http://msawarenessgallery.blogspot.com/ I feel like I just found a four-leaf clover.
That's right, laugh if you must, I am a reader of instructions. Measure twice, cut once, I say. I read the warnings on light bulbs and directions on instant oatmeal, that's right---I said it.
Unfortunately, while I am reading page one, my co-horts are usually done with bulb installation, oatmeal cooking, and various assemblies...I find it despicable! Some American, well, some Asian person or other worldly human took the time to compose instructions and by GOD I'm going to honor their hard work.
Uh-hem, I did find page one a bit disturbing, though I swear the room seemed to swirl with laughter as I read...(You might have to enlarge the small print.)
If you doubt that, note that I am now FOLLOWING MY OWN BLOG! Holy Stupidity!
My newest walking aid has arrived via UPS. It was in the biggest box I have ever received. I once worked in a box factory and this definitely would have been an A-Level job.
Where would our life be without boxes? As a child I LOVED boxes, any shape or size. Animals love boxes, just plop a box in the middle of your main room at home and watch what your pet does. (If you have an ant farm...not so much, but maybe.) Bring a sealed box home and set it on the table. Watch your spouse. Throw a box out your car window while passing a police station, drop one in an airport, place one in front of Nordstrom's in Seattle and watch live TV news coverage as a robot attacks it. (Please, I'm not suggesting you do these things, just THINK about the consequences of boxes. I CAN'T go back to prison!) Then there are the holiday boxes that fill us with joy. Okay, you get the idea.
So, yes, I was excited beyond sanity to get this huge box, my friend Angie, who offered to assemble the contents---not so much. You see, Diane thought the ad said the device weighed one pound, later, after telling the world (HER world, much smaller than THE world, but riots are quite bad, coups always possible) about the lightweight creature, but the ad read "100 lbs."
OK, fine, HEY, I have MS, shrinking brain, black holes, lost cells, PLUS I'm FRAKKING FIFTY two; ANYHOO---day one: open the box. Pandora, look out!
"When I was just a little girl
I asked my mother, what will I be?
Will I be pretty, will I be rich?
Here's what she said to me.
Que Sera, Sera,Whatever will be, will be.
The future's not ours, to see.
,Que Sera, Sera,What will be, will be.
When I was young, I fell in love.
I asked my sweetheart what lies ahead.
Will we have rainbows, day after day?
Here's what my sweetheart said.
Que Sera, Sera,Whatever will be, will be.
The future's not ours, to seeQue Sera, Sera.
What will be, will be.
One week my great aunt Vi decided to wallpaper her bedroom in red velvet patterned paper. She and her longtime companion , Ivah, were always wall-papering or painting or in some way redecorating their jointly owned three-apartment house. Aunt Vi also put down red carpet, bought a red velvet chair, red drapes and a RED bulb for her red swag lamp. She had many friends and sitting on the arm of her chair are two Amish, carved wood dolls. Is she great or what?
Why Repair Of Brain's Wiring FailsScienceDaily (July 1, 2009) — Scientists have uncovered new evidence suggesting that damage to nerve cells in people with multiple sclerosis accumulates because the body's natural mechanism for repair of the nerve coating called "myelin" stalls out.The study, published July 1, 2009, in the print edition of Genes & Development, was conducted by scientists at the University of California, San Francisco and University of Cambridge. The research was led by co-senior investigator David Rowitch, MD, PhD, a Howard Hughes Medical Institute investigator at UCSF.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."To glean further evidence about Wnt's role, the researchers hyperactivated the Wnt pathway in the oligodendrocytes of mice, which caused a profound delay in repair. Further analysis suggested that the Wnt pathway activation was creating a roadblock that prolonged oligodendrocyte precursor development."While the animals eventually showed repair, it was delayed compared to normal mice," says Fancy. The researchers also tested human tissue for the presence of Tcf4, and found the protein in areas damaged by MS but not in healthy white matter. Further, the researchers examined available data from another study and found that many signaling molecules of the Wnt pathway are overactive in lesions of patients with MS."This is an important step that we hope will lead to targeted therapies involving the repair process," says co-senior author Robin Franklin of the University of Cambridge.Now the team is starting to examine some of the other genes it found to be active in the myelin repair process, and is developing new mouse models to help test potential therapies that might manipulate the Wnt pathway to improve myelin repair. Given the pathway's role in so many different processes, however, Rowitch cautioned that targeting Wnt could cause unintended side effects.The new work may also have implications for another neurological disease, periventricular leukomalacia, which can lead to cerebral palsy in extremely premature infants, says Rowitch. Recent studies by Rowitch and colleagues show a similar inability of oligodendrocytes to perform their important repair function."The researchers have made an encouraging finding that could open a new window into the cause of failed neural repair in multiple sclerosis," says Dr. Patricia O'Looney, Vice President of BioMedical Research at the National Multiple Sclerosis Society. "Understanding such mechanisms should help advance the efforts to find valuable treatments for this debilitating disease."
The work was funded by the National Multiple Sclerosis Society, the United Kingdom Multiple Sclerosis Society and the National Institutes of Health and Howard Hughes Medical Institute.Co-authors of the study were Sergio E. Baranzini, Karen-Amanda Irvine and Nader Sanai, of UCSF, Chao Zhao of University of Cambridge and Dong-In Yuk of Dana-Farber Cancer Institute.
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