Way too hot!
Hi everyone! Long time no posting... Tsk. Sorry about that! Living life a little bit too much I guess :) So, ummm, it's really hot here in Vancouver. Seriously hot. It went up to 35 degrees yesterday. Unbearable when you can't have AC! My condo complex doesn't allow for the unsightly look of AC units in the windows which really warrants running for council to change that considering we have this weather for another week.
A new thing happened yesterday. At noon, my body just quit. I could not stay awake or move really and just crashed out on the couch for about an hour. I felt better afterwards and thank god I wasen't working, but it was a bit unnerving. I haven't felt that before unless it was when mowing the lawn or exerting energy in some way. Weird stuff.
I have a few medical postings that I'll try to get to in the next week! Hope your all enjoying your summers.
Tuesday, July 7, 2009
Okay, I'll admit it.
A new thing happened yesterday. At noon, my body just quit. I could not stay awake or move really and just crashed out on the couch for about an hour. I felt better afterwards and thank god I wasen't working, but it was a bit unnerving. I haven't felt that before unless it was when mowing the lawn or exerting energy in some way. Weird stuff.
I have a few medical postings that I'll try to get to in the next week! Hope your all enjoying your summers.
Okay, I'll admit it.
I joined the masses and am now on Twitter. My name there is of course RestPeriod. Come find me if you like! I'm mostly just randomly posting about the stuff in my life related to my MS. :) Hope to see you there!
Friday, July 3, 2009
Why repair of brain's wiring fails
Why repair of brain's wiring fails
That darn Myelin... why can't it just repair it's self? Perhaps they've found out why!
"The investigation, conducted in mice and in human tissue, showed that repair of nerve fibers is hampered by biochemical signals that inhibit the development of cells known as oligodendrocytes, which function as repair workers in the brain.
Oligodendrocytes form a protective sheath, known as myelin, that insulates the fibrous cables, or axons, radiating from nerve cells. In multiple sclerosis, the immune system's T cells and B cells attack oligodendrocytes, ultimately damaging the myelin sheath to the point that the electrical signals transmitted by the axons beneath it are disrupted.
Remarkably, the brain generally is able to recruit fresh, immature oligodendrocytes to the myelin sheath to repair the damage, for a time. This explains why, in the most common form of the disease, known as relapsing remitting MS, the symptoms -- which range from tingling and numbness in the limbs to loss of vision and paralysis -- disappear or are greatly reduced, for some times months or years at a time.
Ultimately, however, the repair process falters and the disease progresses. In their study, the team set out to see if they could determine what was slowing down myelin repair. They lesioned a small region of white matter in healthy mice, then monitored the repair process, examining the tissue after five, 10, and 14 days.
To find out which genes were contributing to three key stages in the repair process – the recruitment of oligodendrocyte precursors to the site of injury, the maturation of those cells into functional oligodendrocytes, and the formation of a new myelin sheath -- they measured the activity of 1,040 genes. All of the genes they studied encode transcription factors, which regulate the activity of other genes. Their experiments showed that 50 transcription factors are working during key steps in myelin repair.
The team then honed in on a gene called Tcf4, because its expression was strong in damaged areas where repair attempts were under way.
Tcf4 is involved in a cascade of biochemical events known as the Wnt (pronounced "wint") pathway, whose importance has been well recognized in normal development of many tissues, including the brain. Until now, however, Wnt had not been linked to myelin production or repair.
"This is the first evidence implicating the Wnt pathway in multiple sclerosis," says lead author Stephen P.J. Fancy, PhD, a postdoctoral fellow in the Rowitch lab. "We consider this an exciting development in our efforts to understand why the repair process often fails in the disease."
Two Genes for MS!
"The investigation, conducted in mice and in human tissue, showed that repair of nerve fibers is hampered by biochemical signals that inhibit the development of cells known as oligodendrocytes, which function as repair workers in the brain.
Oligodendrocytes form a protective sheath, known as myelin, that insulates the fibrous cables, or axons, radiating from nerve cells. In multiple sclerosis, the immune system's T cells and B cells attack oligodendrocytes, ultimately damaging the myelin sheath to the point that the electrical signals transmitted by the axons beneath it are disrupted.
Remarkably, the brain generally is able to recruit fresh, immature oligodendrocytes to the myelin sheath to repair the damage, for a time. This explains why, in the most common form of the disease, known as relapsing remitting MS, the symptoms -- which range from tingling and numbness in the limbs to loss of vision and paralysis -- disappear or are greatly reduced, for some times months or years at a time.
Ultimately, however, the repair process falters and the disease progresses. In their study, the team set out to see if they could determine what was slowing down myelin repair. They lesioned a small region of white matter in healthy mice, then monitored the repair process, examining the tissue after five, 10, and 14 days.
To find out which genes were contributing to three key stages in the repair process – the recruitment of oligodendrocyte precursors to the site of injury, the maturation of those cells into functional oligodendrocytes, and the formation of a new myelin sheath -- they measured the activity of 1,040 genes. All of the genes they studied encode transcription factors, which regulate the activity of other genes. Their experiments showed that 50 transcription factors are working during key steps in myelin repair.
The team then honed in on a gene called Tcf4, because its expression was strong in damaged areas where repair attempts were under way.
Tcf4 is involved in a cascade of biochemical events known as the Wnt (pronounced "wint") pathway, whose importance has been well recognized in normal development of many tissues, including the brain. Until now, however, Wnt had not been linked to myelin production or repair.
"This is the first evidence implicating the Wnt pathway in multiple sclerosis," says lead author Stephen P.J. Fancy, PhD, a postdoctoral fellow in the Rowitch lab. "We consider this an exciting development in our efforts to understand why the repair process often fails in the disease."
Two Genes for MS!
The research is working! Two genes were found to be linked to MS.
"The newly discovered gene locations in chromosomes 12 and 20, offer very promising targets which indicate susceptibility to MS," says Professor Kilpatrick.
"They also reveal a link between genetic susceptibility to MS and other autoimmune diseases including Type 1 diabetes, Rheumatoid Arthritis and Graves' Disease and the also the potential involvement of Vitamin D metabolism in the risk of developing these diseases."
"These results are like the key in the door – leading us to where to look for MS susceptibility," explains Professor Trevor Kilpatrick.
"The newly discovered gene locations in chromosomes 12 and 20, offer very promising targets which indicate susceptibility to MS," says Professor Kilpatrick.
"They also reveal a link between genetic susceptibility to MS and other autoimmune diseases including Type 1 diabetes, Rheumatoid Arthritis and Graves' Disease and the also the potential involvement of Vitamin D metabolism in the risk of developing these diseases."
"These results are like the key in the door – leading us to where to look for MS susceptibility," explains Professor Trevor Kilpatrick.