As a general rule, hurdling a hurdle presents you with another, different hurdle. Such is progress - but the space between two hurdles is better than the one you just came from. Knowing that the space beyond is better yet, off you go again, at a run and aimed at the next challenge that has presented itself. In that spirit, here is a slice of the way in which science is just this - or, in the words of a cynic, "something like knocking down an infinite series of unevenly spaced brick walls with your head."
Brain cells derived from human embryonic stem cells improved the condition of rats with Parkinson's-like symptoms dramatically, but the treatment caused a significant problem - the appearance of brain tumors - that scientists are now working to solve.
"The results are a real cause for optimism," said Goldman. "These animals with severe Parkinson's symptoms had a dramatically improved outcome after treatment. Now we have a new problem to work on, how to achieve the same benefit without creating tumors. But we expect to be able to solve this problem within the next year or two, using new approaches to cell sorting that we've been developing."
Scientists are attempting to produced controlled growth - which is what embryonic stem cells do in nature. Cancer is nothing more than uncontrolled growth; a sign that the work to be done here is (much as expected in the scientific community, if not in the popular press) much more than simply dropping cells into place and standing back to watch. Regenerating the neurons that die in Parkinson's disease is more than anyone could do just a few short years ago - and a solution to the problem of cancerous growth in the controlled use of embryonic stem cells will come in the years ahead. Hurdles after hurdles, and each leap to a place better than the last.
Two models have been proposed for how calorie restriction (CR) enhances replicative longevity in yeast: (i) suppression of rDNA recombination through activation of the sirtuin protein deacetylase Sir2 or (ii) decreased activity of the nutrient-responsive kinases Sch9 and TOR. We report here that CR increases lifespan independently of all Sir2-family proteins in yeast. Furthermore, we demonstrate that nicotinamide, an inhibitor of Sir2-mediated deacetylation, interferes with lifespan extension from CR, but does so independent of Sir2, Hst1, Hst2, and Hst4. We also find that 5 mm nicotinamide, a concentration sufficient to inhibit other sirtuins, does not phenocopy deletion of HST3. Thus, we propose that lifespan extension by CR is independent of sirtuins and that nicotinamide has sirtuin-independent effects on lifespan extension by CR.
It was coming time for another round of stirring the calorie restriction research pot, and thereby complicating the picture. Here we have a claim that sirtuins really aren't the root mechanism for life extension via CR in yeast. All sorts of interesting and complicating findings are being made in yeast - not to mention human genetic studies - with regard to the mechanisms of calorie restriction; it is by no means certain that sirtuins are the end of the story in mammals, for all that Sirtris and others are achieving good results. The pool of knowledge is growing rapidly, however, and answers will be found.