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We help you stay up to date with the most interesting news in medicine, politics and the healthy life extension community. You can help us by contacting us when you see interesting items online. You can search past news postings through Google by using the form to the right.
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| Discover Magazine looks at one of the noteworthies of the stem cell research community: "The value of therapeutic cloning has long been clear to Lanza, who did his early work with South African heart transplant pioneer Christiaan Barnard. Starting from those early days, Lanza understood that the barrier to tissue transfer was rejection by the recipient. From an entire organ to a dose of embryonic stem cells, if the tissue's DNA came from anyone else, the transplant would be rejected without the aid of harsh immunosuppressive drugs. 'The treatment could be worse than the problem,' Lanza found. But embryonic clones, the source of an endless supply of stem cells imprinted with one's personal DNA, could alter the equation in favor of the patient and augur a paradigm shift in medicine on par with the changes brought about by antibiotics and vaccines ... With the ability to become all of the blood cells - including your immune cells, red blood cells, all of your blood system, as well as vasculature, [hemangioblasts] have been biology's holy grail. What we discovered is that we can create literally millions or billions of these from human embryonic stem cells. ... we can use transient, intermediate cells like hemangioblasts as a toolbox to fix the adult so you don't have to have limbs amputated, so you may not have to go blind, to prevent heart attacks." |
| From the Technology Review: "While all animals can regenerate tissue to a certain extent - we can grow muscle, bone, and nerves, for example - salamanders and newts are the only vertebrates that can grow entire organs and replacement limbs as adults. When a leg is lost to injury, cells near the wound begin to dedifferentiate, losing the specialized characteristics that made them a muscle cell or bone cell. These cells then replicate and form a limb bud, or blastema, which goes on to grow a limb the same way that it forms during normal development. Scientists have identified some of the molecular signals that play a key role in the process, but the genetic blueprint that underlies regeneration remains unknown. Researchers hope that by uncovering these molecular tricks, they can ultimately apply them to humans to regrow damaged heart or brain tissue, and maybe even grow new limbs. ... One of the key questions yet to be answered is whether the salamander has unique genetic properties that enable regeneration, or whether all animals have that innate capability. ... If we come up with some totally unique gene only present in [salamanders], that would make it really hard to replicate." |
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| At first glance, Laron dwarfs appear to be the Ames dwarf mice of the human world - long-lived and resistant to cancer, due to a genetic mutation that suppresses the somatotrophe axis: "There are a little more than 300 people in the world with the condition Laron dwarfism, a third of whom live in remote villages in Ecuador's southern Loja province. Sufferers of Laron - believed to be caused by inbreeding - lack a hormone called Insulin-like Growth Factor 1, or IGF1. Research [suggests] this is the reason for their longevity and apparent immunity to cancer. ... We've discovered that people with Laron simply don't get cancer. Cancer can be detected in their relatives of a normal size, but never in my patients - not one single case. ... Laboratory work in mice, flies and worms has shown that if IGF1 is removed, the animals tend not to get cancer and to live longer. This is now mirrored in recent research into small humans, who turn out to have little or no IGF1." There are a few large factual mistakes in the article, as might be expected given the source, but it is most interesting to see this work in mice translate so faithfully to humans. |
| What does nuclear DNA damage have to do with aging? The correlation is clearly there - older animals have more random nuclear DNA damage - but the mechanism by which increased damage might lead to some portion of degenerative aging is up for debate. A recent paper shows that the correlation extends to calorie restriction and some genetic manipulations that extend life: "Genetic instability has been implicated as a causal factor in cancer and aging. Caloric restriction (CR) and suppression of the somatotroph axis significantly increase life span in the mouse and reduce multiple symptoms of aging, including cancer. To test if in vivo spontaneous mutation frequency is reduced by such mechanisms, we crossed long-lived Ames dwarf mice with a C57BL/6J line [to] measure mutant frequencies. ... Four cohorts were studied: (1) ad lib wild-type; (2) CR wild-type; (3) ad lib dwarf; and (4) CR dwarf. ... results indicate that two major pro-longevity interventions in the mouse are associated with a reduced mutation frequency. This could be responsible, at least in part, for the enhanced longevity associated with Ames dwarfism and CR." |
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| From the Hindustan Times: "Half a dozen eye hospitals in India are collaborating with a research centre in Chennai to create the inner layer of the cornea, the vital window of the human eye. ... Nichi-In Centre for Regenerative Medicine (NCRM) hopes to make corneal endothelium (inside cell layer) available on a commercial scale ... About 100,000 people are in need of eye transplant every year, yet only about 10,000 are able to get donated eyes. The wait for a donor can be endless for the other 90,000. Imagine what a boon it will be if an eye stem cell bank could provide these lab generated endothelial layer of the cornea ... The eye has three main parts. The first is the cornea, which is a transparent film like structure that transmits light into the eye. The other two are the lens and retina. During eye transplant, only the cornea is taken from the donor, not the whole eye. ... Nichi-In is now growing the animal and human corneal inner layer cells on a nano-scaffolding. The research centre is hoping to begin phase I clinical trials on humans in six months." |
| Open science, analogous to open source software development, is the way of the future. It greatly increases diversity and speed of work by lowering the cost of information, and thereby allowing many more people to participate in research. In a world in which information transmission is easy, it makes no sense to lock up scientific data. Publish early, publish often should be the mantra. From Ouroboros: "The world implied by these concepts is one of radical sharing, in which credit still goes where credit is due but by dramatically different mechanisms. Open science isn’t so much 'pay it forward' (though there is a bit of that) as an effort to create a (scientific) world in which no one is paying at all, a world in which there's no incentive to withhold or protect ownership of data. The science fiction writer Iain M. Banks once wrote that 'money implies poverty' - indeed, many of the current models of data ownership and publication, and their accompanying 'currencies' of proprietorship, prestige and closed-access publication, imply a world in which data is scarce and must be hoarded. But data is not scarce anymore." |
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| Via Depressed Metabolism, arguments for a present focus on the development of cryonics over the development of rejuvenation medicine: "In his article 'Why Cryonics Will Probably Help You More Than Antiaging' (2004), cryonics activist Thomas Donaldson contrasts cryonics with antiaging as a means to life extension and argues that a major advantage of cryonics is that cryobiology research can move at a much faster pace than anti-aging research, especially as it pertains to humans ... Not only that, but its progress almost totally lacks the problems of proving that an advance has happened. The state of a brain, or even a section of brain, after vitrification and rewarming to normal temperature, shows directly whether or not the method used improved on previous methods. ... cryonic suspension able at least to preserve our brains in a reversible form, allowing restoration of vital functions, looks likely to come much sooner [than rejuvenation medicine]." Which is all true - but problems left to other people to solve have a way of remaining unsolved. We should work on both cryonics and rejuvenation medicine, not leave the latter for future generations. |
| The Methuselah Foundation is asking supporters to vote for aging science in the Amex Members Project program: "we are supporting a project named 'Undergrads Against Age Related Disease,' submitted as part of the Amex Members Project initiative. In order to move forward, this project must obtain more than 2000 votes in the next 2 weeks - by September 1st, 2008. You can help by voting: it's free and won't take more than a few minutes. We just need you to go to the Members Projects website and nominate the "Undergrads Against Age Related Disease" project. You don't need to be an Amex card holder, but you do need to be a US resident." From the project description: "a program that utilizes college undergraduates to perform research in a variety of scientific venues surrounding fighting age related diseases such as Alzheimer's, Parkinson's, Heart Disease, [Cancer, and] overall extension of healthy human life. Hiring researchers is exceedingly expensive. By outsourcing projects to undergraduate students, laboratory use and labor costs are negligible, and the students receive college credit for their work." |
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| An important aspect of immune system aging is the lack of naive T cells resulting from long periods of chronic infection by viruses like cytomegalovirus. What if we could reconfigure the immune system to behave more rationally when presented with recurring threats, and thus not exhaust its resources? That might be a possibility: "preventing white blood cells' circulation by trapping them in the lymph nodes can help mice get rid of a chronic viral infection ... laboratory mice can fight off infection by the Armstrong strain of lymphocytic choriomeningitis virus (LCMV), but are vulnerable to chronic infection by a variant called clone 13. ... infecting mice with the Armstrong strain sequesters white blood cells in the lymph nodes, while clone 13 does so less stringently. ... Our hypothesis was that if we could artificially induce conditions like those produced by the Armstrong strain, it would help the immune system clear an infection by clone 13 ... an experimental drug called FTY720 [prevents] white blood cells from leaving lymph nodes ... Even if mice have a stable chronic LCMV clone 13 infection, treatment with FTY720 can still improve their immune response against LCMV enough to have them rid it from their systems ... FTY720 appears to prevent 'exhaustion' in the group of white blood cells called CD8+ T cells." |
| From Ouroboros: "Welcome to the second installation of Hourglass, a blog carnival devoted to the biology of aging. The entries are representatives of the excellent (and growing) community of bloggers who are writing about biogerontology, lifespan extension technologies, and aging in general. ... Anne C. shares a parable about taking care of her friend Nigel the Fish and what that led her to realize about longevity: specifically, that environment is critical, and that the combination of extrinsic factors that one might collectively term 'nurture' can make all the difference between a short unhappy life and a long fulfilled one. ... Old and damaged cells enter a permanent growth arrest known as senescence, which is both good (because they can’t initiate tumors) and bad (because persistent senescent cells behave in a ridiculously antisocial manner, secreting growth factors and proteases that both encourage nearby tumors to metastasize and degrade tissue function). ... At his new site Anti-Ageing Research, Dominick Burton discusses ways in which specifically targeted cancer therapies might be adapted to attack senescent cells instead." |
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| Laboratory tissue engineering continues to improve in sophistication, as noted by the New Scientist: "only now have researchers managed to make different tissues blend into one another, as they do naturally in the body. Such gradients are necessary for some structures and organs to function properly ... In the body, gradients like this strengthen the ends of tendons that attach to bones. Currently, lab-grown tendons put into the body often fail at the attachment end because they lack this property ... [the] new technique should lead to more lifelike artificially-grown tendons, and better treatments for injuries like ruptured Achilles tendons. The technique could also be applicable to other tissues, such as blood vessels .. At the heart of the new technique is a gene that triggers the fibroblast cells that make up tendons to start forming bone. The team used viruses carrying that gene to transform a tendon made from normal fibroblasts into one with a gradient of bony properties ... So far, the researchers have shown that tendons made this way are stable when implanted under the skin of rats. The next step is to graft a tendon to connect bone and muscle in a rat and see if it really does perform better." |
| Via Medical News Today, another reminder of the value of exercise: "US scientists comparing middle aged and older regular runners with healthy equivalents for more than 20 years found that vigorous regular exercise was linked to longer life and less disability in old age. ... Fries and his team had 538 members of a nationwide running club and 423 healthy controls from northern California fill in questionnaires every year for as long as they could, from 1984 to 2005 ... The mean disability score was higher for the controls than the runners at all stages of the study and went up with age in both groups, but on average, for runners the onset of disability started later. ... Runners' initial disability was 16 years later than nonrunners ... Runners had a significantly lower risk of having a disability score of 0.5. ... 19 years into the study, 15 per cent of the runners and 34 per cent of the controls had died, and after adjusting for possible confounders, runners showed a greater chance of living longer. ... The differences in disability and longevity between the runner group and the control group continued to diverge at the end of the study, as the participants approached their 80th birthday." |
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| You may recall a solid demonstration that visceral fat tissue negatively affects longevity from earlier this year. The full paper is now open access and available at PubMed Central: "Visceral fat (VF) accretion occurs in obesity and with aging, and a reduction in VF is a common phenotypic change in calorie-restricted [CR] mammals. VF has been shown to be the single most important determinant of metabolic syndrome, and its removal in rats results in improved insulin action and delays the onset of diabetes. Given the hazards associated with abdominal obesity, it seems plausible that the beneficial effects of CR on longevity may be due at least in part to an attenuation of VF. ... Our data clearly demonstrate that in mammals, VF removal and CR are associated with an increase in mean and maximum lifespan. ... The mean and maximum lifespan of CR rats was greater than that seen in VF-removed animals, suggesting that the life-prolonging benefit of CR is mediated in part by pathways other than those modulated by an attenuation of VF. By comparing median lifespans, we estimate that the contribution of CR to longevity in this model was 47 weeks, whereas VF removal was 9.5 weeks, as compared to [ad libitum]-fed rats, suggesting that VF reduction offered approximately 20% of the effect of CR on longevity." |
| ScienceDaily reports on a promising demonstration: "The cells of all organisms have several surveillance systems designed to find, digest and recycle damaged proteins. ... One of these surveillance systems - responsible for handling 30 percent or more of damaged cellular protein - uses molecules known as chaperones to seek out damaged proteins. After finding such a protein, the chaperone ferries it towards one of the cell's many lysosomes ... Dr. Cuervo found that the chaperone surveillance system, in particular, becomes less efficient as cells become older, resulting in a buildup of undigested proteins within the cells. She also detected the primary cause for this age-related decline: a fall-off in the number of lysosomal receptors capable of binding chaperones and their damaged proteins. Could replenishing lost receptors in older animals maintain the efficiency of this protein-removal system throughout an animal's lifespan and, perhaps, maintain the function of the animal's cells and organs as well?" As it turned out, this strategy does indeed work to maintain liver function at young levels in older animals. |
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| Some solid correlations in this paper, but I'm not sold on the suggested mechanism of action. Eating fewer calories definitely slows down the manifestations of aging, but researchers have a way to go yet to fully explain why this is so in each case: "iron accumulates with senescence in several organs, but little is known about iron accumulation in muscle and how it may affect muscle function. In addition, it is unclear if interventions which reduced age-related loss of muscle quality, such as calorie restriction, impact iron accumulation. We investigated non-heme iron concentration, oxidative stress, [and] key indices of sarcopenia (muscle mass and grip strength) in male [rats] fed ad libitum (AL) or a calorie restricted diet ... iron levels in the gastrocnemius muscle of AL rats increased progressively with age. Between 29 and 37 months of age, the non-heme iron concentration increased by approximately 200% in AL-fed rats. Most importantly, the levels of oxidized RNA in gastrocnemius muscle of AL rats were significantly increased as well. The striking age-associated increase in non-heme iron and oxidized RNA levels and decrease in sarcopenia indices were all attenuated in the calorie restriction (CR) rats. These findings strongly suggest that the age-related iron accumulation in muscle contributes to increased oxidative damage and sarcopenia, and that CR effectively attenuates these negative effects." |
| Less chronic inflammation, less cancer: "Cancer is generally recognized as an age-related disease. In fact, incidence and mortality rates of most human cancers increase consistently with age up to 90 years, but they plateau and decline thereafter. A low-grade systemic inflammation characterizes ageing and this pro-inflammatory status underlies biological mechanisms responsible for age-related inflammatory diseases. On the other hand, clinical and epidemiological studies show a strong association between chronic infection, inflammation and cancer and indicate that even in tumours not directly linked to pathogens, the microenvironment is characterized by the presence of a smouldering inflammation, fuelled primarily by stromal leukocytes. ... Centenarians are characterized by a higher frequency of genetic markers associated with better control of inflammation. The reduced capacity of centenarians to mount inflammatory responses appears to exert a protective effect towards the development of those age-related pathologies having a strong inflammatory pathogenetic component, including cancer. All in all, centenarians seem to carry a genetic background with a peculiar resistance to cancer which is also an anti-inflammatory profile." |
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| An interview with Cryonics Institute president and long-time healthy life extension advocate Ben Best can be found at Depressed Metabolism: "I believe that arrogance and complacency are poison for cryonics organizations, and competition is of value in shaking complacency (sometimes). I definitely think that it would be a bad idea for cryonics to have all the eggs in one organizational basket. ... There is already too much vulnerability to lawsuits and legal/political threats. More organizations in more locations (including more countries) would reduce this vulnerability. ... Eliminating or greatly reducing cryoprotectant toxicity would be the greatest possible step toward suspended animation through cryopreservation with vitrification. If suspended animation through cryopreservation became a reality there would be immediate acceptance and adoption by conventional medicine. Patient stabilization would be perfected by researchers all over the world and adopted in hospitals and other medical facilities. I think that too much research effort in cryonics is devoted to whole body vitrification, which is a side issue. Cryoprotectant toxicity needs to be [studied] with experiments directed toward understanding the molecular mechanisms on a theoretical level - not simply trial and error. Whole body vitrification could very well be achieved more quickly if cryoprotectant toxicity was the focus of study." |
| EurekAlert! reminds us of the second main application for stem cell science: researchers "have produced a robust new collection of disease-specific stem cell lines, all of which were developed using the new induced pluripotent stem cell (iPS) technique. ... The cell lines the researchers produced carry the genes or genetic components for 10 different diseases, including Parkinson's Disease, Type I diabetes, Huntington's Disease, Down Syndrome, a form of combined immunodeficiency ('Bubble Boy's Disease'), Lesch-Nyhan syndrome, Gaucher's Disease, and two forms of Muscular Dystrophy, among others. ... the suite of iPS cell lines [marks] an important achievement and a very significant advance for patients suffering from degenerative diseases. These disease-specific iPS cells are invaluable tools that will allow researchers to watch the development diseases in petri dishes, outside of the patients. And we have good reason to believe that this will make it possible to find new treatments, and eventually drugs, to slow or even stop the course of a number of diseases." Advances that reduce the cost of research and increase efficiency will speed further progress. This is an excellent example of the type. |
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| Via Time: "Another more complicated possibility [for women's longevity] is that women have two X chromosomes, while men have one. (Men have an X and a Y.) When cells go through aging and damage, they have a choice in terms of genes - either on one X chromosome or the other. Consider it this way: you have a population of cells, all aging together. In some cells, the genes on one X chromosome are active; in other cells, by chance, the same set of genes, with different variations, are active on the other X chromosome. Don't forget, we all have the same genes - the reason we differ is because we express different variations of those genes, like different colors of a car. Now, if one set of variations provides a survival advantage for the cells versus another, then the cells with the advantage will persist while the other ones will die off, leaving behind more cells with the genes on the more advantageous X chromosome. So, in women, cells can perhaps be protected by a slightly better variation of a gene on the second X chromosome. Men don't have this luxury and don't get this choice." |
| From the Hartford Advocate: "Transhumanism is the idea that it's OK to transcend the limitations of the body and brain ... Technologies, both large and small, could radically change the human experience. The mind reels with possibilities. Could we become cyborgs, with circuitry and metallic components seamlessly integrated into our bodies? Will there be nano-machines with artificial intelligence coursing through our bodies, fixing medical problems? Will we be able to dump our consciousness into computers or other machines? ... The possibilities are endless but, at least for now, human lives are not. ... Slowing body degeneration is a modest goal, and doesn't go far enough for some national anti-aging researchers. Aubrey de Grey, an energetic Englishman with a ZZ Top-length beard, is the chief researcher and evangelist for an anti-aging movement that views aging as a disease that can be cured, and cured soon. ... I think we have a 50 percent chance of getting there in around 25 years, so long as the early proof-of-concept work in mice is well-enough funded for the next 10 years or so." |
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