Hi Gopal,
My Dad had got an EMG done.
Let me get some details from my Mother.
As far as best places to get it done from, I will let you know..But they will be
in Delhi itself.

Let me get some info.
Also, you musta sk your Neurologist. They  usually have such info.

Cheers.
GJ.
--- In ALS_India@yahoogroups.com, Gopala Krishna Gokeda <gokeda@...> wrote:
>
> Hello there,
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
> Can anyone share their experiences about EMG test in India. Where is the best
place in India, to get an EMG test done. I learnt EMG is quite a painful test,
but I want to get a real professional do the test and give the diagnosis. I am
skeptical about various non-experienced and amateur technicians doing the job,
and giving a wrong diagnosis, for sake of money.
> Your inputs are greatly appreciated.
> Thank youGopal 
>

http://www.alscenter.org/news/press/091019.cfm


FROM THE SOCIETY FOR NEUROSCIENCES 39th ANNUAL MEETING IN CHICAGO:
9 a.m., Monday, October 19
McCormick Place, South Hall A Poster Session

Because the inability to breathe is an ultimate cause of death of patients with
ALS, Packard Center scientists are targeting the diaphragm as a therapeutic
target by transplanting stem cells directly into rats' cervical spinal cords,
precisely where the motor neurons that control this respiratory muscle are
located.

"We are transplanting stem cells that will become astrocytes because these cells
play an important role in maintaining the health of motor neurons," says Angelo
Lepore, Ph.D., a postdoctoral fellow in the lab of Packard scientist Nicholas
Maragakis,
M.D.<http://www.hopkinsmedicine.org/neurology_neurosurgery/experts/team_member_p\
rofile/765536147B11BF8F28BBACD5A22525A3/Nicholas_Maragakis>, also an associate
professor of neurology at the Johns Hopkins University School of Medicine.

The team showed that transplanting rat-derived stem cells* into the rodents'
cervical spinal cords helped slow down the decline of diaphragm function and
therefore extended survival in the rat model of ALS. Their findings show that a
targeted delivery of stem cells to the cervical spinal cord is a promising
therapeutic strategy: Even the partial rescue of motor neurons improved
respiratory function.

The work is a follow up to earlier, similarly-positive studies that used stem
cells derived from rat embryos. In this newer research, the stem cells were
created from skin cells of adult rats genetically nudged to go back to a more
unspecialized, less developed stage.

It's a far more useful source of cells, the scientists say, and one that's in
theory more realistic, should the positive results hold down the research
pipeline, for human therapy.

"I think that we first need to examine the potential of human-derived cells
following transplantation before we can say whether this strategy will work in
human patients," Lepore says. "While the initial results are promising, we need
to conduct a number of key experiments before this therapy is translated to the
clinic. That includes testing the efficacy of a similar class of human stem
cells."

* The stem cells, called glial-restricted precursors, or GRPs, came from an
unusual source: the rat's own skin. Fibroblast skin cells were coaxed into
becoming a master pluripotent stem cell by turning on key developmental genes.
These "master," pluripotent stem cells are capable of becoming any tissue. 
They, in turn, were treated to become more specialized, to become cells whose
capabilities are limited to becoming neurons or astrocytes,  their companion
cells.
___________________

About The Robert Packard Center for ALS Research at Johns Hopkins
www.alscenter.org<http://www.alscenter.org>

Located in Baltimore, the Robert Packard Center for ALS Research at Johns
Hopkins is a worldwide collaboration of scientists aimed at developing therapies
and a cure for amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's
disease.

The Center is the only institution of its kind dedicated solely to the disease.
Its research is meant to translate rapidly from the lab bench to the clinic,
largely by eliminating time spent waiting for grants and lowering institutional
barriers to sharing scientific results.

Scientists and clinician members of the Packard Center have moved drugs reliably
and rapidly from preclinical experiments to human trials. Direct or indirect
links to international biotech or pharmaceutical companies bring the
infrastructure and experience needed to make promising drugs into therapies.

Packard scientists are the first to propose and test a combination approach to
drug therapy, a tactic that has worked for AIDS, cancer and other diseases.

ALS is a progressive, disabling neuromuscular disease that causes complete
paralysis and loss of function  –  including the ability to eat, speak and
breathe. ALS progresses quickly and is not curable. Most patients die within
five years of diagnosis.

_________________________________________
Rebecca Berger
Research Program Coordinator
Robert Packard Center for ALS Research at Johns Hopkins
5801 Smith Avenue | McAuley Suite 110
Baltimore, MD 21209
               410.735.7678         410.735.7678  direct
410.735.7680  fax
rberger6@...<mailto:rberger6@...>
www.alscenter.org<http://www.alscenter.org>
www.fiesta5K.org<http://www.fiesta5K.org>

Dear all,
Here's hoping that this Diwali not only brings joy and prosperity to your house
but also best of health for you and your loved ones.

Keep your faith alive. Let's not loose our hope in God and Doctors...
As days go by, we are getting closer and closer to finding a cure for this
disease which has brought all of us together.

God bless all.
Keep smiling...

Regards,
Gaurav.

Before long, Packard Center investigator Jonathan
Glass<http://neurology.emory.edu/Faculty/Glass.htm> should be conducting the
first FDA-approved trial of stem cells for ALS. The Phase I trial - which aims
to test safety of both the cells and the procedure for implanting them -
involves injecting human neural stem cells into patients' spinal cords.

Later trials, if the surgical procedure and cell injections are safe, could be
carried out to show if the cells are effective in spinal cord repair or
regeneration. It's important to know that this first trial is not designed to
determine if the cells will alter disease progression:  Phase 1 trials are
designed only to be sure the procedures and therapies are possible and safe in
humans.

The study site is solely at Emory University where Glass directs their
neuromuscular laboratory. He's also Director of the Emory ALS Center and a
world-respected scientist in that disease. Eva
Feldman<http://www.taubmaninstitute.org/Scholars/feldman.htm>, who directs the
University of Michigan ALS Clinic, is the project's overall leader.

In this first stage, 12 patients will receive from five to ten stem cell
injections to the lumbar spinal cord. The final review comes two years later.

A Maryland-based biotech company, Neuralstem<http://www.neuralstem.com/>, both
launched the research and will provide the human neural stem cells that it uses.
Unlike, say, embryonic stem cells, which have the capacity to become any cell
type, neural stem cells have been nudged a little farther down the developmental
line. The cells appear identical to the semi-specialized stem cells in humans
that go on to become nerve cells.

The original "proof of principle" work - the study that showed this particular
type of neural stem cell might repair the spinal cord, came from Packard-funded
research in 2005. Packard scientist
Vassilis<http://www.hopkinsmedicine.org/stem_cell_research/coaxing_cells/its_all\
_about_networking.html>
Koliatsos<http://www.hopkinsmedicine.org/stem_cell_research/coaxing_cells/its_al\
l_about_networking.html> at Johns Hopkins first showed the stem cells could
survive well in culture and that they could safely be injected into rat models
of ALS (the SOD1 G93A rat). Also, he showed that they could remain stable in the
spinal cord and could morph into neurons.

Most important, the earlier Packard research revealed that the newly created
neurons integrated themselves into natural spinal cord motor neuron circuits.
The grafts - injected only into the lumbar spinal cord and not the entire
diseased organ - delayed the onset of ALS in the rats and extended their life
span almost two weeks.

Later work elsewhere showed the cells could reverse paralysis in rats with
ischemic spastic paraplegia, a more rapid, localized spinal cord damage. Still,
the scientific community realizes that the ability of these models to predict
response in human disease has not yet been firmly established.

As for the present trial, although the FDA approved it this September, no date
has yet been set for its start at Emory. That's because it's awaiting approval
by that university's institutional review board, a process, the Emory web site
states, "could take weeks or months."

Glass has been with the Packard Center since its early days almost a decade ago.
Since its inception, the Center has supported solid, creative stem cell
research. "The development of cellular therapy is exciting," says Jeffrey
Rothstein<http://www.hopkinsmedicine.org/neurology_neurosurgery/experts/team_mem\
ber_profile/1204BCCE82BA0CC842233EB2897C0246/Jeffrey_Rothstein>, Packard
director. "The lessons we have collectively learned over the last 10 years from
animal research tell us that the human trials must be very carefully designed
and executed - even the novel surgical approaches by which the cells are
delivered.

"We all hope that this first clinical trial will provide insight in how to carry
out cellular therapy."

Meanwhile, research with another stem cell type, those that give rise to the key
spinal cord cells, astrocytes, is moving closer to human trials under Center
investigator, Nicholas
Maragakis<http://www.hopkinsmedicine.org/neurology_neurosurgery/experts/team_mem\
ber_profile/765536147B11BF8F28BBACD5A22525A3/Nicholas_Maragakis>, in conjunction
with Q Therapeutics<http://www.qthera.com/>, a Utah biotech firm.

"We're not all about stem cells, however," adds Rothstein. "The Packard Center's
translational program focuses on the early development of a variety of
approaches to ALS treatment that includes novel drugs, gene inactivation, and
cellular therapy."

New Study Shows Agent Can Improve Muscle Strength, Size, in Mouse ALS Model
http://www.alscenter.org/news/briefs/090722.cfm

Work adds support to the principle in ongoing human trials.

It's not a cure. But a new tactic to improve quality of life for ALS patients -
one that significantly slows muscle wasting and resulting loss of strength - has
moved forward in the therapy pipeline, thanks to a ground-laying Packard Center
and pharmaceutical company collaborative study.

The work helps support clinical trials that are underway.

In a new study, a research team led by Packard scientists Brett Morrison and
Kathryn Wagner at Johns Hopkins and including industry researchers from
Acceleron Pharma in Massachusetts, found that injecting ALS mice with an agent
that counters the body's own brakes on muscle growth clearly keeps muscles
larger and stronger, either before or after disease symptoms appear.

"What we're doing doesn't prevent motor neuron loss," says Morrison. "But it
does allow existing mouse neurons to innervate muscles that are larger and
stronger. It's compensating, really. And it seems to hide the animals'
deterioration longer."

The work was reported in a recent issue of Experimental Neurology.

In the study, SOD1 mice that mimic one type of ALS in humans were injected with
a mouse version of a soluble protein called ACE031. The protein is a red herring
of sorts, designed to attract natural molecules like myostatin and keep them
from reaching their normal muscle targets. Myostatin and its relatives are part
of an internal check and balance system. The molecules' role is to rein in
muscle growth.

By keeping myostatin tied up, the body is then free to rebuild muscle tissue.

And even though slowing muscle wasting doesn't prevent death, the value of doing
that looks increasingly important to maintain quality of life in patients.
Muscles are important players in energy metabolism as well as in movement.

In the study's first part, ALS mice received rodent ACE031 some 20 days before
symptoms typically appear. Their body weight increased and stayed at that level
until the animals' death. "Remarkably, the animals actually gained strength for
a time after symptoms appeared," Morrison says. That's a time when strength
begins to decline in their untreated mouse counterparts. Test mice were 35
percent stronger. Toward the end of their lives, however, that strength declined
at a slightly faster rate than in control animals - what you'd expect when the
number of motor neurons contacting a larger muscle drops past a certain point.

As for animals injected just as their symptoms were beginning, the figures at
first look less impressive, says Morrison: Muscle strength is only 7 percent
greater than in untreated mice.

"But this means that ACE031 was able to reverse the initial loss of strength and
still go on to increase it."

The timing of the study is especially good, the researchers say, because it
comes as Acceleron just finished the first of its Phase I trials of human ACE031
in healthy human subjects. Phase I trials are designed to show if a treatment is
safe and that people tolerate the trial dosage. Jas Seehar, CSO of Acceleron
Pharma reported at the Parent Project Muscular Dystrophy meeting this June in
Atlanta that ACE031 wasn't toxic and was tolerated.

"Further," says Wagner, "even though Phase I trials aren't designed to show if
an agent actually works, the company reported a demonstrated increase in muscle
mass from a single ACE031 injection. That looks like the first definitive
demonstration that inhibiting myostatin with a drug can increase muscle mass in
people."

New aspects of Acceleron's Phase I trials begin this year.

ACE031 is a human-built molecule whose "business end" is the protein receptor,
found in muscle, for myostatin and its relatives. It has an added bit, part of a
natural antibody that keeps the molecule soluble and prevents it from quickly
deteriorating.

Dear all,

I have some boxes of Rlutek available with me.
Whoever needs it, please send their mailing address.

First Come First serve basis pls.

Thanks and God bless all.

Gaurav..

NEW LOOK AT DATA POLISHES OLD PRINCIPLE FOR ALS THERAPY
http://www.alscenter.org/news/briefs/090430.cfm

A sophisticated new look at an old study that investigated an epilepsy drug as a
possible ALS (Lou Gehrig's disease) therapy - one that got a "thumbs-down"
nearly a decade ago - is now causing researchers to re-think its conclusions.

"This new analysis supports our interest in a potentially good ALS target that
surprised us by not appearing to be much good back then," says Jeffrey
Rothstein, one of the researchers on the original study. Rothstein, a
neurologist/neuroscientist, directs the Packard Center for ALS Research at Johns
Hopkins.

The new data review, presented Tuesday in Seattle by Harvard neurologist Merit
Cudkowicz at the American Academy of Neurology annual meeting, showed survival
in some patients lengthened by 25 percent.

Cudkowicz was also one of the original study researchers.

In the early 2000s, topiramate, an FDA-approved drug for epilepsy was the tested
agent in a clinical trial run by the Northeast ALS Consortium (NEALS) - a
nationwide body of academic clinicians dedicated to improving clinical trials
for the disease. Nearly 300 people with ALS enrolled in the yearlong test of
safety and efficacy, two-thirds of them receiving topiramate.

The idea, says Cudkowicz, who co-directs NEALS, was that topiramate would reduce
excitotoxicity, a highly damaging process that occurs in ALS. "The chosen dosage
was the maximum that people could be given."

Unfortunately, those in the topiramate group of the study lost more weight than
those on a placebo. And though the drug had no apparent effect on survival or
breathing ability - lessened breathing ability marks real decline in ALS - the
group taking topiramate lost arm strength more quickly than the group on the
placebo.

"The trial looked like a failure and that was that," says Rothstein. "Simply
having a bad side effect ended any further consideration of topiramate." As
important: The result also cast doubts on the underlying rationale for trying
the drug.

Earlier, Rothstein had discovered that glutamate, a natural nerve transmitter in
the brain and spinal cord, plays a part in the ALS-caused death of motor
neurons. He and colleagues later found that motor neurons are especially
vulnerable when glutamate acts at specific sites - receptors - in their
membranes. A flood of glutamate "docking" with so-called AMPA/kainate receptors
trips excitotoxicity, an unfortunate chemical cascade that ends in death.

Rothstein and NEALS colleagues Cudkowicz and Jeremy Shefner, looking for drugs
that could block the AMPA/kainate receptors and perhaps rescue motor neurons,
hit upon topiramate. The chemical is thought to quell epilepsy's seizures by
blocking glutamate receptors.

But, after the "failed" topiramate study, many scientists turned away from
AMPA-blocking as a possible route to explore. "That may change," says Cudkowicz.

Recently, neurologist Walter Bradley with the University of Miami queried
Cudkowicz and NEALS, asking whether the weight loss might have caused the
reported muscle weakness, rather than the topiramate itself. Clinicians have
come to believe that weight loss is important in ALS's downward course.

So Cudkowicz pulled the old study data - it's a NEALS policy to purge research
results of any patient IDs and thus make completed study data available to any
researcher - and she and colleagues began a more sophisticated analysis than was
previously possible.

In turning the statistical spotlight on the ALS patients, a comparison of people
in the topiramate group and those on placebo with the same weight loss revealed
that people on the test drug had a 25 percent longer median survival.

The caution in interpreting this, however, is real, say Cudkowicz and Rothstein:
The study is preliminary and needs the peer review that should come with
publishing it.

Also, analysis is ongoing, Cudkowicz explains. The researchers are now applying
techniques that can answer specifically whether topiramate or weight loss cause
the decline in muscle strength.

"This doesn't necessarily prove topiramate is a good therapy for people with
ALS," says Rothstein, "but it does bring drugs that work on AMPA receptors back
into the picture."

Finding a drug that's like topiramate but that doesn't cause weight loss in ALS
patients could be helpful, says Cudkowicz. But because of the weight loss and
potential harm from the existing drug, it is not recommended as a treatment for
the disease, she adds.

"Also," Cudkowicz says, "it's important in studying possible treatments for
people with ALS to test a greater variety of dosages. You don't want to throw
out a drug that might be on a good pathway because you lack sufficient data on
the best dosage."

_________________

The Packard Center contributes financial support to NEALS as well as expertise.
NEALS is the largest ALS clinical consortium worldwide, with more than 50 sites
in the United States and Canada. It engages patients in clinical trials and
improves understanding of clinical aspects of ALS care and management.

Rothstein and Cudkowicz both sit on NEALS' Executive Committee. Packard Center
researchers who are also Johns Hopkins clinical faculty frequently conduct
NEALS-advised trials at the Johns Hopkins ALS clinic.

The original topiramate study was NIH-sponsored, with additional funding from
(the then) Ortho-McNeil Pharmaceuticals and the Muscular Dystrophy Association.

David Schoenfeld of Harvard, collaborated on the new analysis.

Interesting to read.....

Here is the link to the story of Catherine Royce who died on March 30 after
being diagnosed for ALS in 2003.
She chose to die and bring an end to all the pain that she was going thru.
This is a tough story but it is also a fact.

In the story, she discusses what she felt when she had a near death experience
and then how it felt to come back to life.

Must read...
http://www.npr.org/templates/story/story.php?storyId=102923424&sc=emaf

Hope all of you are well.
Tc.
Gaurav.

NEW COMMON PATHWAY IN NEURODEGENERATIVE DISEASE IS A POSSIBLE DOOR TO A POINT OF
NO RETURN
"...more important to medicine, it defines how neurological disease could spread
throughout the nervous system"
http://www.alscenter.org/news/briefs/090410.cfm

A just-out study suggests that what keeps chronic nervous system diseases such
as Alzheimer's, Huntington's and ALS going - until they overcome the internal
protective mechanisms a body can throw at them - may largely come down to poor
conversational skills.

In the current issue of the journal Neuron, a team of Johns Hopkins scientists
reports uncovering a much-sought molecular path that nerve cells (neurons) use
to communicate with their neighboring cells, the astrocytes.

The team also shows how failure of this system could leave the brain and spinal
cord vulnerable in disease.

Astrocytes are the most plentiful central nervous system cells. And while
scientists have known for some time that they're critical for neurons' normal
activity and even for their survival, precisely how the two cell types
communicate hasn't been clear.

"This new work shows that neurons dynamically direct astroglia," says team
leader Jeffrey Rothstein, M.D., Ph.D., "but more important to medicine, it
defines how neurological disease may spread throughout the nervous system."

Rothstein directs The Robert Packard Center for ALS Research at Johns Hopkins.

The focus of the study is on the plentiful neurons that communicate with each
other through the neurotransmitter glutamate. While glutamate is a necessary
excitatory substance in the nervous system, in excess, it overstimulates and
becomes toxic - excitotoxic - to neurons. Fortunately, neighboring astrocytes
can mop up the excess via molecular transporters embedded in their outer
membranes. The chief transporter is a protein called EAAT2.

Earlier Rothstein's group showed that astroglia - and their EAAT2 protein - are
critical for normal neuron activity.  In test rats whose astroglia lack the
EAAT2 equivalent there's not only a flood of toxic glutamate but a resulting
neuron death that leads to paralysis.

Post-mortem studies of patients with ALS and animal models of that disease
frequently reveal a severe loss of EAAT2.

What the new study shows is that neurons themselves direct the creation of EAAT2
in nearby astrocytes.

Here, the scientists devised a microscopic platform containing two tiny
chambers: One held neurons, another astrocytes. In this system, some neurons
could send out their long, thin axon processes through microscopic channels that
ended in astrocytes. Where axons reached close to astrocytes or touched them -
and only there - the astrocytes quickly turned on their genes for the EAAT2
glutamate transporters, the very protein that could protect them from glutamate
excess.

A second elegant but more intricate part of the work revealed that as neurons
sidle up to astrocytes, they very specifically stimulate a tiny part of the
astrocyte gene that turns on EAAT2. This stimulating molecule, called KBBP,
highly regulates the right astrocyte genes that ultimately can keep neurons
operating.

In the study, astrocytes whose KBBP was high bloomed with transporters. This
didn't occur if neurons in the chamber were poisoned.  It also didn't occur if
production of KBBP was blocked.

The researchers next wanted to see if the pathway they'd uncovered was important
in real injuries to the spinal cord or brain. They showed, in rodent models,
that injuring the spinal cord neurons that control movement, whether by trauma
(like spinal cord injury) or poison, plays havoc with nearby astrocytes. When
astrocytes lose the connection with neurons, KBBP drops, they don't make
transporters, there's a flood of glutamate and they themselves begin to sicken.

This accelerates the ongoing injury to neighboring neurons.

And last, animal models of familial ALS proved the principle of
neuron-directs-astrocyte-to-mop-up-glutamate. The models carry a gene that
causes the disease, and as the neurons deterioriate, the astrocytes follow. 
"The loss of the glutamate transporter in these animal models follows the path
of neuron injury; it spreads through the spinal cord," says Rothstein.

Most exciting, Rothstein says, "is that any number of neurodegenerative diseases
appear to hold this downhill process in common, once the disease has started.
"Even when neurons look OK, the conversation between neurons and astrocytes has
fallen off."

"Although many other processes go wrong in the diseases, this common mechanism
appears key to keeping the disease going, to create further injury," Rothstein
adds.

"Understanding this biology gives us new clues to the ways a neuron's
'neighborhood' forces disease to accelerate," says Rothstein. "Fortunately, it
also gives us ideas for roadblocks to slow the process down."

-----------------

This study was supported by The Robert Packard Center for ALS Research, the
National Institutes of Health and the Muscular Dystrophy Association.

The research team includes first author Yongjie Yang, Oguz Gozen, Andrew
Watkins, Ileana Lorenzini, Angelo Lepore, Yuanzheng Gao, Svetlana Vidensky and
Jean Brennan, with the Johns Hopkins School of Medicine, as well as David
Poulsen, from the University of Montana, Missoula, Jeong Won Park and Noo Li
Jeon with the University of California, Irvine, and Michael B. Robinson, with
the University of Pennsylvania.

PACKARD CENTER ANNOUNCES NEW COLLABORATIVE TIES WITH SCOTLAND'S TOP
ALS RESEARCH BODY
Accomplished stem cell researcher is Packard's first grantee with the
MacDonald Centre
http://www.alscenter.org/news/briefs/090409.cfm

Neuroscientist Catherina Becker is the sort of researcher to inspire
optimism in ALS patients and their families, for the possibility of
what's to come.

A scientist with The Euan MacDonald Centre for Motor Neurone Research
at the University of Edinburgh, Scotland, she's expert on zebrafish, the
small, fast-growing and transparent animals that are lately the darling
of scientists who try to model neurodegenerative diseases.

She's written texts on spinal cord regeneration and is equally savvy
about the capabilities of stem cells. That combination puts her in a
peak place to study the repair of spinal cords, whether from accident
injury or ALS.

So why are we writing about Becker in a Packard Center e-article?

For one thing, Becker is one of Packard's newest grantees, poised to
describe her work at the Packard Center's 9th Annual Symposium in April.


Zebrafish, she recently found, can create new motor neurons from stem
cells that normally lie dormant in an adult spinal cord. She has hopes
that what she's now uncovering in zebrafish will lead to therapy for ALS
patients.

But also, as one of some 20 ALS researchers at the MacDonald Centre in
Scotland, Becker and her colleagues extend Packard's scientific reach
internationally in a new collaborative way.  Now the American and
Scottish organizations are formally research partners.

Packard Director Jeff Rothstein has had his eye on the MacDonald Centre
since it opened in 2007. The two MacDonalds who underwrote the Scottish
organization - Donald MacDonald and son Euan - had consulted with
Rothstein after Euan was diagnosed with ALS.

Thus, a new cross-Atlantic tie was formed. And the fact that the
MacDonald family helped raise funds for the Packard Center strengthened
the bond.

Just as Packard's home base is in a haven of stem cell science at Johns
Hopkins, the MacDonald Centre holds close ties with the University of
Edinburgh's Centre for Neuroregeneration and MRC Centre for Regenerative
Medicine, a facility dedicated to developing useful stem cell lines and
exploring their therapeutic possibilities.

Ian Wilmut, for example, who headed the cloning of Dolly the sheep, is
Director of the MRC Centre for Regenerative Medicine. He now
investigates ways to tailor stem cells to heighten chances that the
cause of diseases such as ALS will stand out.

Besides Becker's work, her MacDonald - and now Packard - stem cell
colleagues investigate what turns on dormant stem cells. They explore
how stem cells produce specialized motor neurons, which is also a key to
repair.

To get an idea of the breadth of MacDonald Centre research, click onto:
http://www.euanmacdonaldcentre.com/researchers.html

Situation:
Loss of muscle movement in hand.

What can we do???
Use a smiley soft foam ball and keep on pressing it whenever you or your patient
are free. This helps muscle movement in hand. For PALS who are stong, they can
even try the fist grippers (available in most medical shops dealing in
equipment). You can hold it in your hand and try and close the grip. They are a
little strong and closing the same needs some amount of energy.

3rd method is to use clay balls...readily available in all shops.

The idea is to keep your muscles moving for as long as you can.

More to come..

God bless all.

Gaurav..

Will be done.

Let me know when.

G...

--- In ALS_India@yahoogroups.com, Gopala Krishna Gokeda <gokeda@...> wrote:
>
> Hi Gaurav,
>  
> Thanks for your mail. These injections will be coming from Philippines to
Delhi. A friend's friend is doing this favour to me. If you can send these to
Visakhapatnam, that'll be great. I shall give you more details soon.
>  
> Thanks very much
>  
> Gopal
>  
>
> --- On Tue, 3/10/09, gauravjain_80 <gauravjain_80@...> wrote:
>
>
> From: gauravjain_80 <gauravjain_80@...>
> Subject: [ALS_India] Re: WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A
PACKARD PERSPECTIVE
> To: ALS_India@yahoogroups.com
> Date: Tuesday, March 10, 2009, 3:17 PM
>
>
>
>
>
>
> Dear Gopal,
> My co bro is travelling to US soon (within 15 days or so).
> If you can get the injections couriered to him, he can bring it back to India
and I can forward it to your folks.
>
> Let me know.
>
> Can be done...
>
> G...
> --- In ALS_India@yahoogrou ps.com, "gauravjain_ 80" <gauravjain_ 80@> wrote:
> >
> > Dear Gopal,
> >
> > glad 2 hear that ur mum is doing fine...
> > I was able 2 get Carnitine tabs but nt the injections.
> > Sorry about that.
> > Let me know if you still need the tabs...
> >
> > Tc and keep in touch...
> >
> > G..
> >
> > --- In ALS_India@yahoogrou ps.com, Gopala Krishna Gokeda <gokeda@> wrote:
> > >
> > > Hi Lalit,
> > >
> > > Please feel free to call me. My phone number is 705-293-0323 and
705-888-1246. My mother is doing very well. I am having hard time getting the
carnitine injections to India. I am still working on them.
> > >
> > > Gopal
> > >
> > >
> > >
> > >
> > >
> > > --- On Fri, 3/6/09, Lalit Kumar <lalitgupta907@ > wrote:
> > >
> > > From: Lalit Kumar <lalitgupta907@ >
> > > Subject: Re: [ALS_India] WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION -
A PACKARD PERSPECTIVE
> > > To: ALS_India@yahoogrou ps.com
> > > Date: Friday, March 6, 2009, 10:24 PM
> > >
> > >
> > >
> > >
> > >
> > >
> > >
> > >
> > >
> > >
> > >
> > >
> > > hello gaurav bhaiya
> > > Do you know any thing about gopal's mother...one thing i want to know once
gopal told me about his neighbour in canada that the person was able to cure his
wife from MND by giving injection of l-carnitine. ..Do u know any thing about
this context????? ??Also do u have any phone no 4 contacting him... want to know
about that lady who was able to cure 4m this prob.....can u do any help regardig
this....If gopal got this mail kindly respond me..
> > >
> > >  
> > > thanx
> > >  
> > > lalit
> > >
> > >  
> > > On 3/5/09, gauravjain_80 <gauravjain_ 80@ yahoo.com> wrote:
> > >
> > >
> > >
> > >
> > >
> > > WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A PACKARD PERSPECTIVE
> > > http://www.alscente r.org/news/ briefs/090304. cfm
> > >
> > >
> > > In 2003, when New England ALS scientists announced they'd discovered
> > > another form of familial ALS - the sixth one, and an adult form that
> > > seems to strike harder in the lower extremities and have a somewhat
> > >
> > > faster course - the hope was that the gene for it would soon surface.
> > >
> > > High excitement in the ALS research community always accompanies
> > > finding a new gene: Perhaps this one holds clues to reveal what triggers
> > >
> > > motor neuron death; perhaps this one will spark a really effective
> > > therapy.
> > >
> > > Last week, after a six-year search, the gene was announced by seasoned
> > > collaborators at the University of Massachusetts and Massachusetts
> > >
> > > General Hospital. Another research team at King's College in London
> > > backed up the finding. Found where they'd suspected it, on chromosome
> > > 16, the mutated FUS gene (for "fused in sarcoma") is responsible for
> > >
> > > perhaps 5 percent of familial ALS. And pinpointing it, after a long,
> > > thorough search, would be news enough.
> > >
> > > But this discovery appears to go beyond the usual. Packard scientists
> > > warmly welcome the appearance of m(for mutated) FUS for a key reason: It
> > >
> > > lends clout to a theory about a major destructive process in ALS that's
> > > been gathering evidence at the Packard Center and elsewhere more than a
> > > decade.
> > >
> > > "The fascinating thing about having the FUS gene linked to ALS," says
> > >
> > > Packard Scientific Director Piera Pasinelli, "is that it's yet another
> > > gene that plays a part in RNA processing."
> > >
> > > And having successful functioning of that molecule is crucial for cells
> > > to work normally. By way of background: RNA - specifically the messenger
> > >
> > > RNA molecule - carries DNA's blueprint for assembling proteins into the
> > > cell cytoplasm where their actual assembly occurs. Yet getting RNA to
> > > reflect DNA's "message" accurately, modifying it for efficiency and then
> > >
> > > transporting it from the cell nucleus to the cytoplasm is an involved,
> > > multi-step process. And it's a one that can go awry.
> > >
> > > In 1998, Packard scientists first published the find that some 65
> > > percent ALS patients harbor abnormal messenger RNA molecules,
> > >
> > > specifically in the injured parts of their central nervous systems. But
> > > no one has known the cause of that or what, if any, part it plays in
> > > ALS's downhill course.
> > >
> > > More evidence: Not long ago, Packard researchers helped discover the
> > >
> > > familial ALS4 gene, one for an abnormal form of a protein called
> > > senataxin. Like FUS, the senataxin gene also has an RNA role, overseeing
> > > proper production of messenger RNA from its DNA blueprint.
> > >
> > > And last year, the King's College group showed mutations in yet another
> > >
> > > gene - one called TDP-43 - that appears both in patients with a variety
> > > of different familial ALS types and, amazingly, in sporadic ALS patients
> > > as well. Healthy people lack these mutations. (Last week, Packard
> > > scientist Wim Robberecht and his European team added to that,
> > >
> > > discovering a new variation of the TDP-gene in familial ALS patients.)
> > > *
> > >
> > > Among TDP-43's list of accomplishments? RNA processing.
> > >
> > > All this suggests that flawed RNA metabolism, then, may join ALS's
> > >
> > > seven "ugly stepsisters, " as another of the biological pathways to go
> > > wrong in ALS. (In scientific terms, the seven stepsisters are: oxidative
> > > damage, misfolded protein aggregates, dysfunctional mitochondria,
> > >
> > > defects in motor neuron transport, growth factor deficiency, pathology
> > > of glial cells, glutamate excitotoxicity. )
> > >
> > > What has Packard scientists most engaged, however, is where the flawed
> > > RNA metabolism could lead. It's interesting, for example, that both
> > >
> > > patients with ALS from mTDP-43 and those with ALS from mFUS appear to
> > > show clumps of misfolded proteins - protein aggregates - in central
> > > nervous system cells, early in the disease. "This suggests that these
> > >
> > > aggregates are key agents, that they participate early in the genesis of
> > > ALS," says Packard scientist Phil Wong, who has just made a mouse model
> > > of ALS using a mutant TDP-43 gene.
> > >
> > > So an important next step, both for understanding and for therapy, Wong
> > >
> > > says, is to "see whether these aggregates are indeed critical players or
> > > if, instead, they're just `tombstones' that mark dying motor neurons."
> > > His mouse model should help answer that question.
> > >
> > >
> > > In this, the new "stepsister" may be the most useful. Because it shows
> > > up in both familial and sporadic patients, some researchers are even
> > > speculating that RNA gone awry may be the missing overarching principle
> > >
> > > that tells how the stepsisters are related. In other words, some are
> > > hoping it may be the key process that causes ALS.
> > >
> > > "The new discoveries, we believe, point strongly to flawed RNA
> > > metabolism as a key disease process to imitate in animal models for
> > >
> > > ALS," says Rothstein.
> > >
> > > "It's these tools - the gene-primed model mice and fish and fruit flies
> > > that Packard scientists offer the world's research community - that will
> > > enable us to understand ALS. Ultimately, they'll become the agents we'll
> > >
> > > all use to find effective therapies."
> > >
> > > *Robberecht is already busy making a zebrafish model of ALS using
> > > mutant TDP-43. His Packard colleague J. Paul Taylor, has begun testing a
> > > new TDP-43 fruit fly model.
> > >
> > >
> > > ____________ _________ _________ _____
> > >
> > > About The Robert Packard Center for ALS Research at Johns Hopkins
> > > www.alscenter. org
> > >
> > >
> > > Located in Baltimore, the Robert Packard Center for ALS Research at
> > > Johns Hopkins is a worldwide collaboration of scientists aimed at
> > > developing therapies and a cure for amyotrophic lateral sclerosis (ALS),
> > > also known as Lou Gehrig's disease.
> > >
> > >
> > > The Center is the only institution of its kind dedicated solely to the
> > > disease. Its research is meant to translate rapidly from the lab bench
> > > to the clinic, largely by eliminating time spent waiting for grants and
> > >
> > > lowering institutional barriers to sharing scientific results.
> > >
> > > Scientists and clinician members of the Packard Center have moved drugs
> > > reliably and rapidly from preclinical experiments to human trials.
> > > Direct or indirect links to international biotech or pharmaceutical
> > >
> > > companies bring the infrastructure and experience needed to make
> > > promising drugs into therapies.
> > >
> > > Packard scientists are the first to propose and test a combination
> > > approach to drug therapy, a tactic that has worked for AIDS, cancer and
> > >
> > > other diseases.
> > >
> > > ALS is a progressive, disabling neuromuscular disease that causes
> > > complete paralysis and loss of function - including the ability to eat,
> > > speak and breathe. ALS progresses quickly and is not curable. Most
> > >
> > > patients die within five years of diagnosis.
> > >
> > > ____________ _________ _________ _________ __
> > > Rebecca Berger
> > > Research Program Coordinator
> > > Robert Packard Center for ALS Research at Johns Hopkins
> > > 5801 Smith Avenue | McAuley Suite 110
> > >
> > > Baltimore, MD 21209
> > > 410.735.7678 direct
> > > 410.735.7680 fax
> > > rberger6@jhmi. edu
> > > www.alscenter. org
> > >
> > > www.fiesta5K. org
> > >
> >
>

Dear Gopal,
My co bro is travelling to US soon (within 15 days or so).
If you can get the injections couriered to him, he can bring it back to India
and I can forward it to your folks.

Let me know.

Can be done...

G...
--- In ALS_India@yahoogroups.com, "gauravjain_80" <gauravjain_80@...> wrote:
>
> Dear Gopal,
>
> glad 2 hear that ur mum is doing fine...
> I was able 2 get Carnitine tabs but nt the injections.
> Sorry about that.
> Let me know if you still need the tabs...
>
> Tc and keep in touch...
>
> G..
>
> --- In ALS_India@yahoogroups.com, Gopala Krishna Gokeda <gokeda@> wrote:
> >
> > Hi Lalit,
> >
> > Please feel free to call me. My phone number is 705-293-0323 and
705-888-1246. My mother is doing very well. I am having hard time getting the
carnitine injections to India. I am still working on them.
> >
> > Gopal
> >
> >
> >
> >
> >
> > --- On Fri, 3/6/09, Lalit Kumar <lalitgupta907@> wrote:
> >
> > From: Lalit Kumar <lalitgupta907@>
> > Subject: Re: [ALS_India] WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A 
PACKARD PERSPECTIVE
> > To: ALS_India@yahoogroups.com
> > Date: Friday, March 6, 2009, 10:24 PM
> >
> >
> >
> >
> >
> >
> >
> >
> >
> >
> >
> >
> >             hello gaurav bhaiya
> > Do you know any thing about gopal's mother...one thing i want to know once
gopal told me about his neighbour in canada that the person was able to cure his
wife from MND by giving injection of l-carnitine. ..Do u know any thing about
this context????? ??Also do u have any phone no 4 contacting him... want to know
about that lady who was able to cure 4m this prob.....can u do any help regardig
this....If gopal got this mail kindly respond me..
> >
> >  
> > thanx
> >  
> > lalit
> >
> >  
> > On 3/5/09, gauravjain_80 <gauravjain_80@ yahoo.com> wrote:
> >
> >
> >
> >
> >
> > WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A PACKARD PERSPECTIVE
> > http://www.alscente r.org/news/ briefs/090304. cfm
> >
> >
> > In 2003, when New England ALS scientists announced they'd discovered
> > another form of familial ALS - the sixth one, and an adult form that
> > seems to strike harder in the lower extremities and have a somewhat
> >
> > faster course - the hope was that the gene for it would soon surface.
> >
> > High excitement in the ALS research community always accompanies
> > finding a new gene: Perhaps this one holds clues to reveal what triggers
> >
> > motor neuron death; perhaps this one will spark a really effective
> > therapy.
> >
> > Last week, after a six-year search, the gene was announced by seasoned
> > collaborators at the University of Massachusetts and Massachusetts
> >
> > General Hospital. Another research team at King's College in London
> > backed up the finding. Found where they'd suspected it, on chromosome
> > 16, the mutated FUS gene (for "fused in sarcoma") is responsible for
> >
> > perhaps 5 percent of familial ALS. And pinpointing it, after a long,
> > thorough search, would be news enough.
> >
> > But this discovery appears to go beyond the usual. Packard scientists
> > warmly welcome the appearance of m(for mutated) FUS for a key reason: It
> >
> > lends clout to a theory about a major destructive process in ALS that's
> > been gathering evidence at the Packard Center and elsewhere more than a
> > decade.
> >
> > "The fascinating thing about having the FUS gene linked to ALS," says
> >
> > Packard Scientific Director Piera Pasinelli, "is that it's yet another
> > gene that plays a part in RNA processing."
> >
> > And having successful functioning of that molecule is crucial for cells
> > to work normally. By way of background: RNA - specifically the messenger
> >
> > RNA molecule - carries DNA's blueprint for assembling proteins into the
> > cell cytoplasm where their actual assembly occurs. Yet getting RNA to
> > reflect DNA's "message" accurately, modifying it for efficiency and then
> >
> > transporting it from the cell nucleus to the cytoplasm is an involved,
> > multi-step process. And it's a one that can go awry.
> >
> > In 1998, Packard scientists first published the find that some 65
> > percent ALS patients harbor abnormal messenger RNA molecules,
> >
> > specifically in the injured parts of their central nervous systems. But
> > no one has known the cause of that or what, if any, part it plays in
> > ALS's downhill course.
> >
> > More evidence: Not long ago, Packard researchers helped discover the
> >
> > familial ALS4 gene, one for an abnormal form of a protein called
> > senataxin. Like FUS, the senataxin gene also has an RNA role, overseeing
> > proper production of messenger RNA from its DNA blueprint.
> >
> > And last year, the King's College group showed mutations in yet another
> >
> > gene - one called TDP-43 - that appears both in patients with a variety
> > of different familial ALS types and, amazingly, in sporadic ALS patients
> > as well. Healthy people lack these mutations. (Last week, Packard
> > scientist Wim Robberecht and his European team added to that,
> >
> > discovering a new variation of the TDP-gene in familial ALS patients.)
> > *
> >
> > Among TDP-43's list of accomplishments? RNA processing.
> >
> > All this suggests that flawed RNA metabolism, then, may join ALS's
> >
> > seven "ugly stepsisters," as another of the biological pathways to go
> > wrong in ALS. (In scientific terms, the seven stepsisters are: oxidative
> > damage, misfolded protein aggregates, dysfunctional mitochondria,
> >
> > defects in motor neuron transport, growth factor deficiency, pathology
> > of glial cells, glutamate excitotoxicity. )
> >
> > What has Packard scientists most engaged, however, is where the flawed
> > RNA metabolism could lead. It's interesting, for example, that both
> >
> > patients with ALS from mTDP-43 and those with ALS from mFUS appear to
> > show clumps of misfolded proteins - protein aggregates - in central
> > nervous system cells, early in the disease. "This suggests that these
> >
> > aggregates are key agents, that they participate early in the genesis of
> > ALS," says Packard scientist Phil Wong, who has just made a mouse model
> > of ALS using a mutant TDP-43 gene.
> >
> > So an important next step, both for understanding and for therapy, Wong
> >
> > says, is to "see whether these aggregates are indeed critical players or
> > if, instead, they're just `tombstones' that mark dying motor neurons."
> > His mouse model should help answer that question.
> >
> >
> > In this, the new "stepsister" may be the most useful. Because it shows
> > up in both familial and sporadic patients, some researchers are even
> > speculating that RNA gone awry may be the missing overarching principle
> >
> > that tells how the stepsisters are related. In other words, some are
> > hoping it may be the key process that causes ALS.
> >
> > "The new discoveries, we believe, point strongly to flawed RNA
> > metabolism as a key disease process to imitate in animal models for
> >
> > ALS," says Rothstein.
> >
> > "It's these tools - the gene-primed model mice and fish and fruit flies
> > that Packard scientists offer the world's research community - that will
> > enable us to understand ALS. Ultimately, they'll become the agents we'll
> >
> > all use to find effective therapies."
> >
> > *Robberecht is already busy making a zebrafish model of ALS using
> > mutant TDP-43. His Packard colleague J. Paul Taylor, has begun testing a
> > new TDP-43 fruit fly model.
> >
> >
> > ____________ _________ _________ _____
> >
> > About The Robert Packard Center for ALS Research at Johns Hopkins
> > www.alscenter. org
> >
> >
> > Located in Baltimore, the Robert Packard Center for ALS Research at
> > Johns Hopkins is a worldwide collaboration of scientists aimed at
> > developing therapies and a cure for amyotrophic lateral sclerosis (ALS),
> > also known as Lou Gehrig's disease.
> >
> >
> > The Center is the only institution of its kind dedicated solely to the
> > disease. Its research is meant to translate rapidly from the lab bench
> > to the clinic, largely by eliminating time spent waiting for grants and
> >
> > lowering institutional barriers to sharing scientific results.
> >
> > Scientists and clinician members of the Packard Center have moved drugs
> > reliably and rapidly from preclinical experiments to human trials.
> > Direct or indirect links to international biotech or pharmaceutical
> >
> > companies bring the infrastructure and experience needed to make
> > promising drugs into therapies.
> >
> > Packard scientists are the first to propose and test a combination
> > approach to drug therapy, a tactic that has worked for AIDS, cancer and
> >
> > other diseases.
> >
> > ALS is a progressive, disabling neuromuscular disease that causes
> > complete paralysis and loss of function - including the ability to eat,
> > speak and breathe. ALS progresses quickly and is not curable. Most
> >
> > patients die within five years of diagnosis.
> >
> > ____________ _________ _________ _________ __
> > Rebecca Berger
> > Research Program Coordinator
> > Robert Packard Center for ALS Research at Johns Hopkins
> > 5801 Smith Avenue | McAuley Suite 110
> >
> > Baltimore, MD 21209
> > 410.735.7678 direct
> > 410.735.7680 fax
> > rberger6@jhmi. edu
> > www.alscenter. org
> >
> > www.fiesta5K. org
> >
>

Dear Gopal,

glad 2 hear that ur mum is doing fine...
I was able 2 get Carnitine tabs but nt the injections.
Sorry about that.
Let me know if you still need the tabs...

Tc and keep in touch...

G..

--- In ALS_India@yahoogroups.com, Gopala Krishna Gokeda <gokeda@...> wrote:
>
> Hi Lalit,
>
> Please feel free to call me. My phone number is 705-293-0323 and 705-888-1246.
My mother is doing very well. I am having hard time getting the carnitine
injections to India. I am still working on them.
>
> Gopal
>
>
>
>
>
> --- On Fri, 3/6/09, Lalit Kumar <lalitgupta907@...> wrote:
>
> From: Lalit Kumar <lalitgupta907@...>
> Subject: Re: [ALS_India] WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A 
PACKARD PERSPECTIVE
> To: ALS_India@yahoogroups.com
> Date: Friday, March 6, 2009, 10:24 PM
>
>
>
>
>
>
>
>
>
>
>
>
>             hello gaurav bhaiya
> Do you know any thing about gopal's mother...one thing i want to know once
gopal told me about his neighbour in canada that the person was able to cure his
wife from MND by giving injection of l-carnitine. ..Do u know any thing about
this context????? ??Also do u have any phone no 4 contacting him... want to know
about that lady who was able to cure 4m this prob.....can u do any help regardig
this....If gopal got this mail kindly respond me..
>
>  
> thanx
>  
> lalit
>
>  
> On 3/5/09, gauravjain_80 <gauravjain_80@ yahoo.com> wrote:
>
>
>
>
>
> WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A PACKARD PERSPECTIVE
> http://www.alscente r.org/news/ briefs/090304. cfm
>
>
> In 2003, when New England ALS scientists announced they'd discovered
> another form of familial ALS - the sixth one, and an adult form that
> seems to strike harder in the lower extremities and have a somewhat
>
> faster course - the hope was that the gene for it would soon surface.
>
> High excitement in the ALS research community always accompanies
> finding a new gene: Perhaps this one holds clues to reveal what triggers
>
> motor neuron death; perhaps this one will spark a really effective
> therapy.
>
> Last week, after a six-year search, the gene was announced by seasoned
> collaborators at the University of Massachusetts and Massachusetts
>
> General Hospital. Another research team at King's College in London
> backed up the finding. Found where they'd suspected it, on chromosome
> 16, the mutated FUS gene (for "fused in sarcoma") is responsible for
>
> perhaps 5 percent of familial ALS. And pinpointing it, after a long,
> thorough search, would be news enough.
>
> But this discovery appears to go beyond the usual. Packard scientists
> warmly welcome the appearance of m(for mutated) FUS for a key reason: It
>
> lends clout to a theory about a major destructive process in ALS that's
> been gathering evidence at the Packard Center and elsewhere more than a
> decade.
>
> "The fascinating thing about having the FUS gene linked to ALS," says
>
> Packard Scientific Director Piera Pasinelli, "is that it's yet another
> gene that plays a part in RNA processing."
>
> And having successful functioning of that molecule is crucial for cells
> to work normally. By way of background: RNA - specifically the messenger
>
> RNA molecule - carries DNA's blueprint for assembling proteins into the
> cell cytoplasm where their actual assembly occurs. Yet getting RNA to
> reflect DNA's "message" accurately, modifying it for efficiency and then
>
> transporting it from the cell nucleus to the cytoplasm is an involved,
> multi-step process. And it's a one that can go awry.
>
> In 1998, Packard scientists first published the find that some 65
> percent ALS patients harbor abnormal messenger RNA molecules,
>
> specifically in the injured parts of their central nervous systems. But
> no one has known the cause of that or what, if any, part it plays in
> ALS's downhill course.
>
> More evidence: Not long ago, Packard researchers helped discover the
>
> familial ALS4 gene, one for an abnormal form of a protein called
> senataxin. Like FUS, the senataxin gene also has an RNA role, overseeing
> proper production of messenger RNA from its DNA blueprint.
>
> And last year, the King's College group showed mutations in yet another
>
> gene - one called TDP-43 - that appears both in patients with a variety
> of different familial ALS types and, amazingly, in sporadic ALS patients
> as well. Healthy people lack these mutations. (Last week, Packard
> scientist Wim Robberecht and his European team added to that,
>
> discovering a new variation of the TDP-gene in familial ALS patients.)
> *
>
> Among TDP-43's list of accomplishments? RNA processing.
>
> All this suggests that flawed RNA metabolism, then, may join ALS's
>
> seven "ugly stepsisters," as another of the biological pathways to go
> wrong in ALS. (In scientific terms, the seven stepsisters are: oxidative
> damage, misfolded protein aggregates, dysfunctional mitochondria,
>
> defects in motor neuron transport, growth factor deficiency, pathology
> of glial cells, glutamate excitotoxicity. )
>
> What has Packard scientists most engaged, however, is where the flawed
> RNA metabolism could lead. It's interesting, for example, that both
>
> patients with ALS from mTDP-43 and those with ALS from mFUS appear to
> show clumps of misfolded proteins - protein aggregates - in central
> nervous system cells, early in the disease. "This suggests that these
>
> aggregates are key agents, that they participate early in the genesis of
> ALS," says Packard scientist Phil Wong, who has just made a mouse model
> of ALS using a mutant TDP-43 gene.
>
> So an important next step, both for understanding and for therapy, Wong
>
> says, is to "see whether these aggregates are indeed critical players or
> if, instead, they're just `tombstones' that mark dying motor neurons."
> His mouse model should help answer that question.
>
>
> In this, the new "stepsister" may be the most useful. Because it shows
> up in both familial and sporadic patients, some researchers are even
> speculating that RNA gone awry may be the missing overarching principle
>
> that tells how the stepsisters are related. In other words, some are
> hoping it may be the key process that causes ALS.
>
> "The new discoveries, we believe, point strongly to flawed RNA
> metabolism as a key disease process to imitate in animal models for
>
> ALS," says Rothstein.
>
> "It's these tools - the gene-primed model mice and fish and fruit flies
> that Packard scientists offer the world's research community - that will
> enable us to understand ALS. Ultimately, they'll become the agents we'll
>
> all use to find effective therapies."
>
> *Robberecht is already busy making a zebrafish model of ALS using
> mutant TDP-43. His Packard colleague J. Paul Taylor, has begun testing a
> new TDP-43 fruit fly model.
>
>
> ____________ _________ _________ _____
>
> About The Robert Packard Center for ALS Research at Johns Hopkins
> www.alscenter. org
>
>
> Located in Baltimore, the Robert Packard Center for ALS Research at
> Johns Hopkins is a worldwide collaboration of scientists aimed at
> developing therapies and a cure for amyotrophic lateral sclerosis (ALS),
> also known as Lou Gehrig's disease.
>
>
> The Center is the only institution of its kind dedicated solely to the
> disease. Its research is meant to translate rapidly from the lab bench
> to the clinic, largely by eliminating time spent waiting for grants and
>
> lowering institutional barriers to sharing scientific results.
>
> Scientists and clinician members of the Packard Center have moved drugs
> reliably and rapidly from preclinical experiments to human trials.
> Direct or indirect links to international biotech or pharmaceutical
>
> companies bring the infrastructure and experience needed to make
> promising drugs into therapies.
>
> Packard scientists are the first to propose and test a combination
> approach to drug therapy, a tactic that has worked for AIDS, cancer and
>
> other diseases.
>
> ALS is a progressive, disabling neuromuscular disease that causes
> complete paralysis and loss of function - including the ability to eat,
> speak and breathe. ALS progresses quickly and is not curable. Most
>
> patients die within five years of diagnosis.
>
> ____________ _________ _________ _________ __
> Rebecca Berger
> Research Program Coordinator
> Robert Packard Center for ALS Research at Johns Hopkins
> 5801 Smith Avenue | McAuley Suite 110
>
> Baltimore, MD 21209
> 410.735.7678 direct
> 410.735.7680 fax
> rberger6@jhmi. edu
> www.alscenter. org
>
> www.fiesta5K. org
>

Dear all,
I have a "Respironics Synchrony" Bi Pap Machine and a suction machine
(make is Anand company).
I had bought both of them for my Dad. There is no need as of now and hence both
m/cs are available for sale.

If anyone is interested, please feel free to contact me. I can email the details
to whoever is interested...

I do not intend on making money or profit out of the same. Whatever is the cost
of the m/c in the market, I will obviously give for less than that.


Cheers...
God bless all.

Gaurav..

Hi Lalit.
Hows ur Father doing now?

Feel free to call me if you need any info or help.

You can email Gopal on gokeda@...

I haven't spoken to him since a while now.

Cheers.
G


  --- In ALS_India@yahoogroups.com, Lalit Kumar <lalitgupta907@...> wrote:
>
> hello gaurav bhaiya
> Do you know any thing about gopal's mother...one thing i want to know once
> gopal told me about his neighbour in canada that the person was able to cure
> his wife from MND by giving injection of l-carnitine...Do u know any thing
> about this context???????Also do u have any phone no 4 contacting him...
> want to know about that lady who was able to cure 4m this prob.....can u do
> any help regardig this....If gopal got this mail kindly respond me..
>
> thanx
>
> lalit
>
>
> On 3/5/09, gauravjain_80 <gauravjain_80@...> wrote:
> >
> >   WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A PACKARD PERSPECTIVE
> > http://www.alscenter.org/news/briefs/090304.cfm
> >
> > In 2003, when New England ALS scientists announced they'd discovered
> > another form of familial ALS - the sixth one, and an adult form that
> > seems to strike harder in the lower extremities and have a somewhat
> > faster course - the hope was that the gene for it would soon surface.
> >
> > High excitement in the ALS research community always accompanies
> > finding a new gene: Perhaps this one holds clues to reveal what triggers
> > motor neuron death; perhaps this one will spark a really effective
> > therapy.
> >
> > Last week, after a six-year search, the gene was announced by seasoned
> > collaborators at the University of Massachusetts and Massachusetts
> > General Hospital. Another research team at King's College in London
> > backed up the finding. Found where they'd suspected it, on chromosome
> > 16, the mutated FUS gene (for "fused in sarcoma") is responsible for
> > perhaps 5 percent of familial ALS. And pinpointing it, after a long,
> > thorough search, would be news enough.
> >
> > But this discovery appears to go beyond the usual. Packard scientists
> > warmly welcome the appearance of m(for mutated) FUS for a key reason: It
> > lends clout to a theory about a major destructive process in ALS that's
> > been gathering evidence at the Packard Center and elsewhere more than a
> > decade.
> >
> > "The fascinating thing about having the FUS gene linked to ALS," says
> > Packard Scientific Director Piera Pasinelli, "is that it's yet another
> > gene that plays a part in RNA processing."
> >
> > And having successful functioning of that molecule is crucial for cells
> > to work normally. By way of background: RNA - specifically the messenger
> > RNA molecule - carries DNA's blueprint for assembling proteins into the
> > cell cytoplasm where their actual assembly occurs. Yet getting RNA to
> > reflect DNA's "message" accurately, modifying it for efficiency and then
> > transporting it from the cell nucleus to the cytoplasm is an involved,
> > multi-step process. And it's a one that can go awry.
> >
> > In 1998, Packard scientists first published the find that some 65
> > percent ALS patients harbor abnormal messenger RNA molecules,
> > specifically in the injured parts of their central nervous systems. But
> > no one has known the cause of that or what, if any, part it plays in
> > ALS's downhill course.
> >
> > More evidence: Not long ago, Packard researchers helped discover the
> > familial ALS4 gene, one for an abnormal form of a protein called
> > senataxin. Like FUS, the senataxin gene also has an RNA role, overseeing
> > proper production of messenger RNA from its DNA blueprint.
> >
> > And last year, the King's College group showed mutations in yet another
> > gene - one called TDP-43 - that appears both in patients with a variety
> > of different familial ALS types and, amazingly, in sporadic ALS patients
> > as well. Healthy people lack these mutations. (Last week, Packard
> > scientist Wim Robberecht and his European team added to that,
> > discovering a new variation of the TDP-gene in familial ALS patients.)
> > *
> >
> > Among TDP-43's list of accomplishments? RNA processing.
> >
> > All this suggests that flawed RNA metabolism, then, may join ALS's
> > seven "ugly stepsisters," as another of the biological pathways to go
> > wrong in ALS. (In scientific terms, the seven stepsisters are: oxidative
> > damage, misfolded protein aggregates, dysfunctional mitochondria,
> > defects in motor neuron transport, growth factor deficiency, pathology
> > of glial cells, glutamate excitotoxicity.)
> >
> > What has Packard scientists most engaged, however, is where the flawed
> > RNA metabolism could lead. It's interesting, for example, that both
> > patients with ALS from mTDP-43 and those with ALS from mFUS appear to
> > show clumps of misfolded proteins - protein aggregates - in central
> > nervous system cells, early in the disease. "This suggests that these
> > aggregates are key agents, that they participate early in the genesis of
> > ALS," says Packard scientist Phil Wong, who has just made a mouse model
> > of ALS using a mutant TDP-43 gene.
> >
> > So an important next step, both for understanding and for therapy, Wong
> > says, is to "see whether these aggregates are indeed critical players or
> > if, instead, they're just `tombstones' that mark dying motor neurons."
> > His mouse model should help answer that question.
> >
> > In this, the new "stepsister" may be the most useful. Because it shows
> > up in both familial and sporadic patients, some researchers are even
> > speculating that RNA gone awry may be the missing overarching principle
> > that tells how the stepsisters are related. In other words, some are
> > hoping it may be the key process that causes ALS.
> >
> > "The new discoveries, we believe, point strongly to flawed RNA
> > metabolism as a key disease process to imitate in animal models for
> > ALS," says Rothstein.
> >
> > "It's these tools - the gene-primed model mice and fish and fruit flies
> > that Packard scientists offer the world's research community - that will
> > enable us to understand ALS. Ultimately, they'll become the agents we'll
> > all use to find effective therapies."
> >
> > *Robberecht is already busy making a zebrafish model of ALS using
> > mutant TDP-43. His Packard colleague J. Paul Taylor, has begun testing a
> > new TDP-43 fruit fly model.
> >
> > ___________________________________
> >
> > About The Robert Packard Center for ALS Research at Johns Hopkins
> > www.alscenter.org
> >
> > Located in Baltimore, the Robert Packard Center for ALS Research at
> > Johns Hopkins is a worldwide collaboration of scientists aimed at
> > developing therapies and a cure for amyotrophic lateral sclerosis (ALS),
> > also known as Lou Gehrig's disease.
> >
> > The Center is the only institution of its kind dedicated solely to the
> > disease. Its research is meant to translate rapidly from the lab bench
> > to the clinic, largely by eliminating time spent waiting for grants and
> > lowering institutional barriers to sharing scientific results.
> >
> > Scientists and clinician members of the Packard Center have moved drugs
> > reliably and rapidly from preclinical experiments to human trials.
> > Direct or indirect links to international biotech or pharmaceutical
> > companies bring the infrastructure and experience needed to make
> > promising drugs into therapies.
> >
> > Packard scientists are the first to propose and test a combination
> > approach to drug therapy, a tactic that has worked for AIDS, cancer and
> > other diseases.
> >
> > ALS is a progressive, disabling neuromuscular disease that causes
> > complete paralysis and loss of function - including the ability to eat,
> > speak and breathe. ALS progresses quickly and is not curable. Most
> > patients die within five years of diagnosis.
> >
> > _________________________________________
> > Rebecca Berger
> > Research Program Coordinator
> > Robert Packard Center for ALS Research at Johns Hopkins
> > 5801 Smith Avenue | McAuley Suite 110
> > Baltimore, MD 21209
> > 410.735.7678 direct
> > 410.735.7680 fax
> > rberger6@... <rberger6%40jhmi.edu>
> > www.alscenter.org
> > www.fiesta5K.org <http://www.fiesta5k.org/>
> >
> >
> >
>

WHY THE NEW GENE FINDINGS ARE A CALL TO ACTION - A PACKARD PERSPECTIVE
http://www.alscenter.org/news/briefs/090304.cfm

In 2003, when New England ALS scientists announced they'd discovered
another form of familial ALS - the sixth one, and an adult form that
seems to strike harder in the lower extremities and have a somewhat
faster course - the hope was that the gene for it would soon surface.

High excitement in the ALS research community always accompanies
finding a new gene: Perhaps this one holds clues to reveal what triggers
motor neuron death; perhaps this one will spark a really effective
therapy.

Last week, after a six-year search, the gene was announced by seasoned
collaborators at the University of Massachusetts and Massachusetts
General Hospital. Another research team at King's College in London
backed up the finding.  Found where they'd suspected it, on chromosome
16, the mutated FUS gene (for "fused in sarcoma") is responsible for
perhaps 5 percent of familial ALS.  And pinpointing it, after a long,
thorough search, would be news enough.

But this discovery appears to go beyond the usual.  Packard scientists
warmly welcome the appearance of m(for mutated) FUS for a key reason: It
lends clout to a theory about a major destructive process in ALS that's
been gathering evidence at the Packard Center and elsewhere more than a
decade.

"The fascinating thing about having the FUS gene linked to ALS," says
Packard Scientific Director Piera Pasinelli, "is that it's yet another
gene that plays a part in RNA processing."

And having successful functioning of that molecule is crucial for cells
to work normally. By way of background: RNA - specifically the messenger
RNA molecule - carries DNA's blueprint for assembling proteins into the
cell cytoplasm where their actual assembly occurs. Yet getting RNA to
reflect DNA's "message" accurately, modifying it for efficiency and then
transporting it from the cell nucleus to the cytoplasm is an involved,
multi-step process. And it's a one that can go awry.

In 1998, Packard scientists first published the find that some 65
percent ALS patients harbor abnormal messenger RNA molecules,
specifically in the injured parts of their central nervous systems. But
no one has known the cause of that or what, if any, part it plays in
ALS's downhill course.

More evidence: Not long ago, Packard researchers helped discover the
familial ALS4 gene, one for an abnormal form of a protein called
senataxin. Like FUS, the senataxin gene also has an RNA role, overseeing
proper production of messenger RNA from its DNA blueprint.

And last year, the King's College group showed mutations in yet another
gene - one called TDP-43 - that appears both in patients with a variety
of different familial ALS types and, amazingly, in sporadic ALS patients
as well. Healthy people lack these mutations. (Last week, Packard
scientist Wim Robberecht and his European team added to that,
discovering a new variation of the TDP-gene in familial ALS patients.)
*

Among TDP-43's list of accomplishments? RNA processing.

All this suggests that flawed RNA metabolism, then, may join ALS's
seven "ugly stepsisters," as another of the biological pathways to go
wrong in ALS. (In scientific terms, the seven stepsisters are: oxidative
damage, misfolded protein aggregates, dysfunctional mitochondria,
defects in motor neuron transport, growth factor deficiency, pathology
of glial cells, glutamate excitotoxicity.)

What has Packard scientists most engaged, however, is where the flawed
RNA metabolism could lead.  It's interesting, for example, that both
patients with ALS from mTDP-43 and those with ALS from mFUS appear to
show clumps of misfolded proteins - protein aggregates - in central
nervous system cells, early in the disease.  "This suggests that these
aggregates are key agents, that they participate early in the genesis of
ALS," says Packard scientist Phil Wong, who has just made a mouse model
of ALS using a mutant TDP-43 gene.

So an important next step, both for understanding and for therapy, Wong
says, is to "see whether these aggregates are indeed critical players or
if, instead, they're just `tombstones' that mark dying motor neurons."
His mouse model should help answer that question.

In this, the new "stepsister" may be the most useful. Because it shows
up in both familial and sporadic patients, some researchers are even
speculating that RNA gone awry may be the missing overarching principle
that tells how the stepsisters are related. In other words, some are
hoping it may be the key process that causes ALS.

"The new discoveries, we believe, point strongly to flawed RNA
metabolism as a key disease process to imitate in animal models for
ALS," says Rothstein.

"It's these tools - the gene-primed model mice and fish and fruit flies
that Packard scientists offer the world's research community - that will
enable us to understand ALS. Ultimately, they'll become the agents we'll
all use to find effective therapies."

*Robberecht is already busy making a zebrafish model of ALS using
mutant TDP-43. His Packard colleague J. Paul Taylor, has begun testing a
new TDP-43 fruit fly model.


___________________________________

About The Robert Packard Center for ALS Research at Johns Hopkins
www.alscenter.org

Located in Baltimore, the Robert Packard Center for ALS Research at
Johns Hopkins is a worldwide collaboration of scientists aimed at
developing therapies and a cure for amyotrophic lateral sclerosis (ALS),
also known as Lou Gehrig's disease.

The Center is the only institution of its kind dedicated solely to the
disease. Its research is meant to translate rapidly from the lab bench
to the clinic, largely by eliminating time spent waiting for grants and
lowering institutional barriers to sharing scientific results.

Scientists and clinician members of the Packard Center have moved drugs
reliably and rapidly from preclinical experiments to human trials.
Direct or indirect links to international biotech or pharmaceutical
companies bring the infrastructure and experience needed to make
promising drugs into therapies.

Packard scientists are the first to propose and test a combination
approach to drug therapy, a tactic that has worked for AIDS, cancer and
other diseases.

ALS is a progressive, disabling neuromuscular disease that causes
complete paralysis and loss of function - including the ability to eat,
speak and breathe. ALS progresses quickly and is not curable. Most
patients die within five years of diagnosis.


_________________________________________
Rebecca Berger
Research Program Coordinator
Robert Packard Center for ALS Research at Johns Hopkins
5801 Smith Avenue | McAuley Suite 110
Baltimore, MD 21209
410.735.7678  direct
410.735.7680  fax
rberger6@...
www.alscenter.org
www.fiesta5K.org

To provide relief in night for changing positions:

Use cushions or pillows between legs (place them under knees and feet)

This not only makes your PALS comfortable but will also help them in
moving easily throught out night.

It may happen that with time, your PALS are not able to move their
limbs freely.
Such small adjustments will keep them comfortable thru out the night
and they may not feel the need to change positions.

Hint: Use big pillows and soft cushions for best movement.

More to come from where this one came.

Keep a note.

Cheers.
Gaurav..

(February 26, 2009) - In one of the most significant breakthroughs in
the recent history of ALS research, a consortium of scientists
organized and funded by The ALS Association has discovered a new
gene, ALS6 (Fused in Sarcoma), responsible for about 5 percent of the
cases of inherited ALS. The discovery will provide important clues to
the causes of inherited ALS, which accounts for 10 percent of all
cases, and sporadic ALS, which occurs in individuals with no family
history of the disease and accounts for the other 90 percent of cases
diagnosed.

"This is a momentous discovery in furthering our understanding of
ALS," said Lucie Bruijn, Ph.D., senior vice president of Research and
Development at The ALS Association. "A new gene provides a new piece
of the puzzle we can use to shed light on why ALS develops, and where
to focus our efforts on creating new treatments and finding a cure."

The results of this groundbreaking research are published in the
Friday, February 27 issue of the prestigious journal Science. The
project was led by Tom Kwiatkowski M.D., Ph.D., at Massachusetts
General Hospital, and Robert Brown, M.D., of the University of
Massachusetts School of Medicine, and ALS Association-funded
researchers Caroline Vance, Ph.D., and Christopher Shaw, M.D., of
Kings College in London. The project was supported by a consortium of
leading ALS researchers from around the world, formed as part of The
Association's Gene Identification Project. Their success reflects an
unprecedented effort to accelerate the search for genetic mutations
linked to all forms of ALS.

For more, pls visit:
http://web.alsa.org/site/PageServer?pagename=Breaking_News

Cheers.
Gaurav...

Situation:
Your PALS cannot control their jaw and while yawning they end up
clenching their teeth really hard which may cause pain.

Solution: Keep a towel handy, either with the person who is with the
PALS all the time or on the shoulder of PALS.
The moment you see them yawning etc, quickly put the towel end in
their mouth. This way when they will close their jaw forefully, it
will not hurt.

Personal tip: When my father could not control his jaw and could not
move his hands, we would have a competition as to who will help Dad
the most in not clenching his teeth....And Dad would have to help
each of us win so we would have a good time, even when he was not
well. He would laugh at it too and I would get a glimpse of happiness
in him, even though he was helpless.

Think about it.


Cheers....
Gaurav...

HI all,

Thanks Padma for sharing such good info with every1...
The book behind the movie " SO much So fast" Is " His Brother's
Keeper".

IN India, you can buy it from Infibeam.com or even Landmark Book
stores around the country.

I have ordered it from Infibeam..Will keep every1 updated...

At Infibeam , they have an approx 25% discount...

Cheers.

G...
--- In ALS_India@yahoogroups.com, "Varanasi, Padma"
<padma.varanasi@...> wrote:
>
> If you have not seen it, I highly recommend the film called
> So much so fast. I am not sure if it is available in india yet?
> The film is based on a true story and based on the book His
Brother's
> keeper.  A very moving film and also it gives you an idea of what
research
> is being done on ALS.  It was first aired on the public
television...
>
> - Padma
>
>
> > From: gauravjain_80 <gauravjain_80@...>
> > Reply-To: <ALS_India@yahoogroups.com>
> > Date: Sun, 22 Feb 2009 22:39:07 -0800
> > To: <ALS_India@yahoogroups.com>
> > Subject: [ALS_India] Movies on ALS
> >
> >
> >
> >
> > Here's the link to some movies on ALS:
> >
> > http://www.spout.com/members/0/tags/als-lou-gehrigs-
> > disease/MemberTagFilms.aspx
> >
> > Cheers.
> > G...
> >
> >
> >
> >
>

If you have not seen it, I highly recommend the film called
So much so fast. I am not sure if it is available in india yet?
The film is based on a true story and based on the book His Brother's
keeper.  A very moving film and also it gives you an idea of what research
is being done on ALS.  It was first aired on the public television...

- Padma


> From: gauravjain_80 <gauravjain_80@...>
> Reply-To: <ALS_India@yahoogroups.com>
> Date: Sun, 22 Feb 2009 22:39:07 -0800
> To: <ALS_India@yahoogroups.com>
> Subject: [ALS_India] Movies on ALS
>
>
>
>
> Here's the link to some movies on ALS:
>
> http://www.spout.com/members/0/tags/als-lou-gehrigs-
> disease/MemberTagFilms.aspx
>
> Cheers.
> G...
>
>
>
>

Dear all,

This was aired on Channel 12 news.  It is quite a story of one of our heros.
Yes, we can!  Si se puede!

Check out the link below
http://www.wisn.com/video/18672977/index.html


- Padma

Here's the link to some movies on ALS:

http://www.spout.com/members/0/tags/als-lou-gehrigs-
disease/MemberTagFilms.aspx

Cheers.
G...