Fight Aging! Newsletter, October 22nd 2012

FIGHT AGING! NEWSLETTER
October 22nd 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

- Putting Aside What You'd Rather Be Doing Because You're Dying
- On Chronic Inflammation in Aging
- Considering the Brain
- Discussion
- Latest Headlines from Fight Aging!
    - Spermidine Levels Measured in Centenarians
    - A Small Step Towards Tissue Engineered Kidneys
    - More on Young Blood and Old Mice
    - More Robust Data on the Effect of Mitochondrially Targeted Antioxidants on Fly Life Span
    - The Plasticity of Life Span
    - Overexpression of FGF21 Extends Life in Mice
    - Dopamine and Memory Decline in Aging
    - Another Glenn Foundation Lab Established
    - Commenting on the Late Life Plateau in Aging
    - Investigating Natural Bladder Regeneration in Rats

PUTTING ASIDE WHAT YOU'D RATHER BE DOING BECAUSE YOU'RE DYING

The costs of degenerative aging are all around us, so omnipresent that they are taken for granted. But costs they are, nonetheless:

https://www.fightaging.org/archives/2012/10/putting-aside-what-youd-rather-do-because-youre-dying.php

"Many dubious arguments are fielded in support of aging and involuntary death: every status quo, no matter how terrible, gathers its supporters. This is one of the deeper flaws inherent in human nature, the ability to mistake what is for the most desirable of what is possible. A hundred thousand deaths each and every day and the suffering of hundreds of millions is the proposal on the table whenever anyone suggests that human aging should continue as it is.

"Massive campaigns of giving and social upheaval have been founded on the backs of a hundredth of this level of death and pain - but the world has a blindness when it comes to aging. Such is the power of the familiar and the long-standing: only heretics seek to overturn it, no matter how horrid and costly it is.

"Nonetheless, this is an age of biotechnology in which aging might be conquered. There are plans and proposals, set forth in some detail, and debate over strategy in the comparatively small scientific community focused on aging research. So arguments over whether the development of means of rejuvenation should take place at all, reserved for philosophers and futurists in the past, now have concrete consequences: tens of millions of lives and untold suffering whenever progress is delayed. It should always be feared that a society will somehow turn to block or impede research into therapies for aging - worse and more outright crimes have been committed in the past by the members of so-called civilized cultures.

"One of the arguments put forward in favor of a continuation of aging and mass death is that without the threat of impending personal extinction we'd collapse into stagnation and indolence. As the argument goes, only death and an explicitly limited future gives us the incentive to get anything done, and so all progress depends upon aging to death. I state the proposition crudely, but this is the essence of the thing, flowery language or no.

"This is a terribly wrong way of looking at things: it denies the existence of desire independent of need. It casts us as nothing more than some form of Skinner box, unable to act on our own. This is another example of the way in which many humans find it hard to look beyond what is to see what might be: we live in a state of enforced urgency because we are all dying, because the decades of healthy life are a time of frantic preparation for the decline and sickness that comes later. It is normal, the everyday experience, for all of us to know we are chased by a ticking clock, forced to put aside the things that we would rather do in favor of the things that we must do. We cannot pause, cannot follow dreams, cannot stop to smell the roses.

"Some people seem to manage these goals, but only the lucky few - and then only by twining what they would like to do with what they must do. It's hard to achieve that end, and it is really nothing more than an ugly compromise even when obtained. Yet like so much of what we are forced into by the human condition, it is celebrated. One more way in which what is triumphs over what might be in the minds of the masses.

"Given many more healthy years of life in which to do so, we would lead quite different lives. Arguably better lives, not diverted by necessity into a long series of tasks we do not want to undertake, carried out for the sake of what will come. We could follow desire rather than need: work to achieve the aims that we want to achieve, not those forced on us. Because of aging and death, we are not free while we are alive - and in any collection of slaves there are those who fear the loss of their chains. The longer they are enslaved, the less their vision of freedom. Sadly, in the mainstream of our culture, it is those voices that speak the loudest."

ON CHRONIC INFLAMMATION IN AGING

Researchers believe that chronic inflammation plays an important role in the pace of aging, and that the biology of long-lived mutant mice adds more confirming evidence in support of this view:

https://www.fightaging.org/archives/2012/10/on-inflammation-in-mouse-longevity-mutants.php

"The last 200 years of industrial development along with the progress in medicine and in various public health measures had significant effect on human life expectancy by doubling the average longevity from 35-40 to 75-80. There is evidence that this great increase of the lifespan during industrial development is largely due to decreased exposure to chronic inflammation throughout life. There is strong evidence that exposure of an individual to past infections and the levels of chronic inflammation increase the risk of heart attack, stroke and even cancer.

"During normal aging of rodents and humans there is increased insulin resistance, disruption of metabolic activities and decline of the function of the immune system. All of these age related processes promote inflammatory activity, causing long term tissue damage and systemic chronic inflammation. However, studies of long living mutants and calorie restricted animals show decreased pro-inflammatory activity with increased levels of anti-inflammatory adipokines such as adiponectin. At the same time, these animals have improved insulin signaling and carbohydrate homeostasis that relate to alterations in the secretory profile of adipose tissue including increased production and release of anti-inflammatory adipokines.

"This suggests that reduced inflammation promoting healthy metabolism may represent one of the major mechanisms of extended longevity in long-lived mutant mice and likely also in the human."

CONSIDERING THE BRAIN

A couple of posts from the past week touch on the brain, and efforts to both preserve and understand its workings:

https://www.fightaging.org/archives/2012/10/a-long-discussion-on-what-exactly-needs-to-be-preserved-in-a-stored-brain-in-order-to-preserve-the-mind.php

"But even under the most optimistic of scenarios, such as those in which the SENS program for rejuvenation biotechnology is fully funded starting tomorrow, billions will age to death before the research community can develop the first therapies capable of meaningful rejuvenation. There is something that can be done to address this issue, for all that almost as little effort is made here as for ways to cure aging: long-term preservation of the dead, accomplished in ways that prevent destruction of the fine structures in the brain that store the mind.

"At present, the only way to preserve your mind on death is through cryonics, or low-temperature storage with vitrification of tissue. Legal obstacles make it harder than it needs to be to obtain a good preservation, and as noted above the long-standing cryonics industry is a thin thread rather than the mighty river of effort it would be in a more just and sane world. Billions have died since cryonics became a viable commercial product, of which only a few hundred have been successfully preserved.

"They can wait out the coming decades, wait out the development of medical nanotechnologies that can reverse the processes of cryopreservation. Time is on their side in this age of rapid progress, assuming that the living community of enthusiasts and professionals can continue to ensure a long-term continuity of service.

"A possible future alternative to cryopreservation is plastination, a different methodology for fixing a cell's structure all the way down to the finest details. No organizations analogous to the cryonics industry yet exists to offer plastination services, but that may only be a matter of time. Competition is healthy in any field of human endeavor."

https://www.fightaging.org/archives/2012/10/of-interest-the-human-brain-project.php

"The brain, with its billions of interconnected neurons, is without any doubt the most complex organ in the body and it will be a long time before we understand all its mysteries. The Human Brain Project proposes a completely new approach. The project is integrating everything we know about the brain into computer models and using these models to simulate the actual working of the brain. Ultimately, it will attempt to simulate the complete human brain. The models built by the project will cover all the different levels of brain organisation - from individual neurons through to the complete cortex. The goal is to bring about a revolution in neuroscience and medicine and to derive new information technologies directly from the architecture of the brain.

"The Human Brain Project will impact many different areas of society. Brain simulation will provide new insights into the basic causes of neurological diseases such as autism, depression, Parkinson's, and Alzheimer's. It will give us new ways of testing drugs and understanding the way they work. It will provide a test platform for new drugs that directly target the causes of disease and that have fewer side effects than current treatments. It will allow us to design prosthetic devices to help people with disabilities. The benefits are potentially huge. As world populations grow older, more than a third will be affected by some kind of brain disease. Brain simulation provides us with a powerful new strategy to tackle the problem."

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!

SPERMIDINE LEVELS MEASURED IN CENTENARIANS
Friday, October 19, 2012
https://www.fightaging.org/archives/2012/10/spermidine-levels-measured-in-centenarians.php
Spermidine has been noted to boost autophagy and promote greater longevity to some degree in laboratory animals. Its activities are in the process of being advanced by some researchers as candidate drug mechanisms for slowing aging. Given that, it makes sense for researchers to investigate spermidine levels in longer lived individuals to see if there is any association: "Polyamines (putrescine, spermidine and spermine) are a family of molecules deriving from ornithine, through a decarboxylation process. They are essential for cell growth and proliferation, stabilization of negative charges of DNA, RNA transcription, translation and apoptosis. Recently, it has been demonstrated that exogenously administered spermidine promotes longevity in yeasts, flies, worms and human cultured immune cells. Here, using a cross-sectional observational study, we determined whole-blood polyamines levels from 78 sex-matched unrelated individuals divided into three age groups: group 1 (31-56 years, N=26, mean age: 44.6±6.07), group 2 (60-80 years, N=26, mean age: 68.7±6.07) and group 3 (90-106 years, N=26, mean age: 96.5±4.59). Polyamines total content is significantly lower in group 2 and 3 compared to group 1. Interestingly, this reduction is mainly attributable to the lower putrescine content. Group 2 displays the lowest levels of spermidine and spermine. On the other hand, [nonagenarians and] centenarians (group 3) display significant higher median relative percentage content of spermine with respect to total polyamines, compared to the other groups. For the first time we report polyamines profiles from whole blood of healthy [nonagenarians and] centenarians, and our results confirm and extend previous findings on the role of polyamines in determining human longevity. However, although we found an important correlation between polyamines levels and age groups, further studies are warranted to fully understand the role of polyamines in determining life-span. Also, longitudinal and nutritional studies might suggest potential therapeutic approaches to sustain healthy aging and to increase human life-span."

A SMALL STEP TOWARDS TISSUE ENGINEERED KIDNEYS
Friday, October 19, 2012
https://www.fightaging.org/archives/2012/10/a-small-step-towards-tissue-engineered-kidneys.php
Tissue engineers have been inching closer to building a kidney from stem cells in the past couple of years. Here is a recent example of the ongoing work in this field: "Investigators can produce tissues similar to immature kidneys from simple suspensions of embryonic kidney cells, but they have been unsuccessful at growing more mature kidney tissues in the lab because the kidneys' complicated filtering units do not form without the support of blood vessels. Now, from suspensions of single kidney cells, [researchers] have for the first time constructed "organoids" that can be integrated into a living animal and carry out kidney functions including blood filtering and molecule reabsorption. Key to their success was soaking the organoids in a solution containing molecules that promote blood vessel formation, then injecting these molecules into the recipient animals after the organoids were implanted below the kidneys. The organoids continued to mature and were viable for three to four weeks after implantation."

MORE ON YOUNG BLOOD AND OLD MICE
Thursday, October 18, 2012
https://www.fightaging.org/archives/2012/10/more-on-young-blood-and-old-mice.php
Some of the effects of aging are driven by signaling changes in important parts of our biochemistry - such as in stem cell niches, collections of cells that provide necessary support to the stem cells that maintain and repair tissue. Niches increasingly act to suppress the stem cells they contain in response to rising levels of cellular and other damage connected to aging. The stem cells themselves also suffer damage, and this evolved response is likely a way to minimize the risk of cancer at the cost of maintaining tissues, but the declining function of the stem cells so far seems to be far more a property of signals from the niche. In the course of investigating this and similar effects, researchers have been moving blood between young and old mice. Transfusions and joining the bloodstreams of young and old mice are a way to change the signaling environment in order to see what the effects are. The outcome is that a range of measures of aging are reversed: "Experiments on mice have shown that it is possible to rejuvenate the brains of old animals by injecting them with blood from the young. ... blood from young mice reversed some of the effects of ageing in the older mice, improving learning and memory to a level comparable with much younger animals. [Researchers] connected the circulatory systems of an old and young mouse so that their blood could mingle. This is a well-established technique used by scientists to study the immune system called heterochronic parabiosis. When [researchers] examined the old mouse after several days, [they] found several clear signs that the ageing process had slowed down. The number of stem cells in the brain, for example, had increased. More important, [they] found a 20% increase in connections between brain cells. One of the main things that changes with ageing are these connections, there are a lot less of them as we get older. That is thought to underlie memory impairment - if you have less connections, neurons aren't communicating, all of a sudden you have [problems] in learning and memory. ... the young blood most likely reversed ageing by topping up levels of key chemical factors that tend to decline in the blood as animals age. Reintroduce these and [all] of a sudden you have all of these plasticity and learning and memory-related genes that are coming back."

MORE ROBUST DATA ON THE EFFECT OF MITOCHONDRIALLY TARGETED ANTIOXIDANTS ON FLY LIFE SPAN
Thursday, October 18, 2012
https://www.fightaging.org/archives/2012/10/more-robust-data-on-the-effect-of-mitochondrially-targeted-antioxidants-on-fly-life-span.php
In recent years a few research groups have been working on a class of antioxidant compounds that can be ingested but nonetheless target themselves to mitochondrial in our cells. These compounds extend life in laboratory animals, probably by soaking up reactive free radical compounds emitted by mitochondria in the course of their operation, and thus preventing some of the damage that mitochondria cause to themselves. This damage is significant in aging, one of the root causes of degeneration and age-related disease. It is worth noting that all of the commonly available antioxidant compounds you can buy and ingest do nothing for life span or health, according to many, many studies. They don't target mitochondria, and in fact probably even cause some harm by blocking hormetic processes that use free radical signaling to boost repair mechanisms in tissue. Here is a paper providing more data on the effects of the best known class of mitochondrially targeted antioxidant: "Previously, extremely low [concentrations] of the mitochondria-targeted plastoquinone derivative SkQ1 (10-(6'-plastoquinonyl) decyltriphenylphosphonium) were shown to prolong the lifespan of male and female Drosophila melanogaster by about 10%. Using long-term monitoring of SkQ1 effects on the Drosophila lifespan, we analyzed different integral parameters of Drosophila survival and mortality under SkQ1 treatment. Meta-analysis was used to evaluate the average SkQ1 effect measured in terms of standard deviation. The effect appeared to be 0.25 for females and 0.18 for males. The SkQ1 effects on the Drosophila lifespan were reproducible over six years and showed no relationship to fluctuations in the mean lifespan of the w ( 1118 ) line used in the experiments, methods of preparation and administration of the drug, seasons, or calendar years. Adding SkQ1 to fly food was associated with a reduction in early mortality and a decrease in random variation in lifespan. [The data] indicated that feeding flies SkQ1 reduced the rate of fall of fly vitality and, consequently, slowed aging. These findings indicated that the SkQ1 effect on lifespan was associated with both elevation of life quality and slowing of aging."

THE PLASTICITY OF LIFE SPAN
Wednesday, October 17, 2012
https://www.fightaging.org/archives/2012/10/the-plasticity-of-life-span.php
We live longer than our ancestors thanks to our greater wealth and more advanced technology: risk of death is reduced at all ages, the level of damage suffered due to infectious disease and other causes is lowered throughout life, and inroads made into means of alleviating age-related disease. When it comes to effects across a life span, however, our extended lives are so far largely incidental, a side effect of improvements in medicine and quality of life that were introduced to satisfy other, more short-term goals. This shows that aging and life span is very plastic - it can be changed, and is very readily changed. On the other hand, it tells us next to nothing about what lies ahead, as the rejuvenation biotechnology of the future will be an entirely different beast from the medicine of the past. Only now is the research community deliberately trying to manipulate the processes of aging, or repair the biological damage that causes degeneration. Given this shift in what is possible, projecting past trends to the future is unwise: the deliberately engineered changes in longevity of tomorrow will not look like the incidental benefits that slowed aging yesterday. Here is an article on recent research that seeks to quantify the degree of improvement in human life expectancy that has occurred in recent centuries - you might want to look at the paper itself since it is open access. "It's said that life is short. But people living in developed countries typically survive more than twice as long as their hunter-gatherer ancestors did, making 72 the new 30, according to new research. Most of the decline in early mortality has occurred in the past century, or four generations, a finding that calls into question traditional theories about aging. But there's a larger message from the research: Our estimates about the limits of human lifespans may be too low. The study findings "make it seem unlikely that there is a looming wall of death ... which kills off individuals at a certain age" because of genetic mutations that build up as we age. For example, hunter-gatherer humans were about 100 times more likely to die before age 15 than today's residents of Japan and Sweden. And the study says hunter-gatherers were as likely to die at age 30 as Japanese people are at age 72. But the human lifespan didn't grow gradually over thousands of years. The big jump occurred after 1900 in what the study authors call a "rapid revolutionary leap." In the big picture, the research challenges the idea that genetic mutations over a lifetime prevent humans from living very long ... Without changing our genetic code at all, we have all of this improvement in mortality at these ages where these mutations should kill us off. And we got all this improvement without 'fixing' any of these mutations that are predicted to cause our bodies to break down in various ways."

OVEREXPRESSION OF FGF21 EXTENDS LIFE IN MICE
Wednesday, October 17, 2012
https://www.fightaging.org/archives/2012/10/overexpression-of-fgf21-extends-life-in-mice.php
An enormously complex web of genes and protein machinery controls the operation of metabolism, a layered nest of interactions and feedback loops. It is thus possible for many different genetic alterations to extend life by working through the same basic mechanism. The example here involving fibroblast growth factor 21 is a newly discovered change that seems to work through a known life extension method involving suppression of growth hormone, used in the past to extend life by 60-70% in mice. "Restricting food intake has been shown to extend lifespan in several different kinds of animals. In our study, we found transgenic mice that produced more of the hormone fibroblast growth factor-21 (FGF21) got the benefits of dieting without having to limit their food intake. Male mice that overproduced the hormone had about a 30 percent increase in average life span and female mice had about a 40 percent increase in average life span. FGF21 seems to provide its health benefits by increasing insulin sensitivity and blocking the growth hormone/insulin-like growth factor-1 signaling pathway. FGF21 is a hormone secreted by the liver during fasting that helps the body adapt to starvation. It is one of three growth factors that are considered atypical because they behave like hormones. ... Previous research has found that FGF21 can reduce weight in obese mice. The mice that overproduced FGF21 in this latest study were lean throughout their lives and remained lean even while eating slightly more than the wild-type mice. The hormone does have some downsides: FGF21 overproducers tended to be smaller than wild-type mice and the female mice were infertile. While FGF21 overproducers had significantly lower bone density than wild-type mice, the FGF21-abundant mice exhibited no ill effects from the reduced bone density."

DOPAMINE AND MEMORY DECLINE IN AGING
Tuesday, October 16, 2012
https://www.fightaging.org/archives/2012/10/dopamine-and-memory-decline-in-aging.php
Parkinson's disease is caused by excessive loss of cells in the small population of dopamine-generating neurons. This is an exaggerated version of a loss that we all suffer due to the wear and tear of aging: many age-related conditions are of this nature, aggravated or more rapidly occuring versions of the same damage that everyone suffers. So all people lose some of the cells that generate the neurotransmitter dopamine, just not enough for that loss to become a named and known medical condition. But even this more modest loss of dopamine neurons causes functional decline in the brain, as researchers here demonstrate - with the intent to show that drugs that deliver dopamine to the brain could at least partially compensate for this decline: "Activation of the hippocampus is required to encode memories for new events (or episodes). Observations from animal studies suggest that, for these memories to persist beyond 4-6 hours, a release of dopamine generated by strong hippocampal activation is needed. This predicts that dopaminergic enhancement should improve human episodic memory persistence also for events encoded with weak hippocampal activation. Here, using pharmacological functional MRI (fMRI) in an elderly population in which there is a loss of dopamine neurons as part of normal aging, we show this very effect. The dopamine precursor levodopa led to a dose-dependent (inverted U-shape) persistent episodic memory benefit for images of scenes when tested after 6 hours, independent of whether encoding-related hippocampal fMRI activity was weak or strong (U-shaped dose-response relationship). This lasting improvement even for weakly encoded events supports a role for dopamine in human episodic memory consolidation, albeit operating within a narrow dose range."

ANOTHER GLENN FOUNDATION LAB ESTABLISHED
Tuesday, October 16, 2012
https://www.fightaging.org/archives/2012/10/another-glenn-foundation-lab-established.php
Following on from last week's news, it seems the Glenn Foundation for Medical Research is establishing a brace of new laboratories for the study of aging, joining those formed a few years back. Which is to say that the Foundation is reinforcing some of the existing leading lights in aging and longevity science, and in the process of delivering sizable grants is setting up new, named research centers. This time it's the turn of researchers at the Albert Einstein College of Medicine: " Albert Einstein College of Medicine of Yeshiva University has received a $3 million grant from the Glenn Foundation for Medical Research to establish the Paul F. Glenn Center for the Biology of Human Aging Research. The grant will fund research to translate recent laboratory and animal discoveries into therapies to slow human aging. "Paul F. Glenn has been a visionary in aging research for more than 30 years," said Ana Maria Cuervo, M.D., Ph.D., co-director of the new center, the Robert and Renee Belfer Chair for the Study of Neurodegenerative Diseases, and professor of developmental and molecular biology, of anatomy and structural biology and of medicine at Einstein. "Some of us got to know him when we were still graduate students and he came to scientific conferences to see the data as it was being developed. Paul's personal approach to science has made a big difference to many of us in the field of aging research and has contributed to the career development of many young investigators." The funding, in the form of pilot and feasibility study grants, is targeted to several specific research projects: uncovering the genetic and epigenetic mechanisms that protect humans against aging and age-related diseases, testing the effectiveness of the first-generation pro-longevity therapies, and developing novel preventive and therapeutic interventions against cellular aging in humans." Cuervo, you might recall, led the demonstration of reversal of lysosomal decline in the aging liver a few years back, making old mouse livers function as well as when young.

COMMENTING ON THE LATE LIFE PLATEAU IN AGING
Monday, October 15, 2012
https://www.fightaging.org/archives/2012/10/commenting-on-the-late-life-plateau-in-aging.php
One fairly standard definition for aging is an increase in mortality rate over time. You are said to age if you become increasingly likely to die in any given interval of time. There is an interesting twist, however: researchers have shown that in short-lived species such as flies there appears to be a point in very late life at which mortality rate stops increasing - i.e. aging, by this definition, ceases. There is some debate as to what this tells us, and how useful in might be in terms of informing aging research or practical applications of biotechnology to extend life. For example, the evidence for any such late-life plateau for mortality rates in humans is tenuous to non-existent. Does it even exist outside very short-lived species? Here is a further commentary on late-life plateaus in mortality rate and evolutionary considerations of aging: "Too often, aging is thought of as an inevitable accumulation of damage to cells, as something common to all organisms and across all adult ages, or as a physiological process. These ways of thinking about aging limit aging research. We should instead understand aging as an evolutionarily derived condition, dependent entirely on the pattern of the force of natural selection. In late adult life, the forces of natural selection no longer differentiate between age classes. At these late ages, there is no effective force of natural selection. This leads to a corresponding absence of consistent changes in fecundity and mortality. One prediction of the evolutionary theories is that other fitness characters, such as male virility, should also stabilize in late life. Following the virility of 1000 individual male D. melanogaster, I found that, as expected, male virility also reached a plateau in late life. This result conforms to the predictions of the evolutionary theories of late life. Late life is therefore a period in which mortality, fecundity, and virility all plateau. ... These results suggest that late life physiology is distinct from that of aging, and that the absence of change in the effective forces of selection in late life, leads to paradoxical transitions in physiology as cohorts enter late life. From these results, I infer that the periods of aging and late life are different physiologically as a result of the very different ways in which they experience selective forces."

INVESTIGATING NATURAL BLADDER REGENERATION IN RATS
Monday, October 15, 2012
https://www.fightaging.org/archives/2012/10/investigating-natural-bladder-regeneration-in-rats.php
Important things remain to be learned of the regenerative capacity of various mammal species - such as the way in which rats can regrow large sections of the bladder. Researchers investigate mechanisms of natural regeneration with an eye to finding ways to reproduce exceptional examples of regrowth in human biochemistry. Here, scientists suggest that regeneration of the bladder in rodents is a better avenue of investigation than the well known regeneration of the liver that even we humans are capable of: "Subtotal cystectomy (STC; surgical removal of ~75% of the rat urinary bladder) elicits a robust proliferative response resulting in complete structural and functional bladder regeneration within 8-weeks. ... Although regeneration per se occurs throughout the animal kingdom, there are large disparities in the degree of regeneration observed between species (e.g., amphibian versus mammalian) let alone amid organs (e.g., liver versus kidney). The extensive attention focused on regenerative medicine is understandable given the enormous potential for repair and/or replacement of old, damaged or diseased cells, tissues and organs; such as the diseased and dysfunctional bladders that are the subject of this report. The liver is very efficient in repairing or regenerating its mass, which occurs as a direct result of the proliferation of all the existing cells from the remaining liver remnant, but is mainly driven by mature hepatocytes, which will re-enter the cell cycle to restore the liver. The entire process, which is usually referred to as regeneration, is completed within a couple weeks, depending upon the mammalian species. However, the process is more accurately termed compensatory hyperplasia. These well established observations regarding liver re-growth stand in contrast to rodent bladder regeneration, which occurs over a longer time frame (8 weeks rather than 2 weeks), and moreover, results in a regenerated bladder that structurally and functionally is essentially identical to the native bladder which it replaced. More specifically, the bladder capacity and bladder wall thickness (as well as the presence of all three layers; urothelium, muscularis propria and lamina propria) of the regenerated bladder are indistinguishable from the previous native bladder, and moreover, the animals are entirely continent. To our knowledge, bladder regeneration therefore holds a unique position with respect to its regenerative potential, as there is no other mammalian organ capable of this type of regeneration."

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