[mage lang=”en|es|fr|en” source=”flickr”]anti aging telomerase enzyme[/mage]
[mage lang=”en|es|fr|en” source=”flickr”]telomerase meditation[/mage]
[mage lang=”en|es|fr|en” source=”flickr”]telomerase vaccine[/mage]
[mage lang=”en|es|fr|en” source=”flickr”]telomerase enzyme supplement[/mage]
Telezyme – Telomerase Enzyme supplement that maintains your telomeres
[mage lang=”en|es|fr|en” source=”flickr”]telomerase in mice[/mage]
Watch this remarkable video from ABC Television showing the lab results of two mice.
One was treated with a telomerase suppliment and the other was not. Both mice are the same age and you can see the results of the mouse that was treated showing signs of age reversal.
The mouse’s hair is growing back from where it was once going bald. The grey hairs have been replaced with normal color hair of a younger mouse.
This holds a great deal of promise for human response to telomere suppliment treatments.
Elizabeth Blackburn Part 1 The Roles of Telomeres and Telomerase
[mage lang=”en|es|fr|en” source=”flickr”]telomerase cells[/mage]
what enzyme is present in cancer cells, which, scientists believe, allows the cancer cells to keep growing ?
morphogen, oxytocin, glucagon, telomerase
In normal cells, the telomeres (segment of DNA at the end of the chromosomes) shorten following each cell division thus limiting the life span of the cell. Due to the nature of the lagging strand after each cell division some DNA is lost, once the telomeres are gone, slowly genes of the chromosome disappear until the point that the cell cannot make proteins that it needs to survive, then the cell dies. This is very important in cell ageing. Most fully differentiated somatic cells do not express the enzyme, however, for some reason cancer cells do, thus allowing them to be immortal and replicate indefinetly
Elizabeth Blackburn Part 3 Stress, Telomeres and Telomerase in Humans
[mage lang=”en|es|fr|en” source=”flickr”]telomerase detection[/mage]
[mage lang=”en|es|fr|en” source=”flickr”]telomerase source[/mage]
James Roche Cassidy joins as head of translational medicine – Oncology Nutley, NJ, June 27, 2011 / PRNewswire / – Roche announced today James (Jim) Cassidy, MD, PhD, Roche will join on 1 July as head of translational medicine in oncology discovery and translational area (DTA) pharmaceutical research and early development (Pred). "We are very pleased to join Jim Roche," said Mike Burgess, MD, Ph.D., Global Director, DTA oncology and head of the large molecule …
[mage lang=”en|es|fr|en” source=”flickr”]telomerase process[/mage]
Could increased cell senescence be avoided during healing process by activating the telomerase gene?
During a healing process, our cells divide to repair a damaged area of our body. Telomere sequences are therefore shortened by this process, reducing the lifespan of the newly created cells.
Theoretically, could this be avoided by enabling the telomerase gene in the cells as they reproduce and then disabled upon successful completion of the process or would it be impossible to disable the gene in such a large amount of cells?
(Obviously the cells would need to be monitored to ensure that any defective cells are removed to avoid cancer developing.)
I think, theoretically, this may be feasible. But remember that the effect of activating the telomerase doesn’t apply to all cells. Our body is composed of so many complex tissues and cells. An effect on one cell doesn’t necessarily mean the same effect to all other cells.
Yes, I agree that you must first remove any defective cells to avoid cancer development since activation of telomerase makes some cells immortal (that is, if there are cancer cells, it will multiply and live forever making it hard to destroy them). However, detection of defective cells involves a very tedious and complex process and you might end up destroying the good cells.
Besides, our body needs cell senescence. The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons. Senescence is not universal, and scientific evidence suggests that cellular senescence evolved in certain species as a mechanism to prevent the onset of cancer. In a few simple species, senescence is negligible and cannot be detected. All such species have no “post-mitotic” cells; they reduce the effect of damaging free radicals by cell division and dilution.
These are just my thoughts. Please feel free to correct me if I misunderstood some of the terms.
What’s a Telomere and Why is it Important to the Aging Process