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:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, February 28, 2013

Tech titans create $3 million 'Breakthrough Prize' for scientists

If we had a Great stroke association they would be pushing their scientists to win these types of prizes. 
http://www.cnn.com/2013/02/20/tech/innovation/zuckerberg-brin-breakthrough-prize/index.html?

Ireland - Stroke services - 'lots done, more to do'

Another indication that they are just improving the status quo, not even thinking about these fourteen objective diagnosis of ischemic vs. hemorrhagic strokes. And no talk about various hyperacute therapies that might stop the neuronal cascade of death.
You Irish readers will need to agressively challenge these ideas. This is way too important to leave it to the stroke medical world, especially when they don't even seem to be up-to-date.  It's your imperative to get this done.
http://www.irishhealth.com/article.html?id=21671

The Shirky Principle as applied to stroke

My head explodes how this precisely describes trying to get the stroke medical world to examine itself.
The Japanese version;
シャーキーの法則  The Shirky Principle

「組織は自分自身がその解決策となるべき問題を維持しようとする。」―― クレイ・シャーキー

こ の意見はすばらしいと思う。これを見て、私は明解なピーターの法則を思い出した。それは、組織にいる人間はその人が無能になる段階まで昇進する、というも のである。その段階になると、その人は過去の業績のおかげで解雇されることはないが、それ以上昇進できなくなって、その無能な状態で滞留する。
"Institutions will try to preserve the problem to which they are the solution." -- Clay Shirky
I think this observation is brilliant. It reminds me of the clarity of the Peter Principle, which says that a person in an organization will be promoted to the level of their incompetence. At which point their past achievements will prevent them from being fired, but their incompetence at this new level will prevent them from being promoted again, so they stagnate in their incompetence.
The Shirky Principle declares that complex solutions (like a company, or an industry) can become so dedicated to the problem they are the solution to, that often they inadvertently perpetuate the problem.
http://www.kk.org/thetechnium/archives/2010/04/the_shirky_prin.php
Ask your doctor how they are not part of the problem. I want reports of exploding heads.
This matches to my earlier post about the non-plasticity of doctors.

Do doctors exhibit plasticity?

Neutrophils Usher Monocytes Into Sites of Inflammation

Our researchers need to understand this if we truly want to prevent strokes and clean up after the damage.
http://circres.ahajournals.org/content/112/5/744.extract.html?etoc
One of the key processes of inflammation is the transmigration of circulating leukocytes across the endothelium. Among the leukocytes, neutrophils and monocytes are large phagocytes that can respond quickly to infection or injury. On sensing danger, neutrophils and monocytes adhere to the endothelium and transmigrate to the adjacent tissue via the coordinated activities of adhesion molecules, integrins, cytokines, and chemokines.1 Once they accumulate, these myeloid cells participate in a myriad of immune inflammatory activities. The importance of this event cannot be understated, especially because the accumulation of leukocytes in tissue is a double-edged sword. On the one hand, coordinated leukocyte accumulation in injured or infected sites is required for effective pathogen elimination and tissue healing. On the other hand, uncontrolled accumulation is a defining feature of chronic diseases, such as atherosclerosis.2 Understanding leukocyte migration is essential to understanding the immune system.
Article, see p 792
Neutrophils and monocytes do not accumulate all at once. In a typical acute inflammatory response, there is a well-defined sequence: neutrophils accumulate first; monocytes accumulate second. Among the monocytes, of which ≥2 subsets circulate in the mouse and human, there is yet another sequence: inflammatory murine Ly-6Chigh monocytes accumulate first and reparative Ly-6Clow monocytes accumulate second.3 This temporal (neutrophil ––> Ly-6Chigh monocyte ––> Ly-6Clow monocyte) hierarchy of accumulation is likely required for an effective innate response. The subsets, which have overlapping but also specialized functions, contribute sequentially to processes that involve pathogen elimination, efferocytosis, restoration of tissue integrity,
Full text at link

IBM's Watson Does Drug Discovery?

Based on this article and the following blog writeup.
http://www.nytimes.com/2013/02/28/technology/ibm-exploring-new-feats-for-watson.html?hp&_r=2&pagewanted=all&

http://pipeline.corante.com/archives/2013/02/28/ibms_watson_does_drug_discovery.php
A Great stroke association would take the 1000+ failed hyperacute drugs and the animal model possibilities and have Dr. Watson come up with which way to go next. That Great stroke association would already have all this data available because researchers would be looking at it all the time.

5 Most Surprising Reasons to Drink Coffee

Have at it. I'm doing this a lot.
http://www.caring.com/articles/5-best-reasons-to-drink-coffee?utm_medium=email&utm_source=suggests&utm_content=20130228
Full content at link.

1. Coffee Slashes Your Risk of Developing Type 2 Diabetes

2. Coffee Can Counter Cancerous Cell Damage

3. Coffee May Lower Your Risk of Dementia

4. Coffee Protects Against Parkinson's Disease

5. Coffee May Buffer Depression



Blocked Heart Arteries May Be Key Risk Factor for Stroke

You might want to talk to your doctor about calcification.
http://www.doctorslounge.com/index.php/news/hd/36102
People with arterial clogs caused by what's known as coronary artery calcification -- calcium deposits in the artery -- are at higher risk for stroke, even if they're otherwise considered to have a low risk, the German researchers found.
The findings are published Feb. 28 in the journal Stroke.
"Stroke risk is tightly aligned with coronary atherosclerosis [hardening of the arteries], showing the closely related nature of cardiovascular and cerebrovascular [brain blood flow] disease," lead investigator Dr. Dirk Hermann, a professor of vascular neurology and dementia at the University Hospital Essen, said in a journal news release.

More at link

Wednesday, February 27, 2013

New Journal: Fatigue: Biomedicine, Health and Behavior

Your doctor is going to have to subscribe to this journal. With a substantial percentage of stroke patients having fatigue, maybe someone will determine why it occurs after stroke. A Great stroke association would solve this.
You do expect your doctor to solve your fatigue? Don't you?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=128849&CultureCode=en
With peer-reviewed articles on fatigue having increased 90% over the past decade ­– and nearly 1,000 papers on the topic published in 2011 alone ­– the time is right for Routledge’s new journal, Fatigue: Biomedicine, Health & Behavior.
Sponsored by the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFS/ME) and supported by a distinguished multidisciplinary editorial board of international scientists and clinicians, Fatigue is the first biomedical and behavioral journal focused on fatigue. Editor Fred Friedberg says, ‘We believe that high-quality contributions in the area of fatigue are more likely to be submitted to a journal that clearly recognizes the importance of fatigue as a field of scientific study as well as an important clinical concern.’
The aim of the new journal is to address the symptom of fatigue in medical illnesses, behavioral disorders and specific environmental conditions. These three broad domains are intended to advance interdisciplinary research on causation, pathophysiology, assessment and treatment.
Topics covered by the journal include: fatigue in diseases such as cancer, autoimmune diseases, multiple sclerosis (MS), pain conditions, mood disorders and circulatory diseases. Friedberg and his editorial board will also consider papers on chronic fatigue syndrome (CFS/ME), fibromyalgia, fatigue in sleep, aging, exercise, sport and occupations. As Friedberg notes, ‘More generally Fatigue will publish on the biology, physiology and psychosocial aspects of fatigue as well as assessment and treatment.’
Fatigue will also target both science and practice. Fatigue science focuses on the study of acute and chronic fatigue states in healthy and ill populations. Fatigue practice refers to clinicians, largely physicians, psychologists, physical and occupational therapists and nurses who diagnose, evaluate, treat and provide clinical care for patients with a wide range of fatiguing illnesses and conditions.
The inaugural issue of Fatigue has just been published, and has already attracted attention on Internet fora. In addition to overviews of the subject and the state of current research, the issue includes papers on topics as far-ranging as energy-conservation interventions for patients with CFS/ME, fatigue and circadian-activity rhythms in breast-cancer patients, fatigue and related issues in women with (and without) fibromyalgia, fatigue management in the workplace and fatigue in US railroad workers in safety-sensitive positions.
Fatigue will be published quarterly, in online and hard-copy versions. Significantly, there are no submission fees for authors, who are encouraged to submit original research papers, literature reviews, data-based theoretical papers, short reports, qualitative studies, innovative case studies, expert interactive commentary and letters to the editor.
The next issue of this ground-breaking and timely journal from Routledge and the IACFS/ME will be published in June 2013.

Major Depression Does Respond to 'Minor' Tools

You may need your doctor to push back against this idea for stroke patients.
We need the real thing, accept no substitutes.
Look at the recovery benefits of actual drug prescription first.
http://www.medpagetoday.com/Psychiatry/Depression/37557?
Patients with more severe depression gain as much clinical benefit from low-intensity interventions, such as self-help books and websites, as those with less severe depression, researchers found.
In a meta-analysis, patients who were more severely depressed at baseline had larger treatment effects with low-intensity interventions than those who were less depressed (coefficient -0.1, 95% CI -0.19 to -0.002), reported Peter Bower, PhD, of the University of Manchester in England, and colleagues online in BMJ.
They cautioned, however, that the magnitude of the interaction was small and may not be clinically significant. Still, it is possible that patients with "more severe depression can be offered low-intensity interventions as part of a stepped-care model."
Rest at the link.

The Science Behind Coffee and Why it’s Actually Good for Your Health

Thanks to Billy for pointing this one out. I'm using it for Alzheimers and because I need it to combat my fatigue.
http://lifehacker.com/5986506/the-science-behind-coffee-and-why-its-actually-good-for-your-health

Sweet news for stem cell’s ‘Holy Grail’

In 30 years if we have a Great stroke association pushing this line of research we might have some useful therapy for strokies.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=128826&CultureCode=en
Scientists have used sugar-coated scaffolding to move a step closer to the routine use of stem cells in the clinic and unlock their huge potential to cure diseases from Alzheimer’s to diabetes.
Stem cells have the unique ability to turn into any type of human cell, opening up all sorts of therapeutic possibilities for some of the world’s incurable diseases and conditions. The problem facing scientists is how to encourage stem cells to turn into the particular type of cell required to treat a specific disease.
But researchers at the University of Manchester’s School of Materials and Faculty of Life Sciences have developed a web-like scaffold, coated with long-sugar molecules, that enhances stem-cell cultures to do just this. The scaffold is formed by a process known as ‘electrospinning’, creating a mesh of fibres that mimic structures that occur naturally within the body.
The team’s results – presented in the Journal of Biological Chemistry - are particularly promising, as the sugar molecules are presented on the surface of the fibres, retaining structural patterns important in their function. The sugars are also ‘read’ by the stem cells grown on the surface, stimulating and enhancing the formation of neuronal cell types.
Lead author Dr Catherine Merry, from Manchester’s Stem Cell Glycobiology group, said: “These meshes have been modified with long, linear sugar molecules, which we have previously shown play a fundamental role in regulating the behaviour of stem cells. By combining the sugar molecules with the fibre web, we hoped to use both biochemical and structural signals to guide the behaviour of stem cells, in a similar way to that used naturally by the body. This is the Holy Grail of research into developing new therapeutics using stem cell technology.”
The group anticipate that the combination of the sugar molecules with the fibre web will aid both the growth of stem cells and the formation of different cell types from the stem cell population.
Possible applications include tissue engineering, where the meshes could support cells differentiating to form bone, liver or blood vessels, for example.  The meshes also have potential therapeutic implications in the treatment of diseases such as multiple osteochondroma (MO), a rare disease creating bony spurs or lumps caused by abnormal production of these sugar molecules.
Co-author Professor Tony Day, from Manchester’s Wellcome Trust Centre for Cell-Matrix Research, said: "This cross-faculty collaboration provides exciting new possibilities for how we might harness the adhesive interactions of extracellular matrix to manipulate stem cell behaviour and realise their full therapeutic potential."
The study was funded by the Medical Research Council and Engineering and Physical Sciences Research Council Human Frontiers Scientific Programme.

Biting back - snake venom contains toxic clotting factors

Note that it also contains anti-clotting factors, maybe it can become as useful as vampire bats. Your researcher needs to look into applications for stroke.
Research article here:
http://www.jvat.org/content/19/1/3
Writeup here:
http://www.alphagalileo.org/ViewItem.aspx?ItemId=128792&CultureCode=en
The powerful venom of the saw-scaled viper Echis carinatus contains both anticoagulants and coagulants finds a study published in the launch edition of BioMed Central’s open access journal Journal of Venomous Animals and Toxins including Tropical Diseases (JVATiTD). These may be a source of potent drugs to treat human disease.

The saw-scaled viper family Echis, responsible for most snake attacks on humans, are recognizable by the ‘sizzling’ noise they make, produced by rubbing together special serrated scales, when threatened. Echis venom causes coagulopathy, which can result in symptoms ranging from lack of blood clotting, hemorrhage, renal failure and stroke. 

Researchers from the Razi Vaccine and Serum Research Institute, Iran led by Hossein Zolfagharian noted that treating plasma with venom from  Echis carinatus actually causes it to coagulate. Splitting the venom by ion exchange chromatography showed that then venom contained both coagulants and anticoagulants. The clotting factors alone were toxic to mice.

The diametric effects of snake venom on blood are of interest because of medical applications, and although snakes can be considered as dangerous to humans – they may yet save lives.

In the auspicious Year of the Snake, BioMed Central, the open access publisher, is pleased to announce that the  Journal of Venomous Animals and Toxins including Tropical Diseases (JVATiTD), the official academic journal of the The Center for the Study of Venoms and Venomous Animals (CEVAP) of São Paulo State University (UNESP), based in Brazil, has moved to BioMed Central's open access publishing platform. Also this journal marks growth of BioMed Central’s portfolio of open access journals to 250. 

Along with research into snakes JVATiTD publishes studies into all aspects of toxins, venomous animals, and their derivative products, as well as tropical diseases especially infectious diseases, parasites and immunology.

Muscle, skin and gastrointestinal problems cause a quarter of patients with heart disease and strokes to stop treatment in HPS2-THRIVE trial

I was in the earlier trial - (AIM-HIGH) study  - that just had the niacin, no flushing blocker, I quit the trial I was in because of the exacerbation of existing excema I had on my leg. I was scratching at it until it bled.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=128784&CultureCode=en
The largest randomised study of the vitamin niacin in patients with occlusive arterial disease (narrowing of the arteries) has shown a significant increase in adverse side-effects when it is combined with statin treatment.
Results from the HPS2-THRIVE study (Heart Protection Study 2 – Treatment of HDL to Reduce the Incidence of Vascular Events), including the reasons patients stopped the study treatment, are published online today (Wednesday) in the European Heart Journal [1].
Niacin has been used for decades to help increase levels of “good” HDL cholesterol and to decrease levels of “bad” LDL cholesterol and triglycerides (fats) in the blood in people at risk of cardiovascular problems such as heart disease and stroke. However, it has a number of side-effects including flushing of the skin. Another drug, laropiprant, can reduce the incidence of flushing by blocking the prostaglandin D2 receptor that is involved in the process. Therefore, the HPS2-THRIVE study investigated whether combining extended-release niacin with laropiprant (ERN/LRPT), given in addition to an LDL cholesterol-lowering statin, simvastatin, could reduce the risk of cardiovascular problems in people at high risk due to existing occlusive arterial disease.
A total of 25,673 patients from China, the UK and Scandinavia were randomised between April 2007 and July 2010 to receive either 2g of extended release niacin plus 40 mg of laropiprant or matching placebo. In addition, all participants received intensive LDL cholesterol-lowering therapy with simvastatin (with or without ezetimibe). Researchers from the Clinical Trial Service Unit & Epidemiological Studies Unit (CTSU) at the University of Oxford (UK), who were responsible for designing and conducting the trial and analysing the results, followed the patients for an average of 3.9 years.
By the end of the study, 25% of patients taking ERN/LRPT had stopped their treatment, compared with 17% of patients taking placebo.
Jane Armitage, Professor of Clinical Trials and Epidemiology & Honorary Consultant in Public Health Medicine at the CTSU, said: “The main reason for patients stopping the treatment was because of adverse side-effects, such as itching, rashes, flushing, indigestion, diarrhoea, diabetes and muscle problems. We found that patients allocated to the experimental treatment were four times more likely to stop for skin-related reasons, and twice as likely to stop because of gastrointestinal problems or diabetes-related problems.
“We found that, in the trial as a whole, participants in the experimental arm had a more than four-fold increased risk of myopathy (muscle pain or weakness with evidence of muscle damage) compared with the placebo group. This is highly significant. It appeared that this effect was about three times greater among participants in China than those in Europe, for reasons that are not clear. In the placebo arm (i.e. those on statin-based treatment alone), the statin-related myopathy was more common among participants in China than those in Europe. Therefore – in combination with the greater effect of ERN/LRPT on myopathy in China – the excess number of cases of myopathy caused by ERN/LRPT (though low in both regions) was over ten times greater among participants in China than those in Europe (0.53 percent per year compared to 0.03 percent per year).”
Dr Richard Haynes, Clinical Coordinator at the CTSU, said: “This is the largest randomised trial of extended release niacin treatment and it provides uniquely reliable results on adverse side-effects and the ability of patients to tolerate them. Although 25 percent of patients stopped the treatment early, 75 percent continued on it for approximately four years. Currently, we are analysing the final data on the cardiovascular outcomes from the trial, and once we have these we will know whether or not the benefits of the treatment outweigh the myopathy, skin and gastrointestinal problems.”
The researchers will be presenting full results on the cardiovascular outcomes at the annual meeting of the American College of Cardiology in March and these will be published in another paper afterwards [2].
The co-principal investigator of the study, Dr Martin Landray, Reader in Epidemiology and Honorary Consultant Physician at the CTSU, said: “Previous research had suggested that improving cholesterol levels in high-risk patients might translate into a 10-15 percent reduction in major vascular events such as heart attacks and strokes. In the HPS2-THRIVE study, 3,400 of the 25,673 participants suffered a major vascular event over an average of four years of follow-up. This means the study has excellent statistical power to discover the effectiveness or otherwise of the treatment.”
In an accompanying editorial [3], Professor Ulf Landmesser, of the University Hospital Zurich (Switzerland), points out that although the study showed an increase in myopathy, it also showed that the ERN/LRPT substantially lowered LDL cholesterol and triglycerides by nearly 20%. He writes that these observations “raise important questions as to why niacin/laropiprant did not reduce major cardiovascular events”, and he wonders whether laropiprant “is really biologically inert with respect to atherosclerosis and thrombosis”.
He concludes that “niacin has failed as a valuable ‘partner’ of statin therapy in lipid-targeted approaches to further reduce major cardiovascular events in high-risk patients”. He continues: “At present, statin therapy has been clearly shown to reduce vascular events effectively and is reasonable well tolerated in most patients. We will still have to wait for the results of … ongoing studies to see whether another lipid-targeted intervention can further reduce vascular events in addition to statin therapy.”

Notes:
[1] “HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle, and liver outcomes and reasons for stopping study treatment”, by Richard Haynes, Lixin Jiang, Jemma C. Hopewell, Jing Li, Fang Chen, Sarah Parish, Martin J. Landray, Rory Collins, and Jane Armitage, The HPS2-THRIVE Collaborative Group. European Heart Journal. doi:10.1093/eurheartj/eht055
[2] In December 2012 the pharmaceutical company Merck, which manufactures ERN/LRPT under the trade name Tredaptive and which funded the HSP2-THRIVE study, issued a statement saying the trial had failed to meet its primary endpoint and that “the combination of extended-release niacin and laropiprant to statin therapy did not significantly further reduce the risk of the combination of coronary deaths, non-fatal heart attacks, strokes or revascularizations compared to statin therapy.” ERN/LRPT is not approved for use in the USA, and on January 11, Merck announced that it was “taking steps to suspend the availability of TREDAPTIVE™ (extended-release niacin/laropiprant) tablets worldwide.”
[3] ”The difficult search for a ‘partner’ of statins in lipid-targeted prevention of vascular events: the re-emergence and fall of niacin”, by Ulf Landmesser. European Heart Journal. doi:10.1093/eurheartj/eht064

Tuesday, February 26, 2013

Stanford Health Research Center on Women + Sex Differences in Medicine

I  think we need someone there to ask the questions about - Are there differences in stroke recovery?

March 5th & 6th 2013 - Pre and Symposium Events

Wednesday March 6th NOON-1 p. m. Li Ka Shing: seXX & seXY A Dialogue on the Question of the Female Brain & the Male Brain: Louann Brizendine and Daphna Joel 

Wednesday, March 6th 1.30p.m-5.15 p.m. Li Ka Shing: Basic & Translational Neuroscience Research Symposium: Sex Differences 

https://docs.google.com/spreadsheet/viewform?formkey=dE9sdUFJLXdGVEpGVTN2MFZBUzVZSnc6MQ#gid=0

NSA begging email - What will help you raise stroke awareness? T-shirts? Magnets? Tell us.

My response in one of the open questions. Some day they will finally contact me and ask me to shut up.

If you want support you will have to be survivor focused, support research, have a survivor board of directors and a survivor president
Basic Stationery Top - Redesign 2010
Dear dean,
As a loyal supporter of National Stroke Association, you have been selected to be part of an exclusive study on how we can help you raise awareness about stroke. We want to know what types of items would help you inform others about stroke and how you can become empowered as an individual impacted by it.
As you know, many empowered communities raise awareness about disease states, such as breast cancer, mostly by wearing certain colors or articles of clothing with pride. Things as simple as a polo shirt, a bracelet, a refrigerator magnet or post-it notes can inform others about a cause. National Stroke Association knows that you and others in the stroke community want these types of resources—and we’re committed to providing them.
But we can’t do it without your help. Your input is essential, because your needs determine what we can provide to you. I invite you to help us by participating in a short online survey about the types of items and resources that would help you raise awareness and educate others. You can answer the survey as a survivor, a caregiver,  healthcare professional or a stroke survivor’s loved one.
Take the survey
Thank you for lending your voice to this process. It means more than you can know.
Warm regards,
Pat Riley signature
Patricia Riley
Product Development

Gum disease treatment can lower annual medical costs for people with heart disease and stroke

I don't trust this correlation, if you have gum disease you are already probably in not very good health and don't have the resources to get standard preventative medical treatment. But I know nothing, thats what your doctor is for.
http://news.gnom.es/pr/gum-disease-treatment-can-lower-annual-medical-costs-for-people-with-heart-disease-and-stroke
– The latest findings from a landmark oral health study by United Concordia and Highmark Inc. show that annual medical costs are lower by $2,956 and $1,029 for individuals with heart disease or cerebrovascular disease (stroke), respectively, who are treated for gum disease.

Mediterranean Diet Proven Key In Avoiding Heart Disease And Stroke

I know this is considered the height of prevention but this is just pure laziness because it doesn't require any intellectual work that would be required if they have to find out how to stop the neuronal cascade of death.
http://uinterview.com/news/mediterranean-diet-could-be-key-in-avoiding-heart-disease-and-stroke-6663
The Mediterranean diet, which consists of fresh vegetables, fruits, fish, legumes, nuts and olive oil, has shown to reduce the health risks of cardiovascular disease and stroke.
A five-year dietary experiment carried out in Spain, consisted of three groups — two that followed a variation of a Mediterranean diet and another that followed (or attempted to follow) a low-fat diet. The two former groups were encouraged to eat the foods aforementioned frequently throughout the week, to limit red meat and baked sweets and to have seven glasses of wine with meals per week. The latter group, while also encouraged to eat lean fish, were told to eat pasta and bread, and to stay away from olive oil and nuts.
All of the participants were at higher-than-normal cardiovascular risk — half had Type 2 diabetes, and roughly 80 suffered from hypertension. Throughout the five years of the study, 8 in the Mediterranean diet groups suffered from a heart attack, stroke or cardiovascular death, according to the findings published in The New England Journal of Medicine. Comparatively, a total of 11 on the control diet suffered such an event. These results indicate about a 30% reduction in “events” for those following the Mediterranean diet.
“Really impressive,” Rachel Johnson, a professor of nutrition at the University of Vermont and a spokeswoman for the American Heart Association told The New York Times. “And the really important thing — the coolest thing — is that they used very meaningful endpoints. They did not look at risk factors like cholesterol or hypertension or weight. They looked at heart attacks and strokes and death. At the end of the day, that is what really matters.”
Despite the low-fat dieters clocking in a daily calorie consumption of roughly 1,960 to the Mediterranean dieters 2,200, it proved less beneficial to the participants’ health. However, it is also important to note that there was no reported weight loss associated with the Mediterranean diet, and a majority of the participants were taking statins or blood pressure or diabetes drugs in an ancillary effort to reduce their heart disease risk. “As a doctor it is easier to say take a pill,” Dr. Ramon Estruch, who conducted the study, told the Boston Globe. “But diet is a very powerful effect in protecting against cardiovascular disease.”
The study conducted in Spain, if transferred to the United States, is likely to show even greater results, as a typical Western diet is generally worse than that of those sampled, according to Dr. Miguel Angel Martinez-Gonzalez. “The differences probably would be huge.”

Results of Membrane-activated Chelator Stroke Intervention Randomized Trial of DP-b99 in Acute Ischemic Stroke

A Great stroke association would look at this and determine  why phase II worked and this one failed.
Maybe mouse inflammation not correlating to human inflammation
http://stroke.ahajournals.org/content/44/3/580.short?rss=1

Abstract

Background and Purpose—DP-b99, a lipophilic moderate-affinity chelator of zinc, was postulated to improve recovery after acute ischemic stroke. We evaluated the safety and therapeutic effects of DP-b99 in patients with acute hemispheric ischemic stroke.
Methods—The Membrane-Activated Chelator Stroke Intervention trial was a randomized, double-blind, placebo-controlled, multicenter, parallel-group trial of intravenous DP-b99 administered for 4 consecutive days (NCT00893867). Acute ischemic stroke patients within 9 hours of onset, but untreated by alteplase, with a baseline National Institutes of Health Stroke Scale score of 10 to 16, and evidence of language dysfunction, visual field defect, and neglect were eligible. The primary efficacy analysis compared distributions of functional status measured by modified Rankin score in the intent-to-treat population of patients with any post-treatment outcome, adjusted for initial severity. Functional and neurological recovery were secondary measures. Home time was an exploratory end point.
Results—Enrollment terminated at n=446 after the planned interim analysis determined futility; follow-up continued. Final modified Rankin score distributions were equal between DP-b99 and placebo-treated groups (P=0.10; Padj adjusted for baseline age and National Institutes of Health Stroke Scale=0.21). Fewer patients recovered to modified Rankin score ≤1 in the DP-b99–treated group (45/218; 20.6%) than after placebo (63/219; 28.8%) (P=0.05; Padj=0.10). Similarly, fewer patients attained National Institutes of Health Stroke Scale ≤1 after DP-b99 (42/218; 19.3%) than placebo (56/219; 25.6%; P=0.10; Padj=0.26). Mortality was similar between DP-b99 and placebo intent-to-treat groups (36/218; 16.5% vs 33/219; 15.1%; P=0.68). Home time was unchanged by treatment (median 36 vs 36.5 days; P=0.25).
Conclusions—Despite encouraging preclinical and phase II trial data, DP-b99 shows no evidence of efficacy in treating human ischemic stroke.

Warfarin-induced Venous Limb Gangrene

Ask your doctor what the early symptoms are for this so you can get it treated in time. I'm sure your doctor already warned you about this.
http://europepmc.org/abstract/MED/23198012/reload=0;jsessionid=dP6xnwKxPxeSA8XDQVn9.2
Warfarin is a commonly used anticoagulant that has been associated with several significant cutaneous side effects, most notably warfarin-induced skin necrosis. A lesser known adverse reaction to warfarin is warfarin-induced venous limb gangrene. Both cutaneous adverse effects share the same pathophysiology, but are clinically quite different. The majority of cases of warfarin-induced venous limb gangrene has been in patients with cancer or heparin-induced thrombocytopenia. However, other hypercoagulable disease states, such as the antiphospholipid antibody syndrome, can be associated with venous limb gangrene. In order to increase recognition of this important condition, the authors report a case of warfarin-induced venous limb gangrene in a patient with presumed antiphospholipid antibody syndrome and review the literature on warfarin-induced venous limb gangrene.

Leukoaraiosis, a Common Brain Magnetic Resonance Imaging Finding, as a Predictor of Traffic Crashes

Diffuse white matter abnormalities, possibly from silent strokes.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057255

Abstract

Background

There are no reported studies on the relationship between traffic crashes and brain tissue changes in healthy drivers. The relationship between traffic crashes and leukoaraiosis, a common magnetic resonance imaging finding, was investigated in this study.

Methods

A total of 3,930 automobile drivers (2,037 men and 1,893 women; age, 21–87 years) who underwent brain magnetic resonance imaging as part of total health check-ups and answered a road traffic questionnaire were examined to determine whether asymptomatic leukoaraiosis was associated with various types of traffic crashes. Multiple logistic regression analysis was performed to elucidate the relationship between leukoaraiosis and various types of traffic crashes.

Results

Subcortical leukoaraiosis was diagnosed in 28.52% of all subjects, whereas periventricular leukoaraiosis was diagnosed in 9.57% of all subjects. Adjusted odds ratios for involvement in all types of traffic crashes were not significant for subjects with periventricular leukoaraiosis; however, they were significant for subjects with multiple and large multiple subcortical leukoaraiosis. Adjusted odds ratios for involvement in crashes at crossroads were 1.09 (95% confidence interval [CI], 0.60–2.00) for subjects with single subcortical leukoaraiosis, 3.35 (95% CI, 2.36–4.77) for subjects with multiple subcortical leukoaraiosis, and 2.45 (95% CI, 2.36–4.98) for subjects with large multiple subcortical leukoaraiosis. Periventricular leukoaraiosis was not significantly associated with crossroad crashes. Involvement in crashes of any type, parking lot crashes, and rear-end collisions showed no significant association with either subcortical or periventricular leukoaraiosis.

Conclusions

Multiple subcortical leukoaraiosis, but not periventricular leukoaraiosis, is significantly associated with traffic crashes, in particular, crossroad crashes. This association is independent of sex, age, and driving exposure. To our knowledge, this is the first evidence describing the relationship between brain tissue changes and traffic crashes.

Vascular Elasticity and Grip Strength Are Associated With Bone Health of the Hemiparetic Radius in Chronic Stroke: Implications for Rehabilitation

No clue on how this might be of any use to your doctor or therapist.
http://ptjournal.apta.org/content/early/2013/02/20/ptj.20120378.abstract

Abstract

Background Individuals with stroke often sustain increased bone loss and fracture rate. Increasing evidence has demonstrated a link between cardiovascular health and bone loss in other patient populations.
Objective To compare the bone density and geometry of the radius diaphysis between the two sides in people with chronic stroke and aged-matched controls, and to examine the relationship between the bone strength index of the hemiparetic radius diaphysis and vascular health in people with chronic stroke.
Design This was a case-control study.
Methods The radius diaphysis on both sides was scanned using peripheral quantitative computed tomography in 65 people with chronic stroke and 34 controls. Large and small artery elasticity indices were evaluated using a cardiovascular profiling system.
Results The paretic radius diaphysis had significantly lower value in cortical bone mineral density, cortical thickness, cortical area, bone strength index but greater marrow cavity area than the non-paretic radius diaphysis in the stroke group whereas none of the bone measurements showed significant side-to-side difference in controls. Multiple regression analyses showed that large artery elasticity index and grip strength remained significantly associated with bone strength index of the hemiparetic radius diaphysis, after controlling for age, sex, time since stroke diagnosis, body mass index, physical activity (R2=0.790, p≤0.001).
Limitations This study was cross-sectional and could not establish causality. The radius diaphysis is not the most common site of fracture after stroke.
Conclusions Both the integrity of the vasculature and muscle strength were significantly associated with the bone strength index at the hemiparetic radius diaphysis among people with chronic stroke. The results may be useful in guiding rehabilitative programs for enhancing bone health in the paretic arm following a stroke.

Long Course Hyperbaric Oxygen Stimulates Neurogenesis and Attenuates Inflammation after Ischemic Stroke

Your doctor will need to decipher this and see if the conclusions match the results. I doubt it.
http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/mi/2013/512978.pdf&sa=X&scisig=AAGBfm2LTyPWIJ_t-r0f2O6-52_ql2KWfg&oi=scholaralrt
Several studies have provided evidence with regard to the neuroprotection benefits of hyperbaric oxygen (HBO) therapy in cases
of stroke, and HBO also promotes bone marrow stem cells (BMSCs) proliferation and mobilization. This study investigates the
influence of HBO therapy on the migration of BMSCs, neurogenesis, gliosis, and inflammation after stroke. Rats that sustained
transient middle cerebral artery occlusion (MCAO) were treated with HBO three weeks or two days. The results were examined
using a behavior test (modified neurological severity score, mNSS) and immunostaining to evaluate the effects of HBO therapy
on migration of BMSCs, neurogenesis, and gliosis, and expression of neurotrophic factors was also evaluated. There was a lower
mNSS score in the three-week HBO group when compared with the two-day HBO group. Mobilization of BMSCs to an ischemic
area wasmore improved in long course HBO treatments, suggesting the duration of therapy is crucial for promoting the homing of
BMSCs to ischemic brain by HBO therapies. HBO also can stimulate expression of trophic factors and improve neurogenesis and
gliosis. These effects may help in neuronal repair after ischemic stroke, and increasing the course of HBO therapy might enhance
therapeutic effects on ischemic stroke.

The Relationship of Atherosclerosis to the 10-Year Cumulative Incidence of Age-related Macular Degeneration: The Beaver Dam Studies

So maybe I don't have to worry any more than usual.
http://www.docguide.com/relationship-atherosclerosis-10-year-cumulative-incidence-age-related-macular-degeneration-beaver-da?hash=7e422beb&eid=31292&alrhash=3c9ebc-5aeefe0d7ed0a73e6788dca4998df39c
OBJECTIVE: To describe the relationships of intima-media thickness (IMT), plaque in the carotid artery, angina, myocardial infarction (MI), and stroke to the 10-year cumulative incidence of early and late age-related macular degeneration (AMD) and progression of AMD. DESIGN: Cohort study. PARTICIPANTS: A total of 1700 persons aged 53 to 96 years who participated in both the Epidemiology of Hearing Loss Study and the Beaver Dam Eye Study in 1998-2000, with photographs gradable for AMD at 5-year (2003-2005) and 10-year (2008-2010) follow-up examinations. METHODS: The IMT and presence of plaque were assessed using B-mode ultrasonography of the carotid artery. Presence of angina, MI, and stroke were defined on the basis of a self-reported history of physician diagnosis. The presence and severity of AMD were determined by systematic grading of stereoscopic color fundus photographs. MAIN OUTCOME MEASURES: Age-related macular degeneration. RESULTS: The 10-year cumulative incidence of early AMD was 15.7%, and the 10-year cumulative incidence of late AMD was 4.0%. After adjusting for age, sex, body mass index, smoking status, age-related maculopathy susceptibility 2 (ARMS2) and complement factor H (CFH) genotypes, and other factors, mean IMT was associated with the 10-year incidence of early AMD (odds ratio [OR] per 0.1 mm IMT, 1.11; 95% confidence interval [CI], 1.00-1.21; P = 0.03) and late AMD (OR per 0.1 mm IMT, 1.27; CI, 1.10-1.47; P = 0.001). Mean IMT was associated with the 10-year incidence of pure geographic atrophy (OR per 0.1 mm IMT, 1.31; CI, 1.05-1.64; P = 0.02) but not exudative AMD (OR per 0.1 mm IMT, 1.14; CI, 0.97-1.34; P = 0.11). Similar associations were found for maximum IMT. The number of sites with plaque was related to the incidence of late AMD (OR per 0.1 mm IMT, 2.79 for 4-6 sites vs. none; CI, 1.06-7.37; P = 0.04) but not to early AMD. A history of angina, MI, or stroke was not related to any incident AMD outcome. CONCLUSIONS: In these population-based data, carotid artery IMT and carotid plaques had a weak relationship to the incidence of late AMD that was independent of systemic and genetic risk factors. Angina, MI, and stroke were not related to AMD. It is unclear whether the carotid IMT is a risk indicator of processes affecting Bruch's membrane and the retinal pigment epithelium, or a measure of atherosclerosis affecting susceptibility to AMD. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

The Growing Shortage of Vascular Neurologists in The Era of Health Reform: Planning is Brain! [Special Reports]

Once again the stroke world is not doing any strategic planning, they are assuming that todays processes are what will be available tomorrow. Rather than figuring out that an objective test that doesn't require trained analysis is the logical way to go.  Damn these people have no useable brains at all.
http://stroke.ahajournals.org/cgi/content/short/44/3/822?rss=1

Monday, February 25, 2013

Ateronon Reveals More On Research Confirming That 'Tomatoes Can Reduce The Risk of Strokes In Men'

Of course natural foods are not good enough, you have to buy processed pills equal to 1 kilogram of tomatoes. I guess my pint of grape tomatoes a day is not enough, I don't think I could do 1 kg.
http://world.einnews.com/247pr/331940
A study has revealed men can reduce the risk of suffering a stroke by ensuring they have a tomato rich diet, as it contains the antioxidant lycopene.
The study of over 1,000 men, carried out by Finnish researcher and study author Jouni Karppi*, revealed those with higher blood levels of lycopene were 55% percent less likely to suffer a stroke than men with the lowest amounts.
Men wanting to take serious steps to look after their heart health should not rely on eating tomatoes alone. Tomatoes do have many health benefits but lycopene, which is found in their skin is not easily used and processed by the body in its natural food form.

More at link.

Sunday, February 24, 2013

Cannabinoid Trans-Caryophyllene Protects Brain Cells From Ischemia

Another item to tell my ER doctor to administer to me in the first hours. Damn it had better be a stroke that leaves me lucid since I know otherwise I won't get any of the hyperacute therapies that I have mentioned. I can just see telling my doctor to read my blog and 5 days later comes back and says, 'So what?' ' You expect me to listen to a stroke patient for advice?' 'Why yes, I damn well expect you to listen to me.'
http://www.medicalnewstoday.com/articles/256799.php
The activation of cortical type 2 cannabinoid (CB2) receptors with cannabinoid trans-caryophyllene (TC) is effectively able to facilitate recovery among ischemic brain injury patients, according to a recent study published in The American Journal of Pathology.

TC is derived from the essential oils of the Cannabis sativa plant, but its structure is very different to other classical cannabinoids - it is not associated with any psychoactive side effects.

Researchers conducted tests in both in vivo and in vitro animal models and found that TC is successfully able to protect brain cells from ischemia.
More at link.

Tsc1 (hamartin) confers neuroprotection against ischemia by inducing autophagy

The readable article link is first then comes the abstract itself. Fascinating finding, which should lead directly to research that determines how to add hamartin to your brain, especially for those of us who already had a stroke.
Ability of brain to protect itself from damage revealed
Abstract:
http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3097.html
Previous attempts to identify neuroprotective targets by studying the ischemic cascade and devising ways to suppress it have failed to translate to efficacious therapies for acute ischemic stroke1. We hypothesized that studying the molecular determinants of endogenous neuroprotection in two well-established paradigms, the resistance of CA3 hippocampal neurons to global ischemia2 and the tolerance conferred by ischemic preconditioning (IPC)3, would reveal new neuroprotective targets. We found that the product of the tuberous sclerosis complex 1 gene (TSC1), hamartin, is selectively induced by ischemia in hippocampal CA3 neurons. In CA1 neurons, hamartin was unaffected by ischemia but was upregulated by IPC preceding ischemia, which protects the otherwise vulnerable CA1 cells. Suppression of hamartin expression with TSC1 shRNA viral vectors both in vitro and in vivo increased the vulnerability of neurons to cell death following oxygen glucose deprivation (OGD) and ischemia. In vivo, suppression of TSC1 expression increased locomotor activity and decreased habituation in a hippocampal-dependent task. Overexpression of hamartin increased resistance to OGD by inducing productive autophagy through an mTORC1-dependent mechanism.

Saturday, February 23, 2013

Effect of a Cane on Sit-to-Stand Transfer in Subjects with Hemiparesis

What does your therapist think of this?
http://journals.lww.com/ajpmr/Abstract/2013/03000/Effect_of_a_Cane_on_Sit_to_Stand_Transfer_in.2.aspx

Abstract

Objective: The aim of this study was to determine the effect of using a cane on movement time, joint moment, weight symmetry, and muscle activation patterns during sit-to-stand (STS) transfer in healthy subjects and subjects who have had a stroke.
Design: Nine subjects with hemiparesis (mean [SD] age, 61.11 [12.83] yrs) and nine healthy adults (mean [SD] age, 63.11 [10.54] yrs) were included. The subjects with hemiparesis performed STS transfer in two randomly assigned conditions: (1) without a cane and (2) with a cane. The healthy subjects performed only STS transfer without a cane. A three-dimensional motion system, force plates, and eletromyography were used to examine STS transfer. The symmetry index between the two limbs was calculated.
Results: The movement time of the subjects with hemiparesis in both conditions without a cane and with a cane was longer than that of the healthy subjects without a cane (P < 0.025). However, STS transfer with a cane in the subjects with hemiparesis resulted in shorter movement time, greater knee extensor moment of the paretic limb, and more symmetry of weight bearing than in those without a cane (P < 0.05). The sequence of muscle onset tended to improve with a cane in the subjects with hemiparesis.
Conclusions: Cane use may promote more symmetrical STS transfers rather than compensation by the unaffected limb.

The influence of obesity on structure, biochemistry and function of brain regions involved in cognition

Are your cognition problems due to this latest obesity one rather than your stroke. Your doctor had better know the answer.
http://scholar.google.com/scholar_url?hl=en&q=http://dataspace.princeton.edu/jspui/bitstream/88435/dsp015t34sj614/1/Bocarsly_princeton_0181D_10489.pdf&sa=X&scisig=AAGBfm3_VU255HF84XRDv0wJv03uUxfBxA&oi=scholaralrt
Short Abstract
Obesity is a major public health problem, affecting more than one-third of the U.S. population. Several studies suggest deficits in cognition in obese people and several neuroimaging studies indicate reduced volume of certain brain regions, including the hippocampus and prefrontal cortex. These brain regions are important for cognition and anxiety regulation, and thus structural change in them may contribute to alterations in cognition and mood reported in overweight people. No studies have investigated the effects of weight gain on brain structure and function at a level of analysis that would permit identification of cellular mechanisms, which could lead to
future treatment options. This dissertation uses a rat model of diet-induced obesity (DIO) to explore behavioral, structural and biochemical changes in three brain regions important in cognition: the medial prefrontal cortex (mPFC), perirhinal cortex (PRC), and hippocampus (HIP).
Obese rats performed poorly on cognitive tasks specific to the mPFC and PRC, but not the HIP, compared to normal weight controls. In order to begin to characterize the behavioral differences observed, the influence of obesity on brain volume, dendritic architecture and spine density, as well as on associated pre- and post-synaptic markers in the mPFC, PRC and HIP were determined. Deficits in mPFC and PRC-related tasks were accompanied by decreased dendritic spine density and decreased pre- and postsynaptic markers in the mPFC and PRC. Finally, to identify potential mechanisms that might be driving these results, hormones that have previously been linked to changes in brain structure, and/or metabolism and obesity, were surveyed. While there was no difference in testosterone, glucose or insulin levels between groups, leptin was increased in the DIO model, providing a potential mechanism leading to changes in neurological structure and function. Further, obese rats had decreased peripheral corticosterone levels, a condition previously linked to decreased dendritic architecture, suggesting another potential involved mechanism.  The DIO animal model of obesity has allowed us to look into the cellular changes that underlie alterations in brain structure and function, and provided us with foundational research needed to identify mechanisms for future intervention.

Zinc as mediator of ubiquitin conjugation following Traumatic Brain Injury

I'm sure this might be important to us. Our researchers need to respond. If we had a Great stroke association this would be looked into.
http://www.sciencedirect.com/science/article/pii/S0006899313002035

Abstract

Previous studies have shown that pathological zinc accumulation and deposition of ubiquitinated protein aggregates are commonly detected in many acute neural injuries, such as trauma, epilepsy and ischemia, However, the underlying mechanisms are poorly understood. Here we assessed the effect of zinc on ubiquitin conjugation and subsequent neurodegeration following traumatic brain injury (TBI). Firstly, we found that scavenging endogenous Zn2+ reduced trauma-induced ubiquitin conjugation and protected neurons from TBI insults in rat hippocampus. Secondly, we detected both zinc accumulation and increased ubiquitin conjugated protein following brain trauma in human cortical neurons. Our previous study has shown that zinc can induce ubiquitin conjugation in cultured hippocampal neurons. All these findings indicate that alterations in Zn2+ homeostasis may impair the protein degradation pathway and ultimately cause neuronal injury following traumatic brain injury.

Resveratrol Decreases Noise-Induced Cyclooxygenase-2 Expression in the Rat Cochlea

So maybe resveratrol protects against hearing loss. Of course it doesn't translate the amount the rats got to  how many bottles you would have to drink. I'm at a loss since I don't like red wine since a fishing canoe trip to the BWCA in college. So don't self-prescribe.
http://oto.sagepub.com/content/early/2013/02/02/0194599813475777.abstract

Abstract

Objective Our previous studies have demonstrated the efficacy of resveratrol, a grape constituent noted for its antioxidant and anti-inflammatory properties, in reducing temporary threshold shifts and decreasing cochlear hair cell damage following noise exposure. This study was designed to identify the potential protective mechanism of resveratrol by measuring its effect on cyclooxygenase-2 (COX-2) protein expression and reactive oxygen species (ROS) formation following noise exposure.
Study Design Controlled animal intervention study.
Setting Otology Laboratory, Henry Ford Health System.
Subjects and Methods Twenty-two healthy male Fischer 344 rats (2-3 months old) were exposed to acoustic trauma of variable duration with or without intervention. An additional 20 healthy male rats were used to study COX-2 expression at different time points during and following treatment of 24 hours of noise exposure. Cochlear harvest was performed at various time intervals for measurement of COX-2 protein expression via Western blot analysis and immunostaining. Peripheral blood was also obtained for ROS analysis using flow cytometry.
Results Acoustic trauma exposure resulted in a progressive up-regulation of COX-2 protein expression, commencing at 8 hours and peaking at 32 hours. Similarly, ROS production increased after noise exposure. However, treatment with resveratrol reduced noise-induced COX-2 expression as well as ROS formation in the blood as compared with the controls.
Conclusion COX-2 levels are induced dramatically following noise exposure. This increased expression may be a potential mechanism of noise-induced hearing loss (NIHL) and a possible mechanism of resveratrol’s ability to mitigate NIHL by its ability to reduce COX-2 expression.

Many locked-in syndrome patients happy, study shows

But don't you realize that having their normal interpreter there would bias the results. Chinese will never talk truthfully with an official nearby. Thanks for the tip Amy. I just had to put in my two cents. 
2cents.gif
http://www.nbcnews.com/id/41746257/ns/health-health_care/#.UShf62ev-V4 
You are awake, aware and probably unable to move or talk — but you are not necessarily unhappy, says the largest study of locked-in syndrome ever conducted.
A surprising number of patients with the condition say they are happy, despite being paralyzed and having to communicate mainly by moving their eyes. Most cases are caused by major brain damage, often sustained in traumatic accidents.
As part of the study — published in the online journal BMJ Open on Wednesday, Dr. Steven Laureys of the Coma Science Group at the University Hospital of Liege in Belgium and colleagues sent questionnaires to 168 members of the French Association for Locked-in Syndrome, asking them about their medical history, their emotional state and views on euthanasia.
Sixty-five patients used a scale to indicate their sense of well-being, with 47 saying they were happy and 18 unhappy. They were also asked a variety of questions about their lives, including their ability to get around or participate in social functions, or if they had ever considered euthanasia.
Only a handful of patients said they often had suicidal thoughts. The patients responded to questions largely by blinking.
Adrian Owen, a neuroscientist at the University of Western Ontario in Canada, said of the results: "We cannot and should not presume to know what it must be like to be in one of these conditions."

Petition response: Increasing Public Access to the Results of Scientific Research



A start anyway, I could be really annoying if I have access to full articles. I'd become even more arrogant.
The White House
Increasing Public Access to the Results of Scientific Research
By Dr. John Holdren, Assistant to the President for Science and Technology and Director of the White House Office of Science and Technology Policy
Thank you for your participation in the We the People platform. The Obama Administration agrees that citizens deserve easy access to the results of research their tax dollars have paid for. As you may know, the Office of Science and Technology Policy has been looking into this issue for some time and has reached out to the public on two occasions for input on the question of how best to achieve this goal of democratizing the results of federally-funded research. Your petition has been important to our discussions of this issue.
The logic behind enhanced public access is plain. We know that scientific research supported by the Federal Government spurs scientific breakthroughs and economic advances when research results are made available to innovators. Policies that mobilize these intellectual assets for re-use through broader access can accelerate scientific breakthroughs, increase innovation, and promote economic growth. That’s why the Obama Administration is committed to ensuring that the results of federally-funded scientific research are made available to and useful for the public, industry, and the scientific community.
Moreover, this research was funded by taxpayer dollars. Americans should have easy access to the results of research they help support.
To that end, I have issued a memorandum today (.pdf) to Federal agencies that directs those with more than $100 million in research and development expenditures to develop plans to make the results of federally-funded research publically available free of charge within 12 months after original publication. As you pointed out, the public access policy adopted by the National Institutes of Health has been a great success. And while this new policy call does not insist that every agency copy the NIH approach exactly, it does ensure that similar policies will appear across government.
As I mentioned, these policies were developed carefully through extensive public consultation. We wanted to strike the balance between the extraordinary public benefit of increasing public access to the results of federally-funded scientific research and the need to ensure that the valuable contributions that the scientific publishing industry provides are not lost. This policy reflects that balance, and it also provides the flexibility to make changes in the future based on experience and evidence. For example, agencies have been asked to use a 12-month embargo period as a guide for developing their policies, but also to provide a mechanism for stakeholders to petition the agency to change that period. As agencies move forward with developing and implementing these polices, there will be ample opportunity for further public input to ensure they are doing the best possible job of reconciling all of the relevant interests.
In addition to addressing the issue of public access to scientific publications, the memorandum requires that agencies start to address the need to improve upon the management and sharing of scientific data produced with Federal funding. Strengthening these policies will promote entrepreneurship and jobs growth in addition to driving scientific progress. Access to pre-existing data sets can accelerate growth by allowing companies to focus resources and efforts on understanding and fully exploiting discoveries instead of repeating basic, pre-competitive work already documented elsewhere. For example, open weather data underpins the forecasting industry and provides great public benefits, and making human genome sequences publically available has spawned many biomedical innovations—not to mention many companies generating billions of dollars in revenues and the jobs that go with them. Going forward, wider availability of scientific data will create innovative economic markets for services related to data curation, preservation, analysis, and visualization, among others.
So thank you again for your petition. I hope you will agree that the Administration has done its homework and responded substantively to your request.
Stay Connected
The White House

Southend Hospital to provide specialist care for stroke patients

For you in the UK you'll have to ask what the hell the specialists are going to do in the hyperacute phase(first week) besides tPA. If something is out there it is well hidden. Find out and publish it for all the worlds stroke patients to use.
http://www.echo-news.co.uk/news/local_news/10244859.Southend_Hospital_to_provide_specialist_care_for_stroke_patients/
SOUTHEND would provide specialist treatment for stroke patients under new proposals for the east of England.
The town’s hospital, which already has a first-class stroke unit, is being recommended as one of three future hyper-acute stroke units for Essex.
The others would be Colchester and Chelmsford.
They could each see up to 40 per cent more patients in the first three days following a stroke and will have more specialist stroke physicians available.
All five hospitals in Essex, including Basildon, would continue to have an acute stroke unit.
However, hyper-acute stroke units in the three hospitals would give all patients in Essex immediate access to top stroke specialists 24 hours a day, 7 days a week.
Jacqueline Totterdell, Southend Hospital chief executive, said: “We are delighted that our award winning stroke service has been recognised as a preferred option to become a hyper acute stroke service as part of the on-going review into the provision of stroke services across Essex and the East of England.
“We will work with our colleagues in the clinical commissioning groups and patient and carers across the local area over the coming months to ensure that our excellent service meets their needs and continues to deliver high quality critical care when it is needed the most.”

Sorry, Coffee Lovers: The Antioxidants In Your Cup Of Joe May Not Pack That Many Health Benefits

I'm still going to drink coffee for the Alzheimers benefits.
http://www.blisstree.com/2013/02/21/food/nutrition/coffee-benefits-antioxidants/
In the past ten years or so, “antioxidants” has become THE buzzword in health food marketing. But a new study says that just because a food is antioxidant rich, doesn’t mean it will prevent disease–particularly when it comes to stroke risk and dementia.
Researcher Elizabeth Devore, an epidemiologist at Brigham and Women’s Hospital, has studied the impact of antioxidants and certain compounds on aging and health before. Last year, she published research proving that eating berries can delay cognitive decline. And in the past, she’s analyzed data from the Rotterdam study, comparing reported diets and health data of over 5,000 subjects, all aged 55 and older, whose health and diets were monitored for 14 years. She found that subjects who consumed high amounts of vitamin E were less likely to develop dementia, and subjects whose diets were high in vitamin A were less likely to have a stroke.
In her latest research, she revisited the Rotterdam study to analyze how antioxidants impact stroke risk and likelihood of dementia. Contrary to what food marketers would lead us to believe, she found that there wasn’t much of a connection at all; at least not when looking at the general category of antioxidants.
In the group she studied, most subjects who consumed a high amount of antioxidants were getting them from coffee and tea. While past studies have linked high consumption of coffee and tea to a lower risk of stroke and dementia, those were largely conducted in European countries, where diets also tend to be high in other antioxidant-rich foods, like wine, fruits and vegetables, which leads her to believe that it may not be the antioxidants in coffee that are actually boosting brain health for the people who drink it.
“We’re seeing strong and clear benefits with specific antioxidants but not overall,” she told NPR. “As we’re able to move into these more nontraditional antioxidant foods, we’ll be able to tease out more specific information for people.”
The loose link between antioxidants and proven health benefits has already gotten some food manufacturers in trouble–POM Wonderful, for example, got more than a little slap on the wrist from the U.S. Supreme court for making false claims about the antioxidant benefits of their pomegranate juice. But as researchers do start to tease out the health benefits of certain antioxidants and flavonoids, it might just get harder to justify that double-shot mocha if you’re not getting your share of fruits and vegetables, too.

Fish Oil Injection to Stroke Victims: Remedy for Brain Damage

For this TBI case the fish oil was administered thru a feeding tube.  This is why I'm going to chow down on fish oil for my next stroke. You may have to beat your doctor over the head with these reports to get it. I however won't listen to my doctor, I'll tell him/her what I want done. I guess you shouldn't listen to me, I know nothing.
http://www.medicaldaily.com/articles/14129/20130222/fish-oil-injection-stroke-remedy-brain-damage.htm
A new fish oil remedy may be the key to preventing brain damage after patients suffer from stroke.
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Researchers from Columbia University and Louisiana State University in New York conducted experiments on mice showing that a fish-oil-based drug given within hours of a stroke can help damaged cells stay alive.
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The existing drug used to prevent brain damage in stroke patients has to be given within four hours of a stroke. It breaks up blood clots that block oxygen flow to the brain, but does not keep suffocating cells from dying - which doesn't help patients who need several hours just to get to a hospital from recovering brain functions in the damaged areas.
If it works in humans in the same way, the fish oil drug might be given much later to keep damaged cells alive, which can help patients who don't get to a hospital quickly enough to prevent permanent brain damage.
The drug, a fluid rich in the omega-3 fatty acid docosahexanoic acid (DHA), uses several methods of keeping damaged cells alive, like turning on gene switches that produce protective proteins.
The researcher's work was published in PLOS One earlier this week, entitled "N-3 Fatty Acid Rich Triglyceride Emulsions Are Neuroprotective after Cerebral Hypoxic-Ischemic Injury in Neonatal Mice."
Omega-3 fatty acids are vital for proper brain function, and necessary for nervous system developments. Mostly found in cold water fatty fish like salmon, tuna, and mackerel, omega-3 fatty acids are necessary for a healthy diet and have strong anti-inflammatory effects.
DHA treatment has been shown to be beneficial in the treatment of many inflammatory chronic diseases, like coronary heart disease, asthma, arthritis, and macular degeneration. This study showcases its potential benefit in stroke treatment.
"Stroke is a brain attack that each year kills 130,000 Americans," notes Dr. Nicolas Bazan of Louisiana State University, one of the authors of the study.
"Strokes can occur at any age, including in newborns, with long-term and devastating consequences. DHA is already widely consumed as a dietary supplement in the US, and from a therapeutic point of view, we can now see a light at the end of the tunnel."
According to the Centers for Disease Control and Prevention (CDC), 795,000 Americans have a stroke each year, and stroke causes 1 in every 18 deaths. Stroke is also the single most common cause of long-term disability, and the costs of stroke in the United States were estimated to total nearly $74 billion in 2010.
The researchers hope to develop a drug testable on humans very soon, which would be delivered through an injection in the arm.


Friday, February 22, 2013

Microbubbles improve myocardial remodelling after infarction

Ok, its not just the stroke medical world that is stupid. Throughout this article they never once consider that maybe the gas is the cause of better outcomes. Something similar was tried  for stroke and the assumption was also that the vibration was the effective factor rather that the xenon gas in the bubbles.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=128689&CultureCode=en
Scientists from the Bonn University Hospital successfully tested a method in mice allowing the morphological and functional sequelae of a myocardial infarction to be reduced. Tiny gas bubbles are made to oscillate within the heart via focused ultrasound - this improves microcirculation and decreases the size of the scar tissue. The results show that the mice, following myocardial infarction, have improved cardiac output as a result of this method, as compared to untreated animals. The study is now being presented in the professional journal PLOS ONE.
Every year in Germany, approximately 280,000 people suffer a myocardial infarction; more than 52,000 die as a result. Due to an occluded vessel, parts of the heart muscle no longer have sufficient circulation and the tissue dies off. These regions are not replaced by new heart muscle cells but instead by scar tissue – this generally causes the pump function of the heart to decrease following an infarction. Scientists from the Bonn University Hospital have now successfully tested a new method on mice with which scar tissue can be reduced and cardiac output increased.
Microbubbles are made to oscillate within the heart
“There are attempts to treat the scar tissue with gene therapy or stem cells - by contrast, we have chosen a physical approach to treatment,“ reports Adj. Professor Dr. med. Alexander Ghanem from the Department of Cardiology of the Bonn University Hospital. The researchers injected a total of 17 mice which had previously had a myocardial infarction with microscopically small, gas-filled bubbles in the bloodstream. Once the microbubbles reached the heart, they were made to vibrate there using focused ultrasound. “Through this mechanical stimulation, the circulation of the area of the infarction is improved - and the scar shrinks,“ says the cardiac specialist.
Treated animals demonstrate ameliorated post-infarction remodelling
The scientists compared the results of the mice treated with the microbubbles to those of a control group. Two weeks after the myocardial infarction, there was expected worsening of heart function in the control group due to the maturing of the scar tissue. In contrast, the mice treated with the microbubbles did not develop any cardiac insufficiency. Jonas Dörner, the first author of the study, summarizes the results: “The pumping function was significantly better in the treated animals as compared to the control group; there was also a significantly smaller amount of decayed heart muscle tissue.” Along with the Department of Cardiology, the Departments of Cardiac Surgery and Anesthesiology and the Institute of Physiology took part in the investigations.
Ultrasound treatment stimulates growth hormones
The scientists sought the causes of the positive treatment success which is, however, unexplained to date. Following ultrasound treatment of the mice, it was demonstrated that the amount of the body’s own growth hormones significantly increased in the heart. “This is evidently the reason why the scar formation decreased as a result of the oscillating microbubbles,“ says Dr. Ghanem. The scientists now hope that humans will also be able to eventually be treated with the microbubble-ultrasound method, however further investigations are still needed. “Potentially, all patients who have had an acute myocardial infarction are eligible for this follow-up treatment,“ explains the cardiologist of the Bonn University Hospital. Interestingly, microbubbles are already used as a diagnostic contrast agent.
Patent for novel ultrasound method filed
The study, conducted with support from the BONFOR funding program of the Medical Faculty of Bonn University and the German Heart Foundation [Deutsche Herzstiftung e.V.], gave rise to a patent application. “Together with the company Philips Medical, we developed a novel ultrasonic probe which enables a standardized impulse discharge in the heart,“ reports the cardiologist. The special feature is that two ultrasound sources linked together are contained in one hybrid ultrasonic probe: one with low frequency for the focused stimulation of the microbubbles in the target organ and one with higher frequency for imaging. In this way, it can be very precisely determined where the scar tissue and the microbubbles are located. “This study demonstrates again that university research inspires technological developments in medicine,“ says Dr. Ghanem.