Another cell population thought to be static throughout life turns out to be capable of regeneration and renewal, given the right cues: "Damage to podocytes - a specialized type of epithelial cell in the kidney - occurs in more than 90 percent of all chronic kidney disease. Now researchers [have] uncovered an unexpected pathway that reveals for the first time how these cells may regenerate and renew themselves during normal kidney function. ... Podocytes are found only in the kidney and are an integral structural component of its blood-filtering system. They stand shoulder-to-shoulder in a part of the organ called the glomerulus and wrap their long 'feet' around the semi-permeable capillaries through which blood flows. Narrow slits between the feet allow small molecules, such as water and salts, to pass while blocking large proteins. This filtering process is the first step to forming urine, and it is critically important - even one missing cell can leave a gap that would allow unwanted molecules through the barrier. ... It used to be thought that you were born with podocytes, and you died with the same podocytes - you don't make any more during your lifetime. ... The problem was, such a scenario doesn't make a lot of evolutionary sense - particularly when other epithelial cells routinely regenerate themselves. ... Podocytes may utilize recognized pathways of regeneration to renew themselves throughout life, [and] people suffering from chronic kidney disease may simply have worn out or outpaced their podocytes' capacity for renewal ... Now that the researchers know podocytes have the ability to regenerate in response to common cellular signals, their next step is to learn whether this regeneration occurs in healthy animals and people. ... If we can harness this regeneration, we may one day be able to treat people with chronic kidney disease."

Link: http://www.sciencedaily.com/releases/2011/12/111205102706.htm

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

One of the world's more active tissue engineering research and development groups works on building replacement tracheas from a scaffold and the patient's own cells. They have carried a number of successful transplants in recent years, and seem on a par with Tengion's work on bladders, or the folk producing heart valves for children in terms of outcomes and technological sophistication.

Here's an update on a transplant carried out late last year:

Surgeons in Sweden have replaced the cancerous windpipe of a Maryland man with one made in a laboratory and seeded with the man's cells.

...

"What we did is surgically remove his malignant tumor," Dr. Macchiarini said. "Then we replaced the trachea with this tissue-engineered scaffold." The Y-shaped scaffold, fashioned from nano-size fibers of a type of plastic called PET that is commonly used in soda bottles, was seeded with stem cells from Mr. Lyles's bone marrow. It was then placed in a bioreactor - a shoebox-size container holding the stem cells in solution - and rotated like a rotisserie chicken to allow the cells to soak in.

After two of days, it was installed in Mr. Lyles during an elaborate operation in which it was sutured to his throat and lungs. All told, the treatment cost about $450,000, Mr. Lyles said.

...

Dr. Macchiarini has performed a dozen trachea transplants since 2008, but the first 10 used organs from cadavers in which all the living cells were removed, leaving behind a natural scaffold of cartilage. Donated tracheas are rare, however, and are never a perfect fit. In Mr. Lyle's case, and in the case of an Eritrean man who received a similar transplant last June and is doing well, the synthetic scaffold is made using CT scans of the existing trachea to ensure it matches precisely.

The cost of the first tissue engineered parts will fall dramatically once the procedures become more widespread and the underlying technologies more robust and commoditized. But costs will not fall as far is they would in an actual free market in medicine, and there will be long and unnecessary years of delay - and vast expense for the sponsoring companies - before regulators in wealthy Western countries will approve these new applications of cell science for broad use.

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

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

Here is an open access paper from a researcher who focuses on mTOR and sees aging as almost entirely programmed, not the consequence of stochastic damage. His view as outlined in the paper is analogous to the view of nuclear DNA damage as not being significant over the present human life span. I think he has a very large hill of evidence for the damage-based view of aging to overcome in order to make a convincing point, however, and this should serve as a reminder that there are a great many diverse (but not necessarily well supported) views in the scientific community when it comes to the nuts and bolts of aging: "Aging is defined as a decline caused by accumulation of all sorts of damage, in particular, molecular damage. This statement seemed so obvious that it was not questioned. Yet several lines of evidence rule out molecular damage as a cause of aging. Yes, of course, molecular damage accumulates over time. But this accumulation is not sufficient to cause organismal death. Eventually it would. But the organism does not live long enough, because another cause terminates life first. This cause is aging, a continuation of developmental growth. Definitely, developmental growth is not driven by accumulation of molecular damage, although molecular damage accumulates. Similarly, aging is not driven by damage. Growth is stimulated in part by mitogen- and nutrient-sensing (and other) signaling pathways such as mTOR. Aging, 'an aimless continuation of developmental program', is driven by the same signaling pathways including mTOR. Aging in turn causes damage: not molecular damage but non-random organ damage (stroke, infarction, renal failure and so on) and death. Seemingly, one objection to this concept is that cancer is caused by molecular damage. And cancer is often a cause of death in mammals. So how may one claim that damage does not drive aging, if it is involved in cancer. Let us discuss this."

Link: http://impactaging.com/papers/v3/n12/full/100422.html

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

Algebra Tutor in Baltimore Maryland

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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

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

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

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

Yes, prevention of aging is within our grasp - in the sense that a package of foreseeable medical technologies could enable repair of the low-level biochemical damage that causes aging, and those technologies might take only twenty years or so to develop. Unfortunately, that timeline is dependent on a large amount of funding and a dedicated research community, neither of which presently exists for many of the essential parts of this research program. While the regenerative medicine and cancer research communities are populous, well funded, and achieving progress, very few researchers are presently working on other goals necessary to halt the aging process - such as repair of mitochondrial DNA.

So when I say "within our grasp," I mean "if we all get up and do our part to make it happen." It takes a wave of public interest and advocacy to steer the scientific community and large funding institutions - and they presently need steering towards repair-based strategies to deal with aging, otherwise the first working rejuvenation therapies will arrive too late for those in middle age today.

Here is an article from Ageing Research with a different take on "within our grasp":

Slowly but steadily knowledge about the human body has progressed and new ideas of animal ageing have immerged. The classic model of ageing, based on "accumulation of errors" has become an outdated notion. Instead, evidence suggests that ageing, at least in part, is likely the result of a failure in the function of cells (such as stem cells) required for cellular regeneration. Replacing impaired stem cells with fully functional stem cells should thus prevent/treat age-associated pathologies allowing us to live healthier longer lives.

This sort of viewpoint I see as a dangerous path of complacence. While it is true that (a) regenerative medicine and stem cell science are racing ahead, and (b) the ability to replace tissue, whole organs, or damaged stem cell populations will do much to help, you can't fix aging with stem cells alone.

I've had to make this point with a number of folk who are enthusiastic about progress in regenerative medicine and think that it will enable great extension of human life. Unfortunately this is not the case, as a great deal of degenerative aging is built atop a build-up of waste biochemicals and the body is an integrated system - the health of each of its subsystems impact the others. You can't fix problems in isolation; you can't drop new stem cells into age-damaged stem cell niches, and you can't put a new heart into a body with corroded arteries and expect it to be just fine. If you replace some failing tissue with fresh tissue, that fails to solve a range of other eventually fatal problems.

This is another aspect of the well known factoid regarding cancer research - if you cured cancer and made no other advance in medicine, that state of affairs would add only a couple of years to overall human life expectancy. The people who survived cancer thanks to the miracle therapy would soon be cut down by other conditions of aging. All of the life-span-limiting forms of biological damage have to be repairable before we can greatly extend our lives. There are no short cuts: it doesn't matter how well regenerative medicine is progressing, the other branches of longevity science must also progress rapidly if we are to live longer.

Given that those branches are for the most part not well funded, nor the focus of large and vigorous research communities, this means that we have work to do.

Researchers continue to investigate the link between germ cells and longevity in lower animals. In this open access paper, changes to fat metabolism are implicated as an important mechanism: "Removing the germ line of Caenorhabditis elegans extends its lifespan by approximately 60%. Eliminating germ cells also increases the lifespan of Drosophila, suggesting that a conserved mechanism links the germ line to longevity ... Reproduction and aging are two processes that seem to be closely intertwined. Experiments in Caenorhabditis elegans and Drosophila have shown that depletion of the germ line increases lifespan and that this process depends on insulin and lipophilic-hormone signaling. Recently, it was demonstrated that when germline stem cells (GSCs) cease to proliferate, fat metabolism is altered and this affects longevity. In this study, we have identified a nuclear hormone receptor, NHR-80, that mediates longevity through depletion of the germ line by promoting fatty acid desaturation. ... Our results reinforce the notion that fat metabolism is profoundly altered in response to GSC proliferation, and the data contribute to a better understanding of the molecular relationship between reproduction, fat metabolism, and aging."

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057950/

Researchers continue to dig into the connection between psychological stress and telomere length: "Exercise can buffer the effects of stress-induced cell aging, according to new research ... A growing body of research suggests that short telomeres are linked to a range of health problems, including coronary heart disease and diabetes, as well as early death. ... Telomere length is increasingly considered a biological marker of the accumulated wear and tear of living, integrating genetic influences, lifestyle behaviors, and stress. ... Results support [the] discovery six years earlier in premenopausal women that psychological stress has a detrimental effect on immune cell longevity, as it relates to shorter telomeres. The new study showed, however, that when participants were divided into groups - an inactive group, and an active [group] - only the inactive high stress group had shorter telomeres. The active high stress group did not have shorter telomeres. In other words, stress predicted shorter telomeres in the sedentary group, but not in the active group."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-05/uoc--ber052510.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Via ScienceNews: "In the new study, researchers looked at genetic markers called single nucleotide polymorphisms, or SNPs, in 1,055 centenarians and 1,267 younger people, all of European descent. The scientists found 150 genetic SNP variants linked to extreme longevity. Initially, the team identified only 33 SNPs found more often in people aged 90 to 114 years but not in a control group made up of people who will presumably live an average lifespan. ... biostatistician Paola Sebastiani [devised] a different statistical method to identify additional SNPs that would improve the team's ability to predict longevity. The team tested their predictions on a separate group of centenarians and controls. With the 150 SNPs, the researchers could correctly predict who was a centenarian 77 percent of the time. ... Now on one side, 77 percent is a very high accuracy for a genetic model, which means that the traits that we are looking at have a very strong genetic base ... On the other hand, the 150 SNPs can't explain why the remaining 23 percent of centenarians in the study have reached such ripe old ages. It could mean that those people have other, rare genetic variants or lifestyles responsible for their longevity or some combination of the two."

View the Article Under Discussion: http://www.sciencenews.org/view/generic/id/60772/title/For_most_centenarians,_longevity_is_written_in_the_DNA

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

From the BBC: "A 10-year-old girl has had a major blood vessel in her body replaced with one grown with her own stem cells. ... A vein was taken from a dead man, stripped of its own cells and then bathed in stem cells from the girl, according to a study published in the Lancet. Surgeons said there was a "striking" improvement in her quality of life. This is the latest is a series of body parts grown, or engineered, to match the tissue of the patient. Last year, scientists created a synthetic windpipe and then coated it with a patient's stem cells. ... In this case, other options such as using artificial grafts to bypass the blockage, had failed. ... It used a process known as "decellularisation". It starts with a donor vein which is then effectively put through a washing machine in which repeated cycles of enzymes and detergents break down and wash away the person's cells. It leaves behind a scaffold. This is then bathed in stem cells from the 10-year-old's bone marrow. The end product is a vein made from the girl's own cells. ... The young girl was spared the trauma of having veins harvested from the deep neck or leg with the associated risk of lower limb disorders."

Link: http://www.bbc.co.uk/news/health-18428889

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

Competition drives progress, but put enough humans into any field and the successful groups will start to form cartels in order to keep their leading position without having to compete as hard for it. It is inherent in the human condition that we self-sabotage very well and very aggressively just as soon as we achieve enough success to feel somewhat elevated over our less fortunate peers. Who can even begin to guess how many opportunities have been wasted, how much potential technological progress has been lost thanks to these urges?

The world of technology is now remarkably flat. The majority of the amenities of modern technology are available to the majority of the world: the descendants of peasants can fly for the same cost as the bloodlines of kings, cars and mobile phones are ubiquitous, and holding vast wealth doesn't in fact give a person any great and massive advantage over the middle class - or even the poor in wealthier regions - when it comes to the variety of available medical technology. Every new advance moves rapidly from being comparatively expensive, faulty, and scarce to being comparatively cheap, reliable, and widespread - whether we are talking about air conditioning or heart surgery, though the pernicious effects of regulation slow down the applications of biotechnology to a crawl in comparison to other lines of technological progress.

One of the defining features of our age is the degree to which the very wealthy and the very connected use the same technologies as the rest of us. When new technology is developed we all win - it doesn't matter which research or development group got there first, because we will all have access soon enough. What does matter is how soon that new technology arrives, and that is a function of the size and level of competition in the research and development communities. Michael Batin has this to say, machine translated from the Russian:

In most types of social interactions, people want to be the first. In sport, business, politics, the most coveted, the most honorable place - this place is number 1. This behavior is due to our neurophysiology, our genetics. Often, the winner takes all. During the war, or fight a duel to win - means to survive.

But, in the fight against aging is a totally different situation. We will survive, if any other scientist, institution or fund wins [in the fight against] aging. Yes, these [strangers get] the glory, money and women. At the same time everyone else interested in the victory over the aging gets a chance to live. No amount of money can [be] compared with the value of life. When you're alive, you have the opportunity to achieve whatever you want. When a person is dead, for him [nothing] is possible.

When we see someone [doing better than us to] extend the life of an animal model [and struggle] with aging, [he benefits us] because he can give us life. The more people who are trying to find a cure for old age, the greater our chances of survival, [and] for the return of youth to radical life extension.

The larger the community, the more healthy competition, the better the outcome and the faster the progress towards the end goal. When it comes to the biotechnology of rejuvenation we will either all win together or we all lose together - there is little in the way of middle ground in technological progress. That result is entirely determined by how fast we can create this sort of future medicine, such as that outlined in the SENS proposals.

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

"Very small embryonic-like stem cells" is the name given by one research group to populations of stem cells that they believe sustain adult tissue throughout life, and which retain most of the desired characteristics needed for the first generation of cell-based regenerative therapies. They are thought to be pluripotent, able to give rise to any form of cell, unlike the more limited and better known forms of stem cell identified in adults and used in the development of regenerative therapies. Over at h+ Magazine, there's an interview with Mariusz Ratajczak, one of the researchers involved:

Very small embryonic like stem cells (VSELs) are purified from adult tissues and are potential sources of stem cells for application in regenerative medicine and stem cell therapies. ... A question that is important from the developmental point of view is why pluripotent stem cells, (PSCs) such as VSELs, would reside in adult organs? For many years, it had been accepted that adult tissues contain only tissue-committed stem cells (TCSCs) that have limited possibility of differentiation - for example, epidermal stem cells, hematopoietic stem cells, skeletal muscle stem cells.

Ratajczak has comments on longevity and regenerative medicine - it's always good to see noted researchers stepping up to support the goal of engineered longevity in public, given that it's only been a handful of years since that sort of freedom of opinion became possible for researchers who wished to retain their funding sources. One of the many necessary preconditions for widespread support of longevity science is that researchers must speak out in favor of rejuvenation biotechnology.

I am deeply convinced that regenerative medicine is our key to a better life and our key to extending lifespan. I believe that we will be able to employ [pluripotent stem cells] (e.g., VSELs), isolated from adult tissues, to harness stem cells to regenerate damaged organs. In combination with developing scaffold-technologies, we may be able to generate ex vivo organ fragments or even whole organs and replace organ transplantations with in vitro generated ones.

I should note that Ratajczak presented at the SENS5 conference last year, alongside other researchers bullish on the future of longevity and medical science. In his presentation, he theorizes a direct link between VSELs and aging:

We propose, based on our experimental data in animal models, that gradual decrease in the number of VSELs deposited in adult tissues, which occurs throughout life in an [insulin/insulin growth factor] signaling-dependent manner is an important mechanism of aging.

Which is much the view that the research community has on stem cells as a whole: stem cells and their capacity to maintain tissue decline with age, for reasons that are being explored in detail, and which may in the near future be addressed in a number of different ways.

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

Tissue printing startup Organovo, of the Methuselah Foundation's portfolio of early stage investments, received a new round of funding recently:

Organovo closed a private placement consisting of approximately 6.5 million units of its securities to qualified accredited investors, for total gross proceeds of $6.5 million. "Organovo's advanced bioprinting platform can replicate essential biology for research, drug discovery and development and, eventually, for therapeutic applications," stated Keith Murphy, chief executive officer of Organovo. "We have found success in achieving early revenue through strategic collaborations, and this funding will allow us to extend the reach and uses of 3D bioprinting through growth and innovation in the coming years."

Given that at this stage in their life cycle they are essentially a research equipment manufacturer, that sort of money - while small in terms of medical development in the mainstream - should be enough to get them to the next level. You might recall an h+ Magazine article from a couple of years ago that gives a good overview of what the company aims to achieve:

Dr. Forgacs ultimately foresees fully implantable organs printed from a patient's own cells. "You give us your cells: we grow them, we print them, the structure forms and we are ready to go," he says. "I am pretty sure that full organs will be on the market [one day]." A printed biological heart might not appear exactly like an embryonic heart with a pericardium, two superior atria, and two inferior ventricles. But it will perform the same function: pumping blood throughout the blood vessels.

The second item relates to the preservation of organs for later transplant: this is a big logistical hurdle. A great deal of the processes of present day transplantation and early tissue engineering are completely shaped by our inability to reliably store large, complex tissues for the long term, without damage. The process of decellularization may be a practical way to work around the issue, though it remains to be seen if the economics work out yet: donated organs can be decellularlized, the scaffold stored at low temperature, and then warmed up and repopulated with a patient's cells in a matter of days. Here is a note from ScienceDaily, which leads to an open access research paper that is available in PDF format:

[Researchers] studied various strategies for freeze-drying porcine heart valves. After the cellular material was removed, they freeze-dried the heart valve scaffolds with or without sucrose and hydroxyl ethylene starch, and then compared the stability and elasticity of the freeze-dried scaffolds to assess the effectiveness of these lyoprotectants in preventing degradation of the scaffold. ... Tissue freeze-dried with sucrose alone displayed less porosity compared to tissue freeze-dried with the sucrose/HES mixture, whereas no significant differences in biomechanical properties were observed. Decellularization decreased the elastic modulus of artery tissue. The elastic modulus of freeze-dried tissue without protectants resembled that of decellularized tissue. The elastic modulus values of freeze-dried tissue stabilized by lyoprotectants were greater compared to those of decellularized tissue, but similar to those of native tissue.

Lastly for today, an article on one of the challenges of tissue engineering that people outside the field don't tend to think all that much about, which is that it is exceedingly difficult to convince tissues to form exactly the desired shape, with exactly the right mechanical properties, and with the right cells in the right place in that shape. A lot of researchers are spending a lot of time on determining how to cultivate tissue of the right size and shape; the strategies needed vary greatly by tissue type and other circumstances. In any case, here is an article on tubes:

In another advance for the field, researchers have now demonstrated a strategy to fabricate tubular structures with multiple types of cells as different layers of the tube walls. This method may be widely used in simulation of many tubular tissues and enriches the toolbox for 3D micro/nanofabrication by initially patterning in 2D and transforming it into 3D. ... To demonstrate the capability of their method, the scientists successfully simulated the structure of a human vessel-like structure - the tubular wall has three layers, and in each layer there is one representative type of cells: endothelial cells, smooth muscle cells and fibroblast cells (from inside out).
This kind of tubular structure with multiple types of cells can be applied in tissue engineering such as arterial and venous grafts in vivo. And [the] preparation method of stress-induced rolling membrane can be applied to fabricate other self-assembled 3D structures.

You might compare the methodologies in the technology demonstration quoted above with the approach used in growing mouse teeth to get a sense of just how broad the range of necessary techniques is.

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

The second part of an article in CMAJ that shows off some of the subtle prejudices against cryonics that exist in the medical scientific community (such as in the choice of title) while attempting objectivity: "Although death and taxes are said to be the only two certainties in life, a small but vocal community takes issue with the inclusion of the former. There is, they say, the alternative of cryonics, in which a legally dead person is preserved at -196C in hopes that he will ultimately be revived and rejuvenated, once a cure for his ailment is found. And it's entirely consistent with the basic tenets of medicine, providers argue. ... Although it seems like an unusual and radical idea to many people, I think in the very truest sense of the term, this is conservative medicine. This is literally conserving a patient rather than giving up on them by today's standards of medicine. It's true a doctor can't do anything more for these people, but that doesn't mean the future cannot. ... Those interested in cryonics tend be optimistic, hopeful about technological developments and dissatisfied with an ordinary life span, says Ben Best, president of the Cryonics Institute. ... a miniscule chance is better than none, enthusiasts say. ... Nobody has come up with a better idea yet, so therefore myself, as well as some others, believe that cryonics is simply the second worst thing that can happen. You're going to die. You're going to stop breathing. Whether you be buried or cremated or cryopreserved, it's going to happen. There's nothing we can do about this now, but I know that if I'm cremated or buried, even if technology vastly increased, I'm never coming back. ... Enthusiasts are mystified that only a small segment of the general population has investigated the cryonic option. ... I don't know why there are far more people who don't sign up for cryonics arrangements. It's true that what we do is unorthodox and different, at least in 2012. But there are so many bizarre ideas out there which have no evidence to support them and get many, many people fascinated ... Yet we only have less than 1000 members after 40 years. ... People tend in my experience to kind of rely on this naturalistic [fallacy] that because people have always gotten older and died, therefore they should get older and die as a result of simply living longer."

Link: http://www.cmaj.ca/site/earlyreleases/20mar12_the-church-of-cryopreservation.xhtml

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

Researchers are steadily cataloging the details of age-related changes in stem cells, which seem to have as much to do with the cellular environment as a whole as the cells themselves: "Aging causes phenotypic changes in skeletal muscle progenitor cells (SMPCs) that lead to the loss of myogenicity and adipogenesis. Secreted protein acidic and rich in cysteine (SPARC), which is secreted from SMPCs, stimulates myogenesis and inhibits adipogenesis. The present study aimed to examine whether changes in SPARC expression, its signaling pathway, or both are involved in age-related phenotypic changes in SMPCs. SPARC expression levels were comparable in SMPCs derived from young and old rats. However, when SPARC expression was reduced by a SPARC-specific siRNA, SMPCs from young rats showed reduced myogenesis and increased adipogenesis. In striking contrast, old rats showed little changes in these functions. ... These results suggest that, although SPARC plays a role in regulating SMPC function, SMPCs become refractory to the action of SPARC with age. Our data may explain an age-related shift from myogenesis to adipogenesis, associated with sarcopenia. ... Because SPARC enhances myogenesis and inhibits adipogenesis, we reasoned that its decreased expression or alterations in its signaling pathway in SMPCs contribute to age-related dysfunction of skeletal muscle, such as fatty infiltration and impaired muscle regeneration. The present study shows that the SPARC signaling pathway, rather than the level of its expression in SMPCs changes with age. It should be noted skeletal muscle cell types other than SMPCs, such as myofibers and endothelial cells, express SPARC. Moreover, SPARC expression levels decline with age in the skeletal muscles of mice. This indicates that although SPARC expression in SMPCs is not altered with age, the amount of SPARC available in the SMPC microenvironment would be decreased. Thus, it is possible that in addition to the decreased responsiveness of SMPC to SPARC, the age-related decline of SPARC expression levels in skeletal muscle accelerates age-related phenotypic changes in SMPC."

Link: http://impactaging.com/papers/v4/n1/full/100426.html

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

Prealgebra Tutor in Richmond

Passion: Helping students understand and enjoy a subject area is my passion. I live for the "aha" moment when they "get it" for the first time and that day when I have a formerly math-hating or math-a-phobic student smiling and laughing as they work.

Experience: I worked in the drop-in tutoring center during community college tutoring all math through Calc I, English/Writing, and Speech/Communications. I also worked at a Kumon Math and Reading center with students as young as kindergarten and have worked as a freelance tutor for math, general study skills/all subjects with clients ranging from Junior High School students in need of remedial help to older adult graduate students returning to math or stats after many years. I have worked with students from public, private, and homeschool backgrounds successfully and make sure to keep parents "in the loop" as full partners invested in the student's learning. I have also taught 4-H dog training classes before – nothing phases me after fifteen 8-16 year old 4-H members with their completely untrained dogs show up on the first night! Training dogs and teaching kids to train them has taught me a great deal about how we learn and how to motivate learning.

Further Qualifications: I earned a double-degree in Mathematics and Cognitive Science (the study of how we think, learn, process, remember, and solve problems) with a 3.9+ GPA and am currently in a Master's program studying Mathematics and teaching undergraduate mathematics courses. My future goal is to teach community college and to research the cognitive processes and pedagogy of teaching mathematics.

Contact me

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

Researchers are examining cellular biochemistry in people who belong to long-lived families: "The offspring of nonagenarian siblings suffer less from age related conditions and have a lower risk of mortality compared to their partners. Fibroblast strains derived from such offspring in middle age show different in vitro responses to stress, more stress-induced apoptosis and less senescence when compared to strains of their partners. Aiming to find differences in cellular metabolism in vitro between these fibroblast strains, [cells were] analysed using (1)H nuclear magnetic resonance (NMR)-based metabolic footprinting. ... Strains from offspring and their partners were compared ... The ala-gln and glucose consumption were higher for fibroblast strains derived from offspring when compared to strains of their partners. Also, production of glutamine, alanine, lactate and pyroglutamic acid was found to be higher for fibroblast strains derived from offspring. In conclusion, differences in NMR-based metabolic profiles of human cells in vitro reflect the propensity for human longevity of the subjects from whom these were derived."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22218423

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