Drat the fact that my camera has dead batteries. I would love to show you what I discovered in my back yard.
I have been lamenting ever since the start of summer that I live on a major road that goes through my small town and we don't have a lawn mower or money to buy one or to pay anyone to cut the grass for us.
Because of this, I have tried to time it so that I am only seen outside after dark so I don't have to see the stares of passersby who gawk at the incredible height of my grass which has now V'd off at the top and gone to seed in all its splendid glory.
I try to spend most of my time behind the privacy fence I once attempted unsuccessfully to scale and ended up hanging by my bra from at rush hour for all to see. That way I have my ... privacy ... with my backyard jungle where the waist-high weeds don't bother me nearly as much.
But, as John so often tells me when his eyes glaze over while listening to one of my stories, I guess I need to GET TO THE POINT!
Well, ok, the point is that the other day I decided the only way this last 10lbs is going to leave my body is if I do something proactive like, I don't know, walking. I decided to walk the inner edge of the privacy fence and maybe the tall grass would actually be beneficial by providing some resistance and making me burn more calories.
I have to be careful where I walk. There are pine cones and dead tree branches hiding in the tall grass waiting to trip me up. So I look down.
Funny thing about that. Looking from my back porch around the yard all I can see are flourishing weeds and tall grass that makes me feel ashamed and embarrassed. But when I waded out in it and began making the circuit around the yard, I found so many hidden treasures that mowing would have never allowed to happen.
All the weeds were in full bloom. There are white flowers, yellow flowers, purple flowers and blue flowers all over my back yard that I never knew were there. After making only one revolution of the yard, I had to go inside and get my 10 year old son to come out and join me for the hunt for the elusive flowers.
Some were flat and oval, some were on stalks that bloomed all the way up the stem. Some were little puff ball shaped things. Some were shaped like bells.
It was incredible. It was beautiful. And I never knew it was out there in my back yard.
And it never would have been if I had a lawn mower or could afford to pay someone to cut the grass.
So, once again I am humbly reminded that there are silver linings to everything and many different ways to view any situation.
I was choosing to be embarrassed and stress over the tall grass. Until my eyes were opened to the beauty cradled beneath.
Don't get me wrong... I still wait until after dark to check the mail.
And I would have run out to buy batteries and capture the beauty to share with you, but as I write this John has gone out and fired up the weed eater and decided to tackle the back yard manned only with that insufficient tool.
Our back yard alone has to be nearly a half acre. And he's gallantly swiping back and forth. Vanquishing the tall green foe.
Obliterating the small wonders within.
I wish he would have done the front yard, but no dice. He says he'd rather have tall grass than have anyone who knows him drive by and catch him trying to weed eat the entire thing.
Oh well, it's like my dad said when he built his house and didn't spend much time on it's outer beauty but made the inside look like something out of Better Homes and Gardens... "I'm not spending my time making it look good for the neighbors - I want it to look good for us."
So the back yard is looking pretty good -- even if the neighbors will never know.
Saturday, July 4, 2009
Tuesday, June 30, 2009
Newly discovered brain cell could be key to MS therapies
The article below was passed to me by a dear friend and it sounds both promising and exciting! Read on...
Newly Discovered Brain Cell Could be Key to Multiple Sclerosis Therapies
Institute researchers have identified a type of cell within the human brain that may be a previously unknown precursor to the stem cells that are capable of promoting growth of new neurons. The discovery could lead to new therapies for neurodegenerative diseases such as multiple sclerosis.
Bruce D. Trapp, PhD, Chair of the Institute's Department of Neurosciences and a leading multiple sclerosis researcher, said the cells called beta 4 tubulin (betaT4) are scattered throughout a region of the brain called the subventricular zone. This zone is known to be a source of stem cells capable of regenerating neurons. It is within the cerebrum, the part of the human brain responsible for social interaction, learning, memory, speech and language, and motor functions.
“Strategies for cell replacement to treat neurodegenerative diseases are very attractive and offer therapeutic possibilities. One example is generating the cells needed to replace the myelin that surrounds, protects and nourishes the neurons in the central nervous system. It's the loss of this myelin that causes lesions in multiple sclerosis [MS] brains,” Dr. Trapp said.
Oligodendrocyte progenitor cells (OPCs) generate new oligodendrocytes, which are required to produce myelin. “Unfortunately, OPC growth is limited, so MS lesions often don't remyelinate. Stimulating other types of precursor cells shows great potential in promoting oligodendrocyte production and remyelination in MS patients,” Dr. Trapp said.
Dr. Trapp's research points to betaT4 cells as one of the precursor cells needed for remyelination.
The presence of betaT4 cells in the subventricular zone peaks during the later stages of fetal brain development, but decreases shortly after birth – suggesting the cells' role in forming neurons. Researchers also found that the number of betaT4 cells significantly increases in the subventricular zone that borders MS lesions in the white matter of brains.
“In our research, we observed that the myelin generated by a relatively small number of transplanted betaT4 cells exceeded that of another known progenitor cell,” Dr. Trapp said. “It's still not clear if betaT4 cells are true stem cells or primitive precursors to stem cells, and the potential of stem cell therapeutics to treat neurodegenerative disease requires additional studies of stem cells in human brains.
“But we propose that betaT4 cells represent a cellular source for the latter stages of myelination and neural repair in the central nervous system” he said. “They could be a promising new direction for cell replacement therapies for neurodegenerative disease.”
Dr. Trapp's collaborators include Chuanshen Wu, PhD, Ansi Chang, MD, Maria C. Smith, Roy Won, Xinghua Yin, MD, Susan M. Staugaitis, MD, PhD, and Grahame Kidd, PhD, of the Institute's Department of Neurosciences; Dimitri Agamanolis, MD, of the Department of Pathology at Akron Children's Hospital; and Robert H. Miller, PhD, of the Department of Neurosciences at Case Western Reserve University School of Medicine. The findings appeared in the Journal of Neuroscience ( www.jneurosci.org/ June 16, 2009). The research was supported by grants from the National Institutes of Health's National Institute of Neurological Disorders and Stroke and the National Multiple Sclerosis Society.
Source Article
Newly Discovered Brain Cell Could be Key to Multiple Sclerosis Therapies
Institute researchers have identified a type of cell within the human brain that may be a previously unknown precursor to the stem cells that are capable of promoting growth of new neurons. The discovery could lead to new therapies for neurodegenerative diseases such as multiple sclerosis.
Bruce D. Trapp, PhD, Chair of the Institute's Department of Neurosciences and a leading multiple sclerosis researcher, said the cells called beta 4 tubulin (betaT4) are scattered throughout a region of the brain called the subventricular zone. This zone is known to be a source of stem cells capable of regenerating neurons. It is within the cerebrum, the part of the human brain responsible for social interaction, learning, memory, speech and language, and motor functions.
“Strategies for cell replacement to treat neurodegenerative diseases are very attractive and offer therapeutic possibilities. One example is generating the cells needed to replace the myelin that surrounds, protects and nourishes the neurons in the central nervous system. It's the loss of this myelin that causes lesions in multiple sclerosis [MS] brains,” Dr. Trapp said.
Oligodendrocyte progenitor cells (OPCs) generate new oligodendrocytes, which are required to produce myelin. “Unfortunately, OPC growth is limited, so MS lesions often don't remyelinate. Stimulating other types of precursor cells shows great potential in promoting oligodendrocyte production and remyelination in MS patients,” Dr. Trapp said.
Dr. Trapp's research points to betaT4 cells as one of the precursor cells needed for remyelination.
The presence of betaT4 cells in the subventricular zone peaks during the later stages of fetal brain development, but decreases shortly after birth – suggesting the cells' role in forming neurons. Researchers also found that the number of betaT4 cells significantly increases in the subventricular zone that borders MS lesions in the white matter of brains.
“In our research, we observed that the myelin generated by a relatively small number of transplanted betaT4 cells exceeded that of another known progenitor cell,” Dr. Trapp said. “It's still not clear if betaT4 cells are true stem cells or primitive precursors to stem cells, and the potential of stem cell therapeutics to treat neurodegenerative disease requires additional studies of stem cells in human brains.
“But we propose that betaT4 cells represent a cellular source for the latter stages of myelination and neural repair in the central nervous system” he said. “They could be a promising new direction for cell replacement therapies for neurodegenerative disease.”
Dr. Trapp's collaborators include Chuanshen Wu, PhD, Ansi Chang, MD, Maria C. Smith, Roy Won, Xinghua Yin, MD, Susan M. Staugaitis, MD, PhD, and Grahame Kidd, PhD, of the Institute's Department of Neurosciences; Dimitri Agamanolis, MD, of the Department of Pathology at Akron Children's Hospital; and Robert H. Miller, PhD, of the Department of Neurosciences at Case Western Reserve University School of Medicine. The findings appeared in the Journal of Neuroscience ( www.jneurosci.org/ June 16, 2009). The research was supported by grants from the National Institutes of Health's National Institute of Neurological Disorders and Stroke and the National Multiple Sclerosis Society.
Source Article
RIP Billy Mays
He missed his calling and should have been a comedian. I'd have liked to have seen more of him than just the 2 minutes of yelling at me to buy something.
Loved watching "Pitchmen".
Infomercials just won't ever be the same again.
Monday, June 29, 2009
My next move...
Inspired by all the videos floating around out there as a result of Michael Jackson's untimely death, I have decided this is the next thing I'm going to try to accomplish.
I want to go for my visit to the clinical trial checkup and have the neuro performing the EDSS test ask me to walk for him. I just want to see the look on his face when I pull off the Moon Walk.
I'll probably lose points off the mental stability part of the test (with copious notes accompanying the test outlining my Wacko Jacko impersonation). Heck, they may even admit me for further evaluation, or maybe even halt the clinical trial because of this heretofore unknown side effect.
I just want to see their faces.
And between tests, when I have to walk from one office to another... I'm going to say it's the only way I can now walk. BWAHAHAHA!
I'll be lucky if I can do it at all. So far, in preliminary practice sessions in my hardwood floored hallway and stockinged feet, I have been unsuccessful at recreating this move in a smooth, flowing fashion.
First off, I have to put my hands on either wall to my sides in order to maintain my balance in the starting position, which ends up more reminiscent of Daniel about to pull of the Crane kick in Karate Kid.
Maybe I should just practice that. Then when the doc goes to wack me on the knee with his rubber mallet, I can say it was just my hyper reflexes. Not my fault.
I don't know what is driving me to conquer moonwalking at this time in my life when I couldn't do it back in the 80's.
Maybe I do have some mental deficit.
Or maybe I should just get a life. :-)
Wednesday, June 24, 2009
My own personal update in the FTY720 TRANSFORMS clinical trial
I started in August 07 so that means I have been in this clinical trial for
this long (according to www.wolframalpha.com )
During this time I have never officially had a relapse, although I have informed my trial nurse at least 2 times that I remember that I thought I might possibly be having one.
And lately I have been having not so much of a relapse, but just a recurrence of oldies but goodies. For instance, my legs are doing that fire and ice thing again where my calves feel like they are burning or really cold. The other night they cramped up really badly, too. I remember both of these symptoms from the very last bona fide relapse I did have -- the one from April of 07. It was much more pronounced back then. After having just a taste of it lately I wonder how I made it through life back then where I was in a constant state of misery.
These latest symptoms are only cropping up lately because I'm trying to do too much, or getting myself stressed out, or not getting enough sleep, or a combination of all of them.
They really started right around the time my son was going to graduate from elementary school and I realized he's growing up despite my efforts to keep him forever young so that I, too, shall be. With all the end of year parties, and then the HSV attack which led me to the GYN only to find out I need that ultrasound of the ovarian cyst and getting reprimanded about ovarian cancer, and then over working myself, etc. etc.
Well, these symptoms are like some sort of divining rod or something. When I have all the right circumstances, my legs start to burn and I get that buzzing down my spine and everything starts cramping up. All as if to tell me, "hey now! Take it easy!!" I don't find water, but I do find my body needing rest.
Once I've had a good night's sleep in my recliner (I've been sleeping there for 2 years now [possible Fingolimod side effect alert!!] and, try as I might to go back to a real bed, I just can't do it) I feel all better.
When I tell the trial people about these "almost" relapses, I am asked to grade them on a scale of 1-10 as far as severity goes. It's always been a 1, or 2 at the most, so they end up conveniently forgetting that I called. Nobody ever really checks it out to follow up with poking/prodding/testing to verify whether or not there is disease activity.
So, while the news I posted in my last blog entry is GREAT, I just wonder how many of us have actually had some form of a relapse that went unnoticed.
I still proudly say that I am relapse free after more than 2 years (since April 07) but sometimes I wonder if that's really the case...
Or maybe I'm just being true to my hypochondriacal self?
Only my hairdresser knows for sure. (for your younger people, that's a Clairol commercial from the 70s I think).
I'll have to ask her next time I see her.
Oral Fingolimod Lowers Disease Activity in Patients With MS for Up to 4 Years
Just got this in my alert email today and wanted to share. My favorite part is in green.
Oral Fingolimod Lowers Disease Activity in Patients With MS for Up to 4 Years: Presented at ENS
By Judith Moser, MD
MILAN, Italy -- June 23, 2009 -- Patients with multiple sclerosis (MS) show sustained clinical benefit when treated with the novel sphingosine-1-phosphatase receptor modulator fingolimod (FTY720), according to the extension phase of a multicentre study presented here at the 19th Meeting of the European Neurological Society (ENS).
Ludwig Kappos, MD, Clinic of Neurology, University Hospital Basel, Basel, Switzerland, presented the 4-year follow-up findings of a phase 2 proof-of-concept study investigating oral fingolimod in the treatment of MS here on June 22.
Fingolimod targets MS via the immune system and probably via the central nervous system as well. "The main mode of action pertains to a redistribution of lymphocytes, which normally stay protected in lymph nodes," Dr. Kappos explained.
The core study, which covered the time between baseline and 6 months, compared once-daily fingolimod 1.25 and 5.00 mg with placebo. In the randomised, dose-blind extension study (months 7-48), patients formerly on placebo were rerandomised to once-daily oral fingolimod 1.25 or 5.00 mg so that all patients were on active treatment.
As Dr. Kappos noted, the number of circulating lymphocytes was permanently reduced in all dose groups by approximately 70% throughout the extension period.
Similarly, the number of gadolinium-enhancing lesions remained low in all arms over 48 months. More than 95% of the study population were free of gadolinium-enhancing lesions at the end of the 4-year extension period.
These findings translated into a low annualised relapse rate. Most patients (51%-70%) remained relapse-free for up to 48 months. Furthermore, most patients were free from disability progression at the end of the study.
"Fingolimod was well tolerated," Dr. Kappos reported. "The long-term safety profile was in line with previous findings."
In the group with the highest cumulative dose, a tendency toward higher infection and nasopharyngitis rates was seen. However, serious adverse events were equally distributed between the dose groups.
Blood pressure and pulmonary function measurements remained stable during the extension study. Asymptomatic elevations of liver enzymes were observed in 16% of patients without any evidence of serious drug-induced liver injury.
Seven cases of localised skin cancers, which were detected by regular examination, occurred within the first 36 months. Between months 37 and 48, no new cases were seen. "This indicates a lack of cumulative risk with increasing drug exposure," Dr. Kappos said.
A phase 3 study program is further characterising the efficacy, safety, and tolerability of oral fingolimod in patients with MS.
Funding for this study was provided by Novartis Pharma.
[Presentation title: Majority of Patients With Relapsing Multiple Sclerosis Receiving Oral Fingolimod (FTY720, a Sphingosine-1-Phosphatase Receptor Modulator) Remain Free From Any Inflammatory Activity: Results of a 4-Yr, Phase II Extension. Abstract O21]
Source: http://www.docguide.com/news/content.nsf/news/852571020057CCF6852575DE00716D8A
Oral Fingolimod Lowers Disease Activity in Patients With MS for Up to 4 Years: Presented at ENS
By Judith Moser, MD
MILAN, Italy -- June 23, 2009 -- Patients with multiple sclerosis (MS) show sustained clinical benefit when treated with the novel sphingosine-1-phosphatase receptor modulator fingolimod (FTY720), according to the extension phase of a multicentre study presented here at the 19th Meeting of the European Neurological Society (ENS).
Ludwig Kappos, MD, Clinic of Neurology, University Hospital Basel, Basel, Switzerland, presented the 4-year follow-up findings of a phase 2 proof-of-concept study investigating oral fingolimod in the treatment of MS here on June 22.
Fingolimod targets MS via the immune system and probably via the central nervous system as well. "The main mode of action pertains to a redistribution of lymphocytes, which normally stay protected in lymph nodes," Dr. Kappos explained.
The core study, which covered the time between baseline and 6 months, compared once-daily fingolimod 1.25 and 5.00 mg with placebo. In the randomised, dose-blind extension study (months 7-48), patients formerly on placebo were rerandomised to once-daily oral fingolimod 1.25 or 5.00 mg so that all patients were on active treatment.
As Dr. Kappos noted, the number of circulating lymphocytes was permanently reduced in all dose groups by approximately 70% throughout the extension period.
Similarly, the number of gadolinium-enhancing lesions remained low in all arms over 48 months. More than 95% of the study population were free of gadolinium-enhancing lesions at the end of the 4-year extension period.
These findings translated into a low annualised relapse rate. Most patients (51%-70%) remained relapse-free for up to 48 months. Furthermore, most patients were free from disability progression at the end of the study.
"Fingolimod was well tolerated," Dr. Kappos reported. "The long-term safety profile was in line with previous findings."
In the group with the highest cumulative dose, a tendency toward higher infection and nasopharyngitis rates was seen. However, serious adverse events were equally distributed between the dose groups.
Blood pressure and pulmonary function measurements remained stable during the extension study. Asymptomatic elevations of liver enzymes were observed in 16% of patients without any evidence of serious drug-induced liver injury.
Seven cases of localised skin cancers, which were detected by regular examination, occurred within the first 36 months. Between months 37 and 48, no new cases were seen. "This indicates a lack of cumulative risk with increasing drug exposure," Dr. Kappos said.
A phase 3 study program is further characterising the efficacy, safety, and tolerability of oral fingolimod in patients with MS.
Funding for this study was provided by Novartis Pharma.
[Presentation title: Majority of Patients With Relapsing Multiple Sclerosis Receiving Oral Fingolimod (FTY720, a Sphingosine-1-Phosphatase Receptor Modulator) Remain Free From Any Inflammatory Activity: Results of a 4-Yr, Phase II Extension. Abstract O21]
Source: http://www.docguide.com/news/content.nsf/news/852571020057CCF6852575DE00716D8A
Thursday, June 11, 2009
If you don't have insurance, just don't get sick. Simple.
I'm so sick of this crap. I've been dealing with it (like a LOT of other American's) for years now. A diagnosis of MS that keeps me from being able to get health insurance, thus effectively cutting me off at the knees when it comes to health care.
I just got a call from the imaging center saying that the idea of billing Novartis for the ultrasound I need of my left ovary is "too third party" for them. I can't have it done.
Great. There is a machine in that building and a person who gets paid by the hour to operate it, that is just so close I can smell that stupid gel they smear you with, BUT I can't get it done so I get to just GUESS if I have an ovary-bomb waiting to kill me.
Or, I can pay thru the nose. Money I don't have that I am trying to scrape up to keep from losing my home (a whole different ball of stressful worry wax).
Funny that Novartis' check was good for them last year when they did the first ultrasound that discovered the cyst. You get one new person in the mix and they have no problem telling you NO.
How can one human being sit there and not break down into tears having to tell another that a possibly life-saving procedure that could change the whole direction of the remainder of the other person's life is going to be denied them because they don't have enough pictures of dead presidents hanging around???
This is freaking absurd and God is looking down on us ready to throw up because it makes him so sick to see what we have become as a society. Maybe he should. Maybe it should be a big plague of puke raining down on us all, clogging all the precious machines that only the wealthy are privileged enough to be treated with. Clogging everything and sickening everyone. What would the insurance gods do then?? Go hide under a big red umbrella? I think not.
And they would be running around screaming in fear as the puke slowly killed them. And the rest, like me, would be calmly standing by welcoming them to our world.
there. I feel better.
Maybe I can get someone to loan me the money.
And then I better just pray it turns out to be nothing because if just DIAGNOSING ovarian cancer can be so elusively hard for the uninsured to accomplish, treating it will take an act of... well, God.
I just got a call from the imaging center saying that the idea of billing Novartis for the ultrasound I need of my left ovary is "too third party" for them. I can't have it done.
Great. There is a machine in that building and a person who gets paid by the hour to operate it, that is just so close I can smell that stupid gel they smear you with, BUT I can't get it done so I get to just GUESS if I have an ovary-bomb waiting to kill me.
Or, I can pay thru the nose. Money I don't have that I am trying to scrape up to keep from losing my home (a whole different ball of stressful worry wax).
Funny that Novartis' check was good for them last year when they did the first ultrasound that discovered the cyst. You get one new person in the mix and they have no problem telling you NO.
How can one human being sit there and not break down into tears having to tell another that a possibly life-saving procedure that could change the whole direction of the remainder of the other person's life is going to be denied them because they don't have enough pictures of dead presidents hanging around???
This is freaking absurd and God is looking down on us ready to throw up because it makes him so sick to see what we have become as a society. Maybe he should. Maybe it should be a big plague of puke raining down on us all, clogging all the precious machines that only the wealthy are privileged enough to be treated with. Clogging everything and sickening everyone. What would the insurance gods do then?? Go hide under a big red umbrella? I think not.
And they would be running around screaming in fear as the puke slowly killed them. And the rest, like me, would be calmly standing by welcoming them to our world.
there. I feel better.
Maybe I can get someone to loan me the money.
And then I better just pray it turns out to be nothing because if just DIAGNOSING ovarian cancer can be so elusively hard for the uninsured to accomplish, treating it will take an act of... well, God.
Subscribe to:
Posts (Atom)