chances of becoming ultra-nonagenarians. The different localization of the proteins we found associated with longevity allows us to predict the areas where the uncoupling process may play an important role in survival at very old age.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

From CTV News: "Researchers say they have discovered a new source of stem cells at the back of the eye, which they hope may one day provide a way to repair the damage from age-related macular degeneration, or AMD. ... [Researchers] identified the central nervous system stem cells in a single layer called the retinal pigment epithelium, or RPE, which lies behind the retina. ... The researchers salvaged the stem cells from the RPE layer in the eyes of more than 100 deceased donors, who ranged in age from 22 to 99. But the cells can also be isolated from the fluid surrounding the retina at the back of the eye, meaning they're also accessible in living people. ... You can literally go in and poke a needle in the eye and get these cells from the sub-retinal space. It sounds awful, but retinal surgeons do it every day. ... In culture dishes in the lab, the researchers were able to coax about 10 per cent of the RPE-derived stem cells to grow in the lab. Further prodding caused the cells to differentiate into, or give rise to, a variety of cell types - those that make bone, fat or cartilage. [The researchers] also generated a progenitor cell that carries some characteristics of one type of nervous system cell, although it was not fully differentiated. ... But the fact that we could make these cells that were part-way, that were immature, indicates to us that if we keep on manipulating them, going forward in the future, we should be able to find ways to create other types of central nervous system cells."

Link: http://www.ctv.ca/CTVNews/Health/20120106/macular-degeneration-stemcells-120106/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

One of the predictions of reliability theory as applied to aging is that we are all born with an existing level of damage. One of the ways in which that damage might occur - and "damage" here is a very broad term, which might include suboptimal epigenetic changes - stems from maternal influence while in the womb. For example, researchers "have shown one way in which poor nutrition in the womb can put a person at greater risk of developing type 2 diabetes and other age-related diseases in later life. This finding could lead to new ways of identifying people who are at a higher risk of developing these diseases and might open up targets for treatment. ... The research shows that, in both rats and humans, individuals who experience a poor diet in the womb are less able to store fats correctly in later life. Storing fats in the right areas of the body is important because otherwise they can accumulate in places like the liver and muscle where they are more likely to lead to disease. ... One of the ways that our bodies cope with a rich modern western diet is by storing excess calories in fat cells. When these cells aren't able to absorb the excess then fats get deposited in other places, like the liver, where they are much more dangerous and can lead to type 2 diabetes. ... The team found that this process is controlled by a molecule called miR-483-3p. They found that miR-483-3p was produced at higher levels in individuals who had experienced a poor diet in their mother's wombs than those who were better nourished."

Link: http://www.eurekalert.org/pub_releases/2012-01/babs-hpm010512.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

If research and development in medicine is to move at anywhere near the pace it is capable of, given the rapid progress in all forms of underlying biotechnology, it must find a way to extend beyond the most heavily regulated regions. The most capable and largest research communities, like that based in the US, are also those with the least ability to locally develop their advances into medical products, thanks to the straitjacket of regulation from government bodies like the FDA.

For much of clinical development, this means that the expense imposed by the FDA makes progress either very slow indeed - and lacking in the competitive vigor that characterizes less regulated industries - or simply non-existent where the costs make a business of medicine unprofitable. Much of this weighing down of development is invisible to the casual observer: you cannot see lost opportunities, or count the medical technologies that might already exist if not for decades of the ball and chain of the FDA.

For some potential clinical applications it's worse than that: they are simply forbidden outright, with no path towards becoming permitted. Treatment of aging, development of rejuvenation biotechnology, is one such field in the US. The FDA doesn't recognize aging as a medical condition, and so will not approve treatments aimed to intervene in aging. Given that, raising funds for development of potential longevity science is very hard - there is next to no for-profit funding, and where that funding does exist, the regulatory path to approval steers development away from potentially useful treatments for aging into the sidelines of diabetes therapy or late-stage treatment of other age-related conditions. This effectively prevents any effective path towards longevity-enhancing therapies for healthy people from being followed within the US.

The way out of this mess, short of a revolution or collapse of government, is a systemic extension of the industry of clinical application of longevity science to include regions outside the US. The logical end result of the growing medical tourism industry is better defined roadway of connections and multinational organizations that will usher scientific developments from regions like the US into other parts of the world where they can be offered as clinical treatments. What has happened for stem cell therapies and medical tourism in the past decade is just a tiny beginning, a few first steps towards what must become a much more systematic, high-bandwidth, highly visible, reliable transfer of knowledge and funds - such that the US government can't just shut it down with a few threats of prosecution, such that every life scientist in the US knows how to monetize their research outside the US by shopping around for deals with offshore developers, and such that a large enough and competitive enough marketplace exists to make that shopping around a viable process.

This is a topic I have strong opinions on. So it's pleasing to see other people touching on these themes as well. Here's a post from the IEET blog on the intersection of visions for seasteading and visions for offshore medical tourism and clinical development:

What is the likelihood of seeing research vessels devoted to scientific research outside the bounds of national jurisdiction? The idea of relocating for the sake of circumventing law, in particular the notion of establishing new nations in international waters, is an idea typically initiated with liberty in mind. ... For instance, the idea of ships offering in vitro fertilization, flying Denmark flags, has been proposed to provide UK residents with a service, locally illegal. In the U.S., major delays in safe and effective regenerative medical services are likely. Regenerex, a company offering regenerative stem cell therapies, faces a potential halt in operation by the FDA. The company has been in dispute with the FDA over whether or not stem cell therapies should be considered 'drug' therapies. If the FDA succeeds in this dispute, Regenerex would then be required, by law, to discontinue treatments until appropriate certification is in place, which could be 'staggeringly expensive' and take several years.

Biotech companies researching longevity also inconveniently face roadblocks from the FDA, which only approves drugs aimed at treating diseases in a specific, defined manner. Aging is not currently considered a disease by the FDA, which makes the delay of essential treatment virtually inevitable. The need for extensive reform in policy is a reality of a good deal of near and future medical services, and both businesses and patrons are incentivized by the unique opportunity of circumventing regulatory systems.

I don't think that the sea is the answer on the scale of development industry needed to break loose the FDA's ball and chain - the goal seems to me to more a case of linking existing (land-based) infrastructure and development institutions, creating the roadway of knowledge, deals, and contractual ties, and the community that sustains that roadway.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Type 2 diabetes (T2D) is a lifestyle disease for the vast majority of people - you avoid it by refraining from overeating, becoming fat, and giving up exercise to turn sedentary. But some folk are more likely to succumb than others, given the same lifestyle choices, and different people descend into metabolic syndrome and then type 2 diabetes at different rates. It won't be too many more years before clinics will be able to tell you exactly where you stand on the downward spiral, and what your risks are: research "has provided the first proof of molecular risk factors leading to type 2 diabetes, providing an 'early warning' sign that could lead to new approaches to treating this and other human disease conditions. ... Taking an innovative research direction, [the] research team decided to map DNA methylation variations rather than DNA sequence variations, as was traditionally done. The team undertook a proof-of-concept study among 1,169 type 2 diabetes patients and non-diabetic controls. The results demonstrated the unique abilities of this novel research approach by revealing a clear-cut, disease-predisposing DNA methylation signature. This is a first report in the scientific literature of epigenetic risk factor for T2D. DNA methylation is a naturally occurring mechanism used to regulate genes and protect DNA from some types of cleavage. It is one of the regulatory processes that are referred to as epigenetic, in which an alteration in gene expression occurs without a change in the nucleotide sequence of the DNA. Defects in this process cause several types of disease that afflict humans. ... telltale methylation signature marks were also shown to appear on the DNA of young individuals who latter developed impaired glucose metabolism, even before the appearance of clinical diabetic manifestations."

Link: http://www.sciencedaily.com/releases/2011/12/111228134841.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The onset of Alzheimer's is not a sudden thing, which reinforces the view of it as a lifestyle disease: "The first changes in the brain of a person with Alzheimer's disease can be observed as much as ten years in advance - ten years before the person in question has become so ill that he or she can be diagnosed with the disease. [Researchers] are studying biomarkers - substances present in spinal fluid and linked to Alzheimer's disease. The group has studied close to 140 people with mild memory impairment, showing that a certain combination of markers (low levels of the substance beta-amyloid and high levels of the substance tau) indicate a high risk of developing Alzheimer's disease in the future. As many as 91 per cent of the patients with mild memory impairment who had these risk markers went on to develop Alzheimer's within a ten-year period. In contrast, those who had memory impairment but normal values for the markers did not run a higher risk of getting Alzheimer's than healthy individuals. ... This is a very important finding with regard to the development of new therapies against the disease. All prospective therapies have so far shown to be ineffective in stopping the disease, and many people are concerned that the pharmaceutical companies will give up their efforts in this field. But these failures may depend on the fact that the new therapies were initiated too late. When a patient receives a diagnosis today, the damage has already gone too far." I'm not sold on this last comment, given the evidence suggesting that Alzheimer's symptoms are reversible.

Link: http://www.lunduniversity.lu.se/o.o.i.s?id=24890&news_item=5773

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The onset of Alzheimer's is not a sudden thing, which reinforces the view of it as a lifestyle disease: "The first changes in the brain of a person with Alzheimer's disease can be observed as much as ten years in advance - ten years before the person in question has become so ill that he or she can be diagnosed with the disease. [Researchers] are studying biomarkers - substances present in spinal fluid and linked to Alzheimer's disease. The group has studied close to 140 people with mild memory impairment, showing that a certain combination of markers (low levels of the substance beta-amyloid and high levels of the substance tau) indicate a high risk of developing Alzheimer's disease in the future. As many as 91 per cent of the patients with mild memory impairment who had these risk markers went on to develop Alzheimer's within a ten-year period. In contrast, those who had memory impairment but normal values for the markers did not run a higher risk of getting Alzheimer's than healthy individuals. ... This is a very important finding with regard to the development of new therapies against the disease. All prospective therapies have so far shown to be ineffective in stopping the disease, and many people are concerned that the pharmaceutical companies will give up their efforts in this field. But these failures may depend on the fact that the new therapies were initiated too late. When a patient receives a diagnosis today, the damage has already gone too far." I'm not sold on this last comment, given the evidence suggesting that Alzheimer's symptoms are reversible.

Link: http://www.lunduniversity.lu.se/o.o.i.s?id=24890&news_item=5773

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Exercise mimetics are drugs that can replicate some fraction of the beneficial effects of exercise; their development is in the early stages. I don't think it's too far-fetched to suggest that the next ten years of exercise mimetic development will look a lot like the last ten years of calorie restriction mimetic development. In other words there will be a couple of well-funded, well-hyped lines of research that fizzle out with nothing to show for it, some solid advances towards identifying mimetics that, for one reason or another, aren't terribly practical for clinical development, and all of that against a backdrop of across-the-board progress in understanding metabolic processes that relate to exercise and its long-term effects. But, you'll note, no actual products that are legally available for use by healthy people.

Absent the straitjacket regulation it would be a whole other story when it came to products and product development, of course, but we live in a world of centralized control and socialism for medicine for those regions that also boast the most active and capable research communities. It's unfortunate, and it needs to change.

In any case, here is an example of the sort of early stage work that will lead to exercise mimetic development. If you cast your mind back ten years or so, you'll see it looks just like the sort of research taking place into the mechanisms of calorie restriction back then.

We take it for granted, but the fact that our muscles grow when we work them makes them rather unique. Now, researchers have identified a key ingredient needed for that bulking up to take place. A factor produced in working muscle fibers apparently tells surrounding muscle stem cell "higher ups" that it's time to multiply and join in. ... In other words, that so-called serum response factor (Srf) translates the mechanical signal of work into a chemical one.

"This signal from the muscle fiber controls stem cell behavior and participation in muscle growth," says Athanassia Sotiropoulos of Inserm in France. "It is unexpected and quite interesting." It might also lead to new ways to combat muscle atrophy. ... Srf works through a network of genes, including one known as Cox2. That raises the intriguing possibility that commonly used Cox2 inhibitors - think ibuprofen - might work against muscle growth or recovery, Sotiropoulos notes. ... "It may be difficult to find a beneficial amount of Srf," she says. "Its targets, interleukins and prostaglandins, may be easier to manipulate."

And so this will lead to a tree of research spanning the next few years, in parallel to a web of other, similar spreading investigations of proteins and genes and their effects on exercise.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

From Big Think: "The loss of a human limb is a tragedy. We know that once they're gone, mammalian arms and legs can't ever be restored. But if you cut off a salamander's leg - or tail - it will reappear in just a few weeks. ... Now, a new generation of longevity-seekers hopes to apply the power of amphibians like the salamander, the axlotl, and the worm to human medicine. ... In the future, if we had the ability to grow a brand new heart or parts of hearts with that person's very own adult stem cells, then when we know that they have heart disease, we could just replace the heart. All of those [costly] visits to the hospital, all of the drugs, won't be required. ... Better tools will enable us to repair people rather than just sort of patching them up for a little while until they get sicker and sicker. ... Over the past few decades, scientists have begun to understand exactly how the regeneration process works in nature. When a salamander is injured, a clump of cells called a blastomea forms at the site of the wound. Like embryonic stem cells, the blastomea are especially plastic. These cells are then triggered to de-differentiate and re-initiate growth. ... Debate remains over whether they're fully pluripotent, meaning that they have the ability to form any type of tissue, or whether the cellular dynamics merely have to be reprogrammed. ... The trick, of course, is applying this knowledge to human anatomy."

Link: http://bigthink.com/ideas/41794

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Two supercentenarian genomes have been sequenced, and suggest that - as always - the roots of variations in human longevity are more complex than we'd like them to be: "Supercentenarians (age 110+ years old) generally delay or escape age-related diseases and disability well beyond the age of 100 and this exceptional survival is likely to be influenced by a genetic predisposition that includes both common and rare genetic variants. In this report, we describe the complete genomic sequences of male and female supercentenarians, both age >114 years old. We show that: (1) the sequence variant spectrum of these two individuals' DNA sequences is largely comparable to existing non-supercentenarian genomes; (2) the two individuals do not appear to carry most of the well-established human longevity enabling variants already reported in the literature; (3) they have a comparable number of known disease-associated variants relative to most human genomes sequenced to-date; (4) approximately 1% of the variants these individuals possess are novel and may point to new genes involved in exceptional longevity; and (5) both individuals are enriched for coding variants near longevity-associated variants that we discovered through a large genome-wide association study. These analyses suggest that there are both common and rare longevity-associated variants that may counter the effects of disease-predisposing variants and extend lifespan. The continued analysis of the genomes of these and other rare individuals who have survived to extremely old ages should provide insight into the processes that contribute to the maintenance of health during extreme aging."

Link: http://dx.doi.org/10.3389/fgene.2011.00090

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm