While it is commonly known that mammals, after a certain young age, will never regenerate or increase the number of motor neurons that we have. Brain and other neurons regenerate for life, but motor neurons are a special type. However, the zebrafish is one animal that can regenerate new motor neurons throughout its life.
By blocking a signal protein called Notch 1, laboratory models suggest that production of motor neurons could be increased, and thus regeneration. Progenitor cells, more specifically, are what they are targeting. Mammals, including humans have these which can turn into motor neurons, however, as it stands, there's nothing to tell them to form motor neurons. With the blockage of Notch 1, researchers are hopeful that they can stimulate the growth of progenitor cells into motor neurons for regeneration of damaged neurons that have led to paralysis.
Work on some knowledge here:
http://www.spinalcordinjury-paralysis.org/research/2012/03/07/fish-model-suggests-motor-neuron-regeneration
For The Cure
Thursday, March 8, 2012
Monday, March 5, 2012
Old Hypothesis Ruled Out for Cause of M.S.
Multiple Sclerosis was once thought to be caused by a break down of oligodendocytes, which create the myelin sheathing that surrounds nerves. This myelin acts as an insulator on our nerve cells, called neurons, that help to transmit nervous impulses at a faster, more efficient rate. And this break down in turn created a break down in the myelin from an autoimmune response that broke down the myelin. Essentially, the body was attacking its own myelin.
However, that hypothesis has been refuted through experiments conducted on mice. Researchers, through genetic manipulation, damaged oligodendrocytes and waited for the immune response; but the response never came. Therefore, it has been posited that the damaging of oligodendrocytes did not lead to an autoimmune response, a reaction, but that the autoimmune response was actually the cause independent of oligodendrocyte breakdown.
Look into this process at this locale:
http://www.medicalnewstoday.com/releases/242205.php
However, that hypothesis has been refuted through experiments conducted on mice. Researchers, through genetic manipulation, damaged oligodendrocytes and waited for the immune response; but the response never came. Therefore, it has been posited that the damaging of oligodendrocytes did not lead to an autoimmune response, a reaction, but that the autoimmune response was actually the cause independent of oligodendrocyte breakdown.
Look into this process at this locale:
http://www.medicalnewstoday.com/releases/242205.php
Tuesday, February 28, 2012
A Map Toward the Road to an M.S. Cure? This is Way More Than Some Yellow Brick Road
The Scripps Research Institute has discovered a receptor, S1P1 receptors to be more precise, that could be a road map to lead the way towards an M.S. cure as well as cures for other diseases. Well, it's actually more of a fully enhanced, virtual image at this time, however this receptor is critical in the onset and progression of multiple sclerosis and other diseases. Yet, don't let that sway your view on this receptor, it is vital towards good health, such as the release of white blood cells.
Understanding its structure is pivotal to understanding certain facets of health, as well as, sickness. Small changes within this structure can have profound effects. So, scientists are hopeful that the study of S1P1 will not only let them determine the onset and spread of diseases in and of itself, but also to similar other structures that play a part. Why only know the road that you're on, when you can know the entire countryside?
The hopes are that one day, researchers and the medical industry will know exactly how to decimate this deadly disease along with others in which S1P1 plays a part.
There's so much more for you to get into here:
http://www.scripps.edu/newsandviews/e_20120227/rosen-stevens.html
Understanding its structure is pivotal to understanding certain facets of health, as well as, sickness. Small changes within this structure can have profound effects. So, scientists are hopeful that the study of S1P1 will not only let them determine the onset and spread of diseases in and of itself, but also to similar other structures that play a part. Why only know the road that you're on, when you can know the entire countryside?
The hopes are that one day, researchers and the medical industry will know exactly how to decimate this deadly disease along with others in which S1P1 plays a part.
There's so much more for you to get into here:
http://www.scripps.edu/newsandviews/e_20120227/rosen-stevens.html
Tuesday, February 21, 2012
Further Findings Into Stopping Muscular Dystrophy
Way back last month, I wrote about a protein known as Dystrophin that was lacking in those with Duchenne and how researchers had found a way to produce more of this protein to help those with the disease. Well, even more good news is occurring as researchers have now identified a protein known as Biglycan. This protein stabilizes synapses at the neuromuscular junction between muscle and bone. This helps us control movement as well as ensure the health of motor neurons and muscles alike.
The way this relates to Dystrophin is that Biglycan promotes Utrophin which takes over for Dystrophin. Therefore, both promoting Dystrophin and also Utrophin can be a double pronged attack that could someday lead to the end of Duchenne and other types of muscular dystrophy.
Another role of Biglycan is that it binds and targets an receptor enzyme known as MuSK that regulates the building and stability of the neuromuscular junction.
This should lead to testing on animal models in the near future; a necessary precursor to human trials.
Soak up some knowledge here:
http://www.medicalnewstoday.com/releases/241680.php
The way this relates to Dystrophin is that Biglycan promotes Utrophin which takes over for Dystrophin. Therefore, both promoting Dystrophin and also Utrophin can be a double pronged attack that could someday lead to the end of Duchenne and other types of muscular dystrophy.
Another role of Biglycan is that it binds and targets an receptor enzyme known as MuSK that regulates the building and stability of the neuromuscular junction.
This should lead to testing on animal models in the near future; a necessary precursor to human trials.
Soak up some knowledge here:
http://www.medicalnewstoday.com/releases/241680.php
Thursday, February 16, 2012
New Blood Test Could Act as Biopsy Lite
Scientists that the Scripps Research Institute have discovered a way to use an advanced blood test to detect CTC's, or circulating tumor cells, that break away from solid tumors in the blood stream. It will allow doctors to monitor, predict, and understand the progression of tumors much better than they do at this time.
The HD-CTC test isolates cancer cells in differentiation from red and white blood cells that are healthy. They then use digital microscopes and image-processing algorithms to study the morphologies, which are the size and shape of the cells to fully differentiate the cancer cells from the regular cells.
5 new studies from California and the Netherlands have shown the accuracy and effectiveness both in identifying cancer cells but also one day they hope to be able to early diagnose patients with cancer as well as improving the research within a lab setting.
Discover the wonders here:
http://www.scripps.edu/news/press/20120202kuhn.html
The HD-CTC test isolates cancer cells in differentiation from red and white blood cells that are healthy. They then use digital microscopes and image-processing algorithms to study the morphologies, which are the size and shape of the cells to fully differentiate the cancer cells from the regular cells.
5 new studies from California and the Netherlands have shown the accuracy and effectiveness both in identifying cancer cells but also one day they hope to be able to early diagnose patients with cancer as well as improving the research within a lab setting.
Discover the wonders here:
http://www.scripps.edu/news/press/20120202kuhn.html
Tuesday, February 14, 2012
Who Would Have Thought; Using Your Own Heart Cells Could Help Repair It?
Ok, enough with the sarcasm, this is actually good news. Researchers have figured a way to use stem cells from your own heart muscle, to help your heart to develop new heart cells after a heart attack. In fact, this will lessen the scars that people have after suffering a myocardial infarction (heart attack). They found that the average patient treated in this manner, lessened their scarring from 24% of the heart, to 12% of the heart. Approximately a 50% reduction in scar size. This took one year of treatment and healing of course.
This news challenges the held belief that once tissue of the heart was lost, it was gone permanently and the scarring was there to stay. Apparently, that has changed, not just in theory, but in applied reality as well. The technology is currently under application of a patent and may soon become a regular treatment option. No timetable has been set, but that still doesn't take into account the good news.
Extra, Extra, Read ALL ABOUT IT:
http://www.sciencedaily.com/releases/2012/02/120213185441.htm
This news challenges the held belief that once tissue of the heart was lost, it was gone permanently and the scarring was there to stay. Apparently, that has changed, not just in theory, but in applied reality as well. The technology is currently under application of a patent and may soon become a regular treatment option. No timetable has been set, but that still doesn't take into account the good news.
Extra, Extra, Read ALL ABOUT IT:
http://www.sciencedaily.com/releases/2012/02/120213185441.htm
Friday, February 3, 2012
National Cancer Day is Upon US
Short post today. Let's all remember those that have Cancer, have lost the fight against Cancer, and keep them in our hearts, prayers, and minds. We're going to keep up the fight against this disease and we're going to beat it through helping those that research the cure. Remember that we can beat this on National Cancer Day. If you know someone, give them a call, or better yet, see them if you can and show your support. Goodnight all.
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