Another email from the NSA that totally misses the points.
1. We have no fast and objective way to diagnose stroke. So you can get them to the ER very fast and the doctors there may not be able to tell for sure what is going on. One of these 17 ways still need to be be proven for fast and objective diagnosis.
2. tPA at 12% efficacy is a failure
But they need to issue press releases to give the impression of action without doing a damn thing.
And they consider themselves a stroke association.
http://nsa.convio.net/site/MessageViewer?dlv_id=33243&em_id=24181.0
I suppose I shouldn't get mad at this anymore, it's not like they will ever stoop to actually listening to stroke survivors and caregivers.
Monday, March 31, 2014
‘Electronic skin' equipped with memory
This would be perfect for monitoring our movements so we could precisely tell what's wrong with them. And every neurologist should have that exact same thought and create a project to implement this for their patients.
I know that is a stupid dream but somehow we have to prove that our neurologists know nothing about stroke recovery.
http://www.nature.com/news/electronic-skin-equipped-with-memory-1.14952
I know that is a stupid dream but somehow we have to prove that our neurologists know nothing about stroke recovery.
http://www.nature.com/news/electronic-skin-equipped-with-memory-1.14952
Stop Waiting on Your Dream: Take Tiny Steps to Make “Someday” Now
This Tiny Buddha post seems written exactly for me.
My relationship wasn’t working.
I hated my job.
Stop Waiting on Your Dream: Take Tiny Steps to Make “Someday” Now
My relationship wasn’t working.
I hated my job.
Stop Waiting on Your Dream: Take Tiny Steps to Make “Someday” Now
Prevent a stroke—free stroke awareness seminar - Houston,TX
You'll have to go and challenge everything they say because they are just going to give you the simplistic crap ideas. Why don't they list any of these 11 Stroke risk reduction ideas?
Do they even have actual research articles to back them up. You won't hear any proof behind their comments.
http://www.yourhoustonnews.com/ranch/living/prevent-a-stroke-free-stroke-awareness-seminar/article_584a46c4-eb19-53ff-aaa1-d318835c27e8.html
While diseases such as heart disease and breast cancer seem to get the bulk of attention these days, don’t forget about the third leading cause of death in this country and the No. 1 cause of disability: stroke.
About 80 percent of strokes(proof?) are preventable simply by lowering risk factors, according to the National Stroke Association. In addition, risk factors for stroke are often intertwined, so treating one of them can often positively affect another. For example, quitting smoking can bring down blood pressure. James Ling, M.D., board certified neurologist on staff at Houston Methodist Sugar Land Hospital, identified the following steps you can take to reduce your stroke risk:
• Eat your fruits and veggies. Experts recommend
five or more servings a day. You should also be getting at least six
servings of grains a day, eating fish like albacore tuna and salmon
twice a week and including fat-free dairy products, beans, lean meats
and skinless poultry into your everyday diet. Limit foods high in
saturated fats, trans fats, cholesterol and calories. High cholesterol
is a risk factor for stroke.
• Move, move, move. Lace up your shoes and hit the pavement for at least 30 minutes on most or all days. If you need to lose weight, increase that activity time to at least 60 minutes.
• Lower your blood pressure. You’ll only know you have high blood pressure – 140/90 mm Hg or higher – if you get it checked. A healthy diet that limits daily salt intake to 2,300 mg (about one teaspoon) or less and regular exercise can often bring down the numbers. If not, you may need medication.
• Butt out. Nicotine and carbon monoxide damage your cardiovascular system, so talk with your health care provider today about quit-smoking aids such as patches and medications.
• Control your diabetes. Having diabetes increases your stroke risk, but uncontrolled diabetes puts you at an even greater risk. Make sure to keep your blood sugar levels under control and visit regularly with your health care provider to stay on top of the disease.
Advancing age, a family history, being male, being of African-American descent and
having had a prior stroke are all risk factors you can’t control. But by taking the measures listed above, you can help reduce your risks.
FREE SEMINAR
Join us on Wednesday, May 21, for a free seminar on stroke awareness presented by James Ling, M.D. The presentation starts at 6 p.m. and will be held at Houston Methodist Sugar Land Hospital’s Conference Center. Call 281-274-7500 or register online at houstonmethodist.org/events to reserve a seat.
Do they even have actual research articles to back them up. You won't hear any proof behind their comments.
http://www.yourhoustonnews.com/ranch/living/prevent-a-stroke-free-stroke-awareness-seminar/article_584a46c4-eb19-53ff-aaa1-d318835c27e8.html
While diseases such as heart disease and breast cancer seem to get the bulk of attention these days, don’t forget about the third leading cause of death in this country and the No. 1 cause of disability: stroke.
About 80 percent of strokes(proof?) are preventable simply by lowering risk factors, according to the National Stroke Association. In addition, risk factors for stroke are often intertwined, so treating one of them can often positively affect another. For example, quitting smoking can bring down blood pressure. James Ling, M.D., board certified neurologist on staff at Houston Methodist Sugar Land Hospital, identified the following steps you can take to reduce your stroke risk:
Advertisement
• Move, move, move. Lace up your shoes and hit the pavement for at least 30 minutes on most or all days. If you need to lose weight, increase that activity time to at least 60 minutes.
• Lower your blood pressure. You’ll only know you have high blood pressure – 140/90 mm Hg or higher – if you get it checked. A healthy diet that limits daily salt intake to 2,300 mg (about one teaspoon) or less and regular exercise can often bring down the numbers. If not, you may need medication.
• Butt out. Nicotine and carbon monoxide damage your cardiovascular system, so talk with your health care provider today about quit-smoking aids such as patches and medications.
• Control your diabetes. Having diabetes increases your stroke risk, but uncontrolled diabetes puts you at an even greater risk. Make sure to keep your blood sugar levels under control and visit regularly with your health care provider to stay on top of the disease.
Advancing age, a family history, being male, being of African-American descent and
having had a prior stroke are all risk factors you can’t control. But by taking the measures listed above, you can help reduce your risks.
FREE SEMINAR
Join us on Wednesday, May 21, for a free seminar on stroke awareness presented by James Ling, M.D. The presentation starts at 6 p.m. and will be held at Houston Methodist Sugar Land Hospital’s Conference Center. Call 281-274-7500 or register online at houstonmethodist.org/events to reserve a seat.
Ageing: Genetic rejuvenation of old muscle
I attribute my relatively decent ability to do most things(I'm not even close to recovery) to my previous excellent physical shape. For others and older persons this rejuvenation seems likely to be required as a first step in your stroke rehabilitation.
Deric Bownds blogging about it here:
Mechanism of muscle decay on aging, and its reversal.
The abstract this is all based upon here:
http://www.nature.com/nature/journal/v506/n7488/full/nature13058.html
Deric Bownds blogging about it here:
Mechanism of muscle decay on aging, and its reversal.
The abstract this is all based upon here:
http://www.nature.com/nature/journal/v506/n7488/full/nature13058.html
Article preview View full access options
Ageing: Genetic rejuvenation of old muscle
- Nature
- 506,
- 304–305
- doi:10.1038/nature13058
- Published online
In advanced age, the stem cells
responsible for muscle regeneration switch from reversible quiescence to
irreversible senescence. Targeting a driver of senescence revives
muscle stem cells and restores regeneration. See Article p.316
Subject terms:
Read the full article
Additional access options:
Aquarius 1/20-2/18
My horoscope for the day.
From .tattoostime.com
From .tattoostime.com
Your
belief in yourself is striking, and it is guiding you toward a new kind
of freedom. You may find that your energy is unwilling to be cooped up
for even one minute, so sneak away and be free.
So I guess my arrogance is ordained by the stars.
FDA clears medical device developed by OHSU and AMES Technology, Inc. for muscle and joint rehabilitation
Vibration once again. Maybe it is useful. What does your doctor and therapist think? Do they think at all?
Previous vibration posts so your doctor doesn't even have to do any research or thinking.
1. Effects of whole-body vibration on muscle architecture, muscle strength, and balance in stroke: A randomized controlled trial
2. Vibrating Glove May Enhance Sense of Touch
3. No specific effect of whole-body vibration training in chronic stroke: a double-blind randomized controlled study.
4. Efficacy of whole body vibration exercise in older people: a systematic review
5. Quicker and easier rehabilitation following a stroke - vibration
6. Vibration and stroke rehab
7. Vibrostimulation in Bobsleigh
8. 7-speed Secret Love Finger Fun Vibrator Vibration Massager with Sexy Dice
9. Foot drop - Step Sensor by Brownmed
10. Touchy-feely options for stroke rehabilitation
11. Stroke rehab glove combines mental practice and muscle stimulation to improve hand function
And the newest one here:
http://www.ohsu.edu/xd/about/news_events/news/2013/05-30-fda-clears-medical-devic.cfm
The Food and Drug Administration today granted 510(k) clearance to a muscle and joint rehabilitation medical device developed by OHSU Scientist Dr. Paul Cordo, Ph.D., and AMES Technology, Inc.
AMES is an Oregon Health & Science University spinoff company established to transform Dr. Cordo's OHSU research findings into a rehabilitation medical device for use in hospitals and clinics. Today's FDA clearance allows AMES to market and sell the device. AMES anticipates delivering the device to hospitals and clinics in early 2014. The typical patient population that possibly receive treatment with an AMES Device would include stroke victims and patients with partial injuries to the spinal cord.
The AMES rehabilitation medical device uses robotic technology to assist a patient in moving the affected limb while vibrating the muscle receptors at the same time. During use, the patient’s input effort and other parameters important in therapy are measured and recorded by the AMES Device and displayed to the patient as real-time visual biofeedback. The AMES Device can also perform several diagnostic tests each time a patient is treated by the device to track progress for clinicians and insurance providers.
Dr. Cordo’s research at OHSU involved applying muscle vibration to the receptors in the muscle tendon at the same time as the joint is being moved. This is thought to result in an exaggerated perception of movement of the extremity, in the correct direction, at the time movement is made. The central nervous system monitors the sensory output of the muscles and when a signal is detected, the brain senses that movement, thereby helping guide the motion. AMES has invested in the application of these important findings into a commercial medical device. This resulted in a device that is capable of delivering combination therapy through a series of programmed treatment regimens controlled via computer software.
“Taking stroke as an example, if a person survives the initial injury, the probability is about 50 percent that he or she will never recover any functional use of the affected limb,” said Dr. Cordo, a professor in the OHSU Department of Biomedical Engineering and Chief Technology Officer for AMES. “Clinicians have few options for the most severely disabled people other than working around their disabilities. How many other types of medical conditions can you think of where we give up on curing the worst affected 50 percent of the affected population? We don’t think this is acceptable, so over the last 10 years, we’ve been working to come up with an alternative that is effective with the severely disabled, or at least able to bring them to the point that other therapies will be effective. The AMES rehabilitation device is the product of that decade of work.”
Current research shows that muscle vibration can help the brain “locate” the muscles controlling the joint, to reduce joint tightness, and to enhance sensation at the treated joint or joints. This enhanced sensation is thought to help the brain re-establish communication with the affected muscles.
A series of clinical studies with the AMES Device were conducted at multiple sites across the United States, some with chronic and sub-acute stroke patients and some with chronic spinal cord injury victims. These studies have provided clinical evidence that the AMES approach improves movement and strength in people with injuries to the brain and spinal cord, in some cases restoring the ability to carry out independent activities that were previously unattainable. The studies included treating the arm, hand and the leg. Most of the participants who were enrolled in these studies were considered to be very disabled when they started AMES treatment.
Currently, in the United States alone, there are more than 10 million people whose movement is profoundly limited by diseases of and injuries to the brain and spinal cord. About half of these people are so disabled that currently available therapies are not effective in restoring normal movement. Recent rehabilitation research suggests that at least some of these severely disabled people can recover functional movement if the therapy focuses on the fundamental problems that prevent movement, as with the AMES Device.
While the device cannot regain movement for certain types of central nervous system injuries and diseases, such as where the spinal cord is completely severed, the device can assist in regaining some movement in a large number of patients.
"We are very excited about the prospect that AMES technology will improve the lives of thousands of injury and stroke victims,” said Dr. Tim Stout, M.D., Ph.D., M.B.A., OHSU’s Vice President for Technology Transfer and Business Development. “This is revolutionary technology that can change how we treat these patients."
OHSU and Dr. Cordo have a significant financial interest in AMES Technology, Inc., a company that may have a commercial interest in the results of this research and technology. This potential individual and institutional conflict of interest has been reviewed and managed by OHSU.
The AMES device is patented technology and is exclusively licensed worldwide to AMES.
Previous vibration posts so your doctor doesn't even have to do any research or thinking.
1. Effects of whole-body vibration on muscle architecture, muscle strength, and balance in stroke: A randomized controlled trial
2. Vibrating Glove May Enhance Sense of Touch
3. No specific effect of whole-body vibration training in chronic stroke: a double-blind randomized controlled study.
4. Efficacy of whole body vibration exercise in older people: a systematic review
5. Quicker and easier rehabilitation following a stroke - vibration
6. Vibration and stroke rehab
7. Vibrostimulation in Bobsleigh
8. 7-speed Secret Love Finger Fun Vibrator Vibration Massager with Sexy Dice
9. Foot drop - Step Sensor by Brownmed
10. Touchy-feely options for stroke rehabilitation
11. Stroke rehab glove combines mental practice and muscle stimulation to improve hand function
And the newest one here:
http://www.ohsu.edu/xd/about/news_events/news/2013/05-30-fda-clears-medical-devic.cfm
The Food and Drug Administration today granted 510(k) clearance to a muscle and joint rehabilitation medical device developed by OHSU Scientist Dr. Paul Cordo, Ph.D., and AMES Technology, Inc.
AMES is an Oregon Health & Science University spinoff company established to transform Dr. Cordo's OHSU research findings into a rehabilitation medical device for use in hospitals and clinics. Today's FDA clearance allows AMES to market and sell the device. AMES anticipates delivering the device to hospitals and clinics in early 2014. The typical patient population that possibly receive treatment with an AMES Device would include stroke victims and patients with partial injuries to the spinal cord.
The AMES rehabilitation medical device uses robotic technology to assist a patient in moving the affected limb while vibrating the muscle receptors at the same time. During use, the patient’s input effort and other parameters important in therapy are measured and recorded by the AMES Device and displayed to the patient as real-time visual biofeedback. The AMES Device can also perform several diagnostic tests each time a patient is treated by the device to track progress for clinicians and insurance providers.
Dr. Cordo’s research at OHSU involved applying muscle vibration to the receptors in the muscle tendon at the same time as the joint is being moved. This is thought to result in an exaggerated perception of movement of the extremity, in the correct direction, at the time movement is made. The central nervous system monitors the sensory output of the muscles and when a signal is detected, the brain senses that movement, thereby helping guide the motion. AMES has invested in the application of these important findings into a commercial medical device. This resulted in a device that is capable of delivering combination therapy through a series of programmed treatment regimens controlled via computer software.
“Taking stroke as an example, if a person survives the initial injury, the probability is about 50 percent that he or she will never recover any functional use of the affected limb,” said Dr. Cordo, a professor in the OHSU Department of Biomedical Engineering and Chief Technology Officer for AMES. “Clinicians have few options for the most severely disabled people other than working around their disabilities. How many other types of medical conditions can you think of where we give up on curing the worst affected 50 percent of the affected population? We don’t think this is acceptable, so over the last 10 years, we’ve been working to come up with an alternative that is effective with the severely disabled, or at least able to bring them to the point that other therapies will be effective. The AMES rehabilitation device is the product of that decade of work.”
Current research shows that muscle vibration can help the brain “locate” the muscles controlling the joint, to reduce joint tightness, and to enhance sensation at the treated joint or joints. This enhanced sensation is thought to help the brain re-establish communication with the affected muscles.
A series of clinical studies with the AMES Device were conducted at multiple sites across the United States, some with chronic and sub-acute stroke patients and some with chronic spinal cord injury victims. These studies have provided clinical evidence that the AMES approach improves movement and strength in people with injuries to the brain and spinal cord, in some cases restoring the ability to carry out independent activities that were previously unattainable. The studies included treating the arm, hand and the leg. Most of the participants who were enrolled in these studies were considered to be very disabled when they started AMES treatment.
Currently, in the United States alone, there are more than 10 million people whose movement is profoundly limited by diseases of and injuries to the brain and spinal cord. About half of these people are so disabled that currently available therapies are not effective in restoring normal movement. Recent rehabilitation research suggests that at least some of these severely disabled people can recover functional movement if the therapy focuses on the fundamental problems that prevent movement, as with the AMES Device.
While the device cannot regain movement for certain types of central nervous system injuries and diseases, such as where the spinal cord is completely severed, the device can assist in regaining some movement in a large number of patients.
"We are very excited about the prospect that AMES technology will improve the lives of thousands of injury and stroke victims,” said Dr. Tim Stout, M.D., Ph.D., M.B.A., OHSU’s Vice President for Technology Transfer and Business Development. “This is revolutionary technology that can change how we treat these patients."
OHSU and Dr. Cordo have a significant financial interest in AMES Technology, Inc., a company that may have a commercial interest in the results of this research and technology. This potential individual and institutional conflict of interest has been reviewed and managed by OHSU.
The AMES device is patented technology and is exclusively licensed worldwide to AMES.
Sunday, March 30, 2014
Walking the trails again
It hit 50 degrees today so I went for an hour long walk. Probably 50% still had some snow on it. Luckily it was soft, I would slide with my left foot down the snow until it hit ground. Came close numerous times to rolling the ankle. It was excellent therapy. Saw deer tracks and turkey tracks. I've seen numerous deer but have yet to be scared by an exploding turkey taking off next to the trail.
Cell-saving drugs could reduce brain damage after stroke
I originally wrote about this in Sept. 2011
And if we had a great stroke association a request for proposal would have gone out to stroke researchers the next week, asking for translational research projects that would solve this problem. But instead we have press release organizations. So you as a survivor will not be helped by the time you have your next stroke.
http://www.sciencedaily.com/releases/2014/03/140326153721.htm?
And if we had a great stroke association a request for proposal would have gone out to stroke researchers the next week, asking for translational research projects that would solve this problem. But instead we have press release organizations. So you as a survivor will not be helped by the time you have your next stroke.
http://www.sciencedaily.com/releases/2014/03/140326153721.htm?
Date:
March 26, 2014
Source:
University College London
Summary:
Long-term
brain damage caused by stroke could be reduced by saving cells called
pericytes that control blood flow in capillaries, reports a new study.
The results show not only that pericytes are the main regulator of blood
flow to the brain, but also that they tighten and die around
capillaries after stroke. This significantly impairs blood flow in the
long term, causing lasting damage to brain cells.
Long-term
brain damage caused by stroke could be reduced by saving cells called
pericytes that control blood flow in capillaries, reports a new study
led by scientists from UCL (University College London).
Until
now, many scientists believed that blood flow within the brain was
solely controlled by changes in the diameter of arterioles, blood
vessels that branch out from arteries into smaller capillaries. The
latest research reveals that the brain's blood supply is in fact chiefly
controlled by the narrowing or widening of capillaries as pericytes
tighten or loosen around them.
The study, published this week in Nature, shows not only that pericytes are the main regulator of blood flow to the brain, but also that they tighten and die around capillaries after stroke. This significantly impairs blood flow in the long term, causing lasting damage to brain cells. The team of scientists from UCL, Oxford University and the University of Copenhagen showed that certain chemicals could halve pericyte death from simulated stroke in the lab, and hope to develop these into drugs to treat stroke victims.
"At present, clinicians can remove clots blocking blood flow to the brain if stroke patients reach hospital early enough," explains Professor David Attwell of UCL's Department of Neuroscience, Physiology & Pharmacology, who led the study. "However, the capillary constriction produced by pericytes may, by restricting the blood supply for a long time, cause further damage to nerve cells even after the clot is removed. Our latest research suggests that devising drugs to prevent capillary constriction may offer new therapies for reducing the disability caused by stroke."
"This discovery offers radically new treatment approaches for stroke," says study co-author Professor Alastair Buchan, Dean of Medicine and Head of the Medical Sciences Division at Oxford University. "Importantly, we should now be able to identify drugs that target these cells. If we are able to prevent pericytes from dying, it should help restore blood flow in the brain to normal and prevent the ongoing slow damage we see after a stroke which causes so much neurological disability in our patients."
The new research also gives insight into the mechanisms underlying the use of functional magnetic resonance imaging to detect blood flow changes in the brain.
"Functional imaging allows us to see the activity of nerve cells within the human brain but until now we didn't quite know what we were looking at," explains Professor Attwell. "We have shown that pericytes initiate the increase in blood flow seen when nerve cells become active, so we now know that functional imaging signals are caused by a pericyte-mediated increase of capillary diameter. Knowing exactly what functional imaging shows will help us to better understand and interpret what we see."
The study, published this week in Nature, shows not only that pericytes are the main regulator of blood flow to the brain, but also that they tighten and die around capillaries after stroke. This significantly impairs blood flow in the long term, causing lasting damage to brain cells. The team of scientists from UCL, Oxford University and the University of Copenhagen showed that certain chemicals could halve pericyte death from simulated stroke in the lab, and hope to develop these into drugs to treat stroke victims.
"At present, clinicians can remove clots blocking blood flow to the brain if stroke patients reach hospital early enough," explains Professor David Attwell of UCL's Department of Neuroscience, Physiology & Pharmacology, who led the study. "However, the capillary constriction produced by pericytes may, by restricting the blood supply for a long time, cause further damage to nerve cells even after the clot is removed. Our latest research suggests that devising drugs to prevent capillary constriction may offer new therapies for reducing the disability caused by stroke."
"This discovery offers radically new treatment approaches for stroke," says study co-author Professor Alastair Buchan, Dean of Medicine and Head of the Medical Sciences Division at Oxford University. "Importantly, we should now be able to identify drugs that target these cells. If we are able to prevent pericytes from dying, it should help restore blood flow in the brain to normal and prevent the ongoing slow damage we see after a stroke which causes so much neurological disability in our patients."
The new research also gives insight into the mechanisms underlying the use of functional magnetic resonance imaging to detect blood flow changes in the brain.
"Functional imaging allows us to see the activity of nerve cells within the human brain but until now we didn't quite know what we were looking at," explains Professor Attwell. "We have shown that pericytes initiate the increase in blood flow seen when nerve cells become active, so we now know that functional imaging signals are caused by a pericyte-mediated increase of capillary diameter. Knowing exactly what functional imaging shows will help us to better understand and interpret what we see."
Scientists Convince People Their Hands Are Rocks
And is your doctor using this scientific knowledge to recover your ability to move your hand and fingers? Or do they have rocks for brains?
http://blogs.discovermagazine.com/inkfish/2014/03/28/scientists-convince-people-their-hands-are-rocks/
http://blogs.discovermagazine.com/inkfish/2014/03/28/scientists-convince-people-their-hands-are-rocks/
Efficacy of anti-inflammatory agents to improve symptoms in patients with schizophrenia: an update
A question for your doctor. What inflammation has occurred in your post-stroke brain and what the hell are you doing about it?
At least someone is studying this for other brain diseases.
Efficacy of anti-inflammatory agents to improve symptoms in patients with schizophrenia: an update
At least someone is studying this for other brain diseases.
Efficacy of anti-inflammatory agents to improve symptoms in patients with schizophrenia: an update
The right inferior frontal cortex - The brain’s cognitive brake
I don't believe this area was damaged in my stroke. I would do almost anything prior and now if someone pours more wine in my glass I will never stop them. Do you want to climb 487 steps? Sure.
What is your doctor doing about a stroke protocol if you have such damage?
TheNeurofractal blogger discussing it here:
http://neurofractal.tumblr.com/post/81075417104/the-right-inferior-frontal-cortex-the-brains
The abstract it is based upon here:
Inhibition and the right inferior frontal cortex: one decade on
and here:
The role of the subthalamic nucleus in response inhibition: Evidence from local field potential recordings in the human subthalamic nucleus
What is your doctor doing about a stroke protocol if you have such damage?
TheNeurofractal blogger discussing it here:
http://neurofractal.tumblr.com/post/81075417104/the-right-inferior-frontal-cortex-the-brains
The abstract it is based upon here:
Inhibition and the right inferior frontal cortex: one decade on
and here:
The role of the subthalamic nucleus in response inhibition: Evidence from local field potential recordings in the human subthalamic nucleus
BioSensics LEGSys™ Fast, Easy, Affordable and Portable Gait Analysis
Will your therapist be using this for your objective gait analysis if they don't like the
1. Sensoria™ Fitness Socks or
2. A gait abnormality measure based on root mean square of trunk acceleration or
3. Simulation of normal and pathological gaits using a fusion knowledge strategy or
4. gait monitoring sensor research?
While they may be able to look at your walking and know that it's not correct, that's not good enough. They need to be able to document exactly what is wrong. How the hell else are they going to be able to give you a stroke protocol to correct your gait problems? I still don't walk correctly because my gait was never analyzed and given very specific corrective exercises. This proves exactly why only 10% get close to full recovery.
And just because spasticity is screwing up your gait is not a reason for your therapist not to have walking protocols.
http://www.biosensics.com/legsys-overview/
1. Sensoria™ Fitness Socks or
2. A gait abnormality measure based on root mean square of trunk acceleration or
3. Simulation of normal and pathological gaits using a fusion knowledge strategy or
4. gait monitoring sensor research?
While they may be able to look at your walking and know that it's not correct, that's not good enough. They need to be able to document exactly what is wrong. How the hell else are they going to be able to give you a stroke protocol to correct your gait problems? I still don't walk correctly because my gait was never analyzed and given very specific corrective exercises. This proves exactly why only 10% get close to full recovery.
And just because spasticity is screwing up your gait is not a reason for your therapist not to have walking protocols.
http://www.biosensics.com/legsys-overview/
Evolve your practice with the advantages offered by LEGSys™
Convenience
LEGSys™ is easily portable and can be set up and utilized anywhere.
Conduct gait tests at your office, in patients’ homes, or anywhere in
between.
Independence
With LEGSys™, you control when and where gait-assessments are run. No
longer will you have to rely on outside facilities for quantitative gait
assessment.
Accuracy LEGSys™ gait analysis algorithms have been validated and used in many clinical studies. Read more…
Objectivity LEGSys objectively quantifies your patient’s gait, enabling you to document therapy outcomes and identify effective treatments.
Validity
Illustrate to patients, as well as insurance providers, the efficacy of
your practice and the progress your patients are making with easy to
interpret, measurable results.
Saturday, March 29, 2014
Glia and the Synapse: Plasticity and Disease
A total of 78 pages for your doctor to use to make sure the stroke
protocols being used for your 100% recovery are still correct.
http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/specialissues/753103.pdf&sa=X&scisig=AAGBfm262Frk1J97GgQoqriYmR2udQKgBA&oi=scholaralrt
Department of Neuroscience, School of Medicine, University of Geneva, 1211-CH Geneva, Switzerland
2 Centre for Research in Neuroscience, Department of Neurology and Neurosurgery,
The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, QC, Canada H3G 1A4
3 Biological and Environmental Sciences & Engineering Division, King Abdullah University of Science and Technology,
Thuwal 23955, Saudi Arabia
Correspondence should be addressed to Irina Nikonenko; iryna.nikonenko@unige.ch
Received 3 February 2014; Accepted 3 February 2014; Published 18 March 2014
Copyright © 2014 Irina Nikonenko et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Glial cells play multiple, diverse roles in the central nervous
system (CNS), ranging from the basal support of
neuronal function to close partnership with the synapse.
Growing experimental evidence shows the importance of
glia for proper brain functioning and their involvement in
injury and disease. Astrocytes are the most intriguing cells
among the glial family. It is well known that they provide
energetic substrates to neurons, take up neurotransmitters,
and maintain ion homeostasis. Recent research has revealed
that they can also release gliotransmitters and signaling
molecules as well as maintain and regulate the extracellular
matrix. Structurally, astrocytic fine processes enwrap synaptic
contacts and exhibit remarkable plasticity resulting from
crosstalk between these compartments. These features endow
astrocytes with the ability to sense neuronal activity and integrate
and modulate synaptic transmission, revealing them as
a crucial element inmechanisms of synaptic transmission and
plasticity.
Indeed, astrocyte-synapse interactions are complex and
dynamic andare required fornormal synapticphysiology and
plasticity, as well as for the development and refinement of
the neuronal circuits. Although much progress has recently
been made in our understanding of the cellular andmolecular
mechanisms that underlie neuronal-glial interactions, ongoing
research is adding new information and new questions
regarding the role of glial cells in CNS development, function,
and disease.
In this special issue we collected research and review
articles that focus on glia-synapse interactions with a
particular focus on astrocytes. An important role played by
these cells in regulating long-term potentiation (LTP) and
memory mechanisms in hippocampus is reviewed by Y. Ota
et al. In the review “The role of astrocytes in the regulation
of synaptic plasticity and memory formation,” the authors
presented a summary of receptors and signaling molecules
implicated in LTP. In addition, they propose an integrative
model describing how astrocytes may modulate LTP at the
postsynaptic site. Supported by a growing number of studies,
their model confirms the involvement of the glutamatergic,
cholinergic, and purinergic pathways in the neuron-astrocyte
interactions taking place during synaptic plasticity.Moreover,
this cellular interplay implicates also ephrin signaling and
cytokines. Finally, Y. Ota and coauthors discuss the central
role played by astrocytic calciumand associated gliotransmitters
in hippocampal-dependent memory.
Although the primary function of astrocytes is to take up
glutamate to prevent excitotoxicity, astrocytes are also able to
release this neurotransmitter. This is generally well accepted
even if the mechanisms of release remain uncertain. In this
special issue, a novel mechanism of glutamate release from
astrocytes was studied by C. Cali et al. in the manuscript
“G-protein coupled receptor-evoked glutamate exocytosis from
astrocytes: role of prostaglandins.” They show the role of the
proinflammatorymediator prostaglandin E2 (PGE2) in glutamate
exocytosis fromastrocytes in the intact brain. Inhibition
of cyclooxygenase pathway caused a significant reduction in
the total number of fusion events of VGLUT1-positive glutamate
containing vesicles in astrocytes induced by activation
Hindawi Publishing Corporation
Neural Plasticity
Volume 2014, Article ID 246714, 2 pages
http://dx.doi.org/10.1155/2014/246714
2 Neural Plasticity
of purinergic and glutamatergic receptors. Prostaglandinmediated
signaling is implicated in the later, slower phase
of glutamate release and requires autocrine/paracrine action
of PGE2, suggesting a physiological role for this mediator in
intercellular communication, in addition to its known role in
inflammatory reactions in the brain.
Gliotransmitters glutamate and D-serine have been
shown to modulate NMDA receptors (NMDAR) at extrasynaptic
sites, revealing neuronal NMDAR as active components
of glia to neuron communication. In the review
“GluN3A: an NMDA receptor subunit with exquisite properties
and functions,” L. A. Kehoe et al. discuss recent data
on the GluN3A subunit which provides “nonconventional”
properties to NMDA receptors. Expression of this subunit
in early development helps to shape neuronal networks,
but it may also be implicated in different neuropathologies.
Interestingly, the presence of GluN3 subunit on perisynaptic
astrocytic processes suggests its possible involvement in
neuron-glia interactions, although more research is required
to elucidate this question.
Another mechanism used by astrocytes to regulate
intercellular interactions in the CNS is through secretion
of matricellular proteins. These proteins are nonstructural
molecules that regulate the extracellular matrix and cell-cell
interactions. In the paper “Astrocyte-secreted matricellular
proteins in CNS remodelling during development and disease,”
E. V. Jones and D. S. Bouvier review the roles of matricellular
proteins secreted from developing and reactive astrocytes
in CNS development, injury, and disease and discuss their
potential as therapeutic targets.
In the paper “Astrocyte-synapse structural plasticity,” Y.
Bernardinelli et al. review the data on plasticity of perisynaptic
astrocytic processes (PAPs). The authors discuss electron
and optical microscopy data showing the distribution of fine
astrocytic processes around synapses and overview growing
evidence on PAP structural plasticity. Although the exact
mechanisms and roles of this type of astrocytic plasticity
are still not clear, recent data has revealed a requirement
for neuronal activity and suggests that PAPs may be implicated
in the structural support and plasticity of a synapse,
control of neurotransmission and intersynaptic crosstalk,
energy supply,maintenance of extracellular homeostasis, and
integration of synaptic signals.
The study of glial structural plasticity (such as PAPs)
requires precise quantification of fine processes and their
motility. This challenging task is addressed in the paper
“Improved method for the quantification of motility in glia and
other morphologically complex cells” by M. Sild et al. who
propose and describe in detail a new approach to calculate a
motility index for cells with complex, dynamicmorphologies.
In this special issue, only some aspects out of a broad
range of topics on synapse-glia interactions are highlighted
and discussed. Despite great progress made recently in our
understanding of glia and their role in the CNS, there is still
a long road ahead. We hope that the data presented in this
issue will help the future research in this quickly growing and
important field.
http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/specialissues/753103.pdf&sa=X&scisig=AAGBfm262Frk1J97GgQoqriYmR2udQKgBA&oi=scholaralrt
Department of Neuroscience, School of Medicine, University of Geneva, 1211-CH Geneva, Switzerland
2 Centre for Research in Neuroscience, Department of Neurology and Neurosurgery,
The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, QC, Canada H3G 1A4
3 Biological and Environmental Sciences & Engineering Division, King Abdullah University of Science and Technology,
Thuwal 23955, Saudi Arabia
Correspondence should be addressed to Irina Nikonenko; iryna.nikonenko@unige.ch
Received 3 February 2014; Accepted 3 February 2014; Published 18 March 2014
Copyright © 2014 Irina Nikonenko et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Glial cells play multiple, diverse roles in the central nervous
system (CNS), ranging from the basal support of
neuronal function to close partnership with the synapse.
Growing experimental evidence shows the importance of
glia for proper brain functioning and their involvement in
injury and disease. Astrocytes are the most intriguing cells
among the glial family. It is well known that they provide
energetic substrates to neurons, take up neurotransmitters,
and maintain ion homeostasis. Recent research has revealed
that they can also release gliotransmitters and signaling
molecules as well as maintain and regulate the extracellular
matrix. Structurally, astrocytic fine processes enwrap synaptic
contacts and exhibit remarkable plasticity resulting from
crosstalk between these compartments. These features endow
astrocytes with the ability to sense neuronal activity and integrate
and modulate synaptic transmission, revealing them as
a crucial element inmechanisms of synaptic transmission and
plasticity.
Indeed, astrocyte-synapse interactions are complex and
dynamic andare required fornormal synapticphysiology and
plasticity, as well as for the development and refinement of
the neuronal circuits. Although much progress has recently
been made in our understanding of the cellular andmolecular
mechanisms that underlie neuronal-glial interactions, ongoing
research is adding new information and new questions
regarding the role of glial cells in CNS development, function,
and disease.
In this special issue we collected research and review
articles that focus on glia-synapse interactions with a
particular focus on astrocytes. An important role played by
these cells in regulating long-term potentiation (LTP) and
memory mechanisms in hippocampus is reviewed by Y. Ota
et al. In the review “The role of astrocytes in the regulation
of synaptic plasticity and memory formation,” the authors
presented a summary of receptors and signaling molecules
implicated in LTP. In addition, they propose an integrative
model describing how astrocytes may modulate LTP at the
postsynaptic site. Supported by a growing number of studies,
their model confirms the involvement of the glutamatergic,
cholinergic, and purinergic pathways in the neuron-astrocyte
interactions taking place during synaptic plasticity.Moreover,
this cellular interplay implicates also ephrin signaling and
cytokines. Finally, Y. Ota and coauthors discuss the central
role played by astrocytic calciumand associated gliotransmitters
in hippocampal-dependent memory.
Although the primary function of astrocytes is to take up
glutamate to prevent excitotoxicity, astrocytes are also able to
release this neurotransmitter. This is generally well accepted
even if the mechanisms of release remain uncertain. In this
special issue, a novel mechanism of glutamate release from
astrocytes was studied by C. Cali et al. in the manuscript
“G-protein coupled receptor-evoked glutamate exocytosis from
astrocytes: role of prostaglandins.” They show the role of the
proinflammatorymediator prostaglandin E2 (PGE2) in glutamate
exocytosis fromastrocytes in the intact brain. Inhibition
of cyclooxygenase pathway caused a significant reduction in
the total number of fusion events of VGLUT1-positive glutamate
containing vesicles in astrocytes induced by activation
Hindawi Publishing Corporation
Neural Plasticity
Volume 2014, Article ID 246714, 2 pages
http://dx.doi.org/10.1155/2014/246714
2 Neural Plasticity
of purinergic and glutamatergic receptors. Prostaglandinmediated
signaling is implicated in the later, slower phase
of glutamate release and requires autocrine/paracrine action
of PGE2, suggesting a physiological role for this mediator in
intercellular communication, in addition to its known role in
inflammatory reactions in the brain.
Gliotransmitters glutamate and D-serine have been
shown to modulate NMDA receptors (NMDAR) at extrasynaptic
sites, revealing neuronal NMDAR as active components
of glia to neuron communication. In the review
“GluN3A: an NMDA receptor subunit with exquisite properties
and functions,” L. A. Kehoe et al. discuss recent data
on the GluN3A subunit which provides “nonconventional”
properties to NMDA receptors. Expression of this subunit
in early development helps to shape neuronal networks,
but it may also be implicated in different neuropathologies.
Interestingly, the presence of GluN3 subunit on perisynaptic
astrocytic processes suggests its possible involvement in
neuron-glia interactions, although more research is required
to elucidate this question.
Another mechanism used by astrocytes to regulate
intercellular interactions in the CNS is through secretion
of matricellular proteins. These proteins are nonstructural
molecules that regulate the extracellular matrix and cell-cell
interactions. In the paper “Astrocyte-secreted matricellular
proteins in CNS remodelling during development and disease,”
E. V. Jones and D. S. Bouvier review the roles of matricellular
proteins secreted from developing and reactive astrocytes
in CNS development, injury, and disease and discuss their
potential as therapeutic targets.
In the paper “Astrocyte-synapse structural plasticity,” Y.
Bernardinelli et al. review the data on plasticity of perisynaptic
astrocytic processes (PAPs). The authors discuss electron
and optical microscopy data showing the distribution of fine
astrocytic processes around synapses and overview growing
evidence on PAP structural plasticity. Although the exact
mechanisms and roles of this type of astrocytic plasticity
are still not clear, recent data has revealed a requirement
for neuronal activity and suggests that PAPs may be implicated
in the structural support and plasticity of a synapse,
control of neurotransmission and intersynaptic crosstalk,
energy supply,maintenance of extracellular homeostasis, and
integration of synaptic signals.
The study of glial structural plasticity (such as PAPs)
requires precise quantification of fine processes and their
motility. This challenging task is addressed in the paper
“Improved method for the quantification of motility in glia and
other morphologically complex cells” by M. Sild et al. who
propose and describe in detail a new approach to calculate a
motility index for cells with complex, dynamicmorphologies.
In this special issue, only some aspects out of a broad
range of topics on synapse-glia interactions are highlighted
and discussed. Despite great progress made recently in our
understanding of glia and their role in the CNS, there is still
a long road ahead. We hope that the data presented in this
issue will help the future research in this quickly growing and
important field.
L-21 stokes brain inflammation post stroke
And precisely what is your doctor doing about inflammation post-stroke? ANYTHING AT ALL? Does s/he even know about inflammation?
http://www.nature.com/nri/journal/v14/n4/full/nri3656.html
Much of the secondary tissue damage associated with ischaemic stroke is caused by inflammation, but the factors involved in this neuroinflammation remain unclear. This study showed that interleukin-21 (IL-21) expression is greatly increased in the brain of mice following cerebral ischaemic reperfusion injury, that Il21−/− mice have reduced brain injury,…
http://www.nature.com/nri/journal/v14/n4/full/nri3656.html
- Nature Reviews Immunology
- 14,
- 215
- doi:10.1038/nri3656
- Published online
Much of the secondary tissue damage associated with ischaemic stroke is caused by inflammation, but the factors involved in this neuroinflammation remain unclear. This study showed that interleukin-21 (IL-21) expression is greatly increased in the brain of mice following cerebral ischaemic reperfusion injury, that Il21−/− mice have reduced brain injury,…
Read the full article
Additional access options:
The new bionics that let us run, climb and dance
And if we had a great stroke association we would be working with this to create bionics to help stroke survivors walk properly again. But alas we don't.
http://www.ted.com/talks/hugh_herr_the_new_bionics_that_let_us_run_climb_and_dance?
http://www.ted.com/talks/hugh_herr_the_new_bionics_that_let_us_run_climb_and_dance?
Action Alert - NSA on state stroke legislation
I don't know how many employees the National Stroke Association has but this statement is a total piece of crap. Doesn't anyone there have any functioning brain cells? How come a stroke survivor knows more than all of the NSA put together?
http://www.stroke.org/site/MessageViewer?pw_id=2002&dlv_id=33241&em_id=24166.0
Dear SAN member,
State legislators are busy helping the stroke community with bills covering a variety of issues that affect stroke survivors, their families, caregivers and the healthcare professionals who care for them. If your state is listed below, you can help the whole stroke community by communicating with your state legislators about the stroke-related issues they’re debating. We’ve made it easy to make a big difference.
Better
Stroke Treatment
Stroke systems of care include many elements designed to decrease the time it takes to diagnose a stroke patient and transport that patient to an appropriate healthcare facility for treatment. Some of these elements are: 1) designating facilities that have additional stroke training so that emergency medical personnel can transport stroke patients to these facilities when possible; 2) establishing a system for collecting statewide stroke data to help facilities improve stroke care in the future; and 3) educating emergency medical personnel about stroke so patients can be diagnosed more quickly.
(Absolutely nothing here on solving the neuronal cascade of death problem or how badly tPA works- 12%)
A strong stroke system of care can make a big difference by reducing the impact of stroke when it occurs. Ultimately these policies can give stroke patients in your state a better chance of survival and a better quality of life after stroke.(Not under the current standard of care!!!) If you live in the District of Columbia, Connecticut, Hawaii, Illinois, Massachusetts, Minnesota, New Jersey or Ohio, take action today to help improve stroke care in your state!
http://www.stroke.org/site/MessageViewer?pw_id=2002&dlv_id=33241&em_id=24166.0
Dear SAN member,
State legislators are busy helping the stroke community with bills covering a variety of issues that affect stroke survivors, their families, caregivers and the healthcare professionals who care for them. If your state is listed below, you can help the whole stroke community by communicating with your state legislators about the stroke-related issues they’re debating. We’ve made it easy to make a big difference.
 |
Stroke systems of care include many elements designed to decrease the time it takes to diagnose a stroke patient and transport that patient to an appropriate healthcare facility for treatment. Some of these elements are: 1) designating facilities that have additional stroke training so that emergency medical personnel can transport stroke patients to these facilities when possible; 2) establishing a system for collecting statewide stroke data to help facilities improve stroke care in the future; and 3) educating emergency medical personnel about stroke so patients can be diagnosed more quickly.
(Absolutely nothing here on solving the neuronal cascade of death problem or how badly tPA works- 12%)
A strong stroke system of care can make a big difference by reducing the impact of stroke when it occurs. Ultimately these policies can give stroke patients in your state a better chance of survival and a better quality of life after stroke.(Not under the current standard of care!!!) If you live in the District of Columbia, Connecticut, Hawaii, Illinois, Massachusetts, Minnesota, New Jersey or Ohio, take action today to help improve stroke care in your state!
Is laughter the best medicine? Cartoons could help patients cope with their chronic conditions
How many cartoons and humorous movies does your hospital stock for stroke patients? It must be too unproven and expensive for your hospital.
What's the downside?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140459&CultureCode=en
Researchers from the University of Southampton have shown that cartoons could be a beneficial way of educating patients and empowering them to cope better with their long term conditions.
"Humour is frequently and naturally used by people with chronic illnesses to help them adjust and understand what is happening to them," explains Associate Professor Dr Anne Kennedy, who led the study. "Our study has shown that cartoons could provide clarity to patients and be a way to engage with them. It is an untapped resource and could be a potential approach to support self-management."
Cartoons are already used in patient information but the content is sourced from health professionals rather than directly from patient experience, a unique aspect of the Southampton study.
Published in the Health Services Research journal, the study was carried out under the auspices of National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care (NIHR CLAHRC) Wessex and Greater Manchester. Researchers used patient feedback to create a series of cartoons which demonstrated common experiences, problems and anxieties. The cartoons were incorporated into a guidebook given to patients who have chronic kidney disease. These patients were asked their opinion on the use of cartoons and humour in regular patient information and then asked to evaluate the cartoons drawn for the guidebook.
Results showed a range of feelings towards the cartoons including amusement, recognition, hostility and incentives to action. Overall patients found the cartoons useful in lightening the tone of information and gave patients insight and understanding they had not had before.
Dr Kennedy says health professionals could use the cartoon approach to help their patients engage more in the management of their own conditions.
She says: "Cartoons can be challenging and the difficult emotional responses some pictures evoke could be used to help people adjust to their situation, but they can also be used to dispel misconceptions. The word chronic is often misinterpreted as meaning terminal - reaction to the particular cartoon that demonstrated 'chronic' did prove a bit shocking to some patients but it allowed the word to be talked through and it was a tipping point for patients to better understand what their condition was."
Professor Anne Rogers, NIHR CLAHRC Wessex Research Director, who also worked on the study, adds: "Cartoons, drawn with patient input, have potential to help communicate important advice and help patients self-manage their conditions while boosting moral. More work needs to done in this area to build on our findings and we hope that this knowledge will be used to develop cartoons that reflect patients, experiences and get them thinking about where they can get support to suit their needs."
Cartoon courtesy of Fran Orford - double click to read the caption.
And I love this one that Peter Levine pointed out. Of course it would be too creepy if it was a guy saying that.
What's the downside?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140459&CultureCode=en
Researchers from the University of Southampton have shown that cartoons could be a beneficial way of educating patients and empowering them to cope better with their long term conditions.
"Humour is frequently and naturally used by people with chronic illnesses to help them adjust and understand what is happening to them," explains Associate Professor Dr Anne Kennedy, who led the study. "Our study has shown that cartoons could provide clarity to patients and be a way to engage with them. It is an untapped resource and could be a potential approach to support self-management."
Cartoons are already used in patient information but the content is sourced from health professionals rather than directly from patient experience, a unique aspect of the Southampton study.
Published in the Health Services Research journal, the study was carried out under the auspices of National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care (NIHR CLAHRC) Wessex and Greater Manchester. Researchers used patient feedback to create a series of cartoons which demonstrated common experiences, problems and anxieties. The cartoons were incorporated into a guidebook given to patients who have chronic kidney disease. These patients were asked their opinion on the use of cartoons and humour in regular patient information and then asked to evaluate the cartoons drawn for the guidebook.
Results showed a range of feelings towards the cartoons including amusement, recognition, hostility and incentives to action. Overall patients found the cartoons useful in lightening the tone of information and gave patients insight and understanding they had not had before.
Dr Kennedy says health professionals could use the cartoon approach to help their patients engage more in the management of their own conditions.
She says: "Cartoons can be challenging and the difficult emotional responses some pictures evoke could be used to help people adjust to their situation, but they can also be used to dispel misconceptions. The word chronic is often misinterpreted as meaning terminal - reaction to the particular cartoon that demonstrated 'chronic' did prove a bit shocking to some patients but it allowed the word to be talked through and it was a tipping point for patients to better understand what their condition was."
Professor Anne Rogers, NIHR CLAHRC Wessex Research Director, who also worked on the study, adds: "Cartoons, drawn with patient input, have potential to help communicate important advice and help patients self-manage their conditions while boosting moral. More work needs to done in this area to build on our findings and we hope that this knowledge will be used to develop cartoons that reflect patients, experiences and get them thinking about where they can get support to suit their needs."
Attached files
And I love this one that Peter Levine pointed out. Of course it would be too creepy if it was a guy saying that.
Sensoria™ Fitness Socks
And why hasn't your therapist used this to determine exactly what is wrong with your walking stride? And created stroke protocols to correct those problems. Or did you get useless instructions like I did? 'Walk this way' with no objective analysis of the problems in your gait. You do expect your therapist to solve your problems? Don't you?
http://store.sensoriafitness.com/sensoria-fitness-anklet-and-one-pair-of-socks/#.UzbkFoXYGVk
Sensoria™ socks are infused with proprietary 100% textile sensors. They are paired with a Bluetooth Smart cool and detachable anklet that not only delivers superior accuracy in step counting, speed, calories, altitude and distance tracking, but goes well beyond that to track cadence, foot landing technique and weight distribution on the foot as you walk and run.
Sensoria™ may help you to identifies injury-prone running styles (heel striking, overpronating, etc.), then leverages a mobile app to coach the runner in real-time via audio cues. The Sensoria™ dashboard can also help achieve goals, improve performance and reduce risk of gravitating back to bad tendencies.
http://store.sensoriafitness.com/sensoria-fitness-anklet-and-one-pair-of-socks/#.UzbkFoXYGVk
Sensoria™ socks are infused with proprietary 100% textile sensors. They are paired with a Bluetooth Smart cool and detachable anklet that not only delivers superior accuracy in step counting, speed, calories, altitude and distance tracking, but goes well beyond that to track cadence, foot landing technique and weight distribution on the foot as you walk and run.
Sensoria™ may help you to identifies injury-prone running styles (heel striking, overpronating, etc.), then leverages a mobile app to coach the runner in real-time via audio cues. The Sensoria™ dashboard can also help achieve goals, improve performance and reduce risk of gravitating back to bad tendencies.
Friday, March 28, 2014
Stroke rehab program begins in Mystic - New London, CT
You will need to contact Dr. Neer Zeevi about the goals of the rehab program. Because if you don't he will set the goals as the standard of care today(10% full recovery). That's setting you up for immediate failure. The goal has to be 100% recovery - NOTHING LESS. I don't give a shit about their medical expertise, the goal has to be 100% recovery. Excuses can't be allowed. Its your health, dammit.
http://www.theday.com/article/20140328/BIZ02/303289973/-1/BIZ
Mystic Healthcare Nursing & Rehabilitation Center announced this week that it has opened a new stroke rehabilitation program with Dr. Neer Zeevi, neurohospitalist at Lawrence + Memorial Hospital in New London, as its director. The program specializes in post-stroke care and rehabilitation, focusing on an interdisciplinary approach centering on the patient's health goals and achieving the highest possible quality of life.
Mystic Healthcare is located at 475 High St. For information, visit: www.mystichealthcare.net. To contact the center, call (860) 536-6070, send an email to: info@mystichealthcare.net. The center is part of Ryders Health Management Nursing & Rehabilitation Centers.
http://www.theday.com/article/20140328/BIZ02/303289973/-1/BIZ
Mystic Healthcare Nursing & Rehabilitation Center announced this week that it has opened a new stroke rehabilitation program with Dr. Neer Zeevi, neurohospitalist at Lawrence + Memorial Hospital in New London, as its director. The program specializes in post-stroke care and rehabilitation, focusing on an interdisciplinary approach centering on the patient's health goals and achieving the highest possible quality of life.
Mystic Healthcare is located at 475 High St. For information, visit: www.mystichealthcare.net. To contact the center, call (860) 536-6070, send an email to: info@mystichealthcare.net. The center is part of Ryders Health Management Nursing & Rehabilitation Centers.
A Huntington's Breakthrough?
If we can mange a breakthrough in this, what the hell is preventing a breakthrough in stroke? Other than no strategy/no plan/no innovation?
A blogger discussing it here;
http://pipeline.corante.com/archives/2014/03/28/a_huntingtons_breakthrough.php
The paper this is based upon is here:
Cystathionine γ-lyase deficiency mediates neurodegeneration in Huntington’s disease
A blogger discussing it here;
http://pipeline.corante.com/archives/2014/03/28/a_huntingtons_breakthrough.php
The paper this is based upon is here:
Cystathionine γ-lyase deficiency mediates neurodegeneration in Huntington’s disease
Liquid Water Discovered on Surface of Minnesota
Couldn't help myself, I'm still a Minnesotan at heart, the cold keeps out the riffraff.
Thanks to Doug for finding this.
http://fourthcrown.wordpress.com/2014/03/26/liquid-water-discovered-on-surface-of-minnesota/
Thanks to Doug for finding this.
http://fourthcrown.wordpress.com/2014/03/26/liquid-water-discovered-on-surface-of-minnesota/
The Saturated Fat, Cholesterol, and Statin Controversy: A Commentary from the Journal of the American College of Nutrition
You''l need this understanding to be able to hold a decent conversation with your doctor.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140435&CultureCode=en
A couple lines from it here;
While saturated fats have been blamed for causing CVD, more recent scientific literature points instead to processed sugars, trans-fats, and starchy/processed high-glycemic carbs as the more likely culprits. “Our nutritional courts,” the authors claim, “tried and convicted the wrong man.”
Short version here;
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140435&CultureCode=en
Full text available here;
http://www.tandfonline.com/doi/full/10.1080/07315724.2014.878633
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140435&CultureCode=en
A couple lines from it here;
While saturated fats have been blamed for causing CVD, more recent scientific literature points instead to processed sugars, trans-fats, and starchy/processed high-glycemic carbs as the more likely culprits. “Our nutritional courts,” the authors claim, “tried and convicted the wrong man.”
Short version here;
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140435&CultureCode=en
Full text available here;
http://www.tandfonline.com/doi/full/10.1080/07315724.2014.878633
Stroke patients should receive customized palliative care
What a pile of crap. Providing palliative care means the stroke medical team has given up on recovery. Don't they have any clue that these 31 hyperacute possibilities would be a good starting point? Should these be given that will lessen the disability considerably? Or these 177 possibilities needing research? By doing these I bet the 30-day death rate would be lessened considerably. This is a perfect example of the nocebo effect. Your doctor expects you to die, so you'll have to oblige them and do that.
This stress you are under will start elimination of dendritic spines in the hippocampus. And that is the start of your downward spiral to death.
If this occurs to you your doctors have already given up on your recovery, you need to fire them and go to a more knowledgeable and professional place, you don't want to stay where incompetency rules. You're going to have get into a screaming match with your doctor, because nothing else will cause them to change their practice.
And this was written in the American Heart Association journal Stroke. you can cross the ASA off the list of organizations that support survivors.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140307&CultureCode=en
Don't listen to me, I have no medical training and obviously should not question the medical gods.
And yes I do know that palliative care is not the same as hospice care but it's the slippery slope leading to no useful therapy.
This stress you are under will start elimination of dendritic spines in the hippocampus. And that is the start of your downward spiral to death.
If this occurs to you your doctors have already given up on your recovery, you need to fire them and go to a more knowledgeable and professional place, you don't want to stay where incompetency rules. You're going to have get into a screaming match with your doctor, because nothing else will cause them to change their practice.
And this was written in the American Heart Association journal Stroke. you can cross the ASA off the list of organizations that support survivors.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140307&CultureCode=en
Don't listen to me, I have no medical training and obviously should not question the medical gods.
And yes I do know that palliative care is not the same as hospice care but it's the slippery slope leading to no useful therapy.
Thursday, March 27, 2014
How To Reduce Your Risk Of Stroke With Regular Walks
What a f*cking simplistic answer. That way you can blame the fact that you got a stroke on the patient. I was probably in the best shape of my life and that didn't prevent my stroke, it probably saved my life but that's a different topic. Why don't they put out specific prevention guidelines? Like maybe these 11 Stroke risk reduction ideas.
http://www.huffingtonpost.co.uk/2014/03/27/heart-health-month-stroke-prevention-walk_n_5035405.html
http://www.huffingtonpost.co.uk/2014/03/27/heart-health-month-stroke-prevention-walk_n_5035405.html
Visualizing Cell Signaling: Current Trends and New Technologies
If we had any decent or even adequate neurologists and hospitals this seminar would be required for all stroke medical staff to figure out how neurons signal each other to make neuroplasticity work. But alas, we have idiots instead.
http://webinar.sciencemag.org/webinar/archive/visualizing-cell-signaling
Techniques for the study of intracellular ions are used widely in biology, including for the tracking of calcium waves or ions affecting pH within living cells. The ability to monitor changes in intracellular ion concentrations over time is vital for our understanding of signaling and functional pathways in cellular systems. These pathways are central to many fundamental processes such as muscle contraction and synaptic nerve signal transmission. Ion channels that span the outer cell membrane open or close in response to extracellular and intracellular signals, potentially altering how the cell behaves. These fluctuations can be visualized and quantified using ratiometric microscopy and special fluorescent dyes designed to bind specific ions, such as the FURA-2 indicator dye specific to calcium ions. Changes in the photophysics of the dye as it binds to its target ion allows for quantitation of the bound and unbound ratio, and thus the concentration of the ion under investigation. This webinar will introduce the viewer to the current state of technology in this important field as well as cover the latest advances in microscopy for ion signaling research.
During the webinar, viewers will:
http://webinar.sciencemag.org/webinar/archive/visualizing-cell-signaling
Techniques for the study of intracellular ions are used widely in biology, including for the tracking of calcium waves or ions affecting pH within living cells. The ability to monitor changes in intracellular ion concentrations over time is vital for our understanding of signaling and functional pathways in cellular systems. These pathways are central to many fundamental processes such as muscle contraction and synaptic nerve signal transmission. Ion channels that span the outer cell membrane open or close in response to extracellular and intracellular signals, potentially altering how the cell behaves. These fluctuations can be visualized and quantified using ratiometric microscopy and special fluorescent dyes designed to bind specific ions, such as the FURA-2 indicator dye specific to calcium ions. Changes in the photophysics of the dye as it binds to its target ion allows for quantitation of the bound and unbound ratio, and thus the concentration of the ion under investigation. This webinar will introduce the viewer to the current state of technology in this important field as well as cover the latest advances in microscopy for ion signaling research.
During the webinar, viewers will:
- Learn about current state-of-the-art ion signaling methodologies
- Discover what recent advances have been made in technologies for tracking ion changes, particularly calcium signaling
- Hear how experts in the field are applying these new technologies in the lab today
- Have the opportunity to ask questions of the expert panel live!
Speaker Bios
Mark Hollywood, Ph.D.
Dundalk Institute of Technology
Dundalk, Ireland
Dundalk, Ireland
Dr.
Hollywood undertook his Ph.D. at Queens University in Belfast, Ireland
on the innervation of sheep mesenteric lymphatics. Following graduation
in 1994, he commenced postdoctoral training in the Smooth Muscle Group
and subsequently was offered a lecturer position in the Department of
Physiology in 1995 and a senior lecturer post in 2001. In 2005, Dr.
Hollywood together with his colleagues from the Smooth Muscle Group were
recruited by Dundalk Institute of Technology to set up the Smooth
Muscle Research Centre in Ireland, where he is currently a principal
investigator. Dr. Hollywood’s research interests are focused on (1)
developing novel ion channel modulators to treat overactive bladder and
(2) examining the mechanisms underlying spontaneous activity in urethral
pacemaker cells and how they modulate the bulk smooth muscle. His
laboratory is currently developing a combined patch clamp/confocal
microscopy system that will allow simultaneous imaging of whole-cell
Ca2+ at frame rates in excess of 200 frames per second using
back-illuminated EMCCD cameras, and enable correlation of this data to
the resultant electrical activity observed in isolated urethral
pacemaker cells.
C. Peter Bengtson, Ph.D.
University of Heidelberg
Heidelberg, Germany
Heidelberg, Germany
Dr.
Bengtson has a Ph.D. in neurophysiology from the Department of
Physiology and Pharmacology at the University of Queensland, Australia.
He specializes in both patch clamp electrophysiology and wide-field
microscopy from neurons in brain slices or dissociated cultures. He is
currently a senior postdoctoral fellow in the Department of Neurobiology
in the Interdisciplinary Center for Neuroscience (IZN) at Heidelberg
University where he has worked for over a decade in the laboratory of
Professor Hilmar Bading, primarily investigating the calcium signals and
molecular mechanisms mediating long-term plasticity and memory.
Colin Coates, Ph.D.
Andor Technology
Belfast, Ireland
Belfast, Ireland
Dr.
Coates holds a first-class degree in chemistry, with a postgraduate
degree and postdoctoral research training from Queen’s University
Belfast in Ireland, focusing primarily on time-resolved laser
spectroscopic analysis of photophysical mechanisms. Dr. Coates also has
experience in leading an industrial research and development team that
was involved in developing novel DNA microarray technologies. Dr. Coates
maintains overall product management responsibility for Andor's
research and OEM camera/spectrograph business, encompassing imaging,
spectroscopy, time-resolved, and X-ray product/market segments.
Moderator: Sean Sanders, Ph.D.
Science/AAAS
Washington, DC
Washington, DC
Dr.
Sanders did his undergraduate training at the University of Cape Town,
South Africa, and his Ph.D. at the University of Cambridge, UK,
supported by the Wellcome Trust. Following postdoctoral training at the
National Institutes of Health and Georgetown University, Dr. Sanders
joined TranXenoGen, a startup biotechnology company in Massachusetts
working on avian transgenics. Pursuing his parallel passion for writing
and editing, Dr. Sanders joined BioTechniques as an editor, before
joining Science/AAAS in 2006. Currently Dr. Sanders is the Editor for Custom Publishing for the journal Science and Program Director for Outreach.
Online Resources
Tuesday, March 25, 2014
St Richard’s Hospital under fire for stroke care - Chichester, UK
Every single hospital in the world should be under fire.
1. Using tPA with only 12% efficacy.
2. No fast and objective way to diagnose strokes.
3. Only 10% of stroke patients get to full recovery.
4. Nothing being done in the first week to stop the neuronal cascade of death.
Every hospital and neurologist in the world is incompetent for allowing these problems to fester for years.
http://www.chichester.co.uk/news/local/st-richard-s-hospital-under-fire-for-stroke-care-1-5955892
1. Using tPA with only 12% efficacy.
2. No fast and objective way to diagnose strokes.
3. Only 10% of stroke patients get to full recovery.
4. Nothing being done in the first week to stop the neuronal cascade of death.
Every hospital and neurologist in the world is incompetent for allowing these problems to fester for years.
http://www.chichester.co.uk/news/local/st-richard-s-hospital-under-fire-for-stroke-care-1-5955892
Summary of evidence-based guideline: Complementary and alternative medicine in multiple sclerosis - cannabis use
Of course, no one in the stroke world knows about this unless you tell your doctors. With this your doctor should have the legal ability to prescribe this since nothing else works for spasticity. But what the hell do I know?
http://www.neurology.org/content/82/12/1083.full
The appropriate stuff for us to know:
Results and recommendations: Clinicians might offer oral cannabis extract for spasticity symptoms and pain (excluding central neuropathic pain) (Level A). Clinicians might offer tetrahydrocannabinol for spasticity symptoms and pain (excluding central neuropathic pain) (Level B). Clinicians should counsel patients that these agents are probably ineffective for objective??? spasticity (short-term)/tremor (Level B) and possibly effective for spasticity and pain (long-term) (Level C). Clinicians might offer Sativex oromucosal cannabinoid spray (nabiximols) for spasticity symptoms, pain, and urinary frequency (Level B). Clinicians should counsel patients that these agents are probably ineffective for objective spasticity/urinary incontinence (Level B). Clinicians might choose not to offer these agents for tremor (Level C). Clinicians might counsel patients that magnetic therapy is probably effective for fatigue and probably ineffective for depression (Level B); fish oil is probably ineffective for relapses, disability, fatigue, MRI lesions, and quality of life (QOL) (Level B); ginkgo biloba is ineffective for cognition (Level A) and possibly effective for fatigue (Level C); reflexology is possibly effective for paresthesia (Level C); Cari Loder regimen is possibly ineffective for disability, symptoms, depression, and fatigue (Level C); and bee sting therapy is possibly ineffective for relapses, disability, fatigue, lesion burden/volume, and health-related QOL (Level C). Cannabinoids may cause adverse effects. Clinicians should exercise caution regarding standardized vs nonstandardized cannabis extracts and overall CAM quality control/nonregulation. Safety/efficacy of other CAM/CAM interaction with MS disease-modifying therapies is unknown.
http://www.neurology.org/content/82/12/1083.full
The appropriate stuff for us to know:
Results and recommendations: Clinicians might offer oral cannabis extract for spasticity symptoms and pain (excluding central neuropathic pain) (Level A). Clinicians might offer tetrahydrocannabinol for spasticity symptoms and pain (excluding central neuropathic pain) (Level B). Clinicians should counsel patients that these agents are probably ineffective for objective??? spasticity (short-term)/tremor (Level B) and possibly effective for spasticity and pain (long-term) (Level C). Clinicians might offer Sativex oromucosal cannabinoid spray (nabiximols) for spasticity symptoms, pain, and urinary frequency (Level B). Clinicians should counsel patients that these agents are probably ineffective for objective spasticity/urinary incontinence (Level B). Clinicians might choose not to offer these agents for tremor (Level C). Clinicians might counsel patients that magnetic therapy is probably effective for fatigue and probably ineffective for depression (Level B); fish oil is probably ineffective for relapses, disability, fatigue, MRI lesions, and quality of life (QOL) (Level B); ginkgo biloba is ineffective for cognition (Level A) and possibly effective for fatigue (Level C); reflexology is possibly effective for paresthesia (Level C); Cari Loder regimen is possibly ineffective for disability, symptoms, depression, and fatigue (Level C); and bee sting therapy is possibly ineffective for relapses, disability, fatigue, lesion burden/volume, and health-related QOL (Level C). Cannabinoids may cause adverse effects. Clinicians should exercise caution regarding standardized vs nonstandardized cannabis extracts and overall CAM quality control/nonregulation. Safety/efficacy of other CAM/CAM interaction with MS disease-modifying therapies is unknown.
Medicare Therapy Plateau No Longer Ends Coverage
It seems this was distributed to others, no idea on how this interacts with the $ limit.
But don’t look for an announcement about the changes in the mail, or even a prominent notice on the Medicare website. Medicare officials were required to inform health care providers, bill processors, auditors, Medicare Advantage plans, the 800-MEDICARE information line and appeals judges — but not beneficiaries.
http://newoldage.blogs.nytimes.com/2013/02/04/therapy-plateau-no-longer-ends-coverage/
But don’t look for an announcement about the changes in the mail, or even a prominent notice on the Medicare website. Medicare officials were required to inform health care providers, bill processors, auditors, Medicare Advantage plans, the 800-MEDICARE information line and appeals judges — but not beneficiaries.
http://newoldage.blogs.nytimes.com/2013/02/04/therapy-plateau-no-longer-ends-coverage/
Motor learning: Lining up our sights
Something for our cerebellar dysfunction patients that I'm sure your doctor knows nothing about.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140312&CultureCode=en
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140312&CultureCode=en
Hot nanoparticles for cancer treatments
Who can answer the questions? Can this be used to burn thru clots? How about directing them to the tangles in Alzheimers and destroy them? Who is the futurist in our worlds than can imagine this stuff and get it done? Because we have crap for stroke associations today.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140274&CultureCode=en
Nanoparticles have a great deal of potential in medicine: for diagnostics, as a vehicle for active substances or a tool to kill off tumours using heat. ETH Zurich researchers have now developed particles that are relatively easy to produce and have a wide range of applications.
If you put your hand over a switched-on torch in the dark, it appears to glow red. This is because long-wavelength red light beams penetrate human tissue more effectively than short-wavelength blue light. ETH Zurich researchers exploit this fact in a new kind of nanoparticles: so-called plasmonic particles, which heat up when they absorb near-infrared light. This could enable them to kill tumour tissue with heat, for instance.
Gold is a popular material for nanoparticles used therapeutically, as it is well tolerated and does not usually trigger any undesirable reactions. In the characteristic ball or sphere shape of nanoparticles, however, gold does not have the necessary properties to work as a plasmonic particle that absorbs sufficiently in the near-infrared spectrum of light to heat up. To do so, it needs to be moulded into a special shape, such as a rod or shell, so that the gold atoms adopt a configuration that starts absorbing near-infrared light, thereby generating heat. Producing such nanorods or nanoshells in sufficient amounts, however, is complex and expensive.
Aggregates instead of rods
A team of researchers headed by Sotiris Pratsinis, Professor of Particle Technology at ETH Zurich, has now discovered a trick to manufacture plasmonic gold particles in large amounts. They used their existing know-how on plasmonic nanoparticles (see also: http://www.ethlife.ethz.ch/archive_articles/110512_Plasmonischer_biosensor_su/index_EN) and made sphere-shaped gold nanoparticles that display the desired near-infrared plasmonic properties by allowing them to be aggregated. Each particle is coated with a silicon dioxide layer beforehand, which acts as a placeholder between the individual spheres in the aggregate. Through the precisely defined distance between several gold particles, the researchers transform the particles into a configuration that absorbs near-infrared light and thus generates heat.
“The silicon dioxide shell has another advantage”, explains Georgios Sotiriou, first author on the study and, until recently, a postdoc in Pratsinis’ research group and currently an SNF Fellow at Harvard University: “It prevents the particles from deforming when they heat up.” This is a major problem with nanorods. If the rods lose their shape while heating up, they lose their desired plasmonic properties and are no longer able to absorb enough near-infrared light to generate heat.
The researchers have already tested the new particles on breast cancer cells in a Petri dish and discovered that after exposure to near-infrared light the nanoparticles heated up sufficiently to kill off the cells, while cells survived in control experiments (with particles but without radiation and with radiation but without nanoparticles).
Combination with great potential
To be able to steer the particles specifically towards cancer tissue, the researchers also mixed superparamagnetic iron oxide particles in with the gold particles, which enable the nanoaggregates to be controlled via magnetic fields and may enhance their accumulation in a tumour. Moreover, this opens up the possibility of heating the aggregates in deep layers of tissue that infrared light can no longer reach via magnetic hyperthermia. Here, the heating of the particles is induced by a magnetic field, where the plus and minus poles alternate at a rapid rate.
“A lot of questions still need to be answered before the particles can be used in humans”, says Jean-Christophe Leroux, Professor of Drug Formulation and Delivery at ETH Zurich, who was also involved in the research project. Although gold, silicon dioxide and iron oxide are well tolerated, what happens to the particle aggregates in the body in the course of time – whether they accumulate in the liver or are broken down and excreted, for instance – still needs to be investigated.
The hybrid iron oxide-gold nanoparticles are not only able to kill off tumour cells through heat; they could also be used as a contrast medium for imaging processes in diagnostics by magnetic resonance imaging, as investigated in collaboration with University Hospital Zurich, or as part of a vehicle that carries active substances. “You could even couple the particles with temperature-responsive drug carriers, which would then allow the drug release if a certain temperature were exceeded”, explains Sotiriou. This would allow undesirable side effects on the rest of the body to be reduced or even avoided.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=140274&CultureCode=en
Nanoparticles have a great deal of potential in medicine: for diagnostics, as a vehicle for active substances or a tool to kill off tumours using heat. ETH Zurich researchers have now developed particles that are relatively easy to produce and have a wide range of applications.
If you put your hand over a switched-on torch in the dark, it appears to glow red. This is because long-wavelength red light beams penetrate human tissue more effectively than short-wavelength blue light. ETH Zurich researchers exploit this fact in a new kind of nanoparticles: so-called plasmonic particles, which heat up when they absorb near-infrared light. This could enable them to kill tumour tissue with heat, for instance.
Gold is a popular material for nanoparticles used therapeutically, as it is well tolerated and does not usually trigger any undesirable reactions. In the characteristic ball or sphere shape of nanoparticles, however, gold does not have the necessary properties to work as a plasmonic particle that absorbs sufficiently in the near-infrared spectrum of light to heat up. To do so, it needs to be moulded into a special shape, such as a rod or shell, so that the gold atoms adopt a configuration that starts absorbing near-infrared light, thereby generating heat. Producing such nanorods or nanoshells in sufficient amounts, however, is complex and expensive.
Aggregates instead of rods
A team of researchers headed by Sotiris Pratsinis, Professor of Particle Technology at ETH Zurich, has now discovered a trick to manufacture plasmonic gold particles in large amounts. They used their existing know-how on plasmonic nanoparticles (see also: http://www.ethlife.ethz.ch/archive_articles/110512_Plasmonischer_biosensor_su/index_EN) and made sphere-shaped gold nanoparticles that display the desired near-infrared plasmonic properties by allowing them to be aggregated. Each particle is coated with a silicon dioxide layer beforehand, which acts as a placeholder between the individual spheres in the aggregate. Through the precisely defined distance between several gold particles, the researchers transform the particles into a configuration that absorbs near-infrared light and thus generates heat.
“The silicon dioxide shell has another advantage”, explains Georgios Sotiriou, first author on the study and, until recently, a postdoc in Pratsinis’ research group and currently an SNF Fellow at Harvard University: “It prevents the particles from deforming when they heat up.” This is a major problem with nanorods. If the rods lose their shape while heating up, they lose their desired plasmonic properties and are no longer able to absorb enough near-infrared light to generate heat.
The researchers have already tested the new particles on breast cancer cells in a Petri dish and discovered that after exposure to near-infrared light the nanoparticles heated up sufficiently to kill off the cells, while cells survived in control experiments (with particles but without radiation and with radiation but without nanoparticles).
Combination with great potential
To be able to steer the particles specifically towards cancer tissue, the researchers also mixed superparamagnetic iron oxide particles in with the gold particles, which enable the nanoaggregates to be controlled via magnetic fields and may enhance their accumulation in a tumour. Moreover, this opens up the possibility of heating the aggregates in deep layers of tissue that infrared light can no longer reach via magnetic hyperthermia. Here, the heating of the particles is induced by a magnetic field, where the plus and minus poles alternate at a rapid rate.
“A lot of questions still need to be answered before the particles can be used in humans”, says Jean-Christophe Leroux, Professor of Drug Formulation and Delivery at ETH Zurich, who was also involved in the research project. Although gold, silicon dioxide and iron oxide are well tolerated, what happens to the particle aggregates in the body in the course of time – whether they accumulate in the liver or are broken down and excreted, for instance – still needs to be investigated.
The hybrid iron oxide-gold nanoparticles are not only able to kill off tumour cells through heat; they could also be used as a contrast medium for imaging processes in diagnostics by magnetic resonance imaging, as investigated in collaboration with University Hospital Zurich, or as part of a vehicle that carries active substances. “You could even couple the particles with temperature-responsive drug carriers, which would then allow the drug release if a certain temperature were exceeded”, explains Sotiriou. This would allow undesirable side effects on the rest of the body to be reduced or even avoided.
USPSTF: No Proven Value in Cognition Screening
Sorry, but I vehemently disagree with this. I want to know as soon as possible so I can put my dementia prevention program into overdrive. I think a lot of this is because there is no decent pharmacological intervention and they stupidly have not been reading all the research on small daily activities that can help. They are almost as stupid as the stroke medical world. Throw up your hands in defeat before you have even started the game.
http://www.medpagetoday.com/PrimaryCare/Geriatrics/44914?
Routine screening of all older individuals for cognitive impairment is not supported by the available evidence, the U.S. Preventive Services Task Force (USPSTF) has concluded.
More at link.
http://www.medpagetoday.com/PrimaryCare/Geriatrics/44914?
Routine screening of all older individuals for cognitive impairment is not supported by the available evidence, the U.S. Preventive Services Task Force (USPSTF) has concluded.
More at link.
Multineurons is developing head-worn sensor & iPad app to monitor patients with brain disorders
We most certainly have brain disorders, so what is your doctor doing with this to determine your specific brain problems? Your doctor has to know specifically what damage has occurred. Or how will they come up with the correct stroke protocols to correct the problems and pass on the right prescriptions to the therapists? Because today they know absolutely nothing about your damage and are totally worthless in helping you recover. That statement should create dozens of flame wars in the comments.
http://medcitynews.com/2014/03/multineurons-developing-head-worn-sensor-monitor-patients-brain-disorders/?
http://medcitynews.com/2014/03/multineurons-developing-head-worn-sensor-monitor-patients-brain-disorders/?
A Caregiver’s Wish List for a National Alzheimer’s Agenda
I just wish we had a national stroke agenda - run by survivors, no neurologists need apply.
http://aja.sagepub.com/content/29/2/111?etoc
http://aja.sagepub.com/content/29/2/111?etoc
- Allan S. Vann, EdD1⇑
- Allan S. Vann, EdD 28 Abbey Drive, Commack, NY 11725, USA. Email: acvann@optonline.net
Abstract
When panels are convened to discuss the
best way to deal with Alzheimer’s disease (AD), the panels often consist
of representatives
from government agencies, national Alzheimer’s
organizations, medicine, research, and pharmaceutical companies.
Although each
of these stakeholder groups has much to contribute
to such discussions, too often the voices of caregivers are not heard.
Even the National Alzheimer’s Project Act (NAPA)
Advisory Council has only one full-time 24/7 caregiver as a member. Of
26
voices heard at the NAPA meetings, only 1 can speak
for what life is like for a 24/7 caregiver of a loved one having AD.
This
article provides 10 items that I would raise at
such a meeting based upon my own personal experience and what I have
learned
from others in my weekly spouse caregiver support
group and in my online support groups. Some items suggest funding
priorities,
some suggest changes in how doctors currently
diagnose and treat people with AD and their caregivers, and some suggest
the
need for more caregiver voices to be heard by
government panels and politicians who have the power to effect change.
Monday, March 24, 2014
Usability Evaluation of Digital Games for Stroke Rehabilitation in Taiwan
How many of these games are in your hospital or clinic therapy department? None? Why not?
http://scholar.google.com/scholar_url?hl=en&q=http://www.thinkmind.org/download.php%3Farticleid%3Dachi_2014_15_40_20136&sa=X&scisig=AAGBfm1Jvre7DdXD6pBk_W5h005swQcoUA&oi=scholaralrt
http://scholar.google.com/scholar_url?hl=en&q=http://www.thinkmind.org/download.php%3Farticleid%3Dachi_2014_15_40_20136&sa=X&scisig=AAGBfm1Jvre7DdXD6pBk_W5h005swQcoUA&oi=scholaralrt
Stroke Rehabilitation in China Today
I'm sure your doctor will take the best ideas from here and use them to get to 100% recovery. Ask what the comparison is to all developed countries and to their practice. Only 9 pages, I'm sure they can read 9 pages in English.
http://scholar.google.com/scholar_url?hl=en&q=http://omicsonline.org/open-access/stroke-rehabilitation-in-china-today-2329-9096-S3-005.pdf&sa=X&scisig=AAGBfm3S6-jS5SGlh4iVtHfpAOoCDOLWNA&oi=scholaralrt
http://scholar.google.com/scholar_url?hl=en&q=http://omicsonline.org/open-access/stroke-rehabilitation-in-china-today-2329-9096-S3-005.pdf&sa=X&scisig=AAGBfm3S6-jS5SGlh4iVtHfpAOoCDOLWNA&oi=scholaralrt
Development of a Simple Rehabilitation Device for Hemiparetic Stroke Patients to Perform Reaching Exercises in the Transverse Plane
I'm sure your therapist can figure out how to duplicate this.
http://scholar.google.com/scholar_url?hl=en&q=https://tspace.library.utoronto.ca/bitstream/1807/44072/11/Wasim_Tahir_201403_MHSc_thesis.pdf&sa=X&scisig=AAGBfm05nPI8t_GcTCrsdQ2z39pYN2I08Q&oi=scholaralrt
http://scholar.google.com/scholar_url?hl=en&q=https://tspace.library.utoronto.ca/bitstream/1807/44072/11/Wasim_Tahir_201403_MHSc_thesis.pdf&sa=X&scisig=AAGBfm05nPI8t_GcTCrsdQ2z39pYN2I08Q&oi=scholaralrt
Abstract
Upper-limb hemiparesis caused by stroke can severely limit a survivor's ability to perform activities of daily living. Treatment involves intensive, repetitive therapy that can strain
limited resources.
Rehabilitation devices have been developed to help reduce therapist burden and increase
access to therapy. However, adoption is complicated due to their expense and use of
complex actuators. A rehabilitation tool without actuators was developed to perform reaching
under varying resistance in the transverse plane and measure the reaction force at the handle.
Force measurements from the device were validated through comparison with a standard force
plate. A new method to calculate the center of applied pressure on a spherical handle mounted
on a load cell was developed and validated using 3D modeling.
Finally, a study conducted on healthy subjects demonstrated directional effects on the trajectory length and straightness, while resistance effects were seen for the maximum force, time-to-peak velocity and time-to-peak force.
Subscribe to:
Posts (Atom)