Dr. See-Jins Lab at John Hopkins University School of Medicine has been sucessful in creating a "mighty mutant mice". His lab has come out with a "genetic recipe" of creating a mice which will have 4 times muscle mass than the normal mice.BRAVO!!!
This is clearly evident from the picture on the left. A normal mice and a strong, mutant, muscular mice is seen in every photo.
These mice differ from the normal mice by having almost 73% excess muscle build. The genetic recipe consists of suppressing one protein and overexpressing the other.
These "super-sized, heavy build" mice cannot produce a protein called Myostatin and can produce too much of Follistatin. It is this combined genetic supressiona nd overexpression that has resulted in these mutant mice.
Though the possible molecular mechanism is yet to be elucidated, Dr. See-Jin suggests that Myostatin might restrict muscle development and Follistatin prevents Myostatin from action ,works well in the absence of Myostatin. So he feels there might be more that one mechanism of follistatins action.
Another point to be noted here is that Myostatin is virtually undetectable in Humans and so more targets of Follistatins need to be identified in Humans.But once these targets are identified, then new drugs for muscle development could be produced and this would be hardly resisted by any of the present generation Athletes.
So with this discovery will we have 80 year old Schwazeneggars? The answer from the discoverer was "No".
He says that if new drugs would be discovered then these would prevent muscle weakness in elderly people as well could treat various symptoms of AIDS, Duchennes,Muscle Wasting etc.
However this discovery could pave way for more muscular animals like cattle or sheep to have more muscular and tastier meat.
However there is still a long way to go. But just imagine what would happen if this kind of drug would be available Over the Counter to the public !!!!
Please do send me your comments.
2 comments:
hey... if we need to post to this blog... we needs right to do that... You can allow the people who can post to this blog in your blog settings...
Here is a post that you can put up on the blog for now...
Antibiotics share killing mechanism
Three distinct classes of antibiotics kill bacterial cells with reactive oxygen species
All three major classes of antibiotics share a single mechanism for killing bacterial cells, reports this week's Cell. Although these drugs initially have different effects on bacterial cells, they all converge on a pathway that kills cells by generating highly reactive free radicals.
The results suggest new ways of improving antibiotic effectiveness, the authors say.
"This is one of those neat, unpredictable findings," said Scott Singleton of the University of North Carolina at Chapel Hill, who was not involved in the study. "It's really not just a linear extension of what we knew before."
Drugs that kill bacteria, called bactericidal antibiotics, are grouped into three classes, depending on how the drug damages bacterial cells. One class inhibits DNA replication and repair, another inhibits protein synthesis, and the third prevents cell-wall turnover. "Prior thinking was that cell death arose principally from those interactions and that each [class] acted differently," said senior author James Collins of Boston University.
Earlier this year, Collins's group reported that one class of antibiotics induces production of reactive oxygen species, especially hydroxyl radicals, which cause bacterial cell death by inducing oxidative DNA and protein damage. To see if the other two classes might damage bacteria in the same way, the researchers -- led by Michael Kohanski and Daniel Dwyer, both of Boston University -- exposed Escherichia coli to one of each of the three classes of bactericidal antibiotics.
Using a dye that fluoresces in the presence of hydroxyl radicals, they found that all three antibiotics produced free radicals in E. coli. They also tested antibiotics in another bacterium, Staphylococcus aureus, with the same results. However, when the researchers conducted the same experiment with five bacteriostatic antibiotics, which inhibit bacterial growth without killing the cells, they found no increase in hydroxyl radical levels.
To show that the hydroxyl radicals were responsible for bacterial cell death, the researchers blocked radical formation in one experiment and treated the cells with an antioxidant in another. In both cases, stopping free radical activity increased survival of bacteria treated with any of the three types of antibiotics.
The authors also found that core components of bacterial metabolism -- including the tricarboxylic acid (TCA) cycle and the respiratory electron transport chain -- are required to generate these hydroxyl radicals, showing that all three antibiotics generate hydroxyl radicals through the same mechanism.
Their results do not discount the established mechanisms through which each antibiotic class acts, Collins told The Scientist. But, "in addition to these separate mechanisms, there is a common one that's being induced in all cases."
"It is really quite new and quite startling," said Graham Walker of the Massachusetts Institute of Technology, who was not involved in the work. "This is certainly not what the textbooks say" about antibacterial mechanisms, he said.
The findings help explain results from several studies over the past few decades, Singleton added. Previous studies discovered, for example, that disabling the bacterial DNA damage response can increase the effectiveness of two types of antibiotics. Also, studies found that antibiotic-resistant bacterial mutants had dysfunctions in proteins that generate reactive oxygen species.
Researchers may be able to develop drugs to improve current antibiotics, either by increasing hydroxyl radical production in bacteria or by blocking the bacteria's own damage response systems, Collins said. That might "make antibiotics more effective, which would allow them to work at a lower dose," Singleton agreed.
However, the antibiotic concentrations used in the study were relatively low, said Kim Lewis of Northeastern University in Boston, who was not involved in the work, and it's possible that other mechanisms of cell death might be more important at higher drug concentrations. "But clearly what they discovered seems to be an important component of death," he said.
Ok Thank you sir for the suggestion. I will surely look for that option. Thanks again for that lovely post. I will put it up on the blog.
Thanks.
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