As the Smithsonian notes, "It won't be long before surgeons routinely install replacement body parts created in the laboratory. ... Anthony Atala works in the body shop of the future. ... he and his colleagues use human cells to grow muscles, blood vessels, skin and even a complete urinary bladder. Much of the work is experimental and hasn't yet been tested in human patients, but Atala has implanted laboratory-grown bladders into more than two dozen children and young adults born with defective bladders that don't empty properly, a condition that can cause kidney damage. The bladders were the first lab-generated human organs implanted in people. If they continue to perform well in clinical tests, the treatment may become standard not only for birth defects of the bladder but also for bladder cancer and other conditions. ... Regenerative medicine's once-wild ideas are fast becoming reality. Late last year, Organovo, a biotech company in San Diego, began distributing the first commercially available body-part printer. Yes, you read correctly: a printer for body parts. Using the same idea as an ink-jet printer, it jets laser-guided droplets of cells and scaffold material onto a movable platform. With each pass of the printer head, the platform sinks, and the deposited material gradually builds up a 3-D piece of tissue. Regenerative medicine laboratories around the world have relied on the printer to generate pieces of skin, muscle and blood vessels. Atala's lab has used the technology to construct a two-chambered mouse-size heart in about 40 minutes."

View the Article Under Discussion: http://www.smithsonianmag.com/specialsections/40th-anniversary/97123514.html

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Some people have demonstrably better mitochondrial DNA, others worse. Here, a study shows correlations between some variants and old-age frailty: "Mitochondria contribute to the dynamics of cellular metabolism, the production of reactive oxygen species, and apoptotic pathways. Consequently, mitochondrial function has been hypothesized to influence functional decline and vulnerability to disease in later life. ... mitochondrial DNA (mtDNA) variation was compared in frail and non-frail older adults. Associations of selected SNPs with a muscle strength phenotype were also explored. Participants were selected from the Cardiovascular Health Study (CHS), a population-based observational study ... Three mtDNA SNPs were statistically significantly associated with frailty across all pilot participants or in sex-stratified comparisons." Given the degree to which mitochondrial composition correlates with species life span differences, we should not be surprised to find some variations significant in human life span.

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883558/

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Researchers are gathering evidence to suggest that stem cells from the old are less useful when transplanted - which means that some form of repair or other manipulations may need to be included in future stem cell therapies for the degenerative conditions of aging: "Clinical trials of cardiac cell therapy have indicated limited benefits in aging patients, even though preclinical studies using young animals consistently reported significant improvements. Animal studies have demonstrated reduced efficacy of donor cells isolated from older individuals. Here, we evaluated the effects of donor age on the function of human mesenchymal stem cells (hMSCs) in the context of cell therapy for ischemic cardiomyopathy. ... The regenerative capacity of hMSCs was significantly influenced by age. Transplanting young hMSCs improved functional outcomes after an MI by preventing matrix degradation and promoting angiogenesis. The clinical implication is that aged patients require an optimized source of stem cells for treatment."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20583954

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Crayfish species, like lobsters, appear not to age in any easily measurable way. As for the study of other long-lived species, perhaps there is something to be learned here: "The marbled crayfish is an emerging laboratory model for development, epigenetics and toxicology that produces up to 400 genetically identical siblings per batch. It is easily cultured, has an adult size of 4-9 cm, a generation time of 6-7 months and a life span of 2-3 years. Experimental data and biological peculiarities like isogenicity, direct development, indeterminate growth, high regeneration capacity and negligible senescence suggest that the marbled crayfish is particularly suitable to investigate the dependency of ageing and longevity from non-genetic factors such as stochastic developmental variation, allocation of metabolic resources, damage and repair, caloric restriction and social stress. It is also well applicable to examine alterations of the epigenetic code with increasing age and to identify mechanisms that keep stem cells active until old age. As a representative of the sparsely investigated crustaceans and of animals with indeterminate growth and extended brood care the marbled crayfish may even contribute to evolutionary theories of ageing and longevity. Some relatives are recommended as substitutes for investigation of topics, for which the marbled crayfish is less suitable like genetics of ageing and achievement of life spans of decades under conditions of low food and low temperature. Research on ageing in the marbled crayfish and its relatives is of practical relevance for crustacean fisheries and aquaculture and may offer starting points for the development of novel anti-ageing interventions in humans."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20582627

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Understanding the physical basis of human memory will enable therapies to both enhance youthful memory and reverse its decline with age. From ScienceDaily, an example of present investigations into the biology of memory: "We found one of the key proteins involved in the process of memory and learning. This protein is present in the part of the brain in which memories are stored. We have found that in order for any memory to be laid down this protein, called the M3-muscarinic receptor, has to be activated. We have also determined that this protein undergoes a very specific change during the formation of a memory - and that this change is an essential part of memory formation. In this regard our study reveals at least one of the molecular mechanisms that are operating in the brain when we form a memory and as such this represents a major break through in our understanding of how we lay down memories. This finding is not only interesting in its own right but has important clinical implications. One of the major symptoms of Alzheimer's disease is memory loss. Our study identifies one of the key processes involved in memory and learning and we state in the paper that drugs designed to target the protein identified in our study would be of benefit in treating Alzheimer's disease."

View the Article Under Discussion: http://www.sciencedaily.com/releases/2010/06/100628101450.htm

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Another study to show that transplanting young ovaries into old mice extends life quite significantly: "successful ovarian transplants increased the lifespan of the mice by more than 40% ... All the mice in both experiments that had received transplants resumed the normal reproductive behaviour of young mice. They showed interest in male mice, mated and some had pups. Normally, old mice stay in the corner of the cage and don't move much, but the activity of mice that had had ovarian transplants was transformed into that of younger mice and they resumed quick movements. Furthermore, the lifespan of the mice who received young ovaries was much longer than that of the control mice: the mice that had received two ovaries lived for an average of 915 days, and the mice that had received one ovary, for an average of 877 days. The newest of our data show the life span of mice that received transplants of young ovaries was increased by more than 40%. ... The average normal lifespan for this particular breed of mice [is] 548 days. ... it was not known why the ovarian transplant increased the lifespan of the mice, but it might be because the transplants were prompting the continuation of normal hormonal functions."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-06/esoh-otr062810.php

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Following on from a demonstration of decellularized rat lungs, another team has produced similar work: "Researchers have been able to create tiny mouse lungs in the lab that are able to breathe. The lungs were created with stem cells and attached to a ventilator. ... They used a technique called decellularization, similar to the method used to create a beating mouse heart in a different lab at the University of Minnesota in 2008. In the cancer center, they took a mouse lung and stripped away all its cells. Then, injected the natural framework with stem cells. At first they used fetal mouse lung cells, but this year they had another breakthrough using adult stem cells called 'induced pluriopotent stem cells.' ... That's basically a cell that we can take from anybody and re-program to act like an embryonic stem cell ... The hope is one day human lungs could be re-created for transplant with a greater chance of success. Right now, there is no tissue matching for lung transplants. ... The beauty of that is that you can then create a tissue for an organ that's transplantable that is derived from the patient and therefore would not be recognized as foreign by the immune system and not rejected. By adding the ventilator to make the lungs breathe, the stem cells are further trained to act like lung cells. It's a huge success considering lungs are such complicated organs with some 60 different kinds of cells."

View the Article Under Discussion: http://wcco.com/health/lungs.stem.cells.2.1774895.html

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A review paper: "Mitochondrial disorders can no longer be ignored in most medical disciplines. Such disorders include specific and widespread organ involvement, with tissue degeneration or tumor formation. Primary or secondary actors, mitochondrial dysfunctions also play a role in the aging process. Despite progresses made in identification of their molecular bases, nearly everything remains to be done as regards therapy. Research dealing with mitochondrial physiology and pathology has [greater than 20 years] of history around the world. We are involved, as are many other laboratories, in the challenge of finding ways to fight these diseases. However, our main limitation is the scarcety of animal models required for both understanding the molecular mechanisms underlying the diseases and evaluating therapeutic strategies. This is especially true for diseases due to mutations in mitochondrial DNA (mtDNA), since an authentic genetic model of mtDNA mutations is technically a very difficult task due to both the inability of manipulating the mitochondrial genome of living mammalian cells and to its multicopy nature. This has led researchers in the field to consider the prospect of gene therapy approaches that can roughly be divided into three groups: (1) import of wild-type copies or relevant sections of DNA or RNA into mitochondria, (2) manipulation of mitochondrial genetic content, and (3) rescue of a defect by expression of an engineered gene product from the nucleus (allotopic or xenotropic expression)."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20571866

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A new popular science book on the manipulation of metabolism to slow aging, the author inspired by the Longevity Dividend initiative: "No scientific advances inspire more media hype than ones in gerontology, the study of aging. Even the crustiest editors have been known to turn giddy when new light is shed on the topic and take to blowing raspberries at the Reaper with headlines suggesting immortality elixirs are just around the corner. Biologists aren't so easily wowed, though, and before the mid-1990s they generally saw gerontology as a dismal bog where once-promising peers sank out of sight, or worse, re-emerged clutching beakers of snake oil. ... Studying the details of this inexorable, chaotic decay seemed a waste of time to most life scientists. ... Then in 1988 a miracle happened - the University of Colorado's Thomas Johnson reported that a gene mutation in nematodes could more than double their life spans. Five years later, Cynthia Kenyon at the University of California, San Francisco, nailed a similar worm 'gerontogene' dubbed daf-2. These flabbergasting discoveries revealed that not everything about aging is intractable chaos - worms, at least, apparently possessed gene-encoded modules poised to oppose the ravages of advancing age when activated by a single mutation. Optimists soon speculated that similar modules exist in mammals."

View the Article Under Discussion: http://www.the-scientist.com/news/display/57510/

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From the MIT Technology Review: "Rats genetically engineered to lose their sight can be protected from blindness by injections of human neural stem cells ... a startup in Palo Alto, CA, plans to use the positive results to file for approval from the U.S. Food and Drug Administration to begin human trials. The company is already testing the cells in children with a rare, fatal brain disorder called Batten's disease. ... The company's cells are isolated from human fetal tissue and then grown in culture. To determine whether these cells can protect against retinal degeneration, scientists studied rats that were genetically engineered to progressively lose their photoreceptors - cells in the retina that convert light into neural signals. These animals are commonly used to model macular degeneration and retinitis pigmentosa, two major causes of blindness that result from cell loss in the retina. Researchers injected about 100,000 cells into the animals' eyes when the rats were 21 days old. ... the cells migrate over time, forming a layer between the photoreceptors and a layer of tissue called the retinal pigment epithelium, cells which nourish and support the photoreceptors. ... the cells protected vision in the part of the retina in which they were implanted."

View the Article Under Discussion: http://www.technologyreview.com/biomedicine/25647/?a=f

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Scientific American looks at the state of viral cancer therapies: "The adapted virus that immunized hundreds of millions of people against smallpox has now been enlisted in the war on cancer. Vaccinia poxvirus joins a herpesvirus and a host of other pathogens on a growing list of engineered viruses entering late-stage human testing against cancer. ... After a decade of development of so-called oncolytic viruses, the newest strains hold the most promise yet ... In a two-pronged attack, these viruses specifically target tumor cells while delivering a cargo of immune-boosting genes. In contrast, viruses that cause cancer, such as the human papillomavirus that is responsible for most cases of cervical cancer, disrupt a cell's genome, thereby triggering out-of-control growth. When the engineered viruses recognize and infect cancer cells, they replicate and sometimes destroy their hosts. Several of the viruses also release the gene for granulocyte-macrophage colony-stimulating factor (GM-CSF) an immune system protein. The GM-CSF attracts a swarm of white blood cells and other immune system operatives that mount a further attack on the tumor. ... The vaccinia virus has been developed by the biotechnology company Jennerex ... Later this year, the company plans to launch a phase III clinical trial in advanced liver cancer patients, in which the virus will be added to standard antibody treatment."

View the Article Under Discussion: http://www.scientificamerican.com/article.cfm?id=tumor-virus-vaccines

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A novel methodology in regenerative medicine: "The objective was to evaluate the utility of cryo-preserved human amniotic membrane (HAM) as a support for repairing human articular cartilage injuries, which have a very limited capacity for self-healing ... The results [show] that cryo-preserved HAM is useful as a scaffold for growing human chondrocytes in cell therapy and for repairing human cartilage injuries. ... It provides a more regular surface and fills in the cavities and fissures ... The authors cultivated the chondrocytes (cells that form part of the cartilaginous tissue), isolated from human articular cartilage, on the amniotic membrane over a period of three and four weeks. The amniotic membranes were used to develop 44 repair models of arthritic human articular cartilage in vitro, which was assessed between four and 16 weeks later. The HAM also bonds well with the native cartilage. ... In some models, we could not differentiate between where the native tissue stopped and the neo-synthesised tissue began. ... This tissue had a fibrous appearance and high cellular density (cellularity), which in some cases was greater than that of the actual native cartilage."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-06/f-sf-amu062310.php

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