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October 31, 2003

Medicare Madness

Congress still hasn't come to an agreement on the Medicare bill. Who can be surprised at this point? Frankly, this bill is more about gaining an edge in next year's election than what is best for those who need medical care or what makes the most budgetary sense. If they don't come to an agreement (and I believe they will) watch for a lot of finger-pointing.

Bad news did come out today concerning Medicare. The government announced it is cutting payments (again) to physicians by 4.5 percent. This at the same time they gave themselves a 2 percent pay raise. This does hurt patients. Doctor are increasingly limiting the number of Medicare patients they handle.

A fairly common (and hidden) practice in doctor's offices is when a patient calls in to make an appointment they are asked for their age. If they are over 65 they are told the next available appointment is in 5 to 6 weeks. If they are younger they are told that appoints are available within a few days. This cuts down on the medicade patients. There's no free lunch. If the government doesn't pay enough, the care will suffer. That's wrong.

Posted by Dave at 09:33 PM | Comments (0) | TrackBack

October 30, 2003

BDNF Breakthrough

If BDNF sounds familiar to you it's probably because you've read about it on HD Lighthouse. BDNF, or Brain Derived Neurotrophic Factor, is an important chemical in the brain. Many theorize that boosting BDNF would slow or stop the progression of Huntington's Disease.

As is often the case, research for one disease benefits another disease. Here, researchers investigating Rett Syndrome, a disease where too much BDNF is produced, have identified the gene that regulates BDNF.

Turning this discovery into therapy could not only treat Rett Syndrome (by turning the BDNF off), it could treat Huntington's Disease (by producing more BDNF).

Here is a press release on this discovery from the Rett Syndrome Research Foundation:

Rett Syndrome Research Foundation

RSRF-funded study leads to breakthrough for Rett Syndrome research
A collaborative study between the laboratories of Michael Greenberg of Children's Hospital Boston and Rudolf Jaenisch of the Whitehead Institute of Biomedical Research has resulted in a significant breakthrough. The investigators report in the October 31, 2003 issue of the prestigious journal Science, that the "Rett Syndrome gene", MECP2, regulates expression of the gene encoding brain-derived-neurotrophic factor (BDNF). The study was funded, in part, by the Rett Syndrome Research Foundation (RSRF). A paper by Yi Sun and colleagues of UCLA published in the same issue further corroborates Greenberg's and Janenisch's findings.

Rett Syndrome is a devastating neurological disorder diagnosed almost exclusively in girls. Children with Rett Syndrome (RTT) appear to develop normally until 6 to 18 months of age, when they enter a period of regression, losing speech and motor skills. Most develop repetitive hand movements, irregular breathing patterns, seizures and extreme motor control problems. RTT leaves its victims profoundly disabled, requiring maximum assistance with every aspect of daily living. There is no cure.

Although the protein implicated in RTT, MeCP2, is known, its precise function is not. Past experiments have demonstrated that MeCP2, acting like a biological deadbolt, binds to genes that have undergone methylation (a fundamental biological process in which the cell disables genes it doesn't use by modifying them with a methyl group) preventing them from activating. As a result, scientists theorized that MeCP2 was a "long-range gene repressor."

Jaenisch's lab, with RSRF funding, demonstrated that when MeCP2 is disabled in mice, the animals manifest Rett-like symptoms. The next step was to figure out why this happens and what genes MeCP2 targets.

Concurrently, Greenberg, who is also a professor of neurobiology at Harvard Medical School, was studying a central nervous system gene, BDNF, which is highly active in infants aged 6 to 18 months -- the same age that Rett symptoms first appear. This brain derived neurotrophic factor gene is essential for neural plasticity, learning and memory. BDNF is also implicated in other neurological disorders including Huntington's Disease.

Greenberg noted that BDNF constantly flips back and forth between an "on" state, where it rapidly produces protein, and an "off" state, during which it is silent.

"We knew a lot about how it was turned on," says Greenberg, "but we wanted to know what kept it off."

A graduate student in Greenberg's laboratory, Wen Chen, discovered that MeCP2 controlled the "off" state of BDNF, suggesting that BDNF might contribute to the symptoms seen in RTT. The assumption was that once MeCP2 bound to BDNF, the gene would become permanently inactive. Instead, Chen and post-doctoral fellow, Qiang Chang of the Jaenisch lab, discovered a far more dynamic process.

After the BDNF gene is methylated, MeCP2 does indeed bind to it, shutting the gene off -- but only temporarily. If neurons are excited by any kind of environmental stimuli, MeCP2 immediately detaches, and the BDNF gene begins producing protein. When the stimulus disappears, MeCP2 re-attaches to BDNF, again locking the deadbolt until neuronal stimuli start the process again. Greenberg and Jaenisch say they have never before witnessed this kind of process.

"I find this to be an extremely exciting new development. It is particularly gratifying that RSRF support facilitated the Jaenisch study. RSRF's commitment to funding research into the causes of Rett is clearly beginning to pay off. " says Adrian Bird, of the University of Edinburgh, whose lab discovered MeCP2 more than a decade ago. "To me, what's particularly surprising is that DNA methylation appears to be involved with dynamic regulation of this gene. In the past it has been associated with long term inflexible gene silencing." Bird, Chairman of the RSRF Scientific Advisory Board, has a Perspective article published in the same issue of Science. "It might well be that BDNF is a crucial gene that explains some of the symptoms of Rett patients, but we can't be really sure yet."

The investigators theorize that in Rett patients, mutations in MeCP2 impair its ability to regulate BDNF, and that BDNF's subsequent over-expression may cause Rett symptoms. However, Greenberg points out that BDNF is only one of approximately 300 genes that are controlled by neuronal activity, some of which may also be MeCP2 targets.

The next step, says Greenberg, "is to identify other genes that are regulated by MeCP2," which he says can now can be done on a genome-wide scale. Greenberg was recently awarded a grant by RSRF to support his ongoing research.

"The Greenberg and Sun publications will generate unprecedented attention for RTT in the scientific community. RSRF stands poised to capitalize on any breakthroughs that can be translated into clinical applications for RTT patients." says Monica Coenraads, RSRF VP of Research.

Founded in late 1999, RSRF is the world's only organization devoted exclusively to advancing and supporting biomedical research for RTT. To date, RSRF has committed $4.5 million to fund 45 research projects and scientific meetings.

"RSRF's support of this crucial research underscores our commitment to funding high quality science. In 2002, 98 cents of every dollar went directly to our research program. We are determined to increase our financial commitment to equal the momentum generated by these new developments." says Gordon Rich, RSRF President.

###
For more information on RSRF please visit our website at www.rsrf.org . Investigators interested in joining RSRF's Email broadcast please email monica@rsrf.org with name, institution and area of specialty.

Posted by Dave at 09:47 PM | Comments (0) | TrackBack

October 29, 2003

Bleepin Spammers

Some unethical organizations post commercial advertisements in the comments sections of Blogs. Forcing the bloggers to cover the cost of their advertising. The spammers use computer programs that can post thousands of SPAM's an hour using valuable disk space and bandwidth that the blogger must pay for.

I got hit tonight by a spammer offering prescription Viagra. When I looked up the company I found that this company used a .US domain name and yet they were based in Canada. They are spammers but they used a fake email address so they couldn't be spammed. They were violating several rules that must be met in order to have a .US domain name.

I turned them in to Neustar, the company that handles the .US domain. We'll see if they follow through. Bleepin spammers.

Posted by Dave at 10:05 PM | Comments (0) | TrackBack

HD Disability & Progression

There is an interesting study just published in 'Neurology'. Researchers reviewed the records on over 1000 Huntington's Disease patients. Here's some of what they found:

Chorea (movement) and dystonia (prolonged muscle contraction) are NOT correlated with disability. Weight loss correlated with heavy chorea. Higher CAG counts have a faster progression.

Here's the study abstract with more details:

Neurology. 2003 Oct 28;61(8):1085-92.

Huntington's disease: Clinical correlates of disability and progression.

Mahant N, McCusker EA, Byth K, Graham S.

Department of Neurology (Drs. Mahant and McCusker, and S. Graham) and Westmead Millennium Institute (Dr. Byth), Westmead Hospital.

OBJECTIVE: To define the phenotypic variation in a large population of patients with Huntington disease (HD) and to identity clinical features that predict disability and the rate of disease progression. METHODS: The authors analyzed data on 1,026 patients, followed for a median of 2.7 years, using a mixed effects model. The factors studied included the age at onset, the major clinical feature at onset, the severity of motor and cognitive impairment, and the level of disability.

RESULTS: The mean age at onset was 41.5 (range 8 to 83) years, and patients were enrolled at all stages of disease. Younger onset was associated with more dystonia, less chorea, and a faster rate of motor, cognitive, and functional progression. The rate of progression was not related to the major clinical feature at onset or the sex of the affected parent. Disability correlated with the motor score (excluding chorea and dystonia) and the symbol-digit modalities test. Weight loss correlated with severe chorea. CONCLUSIONS: The rate of progression of HD was significantly more rapid with a younger age at onset. Therefore, CAG repeat length may be an important determinant of not only the age at onset, but also the rate of disease progression. Chorea was associated with weight loss, but chorea and dystonia were not major determinants of disability.

PMID: 14581669

Posted by Dave at 06:10 PM | Comments (0) | TrackBack

October 28, 2003

The State of HD Research

Newsday has a great article on Huntington's Disease. While it does have a couple of minor errors, overall it is a great synopsis on the fight for a cure.

Here are some excerpts:

"There is a lot of excitement," said Dr. Peter Como"

"Several experimental drugs for Huntington's, including riluzole,are now in the final phases of testing. The results may seem like small advances: For example, some patients have recovered the coordination to be able to shave for the first time in years. Others are able to hold a teacup, or stack plates. But these are big things to the 30,000 people in the United States with the disease, and the 150,000 others at immediate genetic risk."

"We finally have some good hypotheses in Huntington's and it has implications for many genetic diseases," added Dr. Chris Ross, a Huntington's disease expert at Johns Hopkins Medical Institutes in Baltimore. "This is a hopeful time."

"In the co-enzyme Q10 trial, almost 400 patients are taking the pill in an attempt to slow progression of the disease, something the substance has done in animal models. The first studies showed modest improvement, and doctors are now enrolling patients for a study using a higher dose."

"(With the PHAROS study) (t)he hope, Como said, is to identify environmental modifiers - such as caffeine consumption, exercise, stress, social support, diet - that may bring on the disease earlier in some or push it back in others."

"But mood, behavior and thought changes are also part of the disease, and there is growing evidence that these more subtle problems begin many years before the physical symptoms. The Pharos study will address this theory."

You can read the whole article here.

Posted by Dave at 06:50 PM | Comments (0) | TrackBack

October 27, 2003

Tips For The Caregiver

Gerri on the Hunt-Dis email list posted a great message a couple of months ago to a caregiver that was faced with many challenges. There was so much wisdom and knowledge in that message that I asked her if I could post part of her message here and she was kind enough to say 'Yes'.

Here's her message with some comments:

While my husband has not yet had the leg cramps and contractions, he is in his 18th year of HD and still doesn't accept that he has it.

Denial, as most caregivers know, is a common symptom.

Actually, about 6 or 7 years ago I decided to just drop the subject, as there was nothing to be gained by that time.

No sense fighting a battle you won't win.

I'd finally established a routine with medications that were working and I (key word: I) just compromised and/or adjusted to everything else.

'Compromise' and 'Adjust' are two of the best tools for effectively coping with the situations caregivers face.

However, in the earlier years there would have been much to gain, not the least of which would have been his cooperation with medications and treatments. He raged and carried on and was often violent.

This is often hidden in the HD community but physical, emotional, and mental abuse is fairly common (and treatable with medications).

Everything was my fault, or our sons. There were some pretty tough and pretty scary times.

Very common when not on medication. I've heard so many people talk about virtually identical experiences. The person with HD really can believe they are 'normal' and their spouse is 'wrong'.

Without going into the grim details, let me say I can well relate to what you are going through. I'm sorry that you are in this position. I think these kinds of behaviors and the denial are about the toughest things to deal with in this disease.

Very true. This is very hard on loved ones, especially spouses.

For starters, (he) clearly needs medication intervention. At the least he needs, perhaps, an anti-psychotic.

I know we live in an age where we tend to take a pill for everything, but medication really is needed in these circumstances. The chemistry in the brain is thrown off and these medications help bring it back to more normal levels. It gives the person with HD (and their family) a degree of normalcy. Studies are even indicating that anti-depressants may help protect the brain against Huntington's Disease.

A good doctor, preferably familiar with HD, will help you through that. ... (doctors can refer you for OT, PT, Speech/Swallowing evaluations and therapies don't forget)

An doctor with active experience with HD makes all the difference in the world. This will make world a world of difference in the quality of care.

I have a few suggestions, from my experience, about other things you can do. I believe that, when faced with such extremes of behavior and symptoms, we have to seek extreme solutions.... devious methods, and whatever works.

Too often caregivers don't do what is best for the patient because of misplaced guilt. If it's in the best interest of the patient you're probably doing the right thing.

Now, without knowing a lot about (him) some of this may not be helpful for your circumstance but here are a few of the things I did with Charlie.

This is great advice...

I lied when necessary... I didn't tell him why we were going to the doctor.

This isn't even a lie. So much of the grief that comes from caregiving goes away when the caregiver learns that sometimes it is best not to provide alternatives or advance notice. Many times a 'matter of fact' statement is accepted without thought, especially if it is said in an ordinary manner.

I would make light of it saying it was a regular checkup, an annual physical, or to check on his ingrown toenail, for example -

Doesn't even have to be a lie, just don't provide the information that makes them uncomfortable. It's less stressful for them.

but I made certain to write out all my concerns for the doctor, in advance, and to instruct the doctor which things could be discussed in front of Charlie.

An experienced doctor is used to working this way. Again, this is a great way to minimize the stress on the patient while giving the doctor the information they need to know.

So, first you have to find the right doctor and maybe have a private appointment with him in advance of him seeing (your spouse).

Visiting in advance is a great suggestion but it is rarely done.

You have to have the full cooperation of the doctor so do some interviewing and don't be afraid to "fire" someone who doesn't get it. I did that a few times too.

Great, great advice. Be willing to fire any medical person who isn't doing the job. There are good one's out there. This is too important to just accept poor medical care.

When Charlie said he didn't have HD and didn't need medication, I said "fine" and gave them to him anyway.

This is where 'guilt' works against the caregiver and the patient. The medications are a critical element care of the patient. And they may also allow you to keep your sanity!

I didn't tell him the truth about what kind of pill I was giving him (for all he knew it was a vitamin)

Again, why distress the person if it isn't necessary. This isn't being 'dishonest' this is being 'caring' and doing what is best for them.

Sometimes I even dissolved or crushed them and put them in his food - the mayonnaise on his sandwich, or in a bite of oatmeal, soup, or applesauce. To make sure he got the bite with the meds in it, I'd put it on a spoon and say, "Here taste this. Is it _______ enough?"

Note: she didn't say "Would you like to try this?" which would probably get a "no". She just went ahead and did it. This technique works in so many circumstances.

There were times with his temper and raging that it worked for me to just put my foot down! When he was in that state there was no reasoning.

The temper and anger have nothing to do with reason and everything to do with biological factors. Trying to reason in these circumstances is futile. It'll just escalate the situation.

He would get out of control, like a little child, and so I would respond like I would to a child. "Screaming is NOT ok!!! You may not scream! Now, sit here and watch TV and calm down!" He would look so surprised at my sternness
that down in his recliner he would plop, and then I would help him find a tv program to watch. It didn't work all the time but when it did, it was such a relief.

Every situation is unique, find what works for you. Note how she didn't provide options, she just stated the way it was going to be. As I've said before, this technique can be effectively used in many circumstances.

But, honestly, the right medications made ALL the difference!!!!

So many caregivers are afraid of medicating their spouses/loved ones. Get over it! It's in the best interest of the person trying to deal with Huntington's Disease.

The thing I want to reiterate is that there almost always is something that can be done, though it isn't easy always to figure out what. What is the alternative, after all?

There are ways and there are people who have been there before you. Support groups (online and in-person) are a great resource for the caregiver.

I'd like to add one thing here:

You, the caregiver, MUST be taken care of first. If you do not take care of yourself then you will be unable to take care of your loved one. Keep a hobby, find ways to continue to do things you enjoy, get help, listen to music, drive, do whatever it takes to keep your sanity. Like on an airplane: Put on your air mask before putting on the air mask....(you know the rest).

Posted by Dave at 09:54 PM | Comments (2) | TrackBack

October 26, 2003

She's A Mommy!

Insomnomaniac Deb has given birth to her daughter Emma and both are well! A few months ago Emma was in a rush to get into this world and when it's finally time she holds out another 60 hours.

Congrats!

Posted by Dave at 07:09 PM | Comments (0) | TrackBack

Therapy Dogs Helping HD Patients

The Waynesboro Record Herald has a wonderful article on the value of therapy dogs. Therapy Dogs, Inc. which trains these animals was founded in 1990 and now has over 4000 members. The therapy dogs provide pure love to those who need it and they can be especially beneficial to those with Huntington's Disease. The article has this example:

"Among those who have been reached by Callie is a 34-year-old woman suffering from Huntington's Chorea, an inherited neurological disease.

"She has seizures and can thrash around. When that happens, Callie can calm her down," said Heater. "In fact, we have been called to come to the nursing home to help her get calm."

"Callie puts herself tightly against the woman, who holds the dog and eventually falls asleep."

Fortunately, there is an organization that is working to match therapy dogs with Huntington's Disease patients across the United States - Generations of Hope. They are working with the various centers around the country to provide this valuable service. You can read more about this on their website (scroll to the bottom).

Some complain (rightfully so) that there isn't enough being done to provide care to those with Huntington's Disease. Generation's of Hope is doing something about it. If you'd like to help Generation's of Hope help others you can visit this page for information on how to donate.

Posted by Dave at 08:35 AM | Comments (0) | TrackBack

October 25, 2003

Testing Positive

HD Lighthouse comes through again with a great article. This time the article is written by Kelly B., a person who has tested 'positive' for the Huntington's Disease gene. This is one of the best articles I've read relating to HD and a valuable resource for those who have taken the predictive test or are thinking about it. Do yourself a favor and go over and read the full article.

Here is a couple of excerpts to tempt you:

"There is life before Huntington's and life after finding out you have Huntington's. While things will never be the same as they were before testing positive, and really, how could they. Life will eventually return to running on an even keel after you have had some time to digest your positive result. "

"I played the "Is this normal, or is this Huntington's" game for awhile. Wondering, for example, if I was just clumsy, or if it was the HD. Until I realized that determining the source would in no way change the bottomline. I am clumsy. Why, made no difference."

"If I could go back to the day I tested positive, I would tell myself the following things:

Want more? You can read the whole article here.

Posted by Dave at 10:28 AM | Comments (0) | TrackBack

Predictive Test For Huntington's Disease

The October 20, 2003 issue of The Scientist has a great article (free registration required) on predictive tests for Huntington's Disease and for Cystic Fibrosis.

Here are some excerpts from the article relating to Huntington's Disease:

"The bench-to-bedside saga of HD serves as a model for the predictive medicine to come. "HD has been predictable longer than any other single-gene disorder, and it is therefore where we have the most experience in predictive testing," says Hayden, whose group tracks HD testing in Canada." ...

"With discovery in 1983 of the HD marker near the causative gene on chromosome 4, an at-risk person whose relatives took the test could know with more than 96% certainty. The gene's discovery itself a decade later raised the predictive power to near 100%." ...

"That newfound certainty frightens people. Many who had indicated before 1983 that they would take a predictive test when it became possible did not do so. The Canadian analysis found an uptake of about 18%; Hayden extrapolates that 50% to 70% of at-risk individuals did not follow through when the hypothetical test became reality. Attitudes in Australia are similar. "While only about 25% of those at-risk have taken the test, fully 100% say that they are pleased that the test is available," says Williamson.

In the United States, uptake is about 5%, says neurology professor Richard Myers, Boston University School of Medicine. "HD testing is by far the most widely used genetic test in the US, with more than 300 presymptomatic tests performed each year. But we don't document them the way the Canadians do, because many people pay out-of-pocket and are very private."

In the Canadian study, more surprising than low uptake was who took the test; it was not predominantly the youngest adults seeking information for starting families, as many researchers expected. Most of the 1,061 tested individuals were between 30 and 40 years old. Only 70 people were older than 60 years, and the oldest was 95. "The most common reason for testing was to resolve uncertainty and plan for the future, careers, and retirement. People wanted to know whether they would need to hire a nurse or could afford to purchase a motor home." says Hayden.

The Canadian group also has studied psychological reactions five years after predictive testing.5 The news is encouraging. "Even those who learned that they had an increased risk resolved the uncertainty, and that improved their well-being, lowered their anxiety, and decreased depression," explains Hayden. The frequency of suicide attempts did not increase after predictive testing, and maybe even decreased. Other risk factors, such as unemployment, onset of symptoms, and history of psychiatric illness were more highly correlated to suicide attempts than to previous testing for HD. But the study has caveats. People likely to respond poorly may have self-selected out of testing, and participants received extensive genetic counseling before and after testing. All of these factors affect uptake."

For those interested in scientific research I highly recommend the online magazine "The Scientist" at http://www.the-scientist.com/. Their website is definitely worth checking out.

Posted by Dave at 10:03 AM | Comments (0) | TrackBack

October 24, 2003

Medicare Bill Postponed (Again)

Earlier this week Congress was anticipating a final Medicare bill by Friday night.

It didn't happen. They're now shooting for middle of next week.

Publicly, the biggest holdup is due to a disagreement between the two parties on what is the best way to control future medicare spending. (Medicare is expected to run large deficits in a few years.)

The Republicans believe that adding a private insurance option as competition will help keep costs down. Democrats believe that the private plans will end up with the healthier patients leaving traditional Medicare with higher per-patient costs.

One item left undecided still is whether American's can purchase their medications from Canada where it is cheaper. On the surface this might seem like a 'no-brainer'...why not allow it? Actually, what is happening now is that American's are footing the bill the bulk of the costs for the worlds research into new cures. Shifting American sales to price controlled countries will reduce spending on research into new medications, especially for 'smaller' diseases such as Huntington's. We need ALL the research dollars possible.

An ABC News article here.

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October 23, 2003

Importance of Living Wills

The Orlando Sentinel has a great article on the importance for all people to have a living will. If you've been putting it off until now, it's time to get one. Here's a couple of excerpts:

"Under the law, all competent adults have the right to make decisions about their health care, including the right to refuse medical treatment. But even people who are no longer able to make their own decisions - maybe they're in a coma or suffering from dementia -- don't lose that right.

The only hitch is, to ensure their wishes are followed, they need to have made them known before they become incapacitated."

And...

"If you never want to be force-fed, say so. If you want every option exhausted, say so."

This advice goes to everybody, not just pHD's.

Posted by Dave at 07:42 PM | Comments (0) | TrackBack

October 22, 2003

Medicare Update

The Washington Post has a surprisingly informative and balanced article on the current state of the Medicare bill. It's worth reading.

The current status of the bill is that it has passed both the House and the Senate. It is currently in the conference committee where they are trying to hammer out the differences between the two bills. They are hoping to have this done by Friday.

The article has some good info on what the final bill will probably entail. It appears there will be some good things and some bad things about the bill. How much of each we won't know until the end. Stay tuned!

Update: More coverage from the New York Times.

Posted by Dave at 09:21 PM | Comments (0) | TrackBack

October 21, 2003

Money Pouring Into Biotech

It's going to take money, a lot of it, to bring new drugs to market for genetic diseases such as Huntington's.

Fortunately, the stock market has been climbing and biotechnology stocks have especially benefited. According to this article from MSNBC:

* Venture capital firm New Enterprise Associates is starting a new biotech fund to raise $1 billion.

* Venture Capital firm Grotech Capital Group is expanding further into biotech.

* Of the 50 new stocks last quarter, 14 were for biopharmaceutical firms.

Huntington's disease is a natural target for these firms. While the market isn't as large as others it is still substantial. Being a single-gene disease, HD offers a quicker time to market. Any company that comes up with an effective treatment or cure for HD will see their stock skyrocket.

Posted by Dave at 07:44 PM | Comments (0) | TrackBack

Attack Update

This website has been unreachable for much of the day. The company that hosts this website has made changes that will make it harder for the pro-terrorist hackers to take us down.

Here's a link to one terrorist supporter talking about this and here's one update from Winds of Change and another.

Update: I'm throwing in a link to Laughing Wolf also (only because he makes a great wine recommendation!)

Update: Irreconcilable Musings has a good post on this. (Hat tip to Captain's Quarters).

Posted by Dave at 06:23 PM | Comments (1) | TrackBack

You're Not Going To Believe This

There has been instances the last couple of days where this website has been effectively knocked off line.

It's not because the bill hasn't been paid, it's because of an Al Qaeda related hacker attack.

I told you you wouldn't believe this!

This blog is hosted with the internet service provider "Hosting Matters", a popular ISP for bloggers. One blog, Internet Haganah, has been involved in shutting down as many as 300 Al Qaeda and terrorism websites around the world. Supporters of some of these shutdown websites have declared a holy war on Internet Haganah and have flooded Hosting Matter's network with a denial of service attack in an attempt to shut the site down.

These attacks end up affecting all of the other websites at Hosting Matters. So far these attacks haven't been covered by the major press but you can read about them Here, Here, Here, Here, and Here.

Update: Hosting Matter's comments on the attacks.

Posted by Dave at 12:52 AM | Comments (0) | TrackBack

October 20, 2003

HDSA Legislative Alert

If you caught this piece here last week you know that there is a genetic anti-discrimination working its way through congress.

We need this bill.

You can help get this bill passed and this alert from HDSA tells you how (special thanks to US Representative Louise Slaughter):

Senate passes S.1053! Genetic Nondiscrimination legislation is half way there! But we still need your help!

On Tuesday, October 14, 2003, the Senate passed S.1053, which directly addressed the issue of genetic discrimination in health insurance and employment. However, the House of Representatives remains reluctant in addressing this important issue. They would prefer to hold “hearings” sometime next year. It is essential that genetic nondiscrimination legislation be passed as soon as possible in order to protect the millions of Americans who suffer from hereditary diseases like Huntington’s Disease.

As you know, US Representative Louise Slaughter has led the fight for passage of legislation like S.1053. HDSA has been in the forefront of this multi-year effort and we urge each of you to now write to your elected representatives to sign the attached letter from Representative Slaughter urging the House leadership to expedite consideration of S.1053, the Genetic Information Nondiscrimination Act.

To find the name and email address of your elected House representatives, please use Econstitutent, the internet advocacy tool that can be accessed through the HDSA national web site (www.hdsa.org). To use, click on “Advocacy” and then “Write your Congressman” and then “Econstituent” (or go here). You will be taken to the home page for this advocacy tool. Enter your zip code and press the enter key. You will be automatically connected to your Senate and House representatives. Click on “contact” for your elected House representative and copy/paste the letter below to your House representative along with the letter from Rep. Slaughter in the message section.

Please take action TODAY!

Letter to your elected representative in the House:

Dear INSERT NAME

I urge you to join with US Representative Louise Slaughter in signing the attached letter to expedite action on S.1053, the Genetic Information Nondiscrimination Act.

On October 14, the Senate passed S.1053 unanimously, marking the first time Congress has addressed directly the issue of genetic discrimination in health insurance and employment. The product of more than two years of intensive negotiations, S.1053 has the support of hundreds of organizations, like the Huntington’s Disease Society of America, as well as the White House, which issued a positive Statement of Administration Policy.

Action is already overdue. Too many Americans fear that a genetic test could be used to deny them health insurance or employment. As a result, they do not participate in genetic research or use genetic testing. If the pace of genetic research is to continue, there must be a law enacted that will protect the individual from genetic discrimination.

Please join with Representative Slaughter to urge the House leadership to address and pass S.1053 as soon as possible by signing the attached letter.

Thank you for your support.

Sincerely,
YOUR NAME

Letter to Speaker of the House
October xx 2003

Dear Mr. Speaker:
We urge you to schedule S.1053, the Genetic Information Nondiscrimination Act, for House consideration as soon as possible.

Earlier this year, the National Human Genome Research Institute announced the complete mapping and sequencing of the human genome. This landmark achievement heralds a new era in medical research, with the potential of major advances in preventing, diagnosing, treating and curing some of the most feared diseases known to humanity. Along with this tremendous promise, however, comes the possibility of the abuse of genetic information.

Every person is estimated to carry between five and fifty genetic mutations that predispose us to serious disorders. As such, we are all potential victims of genetic discrimination. Today no comprehensive federal law bans genetic discrimination in health insurance and employment. As a result, too many Americans are deciding not to take genetic tests because they fear this information could be used to undermine their health coverage or their jobs. This fear is also impacting genetic research, as fewer people are willing to participate in studies. Congress must act to rectify this situation, both to enable our constituents to make the best possible medical decisions for themselves and to preserve the viability of this critical research.

S.1053, the Genetic Information Nondiscrimination Act, represents a reasonable compromise that takes into account both the concerns of patients and the needs of insurers and employers. This bill, which is jointly sponsored by majority ands minority leadership in the Senate, is the product of almost two years of intensive discussion. It also enjoys the strong support of the White House. In the House of Representatives, a more expansive bill, HR1910, has the support of over 220 bipartisan cosponsors and over 300 organizations. Clearly, there is ample support in the House to take up and pass genetic nondiscrimination legislation quickly and easily; S.1053 would be an ideal candidate for consideration on the suspension calendar.

Timely passage of S.1053 would represent a major victory for Congress, the White House ands the American people. We urge you to schedule this legislation for action so that it may be signed by the President before the first session of Congress adjourns.

Sincerely,

Louise Slaughter
Member of Congress Member of Congress

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October 19, 2003

Boosting The Brain

DB's Medical Rants points to an article on CNN's website on exercise boosting memory. Here's an exerpt:

"Now we know that there are many triggers that make parts of the brain regenerate themselves."

One of those triggers may be linked to your fitness level.

"Cardiovascular exercise that's done over a longer period of time will tend to reduce the amount of tissue you lose as you age," says Stan Colcombe, a researcher at the University of Illinois-Urbana.

That includes brain tissue, and losing less of it may mean keeping more precious memories."

This backs up what's been said on this website and on HD Lighthouse's website...you can fight the loss of brain cells due to Huntington's Disease. As mentioned here before, Scott Midyett's exercise program took him from disability to riding a unicycle and competing in triathalons. Brain scans show that he is GAINING brain mass!

Whether it is BDNF or some other chemical protecting and/or generating new brain cells or some other factor increasing the body's ability to cope with HD's protein framents there is clear evidence that exercise does help keep the brain healthy.

Scott started his program just by walking and if you aren't already in some kind of program that keeps you active, walking is a great way to start. Here's a good webpage that will help you start walking.

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October 18, 2003

Another Bit Of The Puzzle

Much of the research into Huntington's Disease the last few years has been focused on the resulting protein 'clumps' within the neural cells. When you read the studies terms such as "gain of function" and "loss of function" are used when debating potential causes for the early cell death.

"Gain of function" theories believe that Huntington's Disease causes a new action in the cell which leads to early cell death. The "loss of function" theories believe that the early cell death is brought on by the cell no longer being able to maintain its health. So which one is right? Probably both of them. There appears to be both actions going on.

Two more common terms used in studies are "wild-type" huntingtin and "mutant" huntingtin. Wild-type refers to the normal huntingtin protein and mutant refers to the huntingtin protein with the long CAG count that causes HD. What many people don't realize is that a person with Huntington's Disease has both type's of the huntingtin protein.

The mutant huntingtin protein causes the protein clumps and the wild-type huntingtin protein performs important functions within the neural cell. So researchers at the Max Planck Institute for Molecular Genetics in Germany decided to find out how the "mutant" huntingtin affected the "wild-type" huntingtin.

So what did they find out? That the "mutant" huntingtin seems to tangle up the "wild type" huntingtin preventing it from doing it's job (loss of function). The cell is then unable to process the resulting 'clump'.

Here's the study abstract:

J Biol Chem. 2003 Oct 17;278(42):41452-61. Epub 2003 Jul 29.

Mutant Huntingtin Promotes the Fibrillogenesis of Wild-type Huntingtin: A POTENTIAL MECHANISM FOR LOSS OF HUNTINGTIN FUNCTION IN HUNTINGTON'S DISEASE.

Busch A, Engemann S, Lurz R, Okazawa H, Lehrach H, Wanker EE.

Max Planck Institute for Molecular Genetics, Ihnestrasse 73, D-14195, Berlin, Germany.

Aggregation of huntingtin (htt) in neuronal inclusions is associated with the development of Huntington's disease (HD). Previously, we have shown that mutant htt fragments with polyglutamine (polyQ) tracts in the pathological range (>37 glutamines) form SDS-resistant aggregates with a fibrillar morphology, whereas wild-type htt fragments with normal polyQ domains do not aggregate. In this study we have investigated the co-aggregation of mutant and wild-type htt fragments. We found that mutant htt promotes the aggregation of wild-type htt, causing the formation of SDS-resistant co-aggregates with a fibrillar morphology. Conversely, mutant htt does not promote the fibrillogenesis of the polyQ-containing protein NOCT3 or the polyQ-binding protein PQBP1, although these proteins are recruited into inclusions containing mutant htt aggregates in mammalian cells. The formation of mixed htt fibrils is a highly selective process that not only depends on polyQ tract length but also on the surrounding amino acid sequence. Our data suggest that mutant and wild-type htt fragments may also co-aggregate in neurons of HD patients and that a loss of wild-type htt function may contribute to HD pathogenesis.

PMID: 12888569

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October 17, 2003

Sodium Butyrate Update

Another fine study has come out indicating that HDAC inhibitors may be effective in treating Huntington's Disease. In this case the HDAC inhibitor, Sodium Butyrate, was tested on the R6/2 HD mice.

The results were very encouraging...the mice gained weight, improved motor skills, and brain deterioration was delayed.

If I'm not mistaken (and I could be on this one) this is the same HDAC inhibitor (or the related Sodium Phenylbutyrate) that is in a Phase I drug trial.

You can read a piece by HD Lighthouse on sodium butyrate here.

Here's the study abstract:

J Neurosci. 2003 Oct 15;23(28):9418-27.

Histone deacetylase inhibition by sodium butyrate chemotherapy ameliorates the neurodegenerative phenotype in Huntington's disease mice.

Ferrante RJ, Kubilus JK, Lee J, Ryu H, Beesen A, Zucker B, Smith K, Kowall NW, Ratan RR, Luthi-Carter R, Hersch SM.

Geriatric Research Education and Clinical Center, Bedford Veterans Affairs Medical Center, Bedford, Massachusetts 01730, USA. rjferr@bu.edu

The precise cause of neuronal death in Huntington's disease (HD) is unknown. Although no single specific protein-protein interaction of mutant huntingtin has emerged as the pathologic trigger, transcriptional dysfunction may contribute to the neurodegeneration observed in HD. Pharmacological treatment using the histone deacetylase inhibitor sodium butyrate to modulate transcription significantly extended survival in a dose-dependent manner, improved body weight and motor performance, and delayed the neuropathological sequelae in the R6/2 transgenic mouse model of HD. Sodium butyrate also increased histone and Specificity protein-1 acetylation and protected against 3-nitropropionic acid neurotoxicity. Microarray analysis showed increased expression of alpha- and beta-globins and MAP kinase phosphatase-1 in sodium butyrate-treated R6/2 mice, indicative of improved oxidative phosphorylation and transcriptional regulation. These findings strengthen the hypothesis that transcriptional dysfunction plays a role in the pathogenesis of HD and suggest that therapies aimed at modulating transcription may target early pathological events and provide clinical benefits to HD patients.

PMID: 14561870

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October 16, 2003

Pyruvate May Be Protective

Pyruvate is an over-the-counter supplement that is claimed to help with weight loss. In the real world it doesn't appear to be very effective in helping people lose weight.

Researchers from the University of British Columbia found that pyruvate protected brain cells in an animal study. But don't go rushing out to buy this supplement. The animal they used is the quinolinic acid rat model. While rats are genetically closer to humans than mice I'm not convinced this quinolinic rat is as good of a model as the R6/2 transgenic mouse for Huntington's Disease.

A couple of important points about the study: The pyruvate was injected and the equivalent dose for a human weighing 150 pounds would be 165-330 grams. A lower dose, that was the human equivalent of 82.5 grams, was NOT effective. Assuming an oral dose of pyruvate was effective (and safe), the equivalent effective dosage would cost over $100 a day!

Here is the study abstract:
Exp Neurol. 2003 Oct;183(2):700-4.

Neuroprotective effects of pyruvate in the quinolinic acid rat model of Huntington's disease.

Ryu JK, Kim SU, McLarnon JG.

Department of Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, V6T 1Z3, Vancouver, BC, Canada

The neuroprotective effects of pyruvate, the end metabolite of glycolysis, were studied in an animal model of Huntington's disease (HD). Intrastriatal injection of quinolinic acid (QA) caused widespread damage to rat striatum as determined from cresyl violet staining and immunohistochemical analysis. Intraperitoneal administration of pyruvate at doses of 500-1000 mg/kg significantly reduced striatal lesions induced by QA. A lower pyruvate concentration of 250 mg/kg was not protective; however, quadruple applications at this dosage was effective in reducing lesion volumes. The protective effects of pyruvate were found over a range of times, from application at the time of QA injection to 1 h post-administration; however, no protection was conferred if pyruvate was applied 30 min prior to QA injection or 3 h post-administration. We also found pyruvate protects different types of striatal neurons against QA toxicity including GABAergic projection neurons, cholinergic interneurons and NADPH-diaphorase interneurons. These results suggest that pyruvate may be effective in reducing neuronal damage in HD.

PMID: 14552912

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October 15, 2003

Creatine Study

Researcher's have conducted a double-blind, placebo controlled one year study on creatine. This is the kind of quality research we need...except for one thing:

The tested dose was 5 grams a day.

Past (lesser quality) studies indicate that the dosage needs to be 10 grams a day in order to be effective in the treatment of Huntington's Disease. In all fairness to the researchers, they used what was considered a standard dose for creatine. The protocol for the study was developed before there was evidence that 10 grams was potentially a more effective dosage.

Let's hope we see a similar study soon with a 10 gram dosage. Here's the study abstract:

Neurology. 2003 Oct 14;61(7):925-930.
Creatine supplementation in Huntington's disease: A placebo-controlled pilot trial.

Verbessem P, Lemiere J, Eijnde BO, Swinnen S, Vanhees L, Van Leemputte M, Hespel P, Dom R.

Exercise Physiology and Biomechanics Laboratory (Drs. Verbessem, Eijnde, Van Leemputte, and Hespel) and Motor Control Laboratory (Dr. Swinnen), Department of Kinesiology, and Adapted Physical Activity and Cardiorespiratory Rehabilitation Unit (Dr. Vanhees), Department of Rehabilitation Sciences, Faculty of Physical Education and Physiotherapy.

OBJECTIVE: To evaluate the effect of creatine (Cr) supplementation (5 g/day) in Huntington's disease (HD). METHODS: A 1-year double-blind placebo-controlled study was performed in 41 patients with HD (stage I through III). At baseline and after 6 and 12 months, the functional, neuromuscular, and cognitive status of the patients was assessed by a test battery that consisted of 1) the Unified Huntington's Disease Rating Scale (UHDRS), 2) an exercise test on an isokinetic dynamometer to assess strength of the elbow flexor muscles, 3) a maximal exercise test on a bicycle ergometer to evaluate cardiorespiratory fitness, and 4) a test to assess bimanual coordination ability. Following the baseline measurements, the subjects were assigned to either a creatine (n = 26) or a placebo group (n = 15). RESULTS: Scores on the functional checklist of the UHDRS (p < 0.05), maximal static torque (p < 0.05), and peak oxygen uptake (p < 0.05) decreased from the start to the end of the study, independent of the treatment received. Cognitive functioning, bimanual coordination ability, and general motor function (total motor scale, UHDRS) did not change from baseline to 1 year in either group. CONCLUSION: One year of Cr intake, at a rate that can improve muscle functional capacity in healthy subjects and patients with neuromuscular disease (5 g/day), did not improve functional, neuromuscular, and cognitive status in patients with stage I to III HD.

PMID: 14557561

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Center Of Excellence Recognized

Today, the Rocky Mountain News devoted an entire column to HDSA's Celebration of Hope dinner that was held in Denver a few weeks ago. The event was a huge success raising $26,000 for the Denver Center of Excellence!

With a paid circulation of several hundred thousand, this Rocky Mountain News article provides excellent exposure for the cause of Huntington's Disease.

I was able to attend the Celebration of Hope dinner and here is what I wrote about it at the time.

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October 14, 2003

Genetic Discrimination Bill Passes

Today the Senate passed a genetic discrimination bill by a vote of 95-0. The bill would prevent insurance companies from denying coverage or raising rates for those who've gotten genetic tests.

The House still needs to pass a comparable bill before it goes to the President for a signature... but this is very encouraging!

One item that is still up for grabs is discrimination in the workplace. At this point it looks like a final bill may include employment protection for those who've taken genetic tests.

Be sure to write your congressperson and let them know how important this issue is to you. Here is an more from ABC News.

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October 13, 2003

Medicare Bill Update

Congress has been trying to get a Medicare bill with better prescription drug benefits to the President's desk for months. The latest self imposed deadline is October 17th.

It appears that a small bit of sanity has struck Congress as more members are now willing to charge the well-to-do and the wealthy more for the drug benefit.

This is an improvement but there is still a good chance that the final version of the bill will ultimately do more harm than good as skyrocketing costs may eventually force program cuts that could hurt the HD community.

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October 12, 2003

Lake Maracaibo, Venezuela

Lake Maracaibo is a valuable part of the Huntington's Disease community. This area in Venezuela has the unfortunate distinction of having the highest prevalence of HD in the world. 10,000 people live in this area and half of them have the HD gene, many have two copies of the gene.

The research that has been done by Dr. Nancy Wexler and her team ultimately led to the discovery of the HD gene and was a critical component of the Human Genome Project.

Here is an article from Business Week on Lake Maracaibo and how Huntington's Disease has affected the region.

Here is an article from Time on how Dr. Wexler's work in Lake Maracaibo advanced research in HD.

Here is an article from the Harvard publication 'Neurotransmitter' on medical treatment in Lake Maracaibo.

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October 11, 2003

Big Gains In HD Research

Researchers at Massachusetts General Hospital (Harvard) have an article published in the journal 'Neuromolecular Medicine' reiterating what's been said on this website and others - that real progress is being made in the search for a treatment for Huntington's Disease.

Here's the key highlight: "(S)tudies...are homing in on the trigger mechanism and the first formative steps that cast HD as a distinct clinical entity. At the same time, assays at the biochemical, cellular, and whole organism levels are starting to yield potential disease modifying genes and candidate drugs."

Here's the whole abstract:

Neuromolecular Med. 2003;4(1-2):7-20.

Huntington's Disease.
MacDonald ME, Gines S, Gusella JF, Wheeler VC.

Molecular Neurogenetics Unit, Center for Human Genetics Research, Massachusetts General Hospital, Charlestown, MA 02129.

Huntington's disease (HD) research is aimed at understanding the root cause of the disorder, for the thrill of uncovering new biology, and for the serious purpose of finding effective therapeutic agents. Molecular genetics has revealed the disease trigger, an inherited unstable CAG expansion in a novel 4p16.3 gene (HD), that lengthens a polyglutamine segment in huntingtin. Now studies with HD patients and model systems that are genetic HD replicas are homing in on the trigger mechanism and the first formative steps that cast HD as a distinct clinical entity. At the same time, assays at the biochemical, cellular, and whole organism levels are starting to yield potential disease modifying genes and candidate drugs. These can be prioritized by testing in a panel of genetic and phenotypic HD mouse models to yield analytical tools for dissecting the early and late stages of the disease process and to maximize the chance of success in trials with HD patients.

PMID: 14528049

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October 10, 2003

A Life Well Lived

After reading this life story of Earlene Mitchell I wish I had met the woman.

You'll feel the same way reading this article from the Deseret News.

Here's a sample...

"The boat? Darlene watched in amazement as Earlene scampered to the banks of the Jordan River and unleashed a small rowboat. As the pair floated down the serene river that morning, Darlene knew that she'd found no ordinary friend."

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October 09, 2003

A Mother's Diet - Epigenics

Dean's World found an interesting article in the New York Times on epigenics - the study of how environmental factors interact with genes in the womb.

Here's a highlight from the article:

"For example, why does one identical twin develop schizophrenia and not the other? Why do certain disease genes seem to affect or "penetrate" some people more than others? Why do complex diseases like autism turn up in more boys than girls?

For answers, epigeneticists are looking at biological mechanisms other than mutation that affect how genes function. One, called methylation, acts like a gas pedal or brake. It can turn gene expression up or down, on or off, depending on how much of it is around and what part of the genetic machinery it affects.

During methylation, a quartet of atoms called a methyl group attaches to a gene at a specific point and induces changes in the way the gene is expressed. "

Wouldn't it be wonderful if researchers found that something in the mother's diet could lower the CAG count in a HD gene-positive baby? Perhaps even reducing the number of children affected by the Juvenile version of Huntington's Disease?

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October 08, 2003

Therapy Dogs For HD

There is a great young HD organization that is working very hard to improve support for families dealing with Huntington's Disease. In addition to starting a retreat for famies and starting up an 800-number support line they are now working to provide Therapy Dogs for those with Huntington's. Visit here and scroll to the bottom to read more about their latest program.

Be sure to tell your friends about Generations of Hope. They need all the support they can get. Visit here to make a donation.

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October 07, 2003

HDDW Update

HD Lighthouse has an update on HD Drug Works, the organization started by Dr. LaVonne Goodman to speed up the process of bringing effective therapies to Huntington's Disease patients.

Here are some of the highlights:
* Thanking Jerry (HD Lighthouse) for all his support
* They will have their own website up later this month
* Their work will be called "HDDW Therapeutic Drug Trials"
* LaVonne is no longer the HDSA Northwest Chapter President
* HDDW is not competing with any other HD organization
* They have three scientific advisors on board so far

Visit HD Lighthouse and read all the details for yourself. HDDW looks to be another great addition to the pantheon of Huntington's Disease organizations.

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October 06, 2003

Fixing The HD Gene

Researchers at the University of Delaware have accomplished something important that may have implications for future Huntington's Disease treatments.

First a quick lesson in HD & DNA 101. The HD gene creates the huntingtin protein (one of 100,000 types of protein) which resides in the middle of the brain cells. With HD, the gene makes the protein with a strand of glutamine (an amino acid) that is too long. The cell can handle the normal, shorter strands in the protein but when the strand gets too long the cell can no longer process the huntington protein properly resulting in early cell death.

These researchers, using a relatively new technique, successfully broke up the long strand of glutamine by changing the code to create leucine in the middle of the strand of glutamine. The theory is that the neural cell will now be able to properly handle the huntingtin protein, stopping the disease.

There are a lot of steps between this finding and a potential treatment for Huntington's Disease (many years), but this is another new potential treatment path.

Here's the study abstract:

Biochem Biophys Res Commun. 2003 Oct 17;310(2):660-6.

Targeted nucleotide exchange in the CAG repeat region of the human HD gene.
Parekh-Olmedo H, Kmiec EB.

Department of Biology, University of Delaware, Delaware Biotechnology Institute, 15 Innovation Way, 19711, Newark, DE, USA

Huntington's disease (HD) is marked by the expansion of a tract of repeated CAG codons in the HD-gene, IT15. Once expressed, the expanded poly Q region of the huntingtin protein (Htt), which is normally soluble, becomes insoluble, leading to the formation of intracellular inclusions and ultimately to neuronal degeneration. Interruption of the pure poly Q tract at the genetic level should undermine the transition from Htt solubility to Htt insolubility. Modified single-stranded oligonucleotides were used to direct the nucleotide exchange of an A residue to a T residue in the second codon of the HD-gene, resulting in the creation of a leucine residue among the poly Q tract. Consistent with results from other groups, we provide evidence that short synthetic DNA molecules can modify the HD-gene directly, preliminarily offering a potential therapeutic approach to Huntington's disease.

PMID: 14521962

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October 05, 2003

Gene's On A Chip

This announcement doesn't have much effect on Huntington's Disease research but it is another significant step in the rapid progression of genetic research.

Affymetrix Inc. and Agilent Technologies have announce a new gene chip that fits portions of virtually the entire human genome onto a dime-sized chip. These chips are used in identifying genetic causes of genes. This is a far cry from what HD researcher's had to do in the 'old' days of genetic research - just a decade ago.

Here's an excerpt from the AP article:

"Researchers even envision a day when pediatricians and other physicians can be armed with the chips, technically called microarrays. The hope is that a drop of a newborn's blood can quickly be converted into a genome on a chip. From there, a doctor could determine the baby's predilection to disease and other genetic traits."

You can read the AP article here (and the original press release).

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October 03, 2003

Fish Oil To The Rescue

HD Lighthouse has just posted another great article, this time on EPA. This one comes from a poster abstract that was to be presented at the postponed 2003 World Congress on Huntington's Disease.

The language in the poster is a little 'thick' and missing some useful details but here's the synopsis:

An individual taking EPA (unstated dosage) was monitored over a six-year period with repeated tests to measure the progression of Huntington's Disease. While the tests scores showed some fluxuation over the period, there was little or no decline in symptoms over the six years.

The researcher(s) concluded that the limited decline over such a long period of time indicated that the EPA was probably the cause of the great results.

This is one more confirmation of the value of taking your fish oil (which contains EPA). While this poster doesn't mention the dosage taken, other studies have been using 2 grams of EPA every day (which is a few fish oil capsules, read the label). As always, speak to your doctor before starting any supplement.

You can read the HD Lighthouse article here.

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October 02, 2003

Terrorists Bomb Again

Animal research was targeted again by domestic terrorists in Pleasanton, California. A splinter group of the Animal Liberation Front called "The Revolutionary Cells" detonated a 10 pound ammonium nitrate bomb strapped with nails at the offices of Shaklee Corporation. This is a much smaller version of the type of bomb that destroyed the Murrah building and killed a 168 people in Oklahoma City a few years ago. Shaklee was targeted because they use Huntingdon Life Sciences for testing. This follows a similar bombing a month before of the medical research company Chiron.

This bombing appears to indicate an escalation in the violence. The Revolutionary Cells statement reads:

"Today, it is 10 pounds, tomorrow 20… until your buildings are nothing more than rubble. No more will all the killing be done by the oppressors, now the oppressed will strike back. ...How are you sleeping? You never know when your house, your car even, might go boom... or maybe it will be a shot in the dark."

The only purpose for using nails in the bomb is to create projectiles that will injure or kill any humans in the vicinity.

Fortunately the terrorists did not affect any medical research this time. Read more information read this earlier piece on the terrorists and this piece on how they are supported by PETA (People for the Ethical Treatment of Animals). Also, here is the news article on this latest bombing and another news article.

This is the group's entire statement on the bombing (Note the statement: "All customers and their families are considered legitimate targets.") :

On the night of September 25th volunteers from the Revolutionary Cells attacked a subsidiary of a notorious HLS client, Yamanouchi. We left an approximately 10lb ammonium nitrate bomb strapped with nails outside of Shaklee Inc, whose CEO is both the CEO for Shaklee and Yamanouchi Consumer Inc. We gave all of the customers the chance, the choice, to withdraw their business from HLS. Now you all will have to reap what you have sown. All customers and their families are considered legitimate targets.

Hey Sean Lance, and the rest of the Chiron team, how are you sleeping? You never know when your house, your car even, might go boom. Who knows, that new car in the parking lot may be packed with explosives. Or maybe it will be a shot in the dark.

We have given all of the collaborators a chance to withdraw from their relations from HLS. We will now be doubling the size of every device we make. Today it is 10lbs, tomorrow 20....until your buildings are nothing more than rubble. It is time for this war to truely have two sides. No more will all of the killing be done by the oppressors, now the oppressed will strike back. We will be non-violent when the these people are non-violent to the animal nations.

In memory of all of those fallen before us in the war for liberation: Jill Phipps (animal activist), Barry Horne (ALF), Olaia Kastresana (ETA), Arkaitz Otazua (ETA), Angayarkanni (LTTE), Babu (LTTE), Bobby Sands (IRA), Patsy O'Hara (INLA), Carlos Guiliani (anti-globilization martyr), Lee Kyung-hae (farmer and anti-globablization victim), and many more on numerous other fronts. We won't forget you, we won't let your deaths be in vain.

Gora Euskadi Ta Askatasuna!
Up the Real IRA!
Long live the Popular Front for the Liberation of Palestine!
Viva La Fuerzas Armadas Revolucionarias de Colombia!
Long live the Frontu Di Liberazione Naziunalista Corsu!
For the creation of Revolutionary Cells!
For Humyn, Earth & Animal Liberation!

Bringing the bomb and the bullet back into amerikan politics, Revolutionary Cells --animal liberation brigade

***

The revolutionary cells exists as a front group for militants across the liberationary movement spectrum. We are anarchists, communists, anti-racists, animal liberationists, earth liberationists, luddites, feminists, queer liberationists, and many more things across various other fronts. Where ever there is oppression there are those unwilling to idly stand by and let it occur, and those people make up the nucleus of the revolutionary cells.

Who are the revolutionary cells? It is an anti-gmo activist destroying a gmo crop, it is a basque youth driving a car packed with explosives destined for a spanish politician, it is a queer bashing back, a rape victim putting a bullet in the rapist, a corsican nationalist planting a bomb at a french bank, it is a cincinatti riot in response to police brutality, an animal liberationist shooting a vivisector dead on his doorstep. In short it is the spirit of resistance realized. It is moving from politics to praxis.

Anyone who takes part in the war against the oppressive heirarchies in this world can consider themselves a member of the Revolutionary Cells.

Revolutionary Cells Guidelines:

1. To take strategic direct action (be it non-violent or not) against the oppressive institutions that permeate the world.

2. Make every effort to minimize non-target casualties, be they human or non-human.

3. Respect a diversity of tactics, whether they be non-violent or not.

4. Any underground activist fighting for the liberation of the humyn, earth or animal nations may consider themselves a Revolutionary Cells volunteer.

Posted by Dave at 07:46 AM | Comments (0) | TrackBack

October 01, 2003

Rating Political Candidates

As you may have noticed (especially those in California) we've entered another political season. At this point we have have at least 11 presidential candidates from the major parties.

As a service to the HD community I will be posting items related to candidates and health care related policies. I am also considering ranking the presidential candidates based on their health care policies. (or lack thereof).

I would like feedback from you, either by adding your comments to this post or by email (dave (at) huntingtons (dot) info), on what the criteria for ranking politicians should be.

The ranking will be ONLY on policies that related to Huntington's Disease which naturally excludes about 99% of the reasons most people choose candidates. Criteria I'm considering include: medicare policies, funding for NIH, funding for rare diseases, disability rule changes, and research.

I will mark candidates down for stringent support of a universal health care system. This may sound counter-intuitive for some but countries that do have a universal health care system consistently ration services to those with incurable diseases such as Huntington's Disease. These countries also sharply reduce their spending on medical research. The HD community cannot afford to be treated worse by the health care system and we definitely need more spending on medical research and care services.

Tell me what your thoughts are on how candidates should be ranked.

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