Regeneration of living tissue in situ and a surprising observation in antisenescence.

07 May 2014

Ordinarily if something happens that causes a chunk of your body to be removed (like, say, a shark bite) there isn't a whole lot that can be done to fill it back in. Scar tissue will form over the wound and skin will eventually cover over it, but that doesn't cause lost muscle and bone to come back. It's kind of scary, when you think about it - what's lost is lost. But that may not be the caes for much longer. A research team active in the field of regenerative medicine at the McGowan Institute for Regenerative Medicine at the University of Pittsburgh have developed a technique in which traumatically lost muscle tissue has been grown back in human subjects. The procedure involves surgery to remove scar tissue that has built up at the trauma site and the implantation of something they refer to as an mammalian extracellular matrix comprised of collagen, structural proteins and polysaccharides (shades of William Gibson, anyone?) upon which cells grow, organize, and connect to one another. Afterward a physical therapy regimen is instituted; the additional metabolic and structural stresses induce the patient's stem cells to infiltrate the MEM, take root, and differentiate into muscle cells. Exercise is continued so that the newly rooted muscle cells will have physical forces to organize them into bundles (because form follows function) and coax them to adhere to one another in a self-reinforcing system. Three of the test subjects suffered injuries during military service; the other two were injured in skiing accidents. Another ten patients are still in process. All of them lost between 60 and 90 percent of their leg muscles and face amputation if the procedure does not work. Increased quality of life aside, three of the five test subjects specifically mentioned regained at least twenty percent of their muscular strength, and all show noticable signs of muscular regeneration.

In other news, a paper was published late last month in the online edition of the Proceedings of the National Academy of Sciences describing the efforts of a resarch team at the Laboratory for Stem Cells and Tissue Engineering at Columbia University. The team, lead by Dr. Gordana Vunjak-Novakovic successfully grew cartilage in bulk quantities in vitro out of mesenchymal stem cells. Cartilage is a pretty simple tissue, structurally speaking - it's comprised of only one kind of cell, it's load-bearing (which means that physics underlying it are fairly well understoood), it doesn't have any nerves or blood vessels running through it, but it's also tricky to grow. Dr. Vunjak-Novakovic's team used a novel technique to cause the stem cells to differentiate and grow in the desired fashion by forcing them to condense and self-organize in an environment much closer to the inside of the body than previously attempted. When tested, the newly cultured cartilage was structurally and mechanically much closer to naturally grown cartilage in situ, with a corresponding degree of compressive strength and amount of lubrication between biosurfaces. Next on their development roadmap is attempting to implant some of the cultured cartilage in a living being. Third is an accidental discovery in the field of anti-senescence, or the combatting of the aging process to prolong health, youth and lifespan. A team at Stanford University discovered by accident that transfusing blood from younger mice into older mice reversed some of the cognitive and physiological deficits that come from aging. The performance of senescent mice (near the end of their natural lifespan) on tests of memory and learning improved markedly, and were reflected in their ability to learn water mazes and associate changes in their environments with electric shocks. The brains of the mice were observed to have stronger dendritic connections than they should have at that age and higher mesurable levels of neurotransmitters associated with the learning process. It was observed in a third experimental series that the senescent test mice were somewhat more capable of extended exercise than they otherwise would have been. It is thought at this time that a protein called Growth Differentiation Factor 11 (common to both humans and mice), which normally occurs in higher concentrations in younger specimens than older ones is implicated in these structural and biochemical alterations. While the evidence for the cognitive improvement is a little sketchy (there are other biochemical factors that could have been at work) there is evidence that higher serum levels of GDF11 were implicated in the physical improvements. It was further observed that heating the mouse blood to a higher temperature than normal (just how high is not mentioned) seems to destroy the properties of the mouse blood in question. The research team hopes to begin human trials of GDF11 concentration modulation techniques within five years.