Saturday, October 11, 2014
The legendary heavyweight was once known as 'The Louisville Lip' because of his fast tongue but is now a virtual mute as his condition deteriorate
Muhammad Ali – once famed for his lightning speed and even faster tongue – is now so ill he can hardly speak, his brother has revealed.
The boxing legend, 72, who has been battling debilitating Parkinson’s disease for years, has become increasingly frail and is now largely housebound.
And fresh health fears were sparked after he was too ill to attend the premiere of a new movie about his life last week and could not take part in any of the filming.
Speaking at the screening of I Am Ali in Hollywood, his brother Rahman, 71, told the Sunday People: “I have not been able to talk to my brother about this because he is sick.
“He doesn’t speak too well. But he is proud that we are here for him. He has given this film his blessing.”
The film focuses on the family life of the charismatic three-time world heavyweight champ nicknamed the Louisville Lip for his infamous wit.
Using Ali’s “audio journals” it presents an intimate portrait of the sporting icon also using interviews with his family and anecdotes from boxers such as Mike Tyson and George Foreman.
His daughter Maryum, 46, was also at the screening. She said of her famous dad: “He has not seen the film yet, but I am very excited for him to see it.
"He is going to love it. I know he is. He is going to cry, he is going to laugh. He will be very proud.”
Director Clare Lewins says Ali’s daughter Hana, 38, plans to show the movie to her father – also known for his pre-fight poems including “float like a butterfly, sting like a bee” – later this month at his Arizona home.
In January, Muhammad’s son Ali Jnr said he believed there was “no chance” of his dad surviving another year.
He said: “I just want, hope and pray to God that this awful disease takes my dad sooner rather than later.
"Take him away from all the suffering he’s in.”
I Am Ali hits UK cinemas on November 28.
http://www.mirror.co.uk/sport/boxing/muhammad-ali-ill-can-barely-4421253#ixzz3FskOrHnL
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Friday, October 10, 2014
TWENTY YEARS WITH PARKINSON'S DISEASE
There are a very limited number of studies on the clinical features of Parkinson's Disease twenty years after onset. So an assessment was carried out for several years on people who had Parkinson's Disease for more than twenty years
Those people considered were those who had Parkinson's
Disease for 20 to 22 years. They were assessed for an average
of nearly four years. Older age at onset and longer duration of
Parkinson's Disease were each associated with a higher
prevalence of major motor and non-motor milestones of
disease disability. Confinement to a wheelchair or bed had by
then occurred in just over 1 in 5 people (21%). Those factors
making confinement to a wheelchair or bed were older age,
postural instability and institutionalisation. Fractures occurred
in 16% of people. Fractures were associated with postural
instability.
The most frequent outcome was death (28%). However, given the age of diagnosis and the duration of Parkinson's Disease this might have been no more than normal. Mortality was associated with male gender, older age, dysphagia (difficulty in swallowing), orthostatic hypotension, postural instability, fractures and institutionalization.
Reference : Journal of Neurology, Neurosurgery and Psychiatry [2014] Oct 3 [Epub ahead of
print] (R.Cilia, E.Cereda, C.Klersy, M.Canesi, A.L.Zecchinelli, C.B.Mariani, S.Tesei,
G.Sacilotto, N.Meucci, M.Zini, C.Ruffmann, I.U.Isaias, S.Goldwurm, G.Pezzoli)
http://www.viartis.net/parkinsons.disease/news/141010.pdf
mail@viartis.net
©2014 Viartis
Nobel Prize in chemistry awarded for microscope breakthrough
Sven Lidin, left , Staffan Nordmark, centre, and Mans Ehrenberg at the Royal Academy of Sciences announce the Nobel Chemistry laureates on Oct. 8, 2014. Americans Eric Betzig and William Moerner and German scientist Stefan Hell won the Nobel Prize in Chemistry for "the development of super-resolved fluorescence microscopy." AP PHOTO/BERTIL ERICSON
STOCKHOLM -- Americans Eric Betzig and William Moerner and German scientist Stefan Hell won the Nobel Prize in chemistry on Wednesday for developing new methods that let microscopes see finer details than they could before.
Their breakthroughs, starting in the 1990s, shattered previous limits on the resolution of optical microscopes, giving scientists improved tools to study diseases such as Parkinson's, Alzheimer's and Huntington's at a molecular level.
The three scientists will split the 8 million-kronor ($1.1 million) award for "the development of super-resolved fluorescence microscopy," which the Royal Swedish Academy of Sciences said has "brought optical microscopy into the nanodimension."
Betzig, 54, works at the Howard Hughes Medical Institute in Ashburn, Virginia. Hell, 51, is director at the Max Planck Institute for Biophysical Chemistry in Goettingen, Germany. Moerner, 61, is a professor at Stanford University in California.
"I was totally surprised, I couldn't believe it," Hell said. "Fortunately I remembered the voice of Nordmark and I realized it was real," he added, referring to Staffan Nordmark of the Royal Swedish Academy of Sciences.
The Nobel judges didn't immediately reach Moerner, who was at a conference in Brazil. He found out about the prize from his wife after she was told by The Associated Press.
"I'm incredibly excited and happy to be included with Eric Betzig and Stefan Hell," Moerner told AP.
For a long time optical microscopes were limited by among other things the wavelength of light. So scientists believed they could never yield a resolution better than 0.2 micrometers.
But helped by fluorescent molecules, the three scientists, working independently, were able to break that limit, taking optical microscopy into a new dimension that made it possible to study the interplay between molecules inside cells, including the aggregation of disease-related proteins, the academy said.
Each of the laureates has used these methods to study tiny components of life. Hell has studied nerve cells to get a better understanding of brain synapses; Moerner has studied proteins related to Huntington's disease; and Betzig has tracked cell division inside embryos, the academy said.
"We can tell whether (individual molecules are) different or whether they're the same. It's very much like asking whether they all march to the same drummer or not," Moerner told the AP. "When you can watch one by one, then we are able to observe exactly when it changes from one state to another."
Tom Barton, president of the American Chemical Society, said the laureates' work allowed progress in many fields because it let scientists see molecules and other features with unprecedented resolution. And for biology, he noted, it allows researchers to study very fine details of living things. In contrast, while an electron microscope can see even finer details, it can't be used on living cells.
"Before maybe we could just see the contours of bacteria but now we can look inside the bacteria and we can see things as small as individual molecules," said Nobel committee member Claes Gustafsson.
"This technique means that suddenly we can start studying details that we could only dream of before. This is really a revolution because as recently as 15 years ago, it was believed to be theoretically impossible to break this barrier," he said.
Last year's chemistry prize went to three U.S.-based scientists who developed powerful computer models that researchers use to understand complex chemical interactions and create new drugs.
This year's Nobel announcements started Monday with U.S.-British scientist John O'Keefe splitting the medicine award with Norwegian couple May-Britt Moser and Edvard Moser for breakthroughs in brain cell research that could pave the way for a better understanding of diseases like Alzheimer's.
On Tuesday, Isamu Akasaki and Hiroshi Amano of Japan and U.S. scientist Shuji Nakamura won physics award for the invention of blue light-emitting diodes - a breakthrough that spurred the development of LED technology that can be used to light up homes and offices and the screens of mobile phones, computers and TVs.
The Nobel Prize in literature will be announced Thursday, followed by the Nobel Peace Prize on Friday and the economics prize on Monday.
The prizes are always handed out in ceremonies on Dec. 10, the date that prize founder Alfred Nobel died in 1896.
Wearable Technology That Feels Like Skin
By
NICK BILTONOCT.
8, 2014
 |
| MC10 is working on attachable computers that look like small rectangular stickers and that can be placed on various parts of the body. |
Credit
John
A. Rogers/The University of Illinois at Urbana-Champaign
When it comes to the
future of computing, there is one major known and a principal unknown.
The
known, with almost guaranteed certainty, is that the next era of computing will be wearables.
The unknown, with commensurate guaranteed uncertainty, is what these wearables
will be and where on your body they will live.
Apple and Samsung, for example, are betting
on the wrist; Google, the face. A slew of tech companies believe clothing will simply become electronic. Yet
there’s a whole new segment of start-ups that believe all of the above are
destined for failure and that we humans will become the actual computers, or at
least the place where the technology will reside.
Their enthusiasm is on an emerging class
of wearable computers that adhere to the skin like temporary tattoos, or attach
to the body like an old-fashioned Band-Aid.
Many
of these technologies don’t look anything like today’s gadgets. Instead, they
are stretchable, bendable and incredibly thin. They can also be given unique
designs, to stand out like a bold tattoo, or to blend in to the color of your
skin.
 |
| MC10 attachable computers. |
Credit
John
A. Rogers/The University of Illinois at Urbana-Champaign
While
these wearables raise novel privacy concerns, their advocates say there
are numerous benefits. Attachable computers will be less expensive to make,
provide greater accuracy because sensors will be closer to a person’s body (or
even inside us) and offer the most utility, as something people won’t forget to
wear.
MC10, a company based in Cambridge, Mass.,
is testing attachable computers that look like small rectangular stickers,
about the size of a piece of gum, and can include wireless antennas, temperature
and heart-rate sensors and a tiny battery.
“Our devices are not like wearables that
are used today, where people wear them for a little bit and then throw them
into a drawer,” said Scott Pomerantz, the chief executive of MC10. “Ours are
always on you. We have the smallest, most flexible, stretchable, wearable
computer, and you can collect all sorts of biometric data tied to your motion.”
MC10 recently teamed up with John A.
Rogers, a professor of materials science and engineering at the
University of Illinois at Urbana-Champaign, who has been working for nearly a
decade to perfect flexible devices that can be worn on the skin or implanted
internally.
How would these gadgets work? Imagine
being able to slap a few Band-Aid-size sensors to your body when you go for a
run, then seeing a micro-level reading of your exercise on your phone.
Maybe you want to figure out which
deodorant would be best for you. This would be done with a sticker that tracks
your sweat level, then emails you a few brand recommendations. Or if you want
to monitor your baby’s breathing, you would stick a little sensor on the baby’s
chest that will alert you to any problems.
 |
| MC10 attachable computers. |
“We’ll
eventually see a more intimate integration of electronics and biological
systems,” Mr. Rogers said in a phone interview. “Without that kind of intimate
physical contact, it’s going to be difficult, or maybe even impossible, to
extract meaningful data.”
The
health applications are enormous. Over the past year, Mr. Rogers and his team
of scientists have been working with patients with Parkinson’s disease to
monitor their motions, dermatologists to treat skin diseases, and beauty
companies like L’Oréal to develop digital stickers that track skin hydration.
Wearable-computer
advocates are also giddy about the infinite style possibilities. “It turns out
that the mechanics of these devices are 100 percent compatible with kids’
standard temporary tattoos,” Mr. Rogers said. Meaning, they can be made to look
like tattoos, with each segment containing different sensors.
Anke Loh, the chairwoman of the fashion
department at the School of the Art Institute of Chicago, has been
experimenting with making the attachable computers look like body art. “You see
these patches and you really want to put them on your skin, even without
knowing what the function is,” Ms. Loh said, noting that most wearable
computers today are clunky and ugly. “There’s a lot of potential to combine
fashion and technology.”
On a more futuristic front, scientists at
the University of Tokyo have been working on an “e-skin,” which, as you may
have guessed, is an electronic skin that sits on top of real skin. It looks
like a flexible and stretchable sheet of plastic wrap, yet contains lots of
health-related sensors.
In another iteration of e-skin, scientists
are working to add a layer of LEDs, turning it into a functional screen that
sits on the body.
Digital skins offer numerous applications,
not only in monitoring a user’s health, but also as a visual user interface.
They can be used on lifelike prosthetics and even replace smartphones one day.
(Imagine your forearm as a touch-screen display.)
But don’t throw aside your smartwatch or
say goodbye to Google Glass just yet. It will be a while before our wearable
future becomes known.
Thursday, October 9, 2014
Drug used for another disease slows progression of Parkinson's
Date:
October 8, 2014
Source:
University of California, Los
Angeles (UCLA), Health Sciences
Summary:
A
drug being evaluated to treat an entirely different disorder helped slow the
progression of Parkinson’s disease in mice, a team of researchers has reported.
Their study found that the drug, AT2101, which has also been studied for
Gaucher disease, improved motor function, stopped inflammation in the brain and
reduced levels of alpha-synuclein, a protein critically involved in
Parkinson's.
A
new study from UCLA found that a drug being evaluated to treat an entirely
different disorder helped slow the progression of Parkinson's disease in mice.
The
study, published in the October edition of the journal Neurotherapeutics,
found that the drug, AT2101, which has also been studied for Gaucher disease,
improved motor function, stopped inflammation in the brain and reduced levels
of alpha-synuclein, a protein critically involved in Parkinson's.
though
the exact cause of Parkinson's is unknown, evidence points to an accumulation
of alpha-synuclein, which has been found to be common to all people with the
disorder. The protein is thought to destroy the neurons in the brain that make
dopamine, a neurotransmitter that helps regulate a number of functions,
including movement and coordination. Dopamine deficiency is associated with
Parkinson's disease.
Gaucher
disease is a rare genetic disorder in which the body cannot produce enough of
an enzyme called β-glucocerebrosidase, or GCase. Researchers seeking genetic
factors that increase people's risk for developing Parkinson's have determined
that there may be a close relationship between Gaucher and Parkinson's due to a
GCase gene. Mutation of this gene, which leads to decreased GCase activity in
the brain, has been found to be a genetic risk factor for Parkinson's, although
the majority of patients with Parkinson's do not carry mutations in the Gaucher
gene.
"This
is the first time a compound targeting Gaucher disease has been tested in a
mouse model of Parkinson's disease and was shown to be effective," said
the study's senior author, Marie-Francoise Chesselet, the Charles H. Markham
Professor of Neurology at UCLA and director of the UCLA Center for the Study of
Parkinson's Disease. "The promising findings in this study suggest that
further investigation of this compound in Parkinson's disease is
warranted."
In
the study, the researchers used mice that were genetically engineered to make
too much alpha-synuclein which, over time, led the animals to develop deficits
similar to those observed in humans with Parkinson's. The researchers found
that the mice's symptoms improved after they received AT2101 for four months.
The
researchers also observed that AT2101 was effective in treating Parkinson's in
mice even though they did not carry a mutant version of the Gaucher gene,
suggesting that the compound may have a clinical effect in the broader
Parkinson's population.
AT2101
is a first-generation "pharmacological chaperone" -- a drug that can
bind malfunctioning, mutated enzymes and lead them through the cell to their
normal location, which allows the enzymes to carry on with their normal work.
This was the first time that a pharmacological chaperone showed promise in a
model of Parkinson's, according to Chesselet.
Parkinson's
disease affects as many as 1 million Americans, and 60,000 new cases are
diagnosed each year. The disorder continues to puzzle scientists. There is no
cure and researchers have been unable to pin down its cause and no drug has
been proven to stop the progression of the disease, which causes tremors,
stiffness and other debilitating symptoms. Current Parkinson's treatments only
address its symptoms.
Story Source:
The
above story is based on materials
provided by University of
California, Los Angeles (UCLA), Health Sciences. Note:
Materials may be edited for content and length.
end
story_source
Journal Reference:
1 Franziska Richter,
Sheila M. Fleming, Melanie Watson, Vincent Lemesre, Lee Pellegrino, Brian
Ranes, Chunni Zhu, Farzad Mortazavi, Caitlin K. Mulligan, Pedrom C. Sioshansi,
Sindalana Hean, Krystal De La Rosa, Richie Khanna, John Flanagan, David J.
Lockhart, Brandon A. Wustman, Sean W. Clark, Marie-Françoise Chesselet. A
GCase Chaperone Improves Motor Function in a Mouse Model of Synucleinopathy.
Neurotherapeutics, 2014; DOI: 10.1007/s13311-014-0294-x
end
journal_references
Cite This Page:
• MLA
APA
Chicago
University of
California, Los Angeles (UCLA), Health Sciences. "Drug used for another
disease slows progression of Parkinson's." ScienceDaily. ScienceDaily, 8
October 2014. <www.sciencedaily.com/releases/2014/10/141008153507.htm
Wednesday, October 8, 2014
What is LSVT LOUD? and What is LSVT BIG?
LSVT LOUD® is an effective speech treatment for individuals with Parkinson disease (PD) and other neurological conditions. LSVT LOUD, named for Mrs. Lee Silverman (Lee Silverman Voice Treatment – LSVT) was developed in 1987 and has been scientifically studied for nearly 20 years with funding support from the National Institute for Deafness and other Communication Disorders (NIDCD) of the National Institutes of Health. Published research data support improvements in vocal loudness, intonation, and voice quality for individuals with PD who received LSVT LOUD, with improvements maintained up to two years after treatment. Recent research studies have also documented the effectiveness of this therapy in improving the common problems of disordered articulation, diminished facial expression and impaired swallowing. Additionally, two brain imaging studies have documented evidence of positive changes in the brain following administration of the therapy.
LSVT LOUD improves vocal loudness by stimulating the muscles of the voice box (larynx) and speech mechanism through a systematic hierarchy of exercises. Focused on a single goal “speak LOUD!” – the treatment improves respiratory, laryngeal and articulatory function to maximize speech intelligibility. The treatment does not train people for shouting or yelling; rather, LSVT LOUD uses loudness training to bring the voice to an improved, healthy vocal loudness with no strain.
Treatment is administered in 16 sessions over a single month (four individual 60 minute sessions per week). This intensive mode of administration is consistent with theories of motor leaning and skill acquisition, as well as with principles of neural plasticity (the capacity of the nervous system to change in response to signals), and is critical to attaining optimal results. The treatment not only simulates the motor system but also incorporates sensory awareness training to help individuals with PD recognize that their voice is too soft, convincing them that the louder voice is within normal limits, and making them comfortable with their new louder voice.
Patients are trained to self-generate the adequate amount of loudness to make their speech understood. While LSVT LOUD has been successfully administered to individuals in all stages of PD, the treatment has been most effective among those who are in early or middle stages of the condition. LSVT LOUD has also been applied to individuals with sub-types of PD (Shy-Drager syndrome, multi-system atrophy and progressive supranuclear palsy), however the largest dataset is for individuals with Idiopathic Parkinson disease (IPD). Recently, LSVT LOUD has been applied to select individuals with stroke, multiple sclerosis, Down syndrome, and cerebral palsy with positive outcomes.
http://www.lsvtglobal.com/patient-resources/what-is-lsvt-loud
LSVT BIG
Recently principles of LSVT LOUD® were applied to limb movement in people with Parkinson disease (LSVT BIG®) and have been documented to be effective in the short term. Specifically, training increased amplitude of limb and body movement (Bigness) in people with Parkinson disease has documented improvements in amplitude (trunk rotation/gait) that generalized to improved speed (upper/lower limbs), balance, and quality of life. In addition, people were able to maintain these improvements when challenged with a dual task.
LSVT BIG can be delivered by a physical or occupational therapist. Treatment is administered in 16 sessions over a single month (four individual 60 minute sessions per week). This protocol was developed specifically to address the unique movement impairments for people with Parkinson disease. The protocol is both intensive and complex, with many repetitions of core movements that are used in daily living. This type of practice is necessary to optimize learning and carryover of your better movement into everyday life!
Start exercising NOW – as soon as possible. Physicians rarely refer their patients to health and fitness programs at diagnosis because medications are very effective early on at alleviating most of the symptoms, and patients experience little change in function. Yet, according to a recent survey it is at the time of diagnosis that patients often begin to consider lifestyle changes and seek education about conventional and complementary/alternative treatment options. Thus referrals to exercise, wellness programs and physical/occupational therapy would be best initiated at diagnosis, when it may have the most impact on quality of life.
http://www.lsvtglobal.com/clinicians
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