Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Saturday, December 31, 2011

Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis

Some day this will all become clear, until then you are basically on your own.

Objective To investigate whether calcium supplements increase the risk of cardiovascular events.

Design Patient level and trial level meta-analyses.

Data sources Medline, Embase, and Cochrane Central Register of Controlled Trials (1966-March 2010), reference lists of meta-analyses of calcium supplements, and two clinical trial registries. Initial searches were carried out in November 2007, with electronic database searches repeated in March 2010.

Study selection Eligible studies were randomised, placebo controlled trials of calcium supplements (≥500 mg/day), with 100 or more participants of mean age more than 40 years and study duration more than one year. The lead authors of eligible trials supplied data. Cardiovascular outcomes were obtained from self reports, hospital admissions, and death certificates.

Results 15 trials were eligible for inclusion, five with patient level data (8151 participants, median follow-up 3.6 years, interquartile range 2.7-4.3 years) and 11 with trial level data (11 921 participants, mean duration 4.0 years). In the five studies contributing patient level data, 143 people allocated to calcium had a myocardial infarction compared with 111 allocated to placebo (hazard ratio 1.31, 95% confidence interval 1.02 to 1.67, P=0.035). Non-significant increases occurred in the incidence of stroke (1.20, 0.96 to 1.50, P=0.11), the composite end point of myocardial infarction, stroke, or sudden death (1.18, 1.00 to 1.39, P=0.057), and death (1.09, 0.96 to 1.23, P=0.18). The meta-analysis of trial level data showed similar results: 296 people had a myocardial infarction (166 allocated to calcium, 130 to placebo), with an increased incidence of myocardial infarction in those allocated to calcium (pooled relative risk 1.27, 95% confidence interval 1.01 to 1.59, P=0.038).

Conclusions Calcium supplements (without coadministered vitamin D) are associated with an increased risk of myocardial infarction. As calcium supplements are widely used these modest increases in risk of cardiovascular disease might translate into a large burden of disease in the population. A reassessment of the role of calcium supplements in the management of osteoporosis is warranted.

Effect of Cranial Osteopathic Manipulative Medicine on Cerebral Tissue Oxygenation

Are we supposed to believe that someone can manipulate our skull enough to create waves in our cerebral spinal fluid? And that that will help us? I think this is what Hercules(Kevin Sorbo) thought helped his recovery.


Context: The use of cranial osteopathic manipulative medicine (OMM) to alter cerebral tissue oxygen saturation could play a role in the maintenance of cerebral homeostasis.
Objective: To examine the effects of cranial OMM on cerebral tissue oxygen saturation (SCTO2) and cardiac autonomic function in healthy adults.
Methods: Cranial OMM augmentation and suppression techniques and sham therapy were randomly applied to healthy adults. During cranial OMM and sham therapy, SCTO2 of the prefrontal cortex was determined bilaterally by using near-infrared spectroscopy. Heart rate, blood pressure, and systemic arterial blood oxygen saturation (SaO2) were also measured. Power spectral analysis was applied to continuous 4-minute R-R intervals. Measurements were made during 2-minute baseline periods, during 4-minute applications of the techniques, and during 5-minute recovery periods.
Results: Twenty-one adults (age range, 23-32 y) participated in the present study. Differences in mean baseline measurements for the augmentation technique, suppression technique, and sham therapy were not statistically significant for heart rate, blood pressure, SaO2, left SCTO2, or right SCTO2. During the suppression technique, there was a statistically significant decrease in both left (slope [standard deviation]= -0.33 [0.08] %/min, R2=0.85, P=.026) and right (slope [standard deviation]=-0.37 [0.06] %/min, R2=0.94, P=.007) SCTO2 with increased cranial OMM time. However, neither the augmentation technique nor the sham therapy had a statistically significant effect on SCTO2. Decreases in normalized low-frequency power of R-R interval variability and enhancements of its high-frequency power were statistically significant (P=.05) during cranial OMM and sham therapy, indicating a decrease in cardiac sympathetic influence and an enhanced parasympathetic modulation.
Conclusion: The cranial OMM suppression technique effectively and progressively reduced SCTO2 in both prefrontal lobes with the treatment time.

Friday, December 30, 2011

Deaths after chiropractic: a review of published cases.

Stay away.

2010 Jul


The aim of this study was to summarise all cases in which chiropractic spinal manipulation was followed by death.


This study is a systematic review of case reports.


Literature searches in four electronic databases with no restrictions of time or language.




Twenty six fatalities were published in the medical literature and many more might have remained unpublished. The alleged pathology usually was a vascular accident involving the dissection of a vertebral artery.


Numerous deaths have occurred after chiropractic manipulations. The risks of this treatment by far outweigh its benefit.

microcurrents toner and lifter - for stroke?

I never saw this device anywhere in stroke rehabilitation so I wonder what caused it to be considered and then dropped. A type of eStim? I wonder if it could be useful to trigger finger contraction? So many questions and no one to ask them about.
Here for the video;

Nuface Microcurrent Toner & Lifter $249

This is the most inexpensive facelift you can get. It uses micro currents to stimulate the muscles and create new muscle memory. It was first used on stroke victims and people with paralysis.. But just as you do with regular body exercise, you have to do this regularly or your muscles will lose their strength. I would suggest getting it done professionally first at a place such as Spa Radiance in San Francisco and then get yourself a home kit for $249. I guarantee you will see your skin lift and muscles in your face tone, no matter what your age.

Elderly Brain Functions Are as Fast as Young Adults with Some Tasks

I'm not elderly yet, or dead. So use some of that brainpower to get stroke rehab/research changed worldwide, we just need to convince all the medical world that they need to re-examine everything they know/don't know about stroke. They are almost all probably younger than us. So we should be able to easily out-think them. Run rings about them logically.

Contrary to popular belief, aging doesn't necessarily lead to slower brain function.

Two Ohio State University psychology professors recently summarized a decade’s worth of research concluding that healthy older people can be trained to respond as quickly in some decision-making tasks as younger adults and children. In fact, their conclusions suggest that when older adults exhibit slower reactions to situations it may be due to a desire to be accurate rather than fast.

“Many people think that it is just natural for older people’s brains to slow down as they age, but we’re finding that isn’t always true,” said Roger Ratcliff, professor of psychology at Ohio State University. “At least in some situations, 70-year-olds may have response times similar to those of 25-year-olds.” Ratcliff’s studies, in collaboration with Gail McKoon, also a psychology professor at Ohio State and co-author, appear in December’s Child Development journal.

For almost 10 years, Ratcliff and his colleagues have studied cognitive processes and aging in their lab. Their work focused primarily on the elderly and young adults comparing cognitive responses. Only recently did they begin to include children in their research. Ratcliff said the results in children are what most scientists would expect: very young children have slower response times and poorer accuracy compared to adults and these improve as children mature.

The more interesting finding, however, is that older adults don’t always have slower brain processes compared to younger people, said McKoon.

“Older people don’t want to make any errors at all and that causes them to slow down. We found that it is difficult to get them out of that habit, but they can with practice,” McKoon said.

Ratcliff, McKoon and others who participated in the studies over the years conducted similar experiments in children, young adults, and the elderly. In one study, participants were seated in front of a computer screen. Asterisks appeared on the screen and the participants had to decide as quickly as possible whether there was a “small” number (31-50) or a “large” number (51-70) of asterisks. They pressed one of two keys on the keyboard, depending on their answer. In another experiment, participants were again seated in front of a computer screen and were shown a string of letters. They had to decide whether those letters represented a word in English or not. Some strings were easy and some were hard. In the child development study, the researchers used the asterisk test on second and third graders, fourth and fifth graders, ninth and tenth graders, and college-age adults. Third graders and college-age adults participated in the word/non-word test as well.

In another study published in the journal Cognitive Psychology, Ratcliff compared college-age subjects, adults aged 60–74, and others aged 75-90 using the asterisk and word/non-word tests. They found that there was little difference in accuracy among the groups, even the oldest of participants.

“For these simple tasks, decision-making speed and accuracy is intact even up to 85 and 90 years old,” McKoon said.

The findings don’t mean there aren’t effects of aging on decision-making speed and accuracy, however. In an article for the Journal of Experimental Psychology, Ratcliff, McKoon and another colleague found that accuracy for “associated memory” does decline as people age. For example, older people were much less likely to remember if they had studied a pair of words together than did younger adults.

Overall, Ratcliff and McKoon’s studies should provide optimism that the cognitive skills of seniors can remain intact and active throughout their later years.

“We’re finding that there isn’t a uniform decline in cognitive processes as people age,” Ratcliff said. “There are some things that older people do nearly as well as young people.”

Systemic Inflammation After Brain Injuries - A Potential Target for Concussion Treatments?

Who is going to see if something like this should be researched for strokes/TBIs?
Traumatic brain injury (TBI) induces an immune response that includes the release of inflammatory mediators (e.g., CCL20) and infiltration of white blood cells into the brain. The spleen is a reservoir of immune cells and plays an important role in systemic immune responses. Identifying specific inflammatory mediators involved in the progression of TBI pathology may help identify a key pathway for therapeutic interventions. Therefore, the purpose of this study was to examine the relationship between the brain’s response to TBI and the systematic immune reaction in a rat model of TBI. Thirty-three rats were concussed utilizing a lateral fluid percussion injury (the link provides video of how the injury was induced [includes surgical footage]). In control animals, the surgery was performed but the lateral fluid percussion injury was not induced. Some animals also had their spleens removed (splenectomy) at the time of the brain injury. One or 2 days after the concussion, the investigators evaluated the thymus, brain, and spleen (in animals where the spleen was not removed). These time points were chosen because they represent a key time during the secondary injury phase when therapuetic agents could block the secondary inflammatory process or promote repair mechanisms. Gene expression of inflammatory mediators (and their receptors) as well as tissue concentrations of CCL20 were evaluated in tissue samples from the spleens. The brain tissues were assessed for signs of degenerating neurons and cell death (apoptosis). The presence of CCL20 protein was also evaluated in the spleen, thymus, and brain tissue using microscopy. The authors found significant amounts of injured neurons within the cerebral cortex, hippocampus, and thalamus both 1 and 2 days after injury compared to the control animals (did not receive concussion injury). There were signs of cell death within the cortex (same side as the impact) and hippocampus at 1 day after the injury but not 2 days after injury compared to the control animals. CCL20 gene expression and protein concentrations were increased in the spleen and thymus 1 day after injury. In contrast, CCL20 was not detected in the brain until 2 days after the injury. Degeneration of neurons were seen in both splenectomy and non-splenectomy rats 1 and 2 days post injury but the splenectomy animals had less neuron degeneration than the animals who still had a spleen. Two days after the injury there were higher levels of CCL20 expression in the brain of animals that still had a spleen compared to splenectomy animals.

This study is important because it demonstrates that there is a systemic inflammatory response to some concussions that can promote secondary brain inflammation and promote neurodegeneration. When the spleen was removed in these animals it reduced the amount of neuron degeneration and the expression of inflammatory mediators in the brain. The authors state “The fact that CCL20 expression is elevated in the spleen and thymus prior to its appearance in the brain, and that brain CCL20 expression is decreased in splenectomised rats provide evidence that a peripheral CCL20 signal mediates the neuropathological response to TBI.” Further investigation are required to determine the mechanism by which CCL20 signals neuron death as well as the exact roles of the spleen and thymus contribute to neuron death. This also supports the idea that after concussions, like many other injuries, it may be important for us to find methods of reducing secondary phases of cell injury. Do you think having a therapeutic agent would change the return to play time of your athlete? Or, would it just assist in alleviating some of the potential secondary effects of a concussion?

Thursday, December 29, 2011

Vegans at Risk for Heart Attacks and Strokes

Maybe a contradiction for the fatty one here:
The vegan one here:

Doctors continue to remind us of the increased cardiovascular risk factors from eating red meat and other animal based products, and suggest we eat more vegetables to maintain good health. Environmentalists inform us how large production cattle ranches wreak havoc on the quality of our air and water, and urge us to go vegetarian. Animal rights activists protest the mistreatment of animals from dairy cows to egg laying chickens, in a concerted effort to promote total veganism.

With all of this anti-meat and animal rights campaigning, one might think eating animal products was just wrong, but new research suggests people who follow a vegan diet are at risk for developing blood clots and atherosclerosis, which are two conditions that can lead to a heart attack or stroke.

The vegan diet is completely free of any kind of animal products. That essentially means a vegan ingests absolutely nothing that comes from or is produced by an animal. Never are eggs, butter, sushi or chicken broth soup for the soul found on the diet list of a vegan. A diet of nuts, seeds and vegetables sounds like it could top the list of what is healthy to eat, yet this type of diet tends to be lacking in several important nutrients. Iron, zinc, vitamin B-12 and omega-3 fatty acids are difficult to acquire on a vegan diet, and these are key nutrients in helping to lower the risk of cardiovascular disease. In addition, a vegan diet is very low in fat and, as a result, these strict vegetarians tend to have higher levels of homocysteine and lower levels of HDL, the good cholesterol, both of which also contribute to the risk of heart disease.

All of these findings, which have appeared in the Journal of Agricultural and Food Chemistry, suggest that to maintain a healthy heart, vegans must at least increase their dietary consumption of omega-3 fatty acids and vitamin B-12. Good sources of these nutrients can be found in nuts, but are more prevalent in meat and oily types of fish like wild salmon and mackerel. While vitamin and mineral supplements do contain everything we need, health experts suggest it is best to derive nutrients from the source.

For most people of average health, eating a little meat and a lot of veggies makes sense. As for the environment, there are sustainable ways to raise fish, beef and pork without harming our precious natural resources. And for the animal rights activists, it is a seriously tough call. Your heart may break when you take that first bite of fish, but at least it will be healthy.

New Blood Test May Rule Out Heart Attacks More Quickly

Hey if they can do this for heart attacks something similar should be found for brain attacks.
A new test measuring levels of troponin I in the blood may help determine whether someone is really having a heart attack earlier than is currently possible.

Troponin I is a protein that is released into the bloodstream when the heart muscle has been damaged such as during a heart attack. The more damage there is to the heart, the more troponin there will be in the blood. Existing tests measure troponin T or troponin I. The new study looked at a highly sensitive type of troponin I test that may be more accurate in less time. The findings appear in the Dec. 28 issue of the Journal of the American Medical Association.

Wednesday, December 28, 2011

Fatty food and brain damage: Study finds connection

But what about this vegan study here:
The fatty one here:

Two new studies show that eating too much fatty food causes brain damage linked to obesity.

US scientists found a sudden change to a high-fat diet triggered inflammation in a key area of rodent brains responsible for regulating body weight. The inflammation produced distinctive scarring similar to that seen in stroke patients - and that brain scarring was then observed in humans who were overweight. While the research does not unequivocally prove brain damage caused by fatty food is linked to obesity, it provides strong indications for further research. More than a third of adults in the U.S. are obese and future exploration on this issue is thus necessary.

Michael Schwartz, who is the director of the University of Washington's Diabetes and Obesity Centre of Excellence said, “It would be unlikely you could injure that part of the brain and not affect the level of bodyweight, because that's what that area does...Fast foods are more likely to do this sort of damage.”

One study found that in the brains of both obese humans and obese rats, neurons around the hypothalamus were damaged by inflammation. High-fat diets have been known to promote inflammation throughout the body, but that usually takes weeks or months to appear. Changes in the brain, however, can happen fast—even within 24 hours.

The second study found that mice on a fatty diet were slow to replace old neurons in the hypothalamus, which could also hamper its function.

Most people have a natural equilibrium bodyweight, and although they can lose or gain kilos by adjusting their diet, their body will tend to return to its natural weight once those restrictions are removed. Thus, obesity is often less a problem of losing weight than of keeping it off. The brain area that regulates metabolism, the hypothalamus, relies on a hormone called leptin to measure the changes in body weight - and leptin is produced in fat. Hypothalamus is an almond-sized area of the brain helps regulate hunger and thirst, as well as sleep and body temperature.

“So you have a situation where if you have an inflammatory response in the hypothalamus you need more leptin to do the same job, and the only way to have more leptin is to have more fat,” Professor Schwartz said. The findings are published in The Journal of Clinical Investigation.

New Clues as to Why Some Older People May Be Losing Their Memory

At one point my doctors told me I must have had several small strokes since I had some small dead spots. I don't think I've lost any memory yet.

ST. PAUL, Minn. – New research links ‘silent strokes,’ or small spots of dead brain cells, found in about one out of four older adults to memory loss in the elderly.

The study is published in the January 3, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology.

“The new aspect of this study of memory loss in the elderly is that it examines silent strokes and hippocampal shrinkage simultaneously,” said study author Adam M. Brickman, PhD, of the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center in New York.

For the study, a group of 658 people ages 65 and older and free of dementia were given MRI brain scans. Participants also underwent tests that measured their memory, language, speed at processing information and visual perception. A total of 174 of the participants had silent strokes.

The study found people with silent strokes scored somewhat worse on memory tests than those without silent strokes. This was true whether or not people had a small hippocampus, which is the memory center of the brain.

“Given that conditions like Alzheimer’s disease are defined mainly by memory problems, our results may lead to further insight into what causes symptoms and the development of new interventions for prevention. Since silent strokes and the volume of the hippocampus appeared to be associated with memory loss separately in our study, our results also support stroke prevention as a means for staving off memory problems,” said Brickman.

The study was supported by the National Institutes of Health.

The American Academy of Neurology, an association of 24,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, brain injury, Parkinson’s disease and epilepsy. For more information about the American Academy of Neurology, visit

'It showed what I always knew - he was really in there': Stroke sufferer, 23, woken up by SLEEPING PILL

Wonder what else it would work on.


Ambien, also called Stilnox, is a prescription medicine used to treat insomnia by initiating sleep.

It contains Zolpidem, which studies have found increases blood flow in the brain, particularly in areas involved in language comprehension - allowing improved function.

Cure? When Sam began taking Ambien he was able to speak again. He now takes it four times a day

Studies into the connection between stroke rehabilitation and Ambien are ongoing.

John White at Moss Rehabilitation Center in Philadelphia is leading a study into the connection.

So far he has found that fewer than 10 per cent of stroke victims respond to the drug - and that Sam's case is extremely rare.

'We’re not able to yet advise families on how to use this drug clinically because the research is in the very early stages,' he told MSNBC.

Is Atherosclerosis an Allergic Disease?

Interesting premise.
That was the title of a recent commentary in Circulation Research by Christoph J. Binder, MD, PhD, and Joseph L. Witztum, MD, from the University of California, San Diego (Circ Res 2011;109:1103-04).

The two commentators were impressed by Wang et. al.'s research showing the involvement of immunoglobulin E (IgE), which plays an important role in allergic reactions, in promoting atherogenesis (J Clin Invest 2011;121:3564-3577).

IgE, in relation to allergic reactions, activates mast cells by binding to IgE's high-affinity receptor FcER1. In addition to allergic responses, mast cells participate in other inflammatory diseases, including atherosclerosis, Wang and colleagues wrote.

For their study, Wang et. al. analyzed serum IgE levels in two separate Chinese populations and found them elevated in patients with myocardial infarction and unstable angina.

Those with acute MIs had the highest levels of IgE, followed by those with unstable angina, and then those with stable angina. In other words, the circulating levels of IgE correlated with plaque instability, Wang and colleagues wrote.

In addition, the investigators found IgE and FcER1 in human atherosclerotic lesions, mostly localized in macrophage-rich areas.

Prior studies had found that people with common allergic diseases such as asthma and allergic rhinitis were more prone to develop atherosclerosis (Arch Intern Med 2005;165:2521-6), suggesting a link.

But such detailed association of IgE with atherosclerosis had not been seen before, Wang et. al. said.

And what it means is not entirely clear, Binder and Witztum wrote in their commentary.

Nevertheless, "the evidence continues to accumulate supporting an important role for immunological mechanisms in all phases of atherosclerosis," the commentators said.

There is a host of "combinatorial groupings" involving IgE and other receptors that contribute to the "pro-atherogenic activity of IgE in humans," including macrophage activation and apoptosis, Binder and Witztum said.

But they focused on the fact that elevated IgE levels typically reflect allergic-type immune responses.

"It would be of great interest to know whether the increased IgE levels were polyclonal or reflected any disease-specific antigens, such as those to oxidation-specific epitopes characterized for IgG and IgM isotypes in humans and murine models of atherosclerosis."

A problem with the current study is that the levels of IgE were low overall. Also, it is unclear whether the IgE levels were a cause or product of the heart disease.

However, the evidence of IgE in atherosclerotic lesions and in serum from patients with unstable plaque "support the notion that such 'minor' immunoglobulin molecules may participate in the activation not only of mast cells, but also other blood-borne inflammatory cells ... during the pathogenesis of human atherosclerosis," Wang and colleagues concluded.

Tuesday, December 27, 2011

Sea snails help scientists explore a possible way to enhance memory

Seems bizarre but anything to help us survivors.

Efforts to help people with learning impairments are being aided by a species of sea snail known as Aplysia californica. The mollusk, which is used by researchers to study the brain, has much in common with other species including humans. Research involving the snail has contributed to the understanding of learning and memory. At The University of Texas Health Science Center at Houston (UTHealth), neuroscientists used this animal model to test an innovative learning strategy designed to help improve the brain's memory and the results were encouraging. It could ultimately benefit people who have impairments resulting from aging, stroke, traumatic brain injury or congenital cognitive impairments.

The proof-of-principle study was published on the Nature Neuroscience website on Dec. 25. The next steps in the research may involve tests in other animal models and eventually humans.

The strategy was used to identify times when the brain was primed for learning, which in turn facilitated the scheduling of learning sessions during these peak periods. The result was a significant increase in memory.

"We found that memory could be enhanced appreciably," said John H. "Jack" Byrne, Ph.D., senior author and chair of the Department of Neurobiology and Anatomy at the UTHealth Medical School.

Building on earlier research that identified proteins linked to memory, the UTHealth investigators created a mathematical model that tells researchers when the timing of the activity of these proteins is aligned for the best learning experience.

Right now, the scheduling of learning sessions is based on trial and error and is somewhat arbitrary. If the model proves effective in follow-up studies, it could be used to identify those periods when learning potential is highest.

"When you give a training session, you are starting several different chemical reactions. If you give another session, you get additional effects. The idea is to get the sessions in sync," Byrne said. "We have developed a way to adjust the training sessions so they are tuned to the dynamics of the biochemical processes."

Two groups of snails received five learning sessions. One group received learning sessions at irregular intervals as predicted by a mathematical model. Another group received training sessions in regular 20-minute intervals.

Five days after the learning sessions were completed, a significant increase in memory was detected in the group that was trained with a schedule predicted by a computer. But, no increase was detected in the group with the regular 20-minute intervals.

The computer sorted through 10,000 different permutations in order to determine a schedule that would enhance memory.

To confirm their findings, researchers analyzed nerve cells in the brain of snails and found greater activity in the ones receiving the enhanced training schedule, said Byrne, the June and Virgil Waggoner Chair of Neurobiology and Anatomy at UTHealth.

"This study shows the feasibility of using computational methods to assist in the design of training schedules that enhance memory," Byrne said.

Other contributors from the UTHealth Department of Neurobiology and Anatomy include lead authors Yili Zhang, Ph.D., research fellow, and Rong-Yu Liu, Ph.D., senior research scientist, as well as George A. Heberton, medical student; Paul Smolen, Ph.D., assistant professor; Douglas A. Baxter, Ph.D., professor; and Len Cleary, Ph.D., professor.

The study, which is titled "Computational Design of Enhanced Learning Protocols," received support from the National Institutes of Health and the Keck Center National Library of Medicine Training Program in Biomedical Informatics of the Gulf Coast Consortia.

Monday, December 26, 2011

Lab-grown glands, eyes and brain parts

Blogger Mo Costandi helps me understand a lot of the neurogenesis/stem cell work done by research labs.
This one has some great ideas needing followup.
A selected paragraph:
Growing a complete, functioning brain is unfeasible, but there is real potential in growing functional neural tissue containing specific types of cells, for transplantation into the human brain. This is one avenue of research that the team are investigating. Last year, they showed that ES cells can be coaxed to differentiate into functional cerebellar Purkinje cells, which integrate themselves into the brain when transplanted into mouse foetuses.

Young blood rejuvenates old brains

The ageing systemic milieu negatively regulates neurogenesis and cognitive function

The scientific post here:

The science blogger writing about it here:

This paragraph was fascinating;

These results suggest that chemicals found in the blood of old mice inhibit the generation of new brain cells, whereas chemicals in the blood of young mice promote it. The researchers then injected blood from young or old mice into young adults. Again, they found that animals injected with old blood had far fewer newborn neurons in the hippocampus than those injected with young blood, confirming that old blood contains soluble factors that inhibit neurogenesis.

Must read stroke book

I just finished reading My Last Degree: A Therapist Goes Home After a Stroke by Rebecca Dutton She is an instructional OT so she has wonderful insights into how to plan your recovery. She also blogs at and posts pictures to describe what she is doing as part of her therapy.
If you really want to get into understanding how therapists think you should read her other book; Clinical Reasoning in Physical Disabilities.
Good stuff for all us survivors. We need more writers, so get out there and write your opus.
Not really sorry Rebecca, your stuff needed more exposure. And you weren't telling us about it.

Improved Understanding Of The Thalamus Offers Potential Stroke Therapy

At least these researchers are thinking about how to help recovery.
The thalamus is the central translator in the brain: Specialized nerve cells (neurons) receive information from the sensory organs, process it, and transmit it deep into the brain. Researchers from the Institute of Toxicology and Genetics (ITG) of KIT have now identified the genetic factors Lhx2 and Lhx9 responsible for the development of these neurons. Their results contribute to understanding the development of the thalamus. In the long term, they are to help healing thalamic strokes.

With 100 billion nerve cells, the brain is the most complex organ in the human body. "We want to understand the development program behind," says Dr. Steffen Scholpp from the ITG. "We want to find out how individual parts of the brain develop, this means, what makes precursor cells build a specialized area such as the thalamus." Scholpp's group at ITG studies the development of the thalamus. "It is the central interface between the brain and the outer world: Everything that is perceived via eyes, ears or the tactile sense has to pass the thalamus before it is routed to the cerebral cortex for further processing."

In the long term, the scientists want to be able to heal damaged brain parts by a tissue replacement therapy. If, for example, brain tissue is damaged after an infarct, the body is not able to regenerate this tissue. "Today, stroke is the most frequent cause of disability acquired at adult age and due to its central role, damage of the thalamus is very serious," emphasizes Steffen Scholpp. "For this reason, we have to find a strategy to activate stem cells such that the damaged tissue can be replaced." Recently, an important step was made by the scientists: By studying zebrafish, they identified Lhx2 and Lhx9, the factors controlling the development of neurons in the thalamus. "Without these factors, the thalamus would accommodate undifferentiated nerve cells only - this means, the precursory cells lack the information required for specialization," explains the biologist. Analysis of brain development in zebrafish allows conclusions to be drawn with respect to the development in all vertebrates, including human. The results of the group are published in the current issue of the PLoS Biology journal.

In the same study, Scholpp and his team identified another factor that acts as "adhesive" in the thalamus: The cell adhesion molecule Pcdh10b ensures development of the thalamus without mixing with the surrounding brain areas. If this factor is lacking, the neurons differentiate, but do not find their target destination. It is now the objective of the researchers to activate these factors in the cultivating dish (in vitro) in undifferentiated cells first for new thalamus tissue to form. In close cooperation with engineers, the biologists are already developing 2-dimensional cell culture systems. In January, they will start a 3D cell cultivation project. "KIT offers excellent opportunities: Parallel to our research, materials researchers work on the development of various biomaterials (biopolymers) which will be tested in the cultivation experiments", says Scholpp.

Dr. Steffen Scholpp thinks that it will be possible to heal stroke patients in the future. "Of course, this will take some years. But it is our ultimate goal to take out quiescent stem cells from a stroke patient and to switch on the specific development biology program in these cells outside of the body. Finally, we plan to bring them back to the position of the damaged tissue. This would be real healing."

Sunday, December 25, 2011

Fast recovery vs. slow rehab

What I wish doctors and researchers would acknowledge is that tPA doesn't work very well. I saw a 32% efficacy in the 3 hour period and 16% efficacy in the 3-4.5 hour period. And besides it doesn't stop the cascade of neuronal death from glutamate poisoning, excitotoxicity and the closed capillaries due to pericytes. My doctor told me I didn't get the fast recovery, I would have to hold out for the slow rehab recovery, and I got it within 90 minutes. In general there is little that can't be massively improved in stroke research and rehabilitation. But first you have to admit that there are problems and try to solve them rather than sticking your head in the sand and saying the solution is to blame the public for not eating and exercising correctly, thus the public is not preventing their own stroke. Someday I'll rant about this in Deans' Stroke Manifesto.
I had to be informed several times during bowling on Friday that I needed to be quiet and bowl. (143,158,105)

Saturday, December 24, 2011

A Signaling Cascade of Nuclear Calcium-CREB-ATF3 Activated by Synaptic NMDA That Protects against Extrasynaptic NMDA Receptor Neuronal Cell Death

This is quite a handful. Followed a calcium tracing book to here.

A Signaling Cascade of Nuclear Calcium-CREB-ATF3 Activated by Synaptic NMDA Receptors Defines a Gene Repression Module That Protects against Extrasynaptic NMDA Receptor-Induced Neuronal Cell Death and Ischemic Brain Damage


Synapse-to-nucleus signaling triggered by synaptic NMDA receptors can lead to the buildup of a neuroprotective shield. Nuclear calcium activating the cAMP response element binding protein (CREB) plays a key role in neuroprotection acquired by synaptic activity. Here we show that in mouse hippocampal neurons, the transcription factor Atf3 (activating transcription factor 3) is a direct target of CREB. Induction of ATF3 expression by CREB in hippocampal neurons was initiated by calcium entry through synaptic NMDA receptors and required nuclear calcium transients and calcium/calmodulin-dependent protein kinase IV activity. Acting as a transcriptional repressor, ATF3 protects cultured hippocampal neurons from apoptosis and extrasynaptic NMDA receptor-induced cell death triggered by bath application of NMDA or oxygen–glucose deprivation. Expression of ATF3 in vivo using stereotaxic delivery of recombinant adeno-associated virus reduces brain damage following a cerebral ischemic insult in mice. Conversion of ATF3 to a transcriptional activator transforms ATF3 into a potent prodeath protein that kills neurons in cell culture and, when expressed in vivo in the hippocampus, ablates the neuronal cell layer. These results link nuclear calcium-CREB signaling to an ATF3-mediated neuroprotective gene repression program, indicating that activity-dependent shutoff of genes is an important process for survival. ATF3 supplementation may counteract age- and disease-related neuronal cell loss caused by a reduction in synaptic activity, malfunctioning of calcium signaling toward and within the nucleus (“nuclear calciopathy”), or increases in death signaling by extrasynaptic NMDA receptors.


The well-being of neurons in the mammalian CNS is dependent on the balance of the activities of the survival-promoting synaptic NMDA receptor and the extrasynaptic NMDA receptor that induces cell death pathways (Hardingham et al., 2002; Hardingham and Bading, 2010). Important for the acquisition of a long-lasting neuroprotective shield following calcium entry through synaptic NMDA receptors is the propagation of calcium signals into the nucleus, the subsequent formation of a nuclear calcium/calmodulin complex, and the initiation of a genomic response (Bading, 2000, Hardingham et al., 2001; 2002; Lee et al., 2005; Papadia et al., 2005; Zhang et al., 2007; 2009; Bengtson et al., 2010). Nuclear calcium is one of the most potent activators of neuronal gene expression and controls a large gene pool that includes a gene program for acquired neuroprotection (Zhang et al., 2009). The transcription factor cAMP response element binding protein (CREB), a key target of nuclear calcium signaling (Hardingham et al., 1997; 2001; Chawla et al., 1998; Zhang et al., 2009), plays an important role in neuronal survival (Mantamadiotis et al., 2002). However, CREB is a multifunctional transcriptional regulator (Mayr and Montminy, 2001; Carlezon et al., 2005) that is also involved in a number of other processes including neuronal plasticity, addiction, neurogenesis, learning, and memory (Carlezon et al., 1998; Silva et al., 1998; Lonze and Ginty, 2002; Zhu et al., 2004; Giachino et al., 2005). CREB signaling may control multiple processes through the activation of target genes, which themselves may encode transcription factors and regulate function-specific genomic subroutines. The concept of a hierarchical transcription factor cascade that starts with a master regulator and branches off to other DNA binding proteins that serve a specific function is not new and has been implemented to control biological processes such as the specification of the body plan and pattern formation in embryonic development (Anderson, 1999; Pearson et al., 2005; Peel et al., 2005; Dequéant and Pourquié, 2008). In this study, we show that the transcriptional repressor ATF3 acts downstream of CREB to mediate the survival function. ATF3 is a direct CREB target that can protect neurons both in vitro and in vivo from death induced by stimulation of extrasynaptic NMDA receptors. CREB-ATF3 signaling, which is controlled by synaptic NMDA receptors and nuclear calcium, represents the core of an activity-regulated survival module that involves the sequential activation of transcriptional induction and gene repression.

Effects of menthol on the triggering of the swallowing reflex in elderly patients with dysphagia

Not sure I'd like the injection into the pharynx. I looked into this from a comment in the book; The design of experiments in neuroscience by Mary Harrington

Friday, December 23, 2011

JAMA Commentary Contends Vitamin Therapy Can Still Reduce Stroke

Ok, lets quit arguing and come to a consensus, lives are at stake.
A commentary by Dr. David Spence of The University of Western Ontario and Dr. Meir Stampfer of the Harvard School of Public Health in today's Journal of the American Medical Association (JAMA) argues that vitamin therapy still has a role to play in reducing stroke.

Vitamin B therapy was once widely used to lower homocysteine levels. Too much of this amino acid in the bloodstream was linked to increased risk of stroke and heart attack. But several randomized trials found lowering homocysteine levels with B vitamins did not result in a cardiovascular benefit. And a study by Dr. Spence, a scientist with the Robarts Research Institute at Western's Schulich School of Medicine & Dentistry, found Vitamin B therapy actually increased cardiovascular risk in patients with diabetic nephropathy.

Dr. Spence says this commentary provides insights that overturn the widespread belief that "homocysteine is dead." He says two key issues have been overlooked in the interpretation of the clinical trials: the key role of vitamin B12, and the newly recognized role of renal failure.

"It is now clear that the large trials showing no benefit of vitamin therapy obscured the benefit of vitamin therapy because they lumped together patients with renal failure and those with good renal function. The vitamins are harmful in renal failure, and beneficial in patients with good renal function, and they cancel each other out," says Dr. Spence, the author of "How to Prevent Your Stroke." The authors also contend most of the trials did not use a high enough dose of vitamin B12.

spnKiX motorized shoes edge closer to production

I know this is quite out there since if you can't walk its unlikely you'd be able to safely balance on these. But anything is possible. Reminds me of the time I brought rollerblades to a PT session.

Peter Treadway's battery-powered motorized shoes - which we first spied as a concept in mid-2010 - are edging closer to production. Called spnKiX, these electric roller-skates have gone through more than thirty prototypes over a five year period to reach the final design and if all goes to plan they will hit the pavement in March 2012.

spnKiX feature a frame made of fiber reinforced nylon that the rider straps on while still wearing their normal shoes. Each "shoe" contains all the electronic parts - there's one in wheel motor and one battery pack for each foot. Gliding is controlled via a wireless handheld remote contro that comes with a simple switch to adjust the speed. There's also a little reflector located on the back of each shoe for safety.

Unless your workplace is close by, the shoes are unlikely to become your new commuting option though. The rechargeable lithium battery is good for only 2-3 miles ride and it takes 2-3 hours to recharge it. The maximum speed is quite impressive (and possibly even a little scary in some situations) at 10 mph. The maker recommends that the rider should be at least sixteen, weighing no more than 180lbs (81kg).

The spnKiX motorized shoes can be pre-ordered for the price of US$375 (the future retail price will be US$649). The first batch of 100 units is slated to be shipped by early March 2012, but this depends on whether the company gathers backing of US$25,000 at the time of writing the project has raised $13,000 with 42 days remaining to reach its goal.

Treadway gives us an insight into the inspiration behind spnKiX in the following video.