Sunday, November 22, 2009
Sunday, November 15, 2009
Friday, January 30, 2009
Stem cells used to reverse MS symptoms
January 30, 2009 — 10:34am ET By John Carroll
From The FierceBioResearcher web site.
Stem cell therapy was able to reverse the neurological damage inflicted by multiple sclerosis, according to a new study. And the procedure, which relies on bone marrow cells, could offer a radically new approach to treating a notoriously drug-resistant condition.
A research team at Chicago's Northwestern University Feinberg School of Medicine injected 21 patients with their own stem cells and also treated them with the drug alemtuzumab, which has demonstrated an ability to halt disease progression. Over a period of three years, 17 of the patients reported an improvement in their symptoms and the rest saw the disease stabilize. None of the volunteers worsened over that period of time.
"These are very encouraging results and it's exciting to see that in this trial not only is progression of disability halted, but damage appears to be reversed," said Dr. Doug Brown, research manager at the MS Society. "Stem cells are showing more and more potential in the treatment of MS and the challenge we now face is proving their effectiveness in trials involving large numbers of people."
None of the therapies in use today can reverse the symptoms of MS.
From The FierceBioResearcher web site.
Stem cell therapy was able to reverse the neurological damage inflicted by multiple sclerosis, according to a new study. And the procedure, which relies on bone marrow cells, could offer a radically new approach to treating a notoriously drug-resistant condition.
A research team at Chicago's Northwestern University Feinberg School of Medicine injected 21 patients with their own stem cells and also treated them with the drug alemtuzumab, which has demonstrated an ability to halt disease progression. Over a period of three years, 17 of the patients reported an improvement in their symptoms and the rest saw the disease stabilize. None of the volunteers worsened over that period of time.
"These are very encouraging results and it's exciting to see that in this trial not only is progression of disability halted, but damage appears to be reversed," said Dr. Doug Brown, research manager at the MS Society. "Stem cells are showing more and more potential in the treatment of MS and the challenge we now face is proving their effectiveness in trials involving large numbers of people."
None of the therapies in use today can reverse the symptoms of MS.
Monday, December 29, 2008
2009 MS WALK FUNDRAISING EFFORT BEGINS NOW!!!!!
I seeking sponsorship of my 2009 MS Walk fundraising campaign. Multiple Sclerosis and its effects have had a significant impact on my personal network. Having Multiple Sclerosis has limited my normal contacts primarily to persons dealing with chronic diseases and disabilities. Fundraising among that demographic is difficult at best.
I am devoting myself to causes for the disabled with particular emphasis on issues relating to Multiple Sclerosis. As a result I am currently serving in the following volunteer capacities:
1. Governor’s Office of Emergency Services SEMS (Standardized Emergency Management System) Specialist Committee for Volunteer Services
2. California Volunteers; Training, Typing, Classification and Credentialing workgroup for Volunteer Disaster Workers
3. National Multiple Sclerosis Society, MS and California Action Networks
4. National Multiple Sclerosis Society, Pacific South Coast Chapter Self Help Support Group Leader
5. National Multiple Sclerosis Society, Pacific South Coast Chapter Government Relations Committee member
6. Committee Chair for the Transportation Sub-Committee of the Pacific South Coast Chapter Government Relations Committee
7. California Neurological Alliance Public Policy Conference attendee and Team Leader for legislative visits conducted as part of the conference
Here are two ways individuals or commercial entities can support me in my efforts:
· Individuals can join my MS Walk team and raise funds yourself @ mswalk.com/msintheoc
· Contribute online to my personal MS Walk effort @ mswalk.com/frank
I welcome any suggestions or in kind donations which can be used in a fundraising effort.
I am devoting myself to causes for the disabled with particular emphasis on issues relating to Multiple Sclerosis. As a result I am currently serving in the following volunteer capacities:
1. Governor’s Office of Emergency Services SEMS (Standardized Emergency Management System) Specialist Committee for Volunteer Services
2. California Volunteers; Training, Typing, Classification and Credentialing workgroup for Volunteer Disaster Workers
3. National Multiple Sclerosis Society, MS and California Action Networks
4. National Multiple Sclerosis Society, Pacific South Coast Chapter Self Help Support Group Leader
5. National Multiple Sclerosis Society, Pacific South Coast Chapter Government Relations Committee member
6. Committee Chair for the Transportation Sub-Committee of the Pacific South Coast Chapter Government Relations Committee
7. California Neurological Alliance Public Policy Conference attendee and Team Leader for legislative visits conducted as part of the conference
Here are two ways individuals or commercial entities can support me in my efforts:
· Individuals can join my MS Walk team and raise funds yourself @ mswalk.com/msintheoc
· Contribute online to my personal MS Walk effort @ mswalk.com/frank
I welcome any suggestions or in kind donations which can be used in a fundraising effort.
Tuesday, November 11, 2008
On This Veteran's Day
I received the following in an email this morning from a fellow veteran with whom I served 40 years ago during the Vietnam era.
We still maintain a fairly extensive mailing list of those that served with us and several of the guys have taken it upon themselves to maintain a database of our locations and contact information.
The email I received read as follows:
Roster update
For all of you who knew Lino Celli I have some bad news. Lino passed away last week at his home in Italy. He had MS for many years and the toll of the long and ugly road called him home. I spent last week with his wife assisting her getting affairs in order. Please pray for Rita and their daughters in these difficult times.
We still maintain a fairly extensive mailing list of those that served with us and several of the guys have taken it upon themselves to maintain a database of our locations and contact information.
The email I received read as follows:
Roster update
For all of you who knew Lino Celli I have some bad news. Lino passed away last week at his home in Italy. He had MS for many years and the toll of the long and ugly road called him home. I spent last week with his wife assisting her getting affairs in order. Please pray for Rita and their daughters in these difficult times.
Saturday, November 01, 2008
Teams Funded by the National MS Society Report on Key Enzymes Related to MS Progression and Nervous System Repair
From the National Multiple Sclerosis Society website.
Two teams of researchers funded by the National MS Society have reported findings on nerve tissue injury and repair that add important information needed to stop MS progression and develop nervous system repair strategies. Isobel Scarisbrick, PhD (Mayo Clinic and Foundation, Rochester, MN) and colleagues have found two enzymes that may serve as markers of progressive MS and nerve fiber injury. Patrizia Casaccia, MD, PhD (Mount Sinai School of Medicine, New York) and colleagues reported that another enzyme is essential for replenishing myelin-making cells that have been depleted by MS. Both teams are continuing these lines of research in hopes of identifying targets for the development of new therapies for MS.
Dr. Scarisbrick reported her team’s findings related to MS progression at the annual meeting of the American Neurological Association (Abstract T-99). Dr. Casaccia’s report on the enzyme critical for repair appeared in Nature Neuroscience (early online publication, August 24, 2008).
Progressive MS and KLK enzymes (Dr. Scarisbrick’s team): Understanding the processes that lead to tissue damage in MS is crucial to feed parallel efforts to protect and repair the brain and spinal cord. Dr. Scarisbrick previously found elevated levels of “KLK6” (a newly identified member of the kallikrein enzyme family) in areas of damage found in tissue samples from people with MS. Now, in a follow-up study, the group has studied the levels of KLK6 and other kallikreins in blood samples taken from 35 people with different clinical courses of MS and 62 controls without MS.
The results show that KLK1 and KLK6 were elevated in people with MS, with the highest levels appearing in people with secondary-progressive MS (a course of MS that initially is relapsing-remitting and then becomes progressive, with or without occasional relapses and minor remissions).
The team also exposed nerve cells isolated from mice to KLK1 or KLK6 in the laboratory, and found that the enzymes promoted nerve cell loss. Dr. Scarisbrick is continuing to study the role of these enzymes in nerve fiber injury and hopes to find a way to target them with therapeutic strategies for people with progressive MS.
Repair and HDAC enzymes (Dr. Casaccia’s team): MS involves immune attacks against brain and spinal cord tissues, primarily myelin, the insulation that surrounds and protects nerve fibers. Several studies have indicated that, early in the disease, immature myelin-making cells – called, “oligodendrocyte progenitors” – are recruited to generate new myelin. A sufficient number of these cells is needed so that progenitors can migrate to the site of myelin damage and develop into myelin-making cells. Then, genes that instruct the formation of myelin components are activated and myelin is formed. In MS, this process fails. Dr. Casaccia is studying whether some molecules may inhibit the activation of the genes that promote myelin formation.
In this study, Dr. Casaccia’s team observed the gene activity during oligodendrocyte development in mice with damaged myelin. They found that enzymes called histone deacetylases (HDACs) were crucial to this process, particularly HDAC1 and HDAC2. Deleting these two enzymes impaired the differentiation of oligodendrocyte progenitors, that is, the process by which these cells develop a more specialized form or function. The team is studying how these findings might be translated into therapeutic strategies.
Two teams of researchers funded by the National MS Society have reported findings on nerve tissue injury and repair that add important information needed to stop MS progression and develop nervous system repair strategies. Isobel Scarisbrick, PhD (Mayo Clinic and Foundation, Rochester, MN) and colleagues have found two enzymes that may serve as markers of progressive MS and nerve fiber injury. Patrizia Casaccia, MD, PhD (Mount Sinai School of Medicine, New York) and colleagues reported that another enzyme is essential for replenishing myelin-making cells that have been depleted by MS. Both teams are continuing these lines of research in hopes of identifying targets for the development of new therapies for MS.
Dr. Scarisbrick reported her team’s findings related to MS progression at the annual meeting of the American Neurological Association (Abstract T-99). Dr. Casaccia’s report on the enzyme critical for repair appeared in Nature Neuroscience (early online publication, August 24, 2008).
Progressive MS and KLK enzymes (Dr. Scarisbrick’s team): Understanding the processes that lead to tissue damage in MS is crucial to feed parallel efforts to protect and repair the brain and spinal cord. Dr. Scarisbrick previously found elevated levels of “KLK6” (a newly identified member of the kallikrein enzyme family) in areas of damage found in tissue samples from people with MS. Now, in a follow-up study, the group has studied the levels of KLK6 and other kallikreins in blood samples taken from 35 people with different clinical courses of MS and 62 controls without MS.
The results show that KLK1 and KLK6 were elevated in people with MS, with the highest levels appearing in people with secondary-progressive MS (a course of MS that initially is relapsing-remitting and then becomes progressive, with or without occasional relapses and minor remissions).
The team also exposed nerve cells isolated from mice to KLK1 or KLK6 in the laboratory, and found that the enzymes promoted nerve cell loss. Dr. Scarisbrick is continuing to study the role of these enzymes in nerve fiber injury and hopes to find a way to target them with therapeutic strategies for people with progressive MS.
Repair and HDAC enzymes (Dr. Casaccia’s team): MS involves immune attacks against brain and spinal cord tissues, primarily myelin, the insulation that surrounds and protects nerve fibers. Several studies have indicated that, early in the disease, immature myelin-making cells – called, “oligodendrocyte progenitors” – are recruited to generate new myelin. A sufficient number of these cells is needed so that progenitors can migrate to the site of myelin damage and develop into myelin-making cells. Then, genes that instruct the formation of myelin components are activated and myelin is formed. In MS, this process fails. Dr. Casaccia is studying whether some molecules may inhibit the activation of the genes that promote myelin formation.
In this study, Dr. Casaccia’s team observed the gene activity during oligodendrocyte development in mice with damaged myelin. They found that enzymes called histone deacetylases (HDACs) were crucial to this process, particularly HDAC1 and HDAC2. Deleting these two enzymes impaired the differentiation of oligodendrocyte progenitors, that is, the process by which these cells develop a more specialized form or function. The team is studying how these findings might be translated into therapeutic strategies.
Saturday, October 18, 2008
Thank You Team Mitsubishi/Nationwide Traffic
On behalf of all those that live with Multiple Sclerosis, I want to thank each of you for your involvement and dedication to the cause.
We will beat this disease! No longer will careers be shortened by MS. No longer will care-givers struggle to fill the needs of both themselves and the person for whom they care. No longer will people have to think about their every move. No longer will there be a need to gain awareness of MS and no longer will there be a need to simply try to make people understand.
And maybe we’ll know why MS exists, what triggers it and why it’s progression can’t be predicted. Maybe we’ll know that there is (or for that matter isn’t) a genetic component. Or, why more women than men are stricken by MS. Why it is more prevalent the farther you go from the equator. We might even know why in some people it effects their balance, some their stamina, some their basic motor skills, some all of the above, and why some seem to lead (normal) productive lives interrupted only by occasional exacerbations that come and go leaving no long term evidence of MS’s flare-up.
MS is a giant question mark. It would be one thing to say there are more questions than answers. With MS there are really only questions, and the questions never stop coming and very few have answers.
So… What you’ve done is significantly help fund the cause. The cause of:
· Research
· Awareness of Multiple Sclerosis
· Advocacy for MS patients, be it Independent Living, Health Care, Medical Insurance, or the Rights of the Disabled.
· Peer self-help. Persons with chronic conditions helping others in the same situation.
· Helping those with MS navigate the Government’s bureaucracy to get Social Security Disability or Supplemental Security Insurance approval.
· Care-giver support.
· Providing a place that people with MS can go to find someone that cares and understands, someone that they can relate to and that doesn’t judge them.
I hope to see each of you out there again next year! If you’ll have me I’d be privileged to be the team’s connection to Multiple Sclerosis, unless of course they find a cure! If that happens I promise to ride with you!
Finally, were it not for the National Multiple Sclerosis Society (funded by events like Bike MS) I’d be very unfulfilled. But, the MS Society gives me the opportunity to reach out to others with MS, advocate for our needs and rights while relating to my fellow MSers and educating the public.
I Sincerely Want To Thank You
Until next year,
We will beat this disease! No longer will careers be shortened by MS. No longer will care-givers struggle to fill the needs of both themselves and the person for whom they care. No longer will people have to think about their every move. No longer will there be a need to gain awareness of MS and no longer will there be a need to simply try to make people understand.
And maybe we’ll know why MS exists, what triggers it and why it’s progression can’t be predicted. Maybe we’ll know that there is (or for that matter isn’t) a genetic component. Or, why more women than men are stricken by MS. Why it is more prevalent the farther you go from the equator. We might even know why in some people it effects their balance, some their stamina, some their basic motor skills, some all of the above, and why some seem to lead (normal) productive lives interrupted only by occasional exacerbations that come and go leaving no long term evidence of MS’s flare-up.
MS is a giant question mark. It would be one thing to say there are more questions than answers. With MS there are really only questions, and the questions never stop coming and very few have answers.
So… What you’ve done is significantly help fund the cause. The cause of:
· Research
· Awareness of Multiple Sclerosis
· Advocacy for MS patients, be it Independent Living, Health Care, Medical Insurance, or the Rights of the Disabled.
· Peer self-help. Persons with chronic conditions helping others in the same situation.
· Helping those with MS navigate the Government’s bureaucracy to get Social Security Disability or Supplemental Security Insurance approval.
· Care-giver support.
· Providing a place that people with MS can go to find someone that cares and understands, someone that they can relate to and that doesn’t judge them.
I hope to see each of you out there again next year! If you’ll have me I’d be privileged to be the team’s connection to Multiple Sclerosis, unless of course they find a cure! If that happens I promise to ride with you!
Finally, were it not for the National Multiple Sclerosis Society (funded by events like Bike MS) I’d be very unfulfilled. But, the MS Society gives me the opportunity to reach out to others with MS, advocate for our needs and rights while relating to my fellow MSers and educating the public.
I Sincerely Want To Thank You
Until next year,
Thursday, October 09, 2008
2007 Most Inspirational Rider
From the Pacific South Coast Chapter's Web Site:
The Land Rover Miramar Bike MS Tour provides the opportunity for any cyclist to ride along the coast with cyclists ranging from beginner to expert, individual to team, and celebrity to family.
For the past few years, a tandem bicycle has made its way up the Torrey Pines Hill pedaled by team "Lloyd's Lagers" fearless leader, Lloyd von Sprecken, and his son, Todd. Lloyd has been inspiring riders with and without multiple sclerosis (MS) for many years. In honor of his commitment to a world free of MS, we created The Lloyd von Sprecken "Most Inspirational Rider Award."
The 2007 Lloyd von Sprecken Most Inspirational Rider Award was presented to Darren Martin. It all started when his short-term memory began to fail. His wife would ask him to go out and get some milk and he would get to the store a quarter-mile away and would have to call her and ask what he was doing there. Darren was diagnosed with MS in 1999.
Before he started getting any exercise, in 2005, he was basically in a chair all day because he was unable to work any longer. According to Darren he used to be in a depressed, miserable mood. Cycling changed his outlook. Darren has this disease, but it's not going to hold him back. He started going to the gym just to get some resistance going and he realized he can sit really well. Darren can sit on a bike and he can pedal, yet he can't stand for any length of time. Darren can't run, he can't jog, but he can ride a bike all day long.
The Land Rover Miramar Bike MS Tour provides the opportunity for any cyclist to ride along the coast with cyclists ranging from beginner to expert, individual to team, and celebrity to family.
For the past few years, a tandem bicycle has made its way up the Torrey Pines Hill pedaled by team "Lloyd's Lagers" fearless leader, Lloyd von Sprecken, and his son, Todd. Lloyd has been inspiring riders with and without multiple sclerosis (MS) for many years. In honor of his commitment to a world free of MS, we created The Lloyd von Sprecken "Most Inspirational Rider Award."
The 2007 Lloyd von Sprecken Most Inspirational Rider Award was presented to Darren Martin. It all started when his short-term memory began to fail. His wife would ask him to go out and get some milk and he would get to the store a quarter-mile away and would have to call her and ask what he was doing there. Darren was diagnosed with MS in 1999.
Before he started getting any exercise, in 2005, he was basically in a chair all day because he was unable to work any longer. According to Darren he used to be in a depressed, miserable mood. Cycling changed his outlook. Darren has this disease, but it's not going to hold him back. He started going to the gym just to get some resistance going and he realized he can sit really well. Darren can sit on a bike and he can pedal, yet he can't stand for any length of time. Darren can't run, he can't jog, but he can ride a bike all day long.
Tuesday, October 07, 2008
It is that time of year again! A random Bike MS Webpage story
...the Cucinotti Family at the 2007 MS Bike Tour...Christian, Giannina (diagnosed with MS in 2003), Peter, Joe, Kylie and Giovanna...please join us again in our fight against MS!
It is that time of year again, to begin fundraising in our battle to find a cure for Multiple Sclerosis. As we continue our battle we call on you all again for support. We understand that there are many great causes out there and we hope you will again consider ours. Our family has been blessed the past two years by all of you. On October 11th and 12th I will again ride my bike 100 miles from O.C. to San Diego to raise money in search of a cure for MS.
Unfortunately for Giannina the disease continues to take its toll on her, although most of the time you wouldn’t know it. She is as beautiful as ever! She continues to have a great attitude while dealing with raising four kids during her sickness. Of course some days are better than others but little by little permanent deficits appear to be taking hold. Giannina’s right leg from the knee down has been 80% numb for the past eight months or so. It’s just part of the hand we are playing. Giannina does not complain and I try not to. Sometimes the reality of all this seems to be harder on me and the kids than it is for Giannina. We often feel so helpless. We just get to watch it all happen. Giannina continues her regiment of medication. The shots are painful and the meds still make her sick but we think it slows the process of the MS.
That is why this time of the year is such a blessing for our family. We get to do our part in raising funds for research centers to continue to look for a cure for this awful disease. MS affects millions of people. We have joined those folks in their battle. We are again asking you to join with us in our struggle to find a cure by donating though my website. If you cannot donate this year we would love your prayers...and we thank you in advance for whatever you wish to do.
Sincerely,
Joe Cucinotti
"Alone we can do so little; together we can do so much."
- Helen Keller
Donate to Joe Cucinotti's Fund Raising effort.
Or, donate to mine. It really doesn't matter we're all working for the same result! My fundraising web page.
It is that time of year again, to begin fundraising in our battle to find a cure for Multiple Sclerosis. As we continue our battle we call on you all again for support. We understand that there are many great causes out there and we hope you will again consider ours. Our family has been blessed the past two years by all of you. On October 11th and 12th I will again ride my bike 100 miles from O.C. to San Diego to raise money in search of a cure for MS.
Unfortunately for Giannina the disease continues to take its toll on her, although most of the time you wouldn’t know it. She is as beautiful as ever! She continues to have a great attitude while dealing with raising four kids during her sickness. Of course some days are better than others but little by little permanent deficits appear to be taking hold. Giannina’s right leg from the knee down has been 80% numb for the past eight months or so. It’s just part of the hand we are playing. Giannina does not complain and I try not to. Sometimes the reality of all this seems to be harder on me and the kids than it is for Giannina. We often feel so helpless. We just get to watch it all happen. Giannina continues her regiment of medication. The shots are painful and the meds still make her sick but we think it slows the process of the MS.
That is why this time of the year is such a blessing for our family. We get to do our part in raising funds for research centers to continue to look for a cure for this awful disease. MS affects millions of people. We have joined those folks in their battle. We are again asking you to join with us in our struggle to find a cure by donating though my website. If you cannot donate this year we would love your prayers...and we thank you in advance for whatever you wish to do.
Sincerely,
Joe Cucinotti
"Alone we can do so little; together we can do so much."
- Helen Keller
Donate to Joe Cucinotti's Fund Raising effort.
Or, donate to mine. It really doesn't matter we're all working for the same result! My fundraising web page.
Monday, September 22, 2008
Laquinimod Demonstrated Significant And Sustained Impact On Multiple Sclerosis Disease Activity
New data from the extension phase of oral laquinimod in relapsing-remitting multiple sclerosis (RRMS) demonstrated a significant reduction in the mean number of gadolinium-enhancing (GdE) lesions in both patients who switched from placebo to laquinimod and patients who continued with their initial laquinimod dose. In RRMS patients who switched from placebo to laquinimod, 52 percent reduction in the mean number of GdE lesions was observed (p<0.0007). The reduction was significant for both patients switching to high-dose (p<0.009) and low-dose laquinimod (p<0.03). In addition, the proportion of patients who switched to active treatment from placebo, and remained enhancing lesion-free, increased from 31 percent to 47 percent (p<0.012), further reinforcing the efficacy of laquinimod on magnetic resonance imaging (MRI) measured disease activity.
Friday, September 19, 2008
Neural Cells Derived From Human Embryonic Stem Cells Reduce Multiple Sclerosis (MS) Symptoms
September 08, 2008 08:56 AM Eastern Daylight Time
Hadassah Hospital Study Shows That Neural Cells Derived From Human Embryonic Stem Cells Reduce Multiple Sclerosis (MS) Symptoms
The Study Data Is Published in the Scientific Journal of PLoS
2008 World Stem Cell Summit
EIN KEREM, Israel--(BUSINESS WIRE)--Hadassah University Hospital and Hadasit, the technology transfer company of Hadassah Medical Organization, announced today that scientists at Hadassah University Hospital have discovered a new application for human embryonic stem cells. They have demonstrated for the first time that transplanted neural cells derived from human embryonic stem cells can reduce the clinical symptoms in animals with a form of multiple sclerosis.
The findings of the study are published in an article titled “Neuroprotective Effect of Transplanted Human Embryonic Stem Cell-Derived Neural Precursors in an Animal Model of Multiple Sclerosis” in the Scientific Journal of PLoS One, a new, high-impact, peer-reviewed, open-access, online publication. Click here to access the article: http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003145.
The data presented in the report are the result of a long-term collaboration between Professor Tamir Ben Hur, director of the Neurological Department at Hadassah Hospital and Professor Benjamin Reubinoff, director of the Human Embryonic Stem Cell Research Center at Hadassah Hospital. Ms. Michal Aharonowiz and Dr. Ofira Einstein both from Hadassah, as well as Professor Hans Lassmann from the University of Vienna also contributed.
“Human embryonic stem cell-derived neural precursors were transplanted into the brains of mice with an experimental form of MS. The grafted human cells integrated in the mice brains and migrated towards the sites of inflammation. They suppressed the inflammatory process in the brain, and consequently protected the animals from demyelination and nerve cell extension (axonal) injury, which are the pathological hallmarks of MS,” said Professor Benjamin Reubinoff.
Multiple sclerosis, the most common cause of neurological disabilities in young adults, is caused by an inflammatory reaction of the patient’s own immune system against the myelin sheath that envelops the nerve processes. The destruction of myelin leads to the degeneration and loss of nerve cells and permanent neurological disabilities. MS affects 2.5 million people worldwide.
“We believe that the encouraging therapeutic effects in the rodent model of MS justify moving ahead to clinical studies. We also anticipate that the anti-inflammatory effect demonstrated in the pre-clinical study may be combined in the future with the use of other human embryonic stem cell derived neural cells to repair the myelin in the brain,” said Professor Reubinoff.
Hadassah Hospital Study Shows That Neural Cells Derived From Human Embryonic Stem Cells Reduce Multiple Sclerosis (MS) Symptoms
The Study Data Is Published in the Scientific Journal of PLoS
2008 World Stem Cell Summit
EIN KEREM, Israel--(BUSINESS WIRE)--Hadassah University Hospital and Hadasit, the technology transfer company of Hadassah Medical Organization, announced today that scientists at Hadassah University Hospital have discovered a new application for human embryonic stem cells. They have demonstrated for the first time that transplanted neural cells derived from human embryonic stem cells can reduce the clinical symptoms in animals with a form of multiple sclerosis.
The findings of the study are published in an article titled “Neuroprotective Effect of Transplanted Human Embryonic Stem Cell-Derived Neural Precursors in an Animal Model of Multiple Sclerosis” in the Scientific Journal of PLoS One, a new, high-impact, peer-reviewed, open-access, online publication. Click here to access the article: http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003145.
The data presented in the report are the result of a long-term collaboration between Professor Tamir Ben Hur, director of the Neurological Department at Hadassah Hospital and Professor Benjamin Reubinoff, director of the Human Embryonic Stem Cell Research Center at Hadassah Hospital. Ms. Michal Aharonowiz and Dr. Ofira Einstein both from Hadassah, as well as Professor Hans Lassmann from the University of Vienna also contributed.
“Human embryonic stem cell-derived neural precursors were transplanted into the brains of mice with an experimental form of MS. The grafted human cells integrated in the mice brains and migrated towards the sites of inflammation. They suppressed the inflammatory process in the brain, and consequently protected the animals from demyelination and nerve cell extension (axonal) injury, which are the pathological hallmarks of MS,” said Professor Benjamin Reubinoff.
Multiple sclerosis, the most common cause of neurological disabilities in young adults, is caused by an inflammatory reaction of the patient’s own immune system against the myelin sheath that envelops the nerve processes. The destruction of myelin leads to the degeneration and loss of nerve cells and permanent neurological disabilities. MS affects 2.5 million people worldwide.
“We believe that the encouraging therapeutic effects in the rodent model of MS justify moving ahead to clinical studies. We also anticipate that the anti-inflammatory effect demonstrated in the pre-clinical study may be combined in the future with the use of other human embryonic stem cell derived neural cells to repair the myelin in the brain,” said Professor Reubinoff.
Friday, August 01, 2008
FDA recommendations for cardiac monitoring of patients with multiple sclerosis (MS) who are treated with Novantrone
Additional Cardiac Monitoring for Patients on Mitoxantrone - from Heartwire — a professional news service of WebMD
Sue Hughes
July 30, 2008 — The FDA has issued an alert informing healthcare professionals about additional recommendations for cardiac monitoring of patients with multiple sclerosis (MS) who are treated with mitoxantrone (marketed as Novantrone and as generics) [1].
In 2005, the labeling for mitoxantrone was changed to recommend that left ventricular ejection fraction (LVEF) be evaluated before initiating treatment and before administering each dose of mitoxantrone to patients with MS. These changes were established in response to postmarketing and case reports in the medical literature that described decreases in LVEF or frank congestive heart failure in patients with MS who had received cumulative doses of mitoxantrone that were lower than 100 mg/m2.
Since that time, the FDA has received information from a postmarketing safety study that demonstrated poor adherence to these recommendations in clinical practice. This study used insurance-claims data and medical-record reviews to examine cardiac monitoring patterns in clinical practice. In this study, it was noted that four patients developed congestive heart failure 4 to 17 months after completing therapy with mitoxantrone.
Given the potential severity of cardiotoxicity and evidence suggesting poor adherence to the recommendations for monitoring cardiac function, the FDA is currently working with the manufacturers of mitoxantrone to remind healthcare professionals of the importance of adhering to the recommendations for patients with MS who are treated with mitoxantrone.
In addition, the FDA and the manufacturers are now advising that all patients with MS who have finished treatment with mitoxantrone receive yearly quantitative LVEF evaluations to detect late-occurring cardiac toxicity.
The FDA has issued the following recommendations for patients treated with mitoxantrone.
For All Patients
Assess signs and symptoms of cardiac disease with a history, physical examination, and ECG before initiating therapy with mitoxantrone.
Perform a baseline quantitative evaluation of LVEF.
For Patients With MS
Patients with a baseline LVEF below the lower limit of normal should not be treated with mitoxantrone.
Patients should be assessed for cardiac signs and symptoms with a history, physical examination, and ECG before each dose.
Patients should undergo a quantitative reevaluation of LVEF before each dose, using the same methodology for each assessment. Additional doses of mitoxantrone should not be administered to patients who have experienced either a drop in LVEF to below the lower limit of normal or a clinically significant reduction in LVEF during mitoxantrone therapy.
Patients should not receive a cumulative mitoxantrone dose greater than 140 mg/m2.
Patients should undergo yearly quantitative LVEF evaluations after stopping mitoxantrone to monitor for late-occurring cardiotoxicity, using the same methodology that was used for assessments that were done during treatment.
For Patients With cancer
The possible danger of cardiac effects in patients previously treated with daunorubicin or doxorubicin should be considered when weighing the benefits and risks of mitoxantrone.
The presence or history of cardiovascular disease, previous or concomitant radiotherapy to the mediastinal/pericardial area, previous therapy with other anthracyclines or anthracenediones, or the concomitant use of other cardiotoxic drugs might increase the risk of cardiac toxicity. LVEF should be monitored regularly after the initiation of therapy in patients with these risk factors.
Sue Hughes
July 30, 2008 — The FDA has issued an alert informing healthcare professionals about additional recommendations for cardiac monitoring of patients with multiple sclerosis (MS) who are treated with mitoxantrone (marketed as Novantrone and as generics) [1].
In 2005, the labeling for mitoxantrone was changed to recommend that left ventricular ejection fraction (LVEF) be evaluated before initiating treatment and before administering each dose of mitoxantrone to patients with MS. These changes were established in response to postmarketing and case reports in the medical literature that described decreases in LVEF or frank congestive heart failure in patients with MS who had received cumulative doses of mitoxantrone that were lower than 100 mg/m2.
Since that time, the FDA has received information from a postmarketing safety study that demonstrated poor adherence to these recommendations in clinical practice. This study used insurance-claims data and medical-record reviews to examine cardiac monitoring patterns in clinical practice. In this study, it was noted that four patients developed congestive heart failure 4 to 17 months after completing therapy with mitoxantrone.
Given the potential severity of cardiotoxicity and evidence suggesting poor adherence to the recommendations for monitoring cardiac function, the FDA is currently working with the manufacturers of mitoxantrone to remind healthcare professionals of the importance of adhering to the recommendations for patients with MS who are treated with mitoxantrone.
In addition, the FDA and the manufacturers are now advising that all patients with MS who have finished treatment with mitoxantrone receive yearly quantitative LVEF evaluations to detect late-occurring cardiac toxicity.
The FDA has issued the following recommendations for patients treated with mitoxantrone.
For All Patients
Assess signs and symptoms of cardiac disease with a history, physical examination, and ECG before initiating therapy with mitoxantrone.
Perform a baseline quantitative evaluation of LVEF.
For Patients With MS
Patients with a baseline LVEF below the lower limit of normal should not be treated with mitoxantrone.
Patients should be assessed for cardiac signs and symptoms with a history, physical examination, and ECG before each dose.
Patients should undergo a quantitative reevaluation of LVEF before each dose, using the same methodology for each assessment. Additional doses of mitoxantrone should not be administered to patients who have experienced either a drop in LVEF to below the lower limit of normal or a clinically significant reduction in LVEF during mitoxantrone therapy.
Patients should not receive a cumulative mitoxantrone dose greater than 140 mg/m2.
Patients should undergo yearly quantitative LVEF evaluations after stopping mitoxantrone to monitor for late-occurring cardiotoxicity, using the same methodology that was used for assessments that were done during treatment.
For Patients With cancer
The possible danger of cardiac effects in patients previously treated with daunorubicin or doxorubicin should be considered when weighing the benefits and risks of mitoxantrone.
The presence or history of cardiovascular disease, previous or concomitant radiotherapy to the mediastinal/pericardial area, previous therapy with other anthracyclines or anthracenediones, or the concomitant use of other cardiotoxic drugs might increase the risk of cardiac toxicity. LVEF should be monitored regularly after the initiation of therapy in patients with these risk factors.
Marijuana impairs thinking in MS patients
By Michelle Rizzo Thursday, Jul. 31, 2008; 6:26 PM
NEW YORK (Reuters Health) -
Patients with multiple sclerosis who smoke marijuana show impaired thinking compared with patients who do not smoke marijuana, according to findings in the journal Neurology.
Frank's editorial comment: Hmmm, how much did that study cost?
NEW YORK (Reuters Health) -
Patients with multiple sclerosis who smoke marijuana show impaired thinking compared with patients who do not smoke marijuana, according to findings in the journal Neurology.
Frank's editorial comment: Hmmm, how much did that study cost?
Adult Stem Cells Reprogrammed To Become Myelin-Making Cells
From Medical News Today
Research published in Nature Neuroscience , electronic publication ahead of print) has shown that adult stem cells in mice that are developing into nerve cells can be redirected to turn into myelin -making cells by changing a single gene . This type of research may some day help repair the damage to myelin which occurs in multiple sclerosis (MS).
In people with MS the immune system can attack both myelin and myelin making cells (oligodendrocytes). Limiting the number of myelin making cells impairs the capacity to repair the damage to myelin. One potential treatment option currently being investigated involves encouraging immature stem cells that reside in the adult brain, called neural stem cells, to move to areas of damage and repair myelin.
When neural stem cells are grown in the laboratory scientists have been able to reprogramme them to develop into several different types of brain cells, including oligodendrocytes. This latest research which took place in The Salk Institute for Biological Studies in California sought to determine if it would be possible to repeat these experiments in the brain.
A gene called Asc1 which is associated with oligodendrocyte development was introduced into the stem cells in the brain and caused neural stem cells to develop into oligodendrocytes.
This study confirms that adult stem cells in the brain retain their ability to be converted to certain other types of brain cells. Further research is needed to determine the significance of these finding to myelin repair in people with MS.
Dr Laura Bell at the MS Society said: 'Finding a way to cause stem cells which are already present in the brain to repair damaged myelin is an attractive potential treatment option for people with MS. This is early research but it is an important step and we look forward to seeing how the work progresses.'
Research published in Nature Neuroscience , electronic publication ahead of print) has shown that adult stem cells in mice that are developing into nerve cells can be redirected to turn into myelin -making cells by changing a single gene . This type of research may some day help repair the damage to myelin which occurs in multiple sclerosis (MS).
In people with MS the immune system can attack both myelin and myelin making cells (oligodendrocytes). Limiting the number of myelin making cells impairs the capacity to repair the damage to myelin. One potential treatment option currently being investigated involves encouraging immature stem cells that reside in the adult brain, called neural stem cells, to move to areas of damage and repair myelin.
When neural stem cells are grown in the laboratory scientists have been able to reprogramme them to develop into several different types of brain cells, including oligodendrocytes. This latest research which took place in The Salk Institute for Biological Studies in California sought to determine if it would be possible to repeat these experiments in the brain.
A gene called Asc1 which is associated with oligodendrocyte development was introduced into the stem cells in the brain and caused neural stem cells to develop into oligodendrocytes.
This study confirms that adult stem cells in the brain retain their ability to be converted to certain other types of brain cells. Further research is needed to determine the significance of these finding to myelin repair in people with MS.
Dr Laura Bell at the MS Society said: 'Finding a way to cause stem cells which are already present in the brain to repair damaged myelin is an attractive potential treatment option for people with MS. This is early research but it is an important step and we look forward to seeing how the work progresses.'
Sunday, July 13, 2008
Best Treatment For MS May Depend On Disease Subtype
Animal studies by University of Michigan scientists suggest that people who experience the same clinical signs of multiple sclerosis (MS) may have different forms of the disease that require different kinds of treatment.
The results, if borne out in further studies, point to a time when doctors will be able to target specific inflammatory processes in the body and more effectively help MS patients, using available drugs and new ones in the pipeline.
Since the 1990s, the treatment picture has brightened for people with multiple sclerosis in its most common form, relapsing-remitting MS. Beta interferon drugs and glatiramer acetate (marketed as Copaxone) have proved effective at decreasing the attack rate and suppressing inflammatory plaque development in many patients with MS. Yet why the drugs help some patients, but not others, has remained a mystery.
The U-M research team conducted the studies in mice that have a disease similar to MS: experimental autoimmune encephalomyelitis or EAE. The team found that different inflammatory chemicals, whose activity is linked to two different types of immune system T cells, could bring on the same paralysis and other MS-like signs. They also showed that drugs that block one of the inflammation pathways were not effective at blocking the other. The results, published online ahead of print, will appear in the July 7 issue of the Journal of Experimental Medicine.
"These two forms of disease differ in the specific anti-inflammatory agents that they are responsive to," says Benjamin Segal, M.D., the study's senior author and the director of the Multiple Sclerosis Center at the U-M Health System.
"We already know that some people respond better to the drugs beta interferon or Copaxone than others. Now we've shown proof that you can cause MS-like syndrome in mice due to qualitatively different types of inflammatory damage. As a result, these two kinds of inflammation likely require different approaches to treatment," says Segal. He directs the Holtom-Garrett Program in Neuroimmunology and is the Holtom-Garrett Family Professor of Neurology at the U-M Medical School.
Context:
MS is an inflammatory disease of the central nervous system believed to be autoimmune in nature. Certain cells in the body's immune system mount an inappropriate response against proteins in the nervous system, in particular myelin, the fatty substance that covers nerve axons. MS affects an estimated 2.5 million people worldwide. Symptoms, which vary widely, include numbness and weakness, incontinence, double vision, tremor, imbalance and pain.
In 85 percent of MS cases, patients begin with what is called a relapsing-remitting form of the disease. Initially, they have attacks in which they experience symptoms for a time, return to normal, then have attacks again. In the last 15 years, several beta interferon drugs and Copaxone have been effective in many patients at limiting the number of attacks. These drugs also can also decrease damage in the brain as visualized on MRI scans.
Research details:
Segal's research team injected one group of mice with an immune system T helper cell, Th1, long believed to play a role in MS, and another group with a T helper cell, Th17, whose potential role in MS has recently come to light. They measured the activity of specific inflammatory agents that are induced by each type of T cell as the immune system mounts its misguided attack on the myelin sheaths of nerve cells.
Both groups of mice developed similarly severe and rapid paralysis. But the researchers found clear differences in the inflammatory agents involved, called cytokines and chemokines, and in the resulting damage to the central nervous system.
Mice injected with Th1 cells showed a pattern of central nervous system inflammation that resembled that of common MS, with lesions filled with macrophages, a type of immune system defender cell. Mice injected with Th17 cells, however, had lesions filled with another immune cell type, neutrophils. In these mice, inflammation reached deep in central nervous system tissues and in the optic nerve.
In both groups of mice, the scientists tested the effects of neutralizing antibody drugs similar to drugs being developed against autoimmune diseases in humans. Some of the drugs inhibited disease in the Th17 mice, but not in the mice receiving Th1 cells. Other drugs were effective against both types of disease.
"That's our proof that these really are different mechanisms of disease," says Mark Kroenke, the study's first author and a Ph.D. student in immunology at U-M.
Implications:
It's not yet known whether the same differences will prove true in people with MS. But the study suggests the need to develop drugs tailored to affect distinct inflammation pathways that might drive different forms of relapsing-remitting MS.
"We speculate at some point being able to identify and measure active inflammatory agents in patients, and to develop customized profiles that would help predict what treatments will be effective," Segal says.
In addition, Segal says, the findings may aid the search for effective drugs for two difficult-to-treat diseases closely related to MS: neuromyelitis optica, which affects the optic nerve and spinal cord, and opticospinal MS, most common in Asia. The pattern of inflammation the team saw in the Th17-injected mice resembled the pattern in these variants of MS.
Other authors include: Anuska V. Andjelkovic, Ph.D., U-M Department of Pathology; and Thaddeus J. Carlson, Ph.D., University of Rochester School of Medicine and Dentistry.
Segal is on the scientific advisory board of the National MS Society, http://www.nationalmssociety.org/index.aspx
This work was supported by grants from the National Multiple Sclerosis Society and the National Institutes of Health.
The results, if borne out in further studies, point to a time when doctors will be able to target specific inflammatory processes in the body and more effectively help MS patients, using available drugs and new ones in the pipeline.
Since the 1990s, the treatment picture has brightened for people with multiple sclerosis in its most common form, relapsing-remitting MS. Beta interferon drugs and glatiramer acetate (marketed as Copaxone) have proved effective at decreasing the attack rate and suppressing inflammatory plaque development in many patients with MS. Yet why the drugs help some patients, but not others, has remained a mystery.
The U-M research team conducted the studies in mice that have a disease similar to MS: experimental autoimmune encephalomyelitis or EAE. The team found that different inflammatory chemicals, whose activity is linked to two different types of immune system T cells, could bring on the same paralysis and other MS-like signs. They also showed that drugs that block one of the inflammation pathways were not effective at blocking the other. The results, published online ahead of print, will appear in the July 7 issue of the Journal of Experimental Medicine.
"These two forms of disease differ in the specific anti-inflammatory agents that they are responsive to," says Benjamin Segal, M.D., the study's senior author and the director of the Multiple Sclerosis Center at the U-M Health System.
"We already know that some people respond better to the drugs beta interferon or Copaxone than others. Now we've shown proof that you can cause MS-like syndrome in mice due to qualitatively different types of inflammatory damage. As a result, these two kinds of inflammation likely require different approaches to treatment," says Segal. He directs the Holtom-Garrett Program in Neuroimmunology and is the Holtom-Garrett Family Professor of Neurology at the U-M Medical School.
Context:
MS is an inflammatory disease of the central nervous system believed to be autoimmune in nature. Certain cells in the body's immune system mount an inappropriate response against proteins in the nervous system, in particular myelin, the fatty substance that covers nerve axons. MS affects an estimated 2.5 million people worldwide. Symptoms, which vary widely, include numbness and weakness, incontinence, double vision, tremor, imbalance and pain.
In 85 percent of MS cases, patients begin with what is called a relapsing-remitting form of the disease. Initially, they have attacks in which they experience symptoms for a time, return to normal, then have attacks again. In the last 15 years, several beta interferon drugs and Copaxone have been effective in many patients at limiting the number of attacks. These drugs also can also decrease damage in the brain as visualized on MRI scans.
Research details:
Segal's research team injected one group of mice with an immune system T helper cell, Th1, long believed to play a role in MS, and another group with a T helper cell, Th17, whose potential role in MS has recently come to light. They measured the activity of specific inflammatory agents that are induced by each type of T cell as the immune system mounts its misguided attack on the myelin sheaths of nerve cells.
Both groups of mice developed similarly severe and rapid paralysis. But the researchers found clear differences in the inflammatory agents involved, called cytokines and chemokines, and in the resulting damage to the central nervous system.
Mice injected with Th1 cells showed a pattern of central nervous system inflammation that resembled that of common MS, with lesions filled with macrophages, a type of immune system defender cell. Mice injected with Th17 cells, however, had lesions filled with another immune cell type, neutrophils. In these mice, inflammation reached deep in central nervous system tissues and in the optic nerve.
In both groups of mice, the scientists tested the effects of neutralizing antibody drugs similar to drugs being developed against autoimmune diseases in humans. Some of the drugs inhibited disease in the Th17 mice, but not in the mice receiving Th1 cells. Other drugs were effective against both types of disease.
"That's our proof that these really are different mechanisms of disease," says Mark Kroenke, the study's first author and a Ph.D. student in immunology at U-M.
Implications:
It's not yet known whether the same differences will prove true in people with MS. But the study suggests the need to develop drugs tailored to affect distinct inflammation pathways that might drive different forms of relapsing-remitting MS.
"We speculate at some point being able to identify and measure active inflammatory agents in patients, and to develop customized profiles that would help predict what treatments will be effective," Segal says.
In addition, Segal says, the findings may aid the search for effective drugs for two difficult-to-treat diseases closely related to MS: neuromyelitis optica, which affects the optic nerve and spinal cord, and opticospinal MS, most common in Asia. The pattern of inflammation the team saw in the Th17-injected mice resembled the pattern in these variants of MS.
Other authors include: Anuska V. Andjelkovic, Ph.D., U-M Department of Pathology; and Thaddeus J. Carlson, Ph.D., University of Rochester School of Medicine and Dentistry.
Segal is on the scientific advisory board of the National MS Society, http://www.nationalmssociety.org/index.aspx
This work was supported by grants from the National Multiple Sclerosis Society and the National Institutes of Health.
Monday, June 30, 2008
ADA Amendments Act of 2008
In a Letter to the Editor of the Orange County Register I wrote:
The ADA Amendments Act of 2008 passed the House of Representatives by a vote of 402 to 17!!!! Great stuff, but…
For those of us that live in California’s 48th Congressional District represented by Congressman John Campbell we should note that our Congressman was one of the 17!
Now I ask, “Congressman Campbell, why?”
The ADA Amendments Act of 2008 passed the House of Representatives by a vote of 402 to 17!!!! Great stuff, but…
For those of us that live in California’s 48th Congressional District represented by Congressman John Campbell we should note that our Congressman was one of the 17!
Now I ask, “Congressman Campbell, why?”
Sunday, June 29, 2008
From the Team Mitsubishi/Nationwide Traffic MS 150 Webpage
Gaining Traction
At this moment in time we have been given great fortune. Our generation above others has been bestowed a deep understanding of the world and the power to do so much. And if we fail to make the most of this moment - if we convert hope and understanding into isolation - if pausing merely leads to complacency - then history can rightly point its finger at each of us.
Action does not have to mean “anything goes”. It need not be morally corrupt. Given a choice, most people want to be thought of a winner and in the right way. We all want to be part of a successful endeavor. We all want meaning, with the freedom to achieve success, not just to survive. We all want the best from life for ourselves, for our families, colleagues, community and society.
Achieving financial objectives and having fun while doing so is one of the fundamentals of why we participate. Beyond the traditional value fun takes on a greater sense. Fun also means enjoying the challenge of involvement, contribution, accomplishment, personal enrichment and satisfaction.
We are identified by a social and ethical balance beyond isolated entities. It’s important not only to have a clear understanding of the “Mission” and role of the NMSS, but also an intense sense of performance. There’s more to performance. A team will provide a wider view- expecting each member to give time and talent to the common cause. Truly “winning” or “success” is from contribution transitioning into a passion to perform. It is this passion that fuels the team and ignites will.
Whatever form winning or success takes on also has to serve the well being of the team. It must also include a process of continual self-improvement. Not as a creed or fixed promise but an attitude. It is about pride, with people knowing that they are pushing themselves to achieve the best that they can. Having genuine interest and excitement in the team’s actions are as important as actual achievement.
In the final analysis, the value of existence is not dependent on crisis - nor should it consist only of dramatic victories. However un-dramatic the pursuit, it must go on. The challenge- to do what we can to create a world free of MS, to be sure is real. Our concepts and definition of this challenge may be very different, but when we give it our all and to the best of our ability it shouldn’t matter what anyone thinks. What matters most is who we are and our expression of life.
For eight years Team Mitsubishi has been part of the “Movement” and we have rallied to the challenge. It started with four riders and every year since we have been in the Top 25 of teams in money raised. We have transitioned into a great group of dedicated people who also enjoy participating. For 2008 the team has been acknowledged as the “Best (Team) Promoting the Mission.” (Of the NMSS)
We dedicate this year’s ride to: Frank Austin- Champion (of MS), Starr Velez, Barbara Ferrante, Matt Bolcer and Kelly Clark and to our family members, friends and co-workers touched by MS.
Together we will end the devastating effects of MS.
At this moment in time we have been given great fortune. Our generation above others has been bestowed a deep understanding of the world and the power to do so much. And if we fail to make the most of this moment - if we convert hope and understanding into isolation - if pausing merely leads to complacency - then history can rightly point its finger at each of us.
Action does not have to mean “anything goes”. It need not be morally corrupt. Given a choice, most people want to be thought of a winner and in the right way. We all want to be part of a successful endeavor. We all want meaning, with the freedom to achieve success, not just to survive. We all want the best from life for ourselves, for our families, colleagues, community and society.
Achieving financial objectives and having fun while doing so is one of the fundamentals of why we participate. Beyond the traditional value fun takes on a greater sense. Fun also means enjoying the challenge of involvement, contribution, accomplishment, personal enrichment and satisfaction.
We are identified by a social and ethical balance beyond isolated entities. It’s important not only to have a clear understanding of the “Mission” and role of the NMSS, but also an intense sense of performance. There’s more to performance. A team will provide a wider view- expecting each member to give time and talent to the common cause. Truly “winning” or “success” is from contribution transitioning into a passion to perform. It is this passion that fuels the team and ignites will.
Whatever form winning or success takes on also has to serve the well being of the team. It must also include a process of continual self-improvement. Not as a creed or fixed promise but an attitude. It is about pride, with people knowing that they are pushing themselves to achieve the best that they can. Having genuine interest and excitement in the team’s actions are as important as actual achievement.
In the final analysis, the value of existence is not dependent on crisis - nor should it consist only of dramatic victories. However un-dramatic the pursuit, it must go on. The challenge- to do what we can to create a world free of MS, to be sure is real. Our concepts and definition of this challenge may be very different, but when we give it our all and to the best of our ability it shouldn’t matter what anyone thinks. What matters most is who we are and our expression of life.
For eight years Team Mitsubishi has been part of the “Movement” and we have rallied to the challenge. It started with four riders and every year since we have been in the Top 25 of teams in money raised. We have transitioned into a great group of dedicated people who also enjoy participating. For 2008 the team has been acknowledged as the “Best (Team) Promoting the Mission.” (Of the NMSS)
We dedicate this year’s ride to: Frank Austin- Champion (of MS), Starr Velez, Barbara Ferrante, Matt Bolcer and Kelly Clark and to our family members, friends and co-workers touched by MS.
Together we will end the devastating effects of MS.
Tuesday, June 24, 2008
Letter to a California State Assemblyman & my personal followup to its author
June 23, 2008
The Honorable Mervyn Dymally
California State Assembly
California State Capitol, Room 6005
Sacramento, CA 95814
Dear Assembly member Dymally:
Re: SB 1198 (Kuehl) Durable Medical Equipment - SUPPORT
A few years ago, you spoke to our organization, Cal Neuro Alliance, at our annual conference in Sacramento. I was very impressed with what you had to say and how you said it. The next day, while at the Capital building, our Advocacy team bumped into you in the hall and your graciousness was impeccable. I am a person with multiple sclerosis and my older brother also has MS.
As I am sure you are aware, SB 1198 is scheduled to be heard in the Assembly Health Committee tomorrow. I urge you to support this important bill which would require health insurers and health plans to offer coverage for durable medical equipment (DME), without a separate benefit cap, as part of their group contracts and policies. This is an important bill that will help disabled people who depend on durable medical equipment to live independent lives.
Multiple sclerosis (MS) is a chronic and often disabling disease of the central nervous system that typically is diagnosed in young adulthood. MS can lead to physical, cognitive and psychiatric symptoms, as well as functional limitations. My brother and I have all those symptoms between us. For many people living with multiple sclerosis, durable medical equipment - especially wheelchairs, scooters and walkers - is critical to their ability to live independently. My brother would be significantly impacted in his personal life if he did not have access to the correct DME. However, private health plans and insurance coverage usually puts lower caps on DME than they place on other medical services. SB 1198 will address this gap in coverage by preventing group health insurance plans from placing special coverage limitations on DME and providing a much needed lifeline for individuals with MS to function at the highest level possible at home, at work, and in the community.
I appreciate your efforts on our behalf. I urge your support of this legislation.
Sincerely,
My email to the author of this letter follows:
First, let me say I am addressing all those addressed in your previous email. Second, I remember first hand and very precisely the graciousness afforded by Assemblyman Dymally during our chance encounter. As the recipient of his gracious deference (it was deference I didn’t expect or solicit) to a man in a wheel chair, I can only echo your praise.
I feel I know without question where Assemblyman Dymally will come down on this issue. The Assemblyman demonstrated all things good during that chance encounter! He took the extra step to help his fellow man! It really didn’t take a lot of effort, but in the busy hustle bustle environment that is the California Capitol Building he took the time to pause and assist his fellow man!
Well done! I commend you for remembering and using that event as a springboard in a letter several years later.
Frank
The Honorable Mervyn Dymally
California State Assembly
California State Capitol, Room 6005
Sacramento, CA 95814
Dear Assembly member Dymally:
Re: SB 1198 (Kuehl) Durable Medical Equipment - SUPPORT
A few years ago, you spoke to our organization, Cal Neuro Alliance, at our annual conference in Sacramento. I was very impressed with what you had to say and how you said it. The next day, while at the Capital building, our Advocacy team bumped into you in the hall and your graciousness was impeccable. I am a person with multiple sclerosis and my older brother also has MS.
As I am sure you are aware, SB 1198 is scheduled to be heard in the Assembly Health Committee tomorrow. I urge you to support this important bill which would require health insurers and health plans to offer coverage for durable medical equipment (DME), without a separate benefit cap, as part of their group contracts and policies. This is an important bill that will help disabled people who depend on durable medical equipment to live independent lives.
Multiple sclerosis (MS) is a chronic and often disabling disease of the central nervous system that typically is diagnosed in young adulthood. MS can lead to physical, cognitive and psychiatric symptoms, as well as functional limitations. My brother and I have all those symptoms between us. For many people living with multiple sclerosis, durable medical equipment - especially wheelchairs, scooters and walkers - is critical to their ability to live independently. My brother would be significantly impacted in his personal life if he did not have access to the correct DME. However, private health plans and insurance coverage usually puts lower caps on DME than they place on other medical services. SB 1198 will address this gap in coverage by preventing group health insurance plans from placing special coverage limitations on DME and providing a much needed lifeline for individuals with MS to function at the highest level possible at home, at work, and in the community.
I appreciate your efforts on our behalf. I urge your support of this legislation.
Sincerely,
My email to the author of this letter follows:
First, let me say I am addressing all those addressed in your previous email. Second, I remember first hand and very precisely the graciousness afforded by Assemblyman Dymally during our chance encounter. As the recipient of his gracious deference (it was deference I didn’t expect or solicit) to a man in a wheel chair, I can only echo your praise.
I feel I know without question where Assemblyman Dymally will come down on this issue. The Assemblyman demonstrated all things good during that chance encounter! He took the extra step to help his fellow man! It really didn’t take a lot of effort, but in the busy hustle bustle environment that is the California Capitol Building he took the time to pause and assist his fellow man!
Well done! I commend you for remembering and using that event as a springboard in a letter several years later.
Frank
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