Maybe this might fix two of the known problems in the neuronal cascade of death. I wonder what strategy is being followed.
1. glutamate poisoning
2. excitotoxicity
Found out this was tested in rats in 2004. This just shows you how fucking poor our stroke leadership and strategy is. 12 years to get to human testing That explains why I haven't written about it, it was before I had my stroke in 2006.
http://www.fau.edu/newsdesk/articles/stroke-treatment.php
A biomedical scientist in the Charles E. Schmidt
College of Medicine at Florida Atlantic University has received a $1.2
million grant from the James and Esther King Biomedical Research
Program, Florida Department of Health, to develop a new and innovative
approach to treat stroke.
Jang Yen (John) Wu, Ph.D., principal investigator and a
senior Schmidt fellow and distinguished professorof biomedical science
in FAU’s College of Medicine, will use a two-pronged approach to treat
stroke in the study. He will preserve and restore brain function by
protecting the brain against stroke induced injury, and also will
stimulate neurogenesis to replenish new brain cells using granulocyte
colony-stimulating factor (GCSF), an FDA-approved drug used to enhance
blood cellular development.
“Many drugs that are designed for stroke intervention
and treatment are based on their anti-oxidative properties or blockers
of calcium channels or glutamate receptors,” said Wu. “However, no
clinically effective therapeutic intervention for stroke has yet been
developed. Furthermore, no non-invasive in vivo procedure is available for monitoring the progression of the treatment for stroke.”
Wu and his collaborators will use gene therapy and a
unique non-invasive MRI monitoring system they developed to observe the
delivery and expression of GCSF, as well as the progression of ischemic
strokes using rodent models of the disease.
“Targeted MRI is highly sensitive and specific when
it is coupled with nanoparticles containing specific oligonucleotide
probes and can be used to track neural progenitor cells in vivo after
gene therapy or stem cell therapy in preclinical and perhaps even
clinical disease models,” said Wu. “Using targeted MRI we will be able
to evaluate the expression of trans genes and brain repair
non-invasively within a living organism.”
Wu anticipates that as a neuroprotectant can
potentially be a powerful growth factor because it is able to preserve
the central nervous system using several overlapping mechanisms that not
only activate cell survival pathways together with suppression of cell
death/apoptotic pathways, but also elicit neurogenesis and angiogenesis.
The Centers for Disease Control and Prevention
estimates that stroke kills almost 130,000 Americans each year, and on
average one American dies from a stroke every four minutes.
Approximately 87 percent of all strokes are ischemic strokes, when blood
flow to the brain is blocked. Stroke is the leading cause of serious
long-term disability and costs the U.S. an estimated $34 billion each
year for healthcare services, medications, and missed days of work.
“The short- and long-term impacts of having a stroke
can be devastating for the individual as well as his or her family,”
said Arthur J. Ross, III, M.D., M.B.A., interim dean and professor in
FAU’s College of Medicine. “We are extremely proud of Dr. Wu’s research
and we are very grateful for receiving this grant from the James and
Esther King Biomedical Research Program. With this grant, Dr. Wu will be
able to develop a novel way to potentially prevent and treat strokes
not only for Florida residents but world-wide.”
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,286 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Wednesday, March 16, 2016
National stroke registries for monitoring and improving the quality of hospital care: A systematic review
Pretty much complete and total crap from the WSO(World Stroke Organization). Monitoring registries, access and care!!! What the hell shit is that? You monitor RESULTS, you fucking idiots.
And Bo Norrving used to be the president of the WSO. You can see why our stroke organizations need to be destroyed.
Someday I'll really tell you what I think.
http://wso.sagepub.com/content/11/1/28.long
Dominique A Cadilhac1,2, Joosup Kim1,2, Natasha A Lannin3,4,Moira K Kapral5, Lee H Schwamm6, Martin S Dennis7,Bo Norrving8 and Atte Meretoja2,9,10
Abstract
Background:
Routine monitoring of the quality of stroke care is becoming increasingly important since patient out-comes could be improved with better access to proven treatments.(There are no proven treatments otherwise known as protocols) It remains unclear how many countries have established a national registry for monitoring stroke care.
Aims:
To describe the current status of national, hospital-based stroke registries that have a focus on monitoring access to evidence-based care and patient outcomes and to summarize the main features of these registries.
Summary of review:
We undertook a systematic search of the published literature to identify the registries that are
considered in their country to represent a national standardized dataset for acute stroke care and outcomes. Our initial keyword search yielded 5002 potential papers, of which we included 316 publications representing 28 national stroke registries from 26 countries. Where reported, data were most commonly collected with a waiver of patient consent(70%). Most registries used web-based systems for data collection (57%) and 25% used data linkage. Few variables weremeasured consistently among the registries reflecting their different local priorities. Funding, resource requirements, and coverage also varied.
Conclusions:
This review provides an overview of the current use of national stroke registries, a description of their common features relevant to monitoring stroke care in hospitals. Formal registration and description of registries would facilitate better awareness of efforts in this field.
And Bo Norrving used to be the president of the WSO. You can see why our stroke organizations need to be destroyed.
Someday I'll really tell you what I think.
http://wso.sagepub.com/content/11/1/28.long
Dominique A Cadilhac1,2, Joosup Kim1,2, Natasha A Lannin3,4,Moira K Kapral5, Lee H Schwamm6, Martin S Dennis7,Bo Norrving8 and Atte Meretoja2,9,10
Abstract
Background:
Routine monitoring of the quality of stroke care is becoming increasingly important since patient out-comes could be improved with better access to proven treatments.(There are no proven treatments otherwise known as protocols) It remains unclear how many countries have established a national registry for monitoring stroke care.
Aims:
To describe the current status of national, hospital-based stroke registries that have a focus on monitoring access to evidence-based care and patient outcomes and to summarize the main features of these registries.
Summary of review:
We undertook a systematic search of the published literature to identify the registries that are
considered in their country to represent a national standardized dataset for acute stroke care and outcomes. Our initial keyword search yielded 5002 potential papers, of which we included 316 publications representing 28 national stroke registries from 26 countries. Where reported, data were most commonly collected with a waiver of patient consent(70%). Most registries used web-based systems for data collection (57%) and 25% used data linkage. Few variables weremeasured consistently among the registries reflecting their different local priorities. Funding, resource requirements, and coverage also varied.
Conclusions:
This review provides an overview of the current use of national stroke registries, a description of their common features relevant to monitoring stroke care in hospitals. Formal registration and description of registries would facilitate better awareness of efforts in this field.
Ipsilesional anodal tDCS enhances the functional benefits of rehabilitation in patients after stroke
You'll have to ask your doctor what ipsilesional and anodal mean since this was obviously not written with laypersons in mind. Not having patients with stroke in the primary cortex seems like cherry picking to a degree that this research is worthless Who approved such research? Stupidity reigns once again.
Ipsilesional anodal tDCS enhances the functional benefits of rehabilitation in patients after stroke
Science Translational Medicine 16 Mar 2016:
Vol. 8, Issue 330, pp. 330re1
DOI: 10.1126/scitranslmed.aad5651
Vol. 8, Issue 330, pp. 330re1
DOI: 10.1126/scitranslmed.aad5651
You are currently viewing the abstract.
View Full Text
View Full Text
Stimulating motor recovery in stroke
Rehabilitation
of movement after stroke requires repeated practice and involves
learning and brain changes. In a new study, Allman et al.
tested whether delivering brain stimulation during a 9-day course of
hand and arm training improved movement in patients after stroke. The
authors found greater improvements in movement in patients who received
real compared to sham (placebo) brain stimulation. Better scores in
patients who received real stimulation were still present 3 months after
training ended. These findings suggest that brain stimulation could be
added to rehabilitative training to improve outcomes in stroke patients.
Abstract
Anodal
transcranial direct current stimulation (tDCS) can boost the effects of
motor training and facilitate plasticity in the healthy human brain.
Motor rehabilitation depends on learning and plasticity, and motor
learning can occur after stroke. We tested whether brain stimulation
using anodal tDCS added to motor training could improve rehabilitation
outcomes in patients after stroke. We performed a randomized, controlled
trial in 24 patients at least 6 months after a first unilateral stroke
not directly involving the primary motor cortex. Patients received
either anodal tDCS (n = 11) or sham treatment (n = 13)
paired with daily motor training for 9 days. We observed improvements
that persisted for at least 3 months post-intervention after anodal tDCS
compared to sham treatment on the Action Research Arm Test (ARAT) and
Wolf Motor Function Test (WMFT) but not on the Upper Extremity
Fugl-Meyer (UEFM) score. Functional magnetic resonance imaging (MRI)
showed increased activity during movement of the affected hand in the
ipsilesional motor and premotor cortex in the anodal tDCS group compared
to the sham treatment group. Structural MRI revealed
intervention-related increases in gray matter volume in cortical areas,
including ipsilesional motor and premotor cortex after anodal tDCS but
not sham treatment. The addition of ipsilesional anodal tDCS to a 9-day
motor training program improved long-term clinical outcomes relative to
sham treatment in patients after stroke.
Smelling farts could be the best thing you do today
Hydrogen sulfide, commonly found in rotten eggs and human flatulence,
could have significant health benefits in small doses, researchers at
the University of Exeter say.
Have fun trying to convince your doctors to allow this. Do not start your own treatment by farting into a paper bag and inhaling that. You have no idea how deadly your farts can be without extensive testing.
http://www.cnet.com/news/how-smelling-farts-could-save-your-life/
It's Friday, and what better way to spend the day that starts with F than talking about Flatulence?
Anyone who has accidentally let one rip in a social situation understands the immediate horror associated with getting caught passing gas. But instead of being ashamed when you fart in public, you should embrace your dirty deed with pride, as you may have just helped saved someone's life. Well, that's what a study currently getting some attention might suggest, but it's more complicated than that.
The study out of the University of Exeter
in the UK found that the hydrogen sulfide gas found in rotten eggs and
flatulence could reduce the risk of cancer, heart attack, strokes,
arthritis, and dementia.
The Exeter scientists created a compound called AP39 that slowly delivers small, concentrated amounts of the gas to mitochondria, the "powerhouses" of cells that take in nutrients, break them down, and create energy. Preventing or reversing mitochondrial damage is considered key to treating a variety of ailments.
"Our results indicate that if stressed cells are treated with AP39, mitochondria are protected and cells stay alive," Professor Matt Whiteman, of the University of Exeter Medical School, said in a statement. The researchers have published their findings in the journal MedChemComm and presented them at the June International Conference on Hydrogen Sulfide in Biology and Medicine in Kyoto, Japan.
Of course, hydrogen sulfide can prove deadly in large doses, meaning that sniffing a fart or two here and there is a much better and safer idea than, say, filling your house with rotten eggs.
So the next time someone lets one go in your presence, consider loudly thanking that person and letting the stink sink in before running in the other direction. Or, since scientists have yet to confirm that smelling farts is as valuable as delivering their compounds straight to cells, at least remember to stop and appreciate that hydrogen sulfide isn't all bad.
Have fun trying to convince your doctors to allow this. Do not start your own treatment by farting into a paper bag and inhaling that. You have no idea how deadly your farts can be without extensive testing.
http://www.cnet.com/news/how-smelling-farts-could-save-your-life/
It's Friday, and what better way to spend the day that starts with F than talking about Flatulence?
Anyone who has accidentally let one rip in a social situation understands the immediate horror associated with getting caught passing gas. But instead of being ashamed when you fart in public, you should embrace your dirty deed with pride, as you may have just helped saved someone's life. Well, that's what a study currently getting some attention might suggest, but it's more complicated than that.
The Exeter scientists created a compound called AP39 that slowly delivers small, concentrated amounts of the gas to mitochondria, the "powerhouses" of cells that take in nutrients, break them down, and create energy. Preventing or reversing mitochondrial damage is considered key to treating a variety of ailments.
"Our results indicate that if stressed cells are treated with AP39, mitochondria are protected and cells stay alive," Professor Matt Whiteman, of the University of Exeter Medical School, said in a statement. The researchers have published their findings in the journal MedChemComm and presented them at the June International Conference on Hydrogen Sulfide in Biology and Medicine in Kyoto, Japan.
Of course, hydrogen sulfide can prove deadly in large doses, meaning that sniffing a fart or two here and there is a much better and safer idea than, say, filling your house with rotten eggs.
So the next time someone lets one go in your presence, consider loudly thanking that person and letting the stink sink in before running in the other direction. Or, since scientists have yet to confirm that smelling farts is as valuable as delivering their compounds straight to cells, at least remember to stop and appreciate that hydrogen sulfide isn't all bad.
Tailored new compound can dramatically reduce brain damage resulting from stroke - hydrogen sulfide inhibition
Now if we had ANY stroke leadership at all we would propose and start research trials in humans. But we don't so we are screwed for at least another 50 years. And if you know you are going to have a stroke you could get pretreatment. Maybe if your are having surgery for an AVM or aneurysm and are worried about having a stroke during surgery. This is not medical advice, ask your doctor these simple questions
http://www.news-medical.net/news/20160310/Tailored-new-compound-can-dramatically-reduce-brain-damage-resulting-from-stroke.aspx
http://www.news-medical.net/news/20160310/Tailored-new-compound-can-dramatically-reduce-brain-damage-resulting-from-stroke.aspx
After suffering a stroke, about three-fourths of patients exhibit
some disability. The extent of a patient's symptoms depends on the
degree and location of brain tissue damage following the stroke event.
This week in ACS Central Science, researchers show that by
using a tailored small molecule to turn off the production of a key
neuromodulator in the brain, they can dramatically reduce brain damage
in stroke models in rats.
The neuromodulator is the gas hydrogen sulfide (H2S). Its production is carefully controlled in the brain. After a stroke, levels of H2S appear to be elevated, leading to brain tissue damage, but the details of how that happens are still a bit of a mystery. So, David B. Berkowitz and coworkers designed a quick way to synthesize molecules they deduced would inhibit the production of H2S. They showed in vitro that these compounds block an enzyme called CBS from making H2S by mimicking one of its other products. Peter T. H. Wong and colleagues then tested the compounds in rats. When the new compound was injected an hour after the simulation of a stroke, the authors observed about a 70 percent reduction in the severity of the observed stroke damage. The results were even more striking with pretreatment. The authors conclude that using molecules like the ones they made will help researchers dissect the mechanism underlying H2S-mediated neuronal damage and will serve as an important starting point for the development of even more drug-like compounds that act in a similar manner.
The neuromodulator is the gas hydrogen sulfide (H2S). Its production is carefully controlled in the brain. After a stroke, levels of H2S appear to be elevated, leading to brain tissue damage, but the details of how that happens are still a bit of a mystery. So, David B. Berkowitz and coworkers designed a quick way to synthesize molecules they deduced would inhibit the production of H2S. They showed in vitro that these compounds block an enzyme called CBS from making H2S by mimicking one of its other products. Peter T. H. Wong and colleagues then tested the compounds in rats. When the new compound was injected an hour after the simulation of a stroke, the authors observed about a 70 percent reduction in the severity of the observed stroke damage. The results were even more striking with pretreatment. The authors conclude that using molecules like the ones they made will help researchers dissect the mechanism underlying H2S-mediated neuronal damage and will serve as an important starting point for the development of even more drug-like compounds that act in a similar manner.
Source:
American Chemical Society
Return to Work Toolkit - stroke rehab
Multiple choices. It would be so much easier to return to work by addressing a major root cause in the first place, dead and damaged neurons that occur during the neuronal cascade of death. But shit, it is much easier and makes people feel like they are helping by doing this crapola rather than solving the real problems in stroke.
This one from the NSA - National Stroke Association:
Return to Work Toolkit - stroke rehab
This one from Heart and Stroke Foundation of Canada:
Back to work
Pedicure again
Just got a pedicure to try to forestall the problem I had last year on vacation where I lost the left big toenail due to massive amounts of walking on the cruise, not tight enough shoes. Leaving Thursday for 8 days in Paris, 7 days driving the French country side. Much wine will be consumed.
Microgliosis in the Injured Brain Infiltrating Cells and Reactive Microglia Both Play a Role
Can't tell if this is any use in our non-existant strategy or rehab. So ask your doctor. Or your stroke association president.
microgliosis
accumulation of microglial cells as a reaction to injury to the parenchyma of the central nervous system, a characteristic of nonsuppurative encephalomyelitis.
Microgliosis in the Injured Brain Infiltrating Cells and Reactive Microglia Both Play a Role
- 1Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, Lanzhou, China
- Shengxiang Zhang, School of Life Sciences, Lanzhou University, No. 222 South Tianshui Road, Lanzhou, Gansu 730000, China. Email: sxzhang@lzu.edu.cn
Abstract
Microgliosis is an intense reaction of CNS
microglia to pathogenic insults. One of the characteristic features of
microgliosis
is an increase in the number of activated microglia
at the site of lesion. Ontogenically, microglia are considered to be of
mesodermal lineage in the adult CNS, but the origin
of the accumulated microglia in pathological conditions remains
controversial.
Some studies indicate that circulating cells from
the bloodstream can infiltrate the CNS and contribute to microglial
pool,
but some studies suggest that local expansion of
reactive microglia is the sole source for parenchymal microglia. Recent
data
suggest that latent progenitors may also exist in
the CNS. Available evidence suggests that multiple sources of microglia
may exist under various neurological conditions. In
this review, we compare the prevalent views and supporting evidence
from
different experimental models and provide an
overview on the origins of microgliosis.
Triciclos Freeway 125cc Wheelchair Motorcycle (Only available in Brazil)
Maybe you want to look up the wheelchair car:
Stuff is out there if only we had a decent stroke association that listed all the possibilities for powered movement. Why hasn't your doctor or therapist given you these possibilities? They are supposed to know everything about stroke rehab.
Or one of these:
http://www.wimp.com/newdevice/
Stuff is out there if only we had a decent stroke association that listed all the possibilities for powered movement. Why hasn't your doctor or therapist given you these possibilities? They are supposed to know everything about stroke rehab.
Texas lawyer building hatchback cars made for people in wheelchairs
Or one of these:
electric attachable handbikes
Turn your wheelchair into a motorcycle
Or this segway like wheelchair:
http://www.wimp.com/newdevice/
Triciclos Freeway 125cc Wheelchair Motorcycle (Only available in Brazil)
Quick Overview
Approximately $12,000. Only
Available in Brazil. United States DOT & EPA bureaucracies make
import impossible. We have already "gone down that road". 45-50 mph,
125 cc, 13" tires.
Does the freedom of the open road call to you? Soon the wind could be whipping through your hair, your cheeks flapping from the ridiculous big smile on your face.
Does the freedom of the open road call to you? Soon the wind could be whipping through your hair, your cheeks flapping from the ridiculous big smile on your face.
New research highlights need to give greater consideration to sleep in stroke care
I was perpetually exhausted while in the hospital, one attempt using finger oximetry that totally missed my sleep apnea. I do wonder if sleeping pills actually create useful sleep. I had them almost every night, nurses would hand them out like candy. We need a stroke protocol here.
Maybe this might help; most of these were written in 2013 which shows you how appallingly slow stroke research is disseminated to clinical practice. That's because we have NO stroke leadership pushing best practices.
Surrey, University of
Researchers identify sleep as a problem in patients with stroke, and highlight the need to give greater consideration to sleep in stroke care, and in particular stroke rehabilitation.
• NICE guideline on stroke rehabilitation does not reference sleep at all
• Sleep essential for learning, mental and physical health
• Stroke care mainly focussed on daytime activity and ignores sleep altogether
Latest findings from the University of Surrey and University of Freiburg all point towards the important role of sleep in patients with stroke. However, at present, sleep is rarely considered in in-patient and community-based stroke care. The team of researchers also found that this is despite a number of studies that highlights patients with stroke often experience difficulties with their sleep.
Patients often report that going to sleep and staying asleep is difficult and aggravates the challenges of coping with everyday activities. But how much do we really know about the sleep of patients with chronic stroke and how their sleep compares to that of other older healthy people? For the first time, the researchers have addressed this question by drawing together all existing research comparing patients with stroke with control populations using polysomnography, the gold standard method to study sleep.
The study, published in the journal PLOS ONE, revealed that sleep is poor in stroke patients, but the research also highlighted the lack of knowledge in particular with regard to older people and chronic patients. For example, the team found no study comparing the sleep physiology of chronic stroke patients with other people in their respective age group. While there is some information on changes of sleep difficulties throughout stroke recovery, how stroke severity, lesion location, and sleep are linked to physical and mental health is generally unexplored.
“Sleep is essential for learning, mental and physical health in everybody but even more so for chronic stroke patients. A comprehensive and holistic understanding of sleep is therefore needed to improve rehabilitation effectiveness and ensure quality long term care,” said lead author Professor Annette Sterr from the University of Surrey.
“However, this link between sleep and stroke has not yet entered clinical practice. The recent guideline for stroke rehabilitation issued by the UK National Institute for Health and Care Excellence (NICE) provides a detailed account of the medical, physical and psychological needs to be met through in-and outpatients stroke care, but these recommendations make no comment on sleep. Moreover, stroke care is focussed on daytime activity and ignores sleep altogether.”
“In the UK, strokes are a major health problem. Every year, around 110,000 people have a stroke in England and it is the third largest cause of death. One key theme emerging through our research is the need to give greater consideration to sleep in stroke care, and in particular in stroke rehabilitation. By doing so this will ensure that each patient is treated fairly and an appropriate course of treatment is planned and implemented.”
Maybe this might help; most of these were written in 2013 which shows you how appallingly slow stroke research is disseminated to clinical practice. That's because we have NO stroke leadership pushing best practices.
How sleep acts as a cleaning system for the brain
http://www.alphagalileo.org/ViewItem.aspx?ItemId=162152&CultureCode=enSurrey, University of
Researchers identify sleep as a problem in patients with stroke, and highlight the need to give greater consideration to sleep in stroke care, and in particular stroke rehabilitation.
• NICE guideline on stroke rehabilitation does not reference sleep at all
• Sleep essential for learning, mental and physical health
• Stroke care mainly focussed on daytime activity and ignores sleep altogether
Latest findings from the University of Surrey and University of Freiburg all point towards the important role of sleep in patients with stroke. However, at present, sleep is rarely considered in in-patient and community-based stroke care. The team of researchers also found that this is despite a number of studies that highlights patients with stroke often experience difficulties with their sleep.
Patients often report that going to sleep and staying asleep is difficult and aggravates the challenges of coping with everyday activities. But how much do we really know about the sleep of patients with chronic stroke and how their sleep compares to that of other older healthy people? For the first time, the researchers have addressed this question by drawing together all existing research comparing patients with stroke with control populations using polysomnography, the gold standard method to study sleep.
The study, published in the journal PLOS ONE, revealed that sleep is poor in stroke patients, but the research also highlighted the lack of knowledge in particular with regard to older people and chronic patients. For example, the team found no study comparing the sleep physiology of chronic stroke patients with other people in their respective age group. While there is some information on changes of sleep difficulties throughout stroke recovery, how stroke severity, lesion location, and sleep are linked to physical and mental health is generally unexplored.
“Sleep is essential for learning, mental and physical health in everybody but even more so for chronic stroke patients. A comprehensive and holistic understanding of sleep is therefore needed to improve rehabilitation effectiveness and ensure quality long term care,” said lead author Professor Annette Sterr from the University of Surrey.
“However, this link between sleep and stroke has not yet entered clinical practice. The recent guideline for stroke rehabilitation issued by the UK National Institute for Health and Care Excellence (NICE) provides a detailed account of the medical, physical and psychological needs to be met through in-and outpatients stroke care, but these recommendations make no comment on sleep. Moreover, stroke care is focussed on daytime activity and ignores sleep altogether.”
“In the UK, strokes are a major health problem. Every year, around 110,000 people have a stroke in England and it is the third largest cause of death. One key theme emerging through our research is the need to give greater consideration to sleep in stroke care, and in particular in stroke rehabilitation. By doing so this will ensure that each patient is treated fairly and an appropriate course of treatment is planned and implemented.”
- Full bibliographic informationPolysomnographic characteristics of sleep in stroke: A systematic review and meta-analysis; Chiara Baglioni, Christoph Nissen, Adrian Schweinoch1, Dieter Riemann, Kai Spiegelhalder, Mathias Berger, Cornelius Weiller, Annette Sterr; PLOS ONE; doi: 10.1371/journal.pone.0148496
Novel blood test for Alzheimer’s diagnosis
Your doctor might want to validate which of these percentages is accurate for their patients
Has your doctor/hospital done anything since these earlier research results?
1. Your 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
Novel blood test for Alzheimer’s diagnosis
Ruhr-Universitaet-Bochum
Today, Alzheimer’s disease is diagnosed too late. In collaboration with a research team at the university and German Center for Neurogenerative Diseases (DZNE) in Göttingen, Researchers at Ruhr-Universität Bochum (RUB) have developed a blood test that may potentially facilitate detection of Alzheimer’s at an early stage. It is based on an immuno-chemical analysis using an infrared sensor.
The sensor’s surface is coated with highly specific antibodies which extract biomarkers for Alzheimer’s from the blood or the cerebrospinal fluid, taken from the lower part of the back (lumbar liquor). The infrared sensor analyses if the biomarkers show already pathological changes, which can take place more than 15 years before any clinical symptoms appear. This method has been featured as the cover story in the internationally renowned academic journal “Biophotonics”, and the results of the study were also published in “Analytical Chemistry”.
In most instances, diagnosis is too late
A major problem of Alzheimer’s disease diagnosis is the fact that, by the time the first clinical symptoms appear, massive irreversible damage to the brain has already occurred. At that point, symptomatic treatment is the only available option. “If we wish to have a drug at our disposal that can significantly inhibit the progress of the disease, we need blood tests that detect Alzheimer’s in its pre-dementia stages,” says Prof Dr Klaus Gerwert, Head of the Department of Biophysics at RUB. “By applying such drugs at an early stage, we could prevent dementia, or at the very least delay its onset,” adds Prof Dr med. Jens Wiltfang, Head of the Department for Psychiatry and Psychotherapy at the University of Göttingen and Clinical Research Coordinator at DZNE Göttingen.
Morbus Alzheimer’s and misfolding of Amyloid beta peptide
For the novel test, the secondary structure of the so-called Amyloid beta peptides serves as biomarker. This structure changes in Alzheimer’s patients. In the misfolded, pathological structure, more and more Amyloid beta peptides can accumulate, gradually forming visible plaque deposits in the brain that are typical for Alzheimer’s disease. This happens more than15 years before first clinical symptoms appear. The pathological beta Amyloid plaques can be temporarily detected by positron emission tomography, short: Amyloid PET; but this procedure is comparatively expensive and is accompanied by radiation exposure.
Patented diagnostic method for Alzheimer’s detection
Together with Prof Dr med. Jens Wiltfang from Göttingen, the team headed by Prof Dr Klaus Gerwert has developed an infrared sensor for detecting misfolding of Amyloid beta peptides as part of the PhD research projects of Andreas Nabers and Jonas Schartner. The infrared sensor extracts the Amyloid beta peptide from body fluids. The method is patent pending. After initially working with cerebrospinal fluid, the researchers subsequently expanded the method towards blood analysis. “We do not merely select one single possible folding arrangement of the peptide; rather, we detect how all existing Amyloid beta secondarystructures are distributed, in their healthy and in their pathological forms,” says Gerwert. Precise diagnostics is not possible until the distribution of all secondary structures is evaluated. Tests that analyse Amyloid beta peptide are already available with so-called enzyme-linked immunosorbent assays (ELISA). They identify the total concentration, percentage of forms of different length, as well as the concentration of individual conformations in body fluids; but they have not, as yet, provided information on the diagnostically relevant distribution of the secondary structures at once. “This is why ELISA tests have not been proven very effective when applied in blood sample analysis in practice,” explains Klaus Gerwert.
First clinical trials completed
Using the methods now developed in Bochum and Göttingen, the researchers have analysed samples from 141 patients. They have achieved a diagnostic precision of 84 per cent in the blood and 90 per cent in cerebrospinal fluid, compared with the clinical gold standard. The test revealed an increase of misfolded biomarkers as spectral shift of Amyloid beta band below threshold, thus diagnosing Alzheimer’s. “What’s unique about it is that this is the only robust label-free test with a single threshold,” as Andreas Nabers describes the result of his dissertation.
A potential sensor for early detection
As part of the published study, the researchers have tested the potential for early detection of Morbus Alzheimer’s on a small group of patients. The results suggest that even in pre-dementia stages, an increased concentration of misfolded Amyloid beta peptides can be detected in body fluids. Thus, Morbus Alzheimer’s may in future be diagnosable in preclinical stages. “The sooner Alzheimer’s is detected, the better the therapy chances. This sensor is an important milestone in the right direction,” adds Prof Dr Jens Wiltfang. Currently, sample analyses for early detection in 800 study participants are being conducted, in order to optimise statistical significance.
http://aktuell.ruhr-uni-bochum.de/pm2016/pm00034.html.en
Has your doctor/hospital done anything since these earlier research results?
1. Your 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
Novel blood test for Alzheimer’s diagnosis
Ruhr-Universitaet-Bochum
Today, Alzheimer’s disease is diagnosed too late. In collaboration with a research team at the university and German Center for Neurogenerative Diseases (DZNE) in Göttingen, Researchers at Ruhr-Universität Bochum (RUB) have developed a blood test that may potentially facilitate detection of Alzheimer’s at an early stage. It is based on an immuno-chemical analysis using an infrared sensor.
The sensor’s surface is coated with highly specific antibodies which extract biomarkers for Alzheimer’s from the blood or the cerebrospinal fluid, taken from the lower part of the back (lumbar liquor). The infrared sensor analyses if the biomarkers show already pathological changes, which can take place more than 15 years before any clinical symptoms appear. This method has been featured as the cover story in the internationally renowned academic journal “Biophotonics”, and the results of the study were also published in “Analytical Chemistry”.
In most instances, diagnosis is too late
A major problem of Alzheimer’s disease diagnosis is the fact that, by the time the first clinical symptoms appear, massive irreversible damage to the brain has already occurred. At that point, symptomatic treatment is the only available option. “If we wish to have a drug at our disposal that can significantly inhibit the progress of the disease, we need blood tests that detect Alzheimer’s in its pre-dementia stages,” says Prof Dr Klaus Gerwert, Head of the Department of Biophysics at RUB. “By applying such drugs at an early stage, we could prevent dementia, or at the very least delay its onset,” adds Prof Dr med. Jens Wiltfang, Head of the Department for Psychiatry and Psychotherapy at the University of Göttingen and Clinical Research Coordinator at DZNE Göttingen.
Morbus Alzheimer’s and misfolding of Amyloid beta peptide
For the novel test, the secondary structure of the so-called Amyloid beta peptides serves as biomarker. This structure changes in Alzheimer’s patients. In the misfolded, pathological structure, more and more Amyloid beta peptides can accumulate, gradually forming visible plaque deposits in the brain that are typical for Alzheimer’s disease. This happens more than15 years before first clinical symptoms appear. The pathological beta Amyloid plaques can be temporarily detected by positron emission tomography, short: Amyloid PET; but this procedure is comparatively expensive and is accompanied by radiation exposure.
Patented diagnostic method for Alzheimer’s detection
Together with Prof Dr med. Jens Wiltfang from Göttingen, the team headed by Prof Dr Klaus Gerwert has developed an infrared sensor for detecting misfolding of Amyloid beta peptides as part of the PhD research projects of Andreas Nabers and Jonas Schartner. The infrared sensor extracts the Amyloid beta peptide from body fluids. The method is patent pending. After initially working with cerebrospinal fluid, the researchers subsequently expanded the method towards blood analysis. “We do not merely select one single possible folding arrangement of the peptide; rather, we detect how all existing Amyloid beta secondarystructures are distributed, in their healthy and in their pathological forms,” says Gerwert. Precise diagnostics is not possible until the distribution of all secondary structures is evaluated. Tests that analyse Amyloid beta peptide are already available with so-called enzyme-linked immunosorbent assays (ELISA). They identify the total concentration, percentage of forms of different length, as well as the concentration of individual conformations in body fluids; but they have not, as yet, provided information on the diagnostically relevant distribution of the secondary structures at once. “This is why ELISA tests have not been proven very effective when applied in blood sample analysis in practice,” explains Klaus Gerwert.
First clinical trials completed
Using the methods now developed in Bochum and Göttingen, the researchers have analysed samples from 141 patients. They have achieved a diagnostic precision of 84 per cent in the blood and 90 per cent in cerebrospinal fluid, compared with the clinical gold standard. The test revealed an increase of misfolded biomarkers as spectral shift of Amyloid beta band below threshold, thus diagnosing Alzheimer’s. “What’s unique about it is that this is the only robust label-free test with a single threshold,” as Andreas Nabers describes the result of his dissertation.
A potential sensor for early detection
As part of the published study, the researchers have tested the potential for early detection of Morbus Alzheimer’s on a small group of patients. The results suggest that even in pre-dementia stages, an increased concentration of misfolded Amyloid beta peptides can be detected in body fluids. Thus, Morbus Alzheimer’s may in future be diagnosable in preclinical stages. “The sooner Alzheimer’s is detected, the better the therapy chances. This sensor is an important milestone in the right direction,” adds Prof Dr Jens Wiltfang. Currently, sample analyses for early detection in 800 study participants are being conducted, in order to optimise statistical significance.
http://aktuell.ruhr-uni-bochum.de/pm2016/pm00034.html.en
- Full bibliographic informationA.
Nabers, J. Ollesch, J. Schartner, C. Kötting, J. Genius, U. Haußmann,
H. Klafki, J. Wiltfang, and K. Gerwert (2016): An infrared sensor
analysing label-free the secondary structure of the Abeta peptide in
presence of complex fluids, Journal of Biophotonics, DOI:
10.1002/jbio.201400145
A. Nabers, J. Ollesch, J. Schartner, C. Kötting, J. Genius, H. Hafermann, H. Klafki, K. Gerwert, and J. Wiltfang (2016): The Amyloid-beta secondary structure distribution in CSF and blood measured by an immuno-IR-sensor: a novel biomarker candidate for Alzheimer’s disease, Analytical Chemistry, Doi: 10.1021/acs.analchem.5b04286
Why P4P(pay for performance) can hurt patient care
I completely and totally disagree where stroke care is concerned. We need to set result goals in recovery not just guidelines to follow. Patients don't give a shit about how they recover they want to recover. Current full recovery of 10% is an appalling failure. Anything to get that higher is worth it even if doctors complain.
Why P4P(pay for performance) can hurt patient care
Why P4P(pay for performance) can hurt patient care
Posttraumatic Stress Disorder: Does the Gut Microbiome Hold the Key?
Since we have a 23% chance of survivors getting PTSD, your doctor should already have stroke protocols to prevent that and be following this with great interest.
Posttraumatic Stress Disorder: Does the Gut Microbiome Hold the Key?
- Sophie Leclercq, PhD1,2
- Paul Forsythe, PhD1,3
- John Bienenstock, MD1,2⇑
- 1McMaster Brain-Body Institute at St Joseph’s Healthcare Hamilton, Hamilton, Ontario
- 2Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario
- 3Firestone Institute for Respiratory Health and Department of Medicine, McMaster University, Hamilton, Ontario
- John Bienenstock, MD, McMaster Brain-Body Institute at St. Joseph’s Healthcare Hamilton, 50 Charlton Avenue East, Hamilton, ON L8 N 4A6, Canada. Email: bienens@mcmaster.ca
Abstract
Gut bacteria strongly influence our
metabolic, endocrine, immune, and both peripheral and central nervous
systems. Microbiota
do this directly and indirectly through their
components, shed and secreted, ranging from fermented and digested
dietary and
host products to functionally active
neurotransmitters including serotonin, dopamine, and γ-aminobutyric
acid. Depression
has been associated with enhanced levels of
proinflammatory biomarkers and abnormal responses to stress.
Posttraumatic stress
disorder (PTSD) appears to be marked in addition by
low cortisol responses, and these factors seem to predict and
predispose
individuals to develop PTSD after a traumatic
event. Dysregulation of the immune system and of the
hypothalamic-pituitary-adrenal
axis observed in PTSD may reflect prior trauma
exposure, especially early in life. Early life, including the prenatal
period,
is a critical time in rodents, and may well be for
humans, for the functional and structural development of the immune and
nervous systems. These, in turn, are likely shaped
and programmed by gut and possibly other bacteria. Recent experimental
and clinical data converge on the hypothesis that
imbalanced gut microbiota in early life may have long-lasting immune and
other physiologic effects that make individuals
more susceptible to develop PTSD after a traumatic event and contribute
to
the disorder. This suggests that it may be possible
to target abnormalities in these systems by manipulation of certain gut
bacterial communities directly through
supplementation or indirectly by dietary and other novel approaches.
Heart Disease and Stroke Statistics—2016 Update
Worthless reams of useless information for survivors. I'll highlight why NOTHING gets done for survivors. Not a single focus is about solving all the problems in stroke for survivors. This is precisely why our stroke associations need to be destroyed and start over with survivors. NOTHING on any BHAG (Big Hairy Audacious Goals), just fucking small shitworthy goals that require nothing in the way of intelligence or innovation.
Other years for your edification, not recovery information.
Heart Disease and Stroke Statistics—2016 Update
Current Status of Cardiovascular Health in the United States (Chapter 2)
-
The concept of cardiovascular health represents a heightened focus for the AHA, with 3 central and novel emphases:
-
—An expanded focus on not only CVD prevention but also promotion of positive cardiovascular health, in addition to the treatment of established CVD
-
—The prioritization of both health behaviors (healthy diet pattern, appropriate energy balance, PA, and nonsmoking) and health factors (optimal blood lipids, blood pressure, glucose levels) throughout the lifespan as primary goals unto themselves
-
—Population-level health promotion strategies to shift the majority of the public toward greater cardiovascular health, in addition to targeting those individuals at greatest CVD risk, because CVD occurs at all risk levels across the population and because healthy lifestyles are uncommon throughout the US population.Heart Disease and Stroke Statistics—2015 Update
-
Other years for your edification, not recovery information.
Heart Disease and Stroke Statistics—2015 Update
Heart Disease and Stroke Statistics—2014 Update
Tuesday, March 15, 2016
Maple Syrup May Protect Brain From Alzheimer’s And Other Neurodegenerative Disease
I'm sure your doctor is following the American Chemical Society’s annual meeting.
You will have to send your doctor after the amounts used.
Remember nothing here can be done without your doctors prescription, you know how dangerous eating food is without your doctors knowledge.
http://www.medicaldaily.com/maple-syrup-alzheimers-disease-brain-health-377846
You will have to send your doctor after the amounts used.
Remember nothing here can be done without your doctors prescription, you know how dangerous eating food is without your doctors knowledge.
http://www.medicaldaily.com/maple-syrup-alzheimers-disease-brain-health-377846
Starting
your day off with a stack of maple syrup-soaked pancakes may help keep
your brain safe from harm. An international team of scientists published
a large body of research to support the beneficial effects of natural
products on neurodegenerative diseases, like Alzheimer’s. The findings, presented at the American Chemical Society’s annual meeting, revealed the potential protective effect maple syrup may have on brain cells against damage.
The team examined the results from 24 different studies that were focused on promoting a healthy brain through diet, and a pattern began to emerge. Researchers found real maple syrup — the kind that comes from the sap of a maple tree — may help prevent two types of proteins found in brain cells from clumping together. When these cellular proteins, beta amyloid and tau peptide, improperly fold and accumulate together they form plaque in the brain, which is a root cause of Alzheimer’s and other brain diseases.
Scientists also found in patients who are already diagnosed with Alzheimer’s that maple syrup extract may be able to prolong the patient’s lifespan by protecting the brain cells from tangling up known as fibrillation. When protein pieces called beta-amyloid clump or tangle together, the small clumps they form may block cell-to-cell signaling, making it difficult for certain brain regions to send messages of communication to other areas. Blockages activate immune system cells that trigger inflammation and destroy disabled cells. Maple syrup’s ability to keep beta-amyloid from sticking together or becoming tangled may be the trick to protect the brain and keep it functioning properly.
"We already know that maple has more than 100 bioactive compounds, some of which have anti-inflammatory properties,” said Serge Beaulieu, the president of the Federation of Quebec Maple Syrup Producers, in a statement. “Brain health is the latest topic of exploration and we look forward to learning more about the potential benefits that maple syrup might have in this area."
Researchers suspect the phenol concentrations found in maple syrup may be the key ingredient. Phenolic compounds found in plants have antioxidant effects, which enable them to capture harmful free radicals before they cause serious damage to cells. Resveratrol is another type of phenolic compound found in grape skins and red wine that has been shown to have anticancer benefits in addition to its neuroprotective effects.
“Natural food products such as green tea, red wine, berries, and pomegranates continue to be studied for their potential benefits in combating Alzheimer's disease," said lead researcher Dr. Navindra P. Seeram, a scientist at Texas State University, in the statement. “And now, in preliminary laboratory-based Alzheimer's disease studies, phenolic-enriched extracts of maple syrup from Canada showed neuroprotective effects, similar to resveratrol, a compound found in red wine.”
Alzheimer’s disease is a progressive condition that gradually worsens over time and causes memory loss, difficulty with language, concentrating, planning, and organizing. According to the Alzheimer’s Association, current treatments cannot stop the disease progression, but they can temporarily slow the worsening of symptoms to improve the quality of life. Using diet to prevent or delay the onset of the neurodegenerative disease may be an effective and inexpensive intervention, however researchers plan to continue their investigation to confirm the benefits.
Source: Weaver D and Seeram NP, et al. American Chemical Society National Meeting & Exposition. 2016.
The team examined the results from 24 different studies that were focused on promoting a healthy brain through diet, and a pattern began to emerge. Researchers found real maple syrup — the kind that comes from the sap of a maple tree — may help prevent two types of proteins found in brain cells from clumping together. When these cellular proteins, beta amyloid and tau peptide, improperly fold and accumulate together they form plaque in the brain, which is a root cause of Alzheimer’s and other brain diseases.
Scientists also found in patients who are already diagnosed with Alzheimer’s that maple syrup extract may be able to prolong the patient’s lifespan by protecting the brain cells from tangling up known as fibrillation. When protein pieces called beta-amyloid clump or tangle together, the small clumps they form may block cell-to-cell signaling, making it difficult for certain brain regions to send messages of communication to other areas. Blockages activate immune system cells that trigger inflammation and destroy disabled cells. Maple syrup’s ability to keep beta-amyloid from sticking together or becoming tangled may be the trick to protect the brain and keep it functioning properly.
"We already know that maple has more than 100 bioactive compounds, some of which have anti-inflammatory properties,” said Serge Beaulieu, the president of the Federation of Quebec Maple Syrup Producers, in a statement. “Brain health is the latest topic of exploration and we look forward to learning more about the potential benefits that maple syrup might have in this area."
Researchers suspect the phenol concentrations found in maple syrup may be the key ingredient. Phenolic compounds found in plants have antioxidant effects, which enable them to capture harmful free radicals before they cause serious damage to cells. Resveratrol is another type of phenolic compound found in grape skins and red wine that has been shown to have anticancer benefits in addition to its neuroprotective effects.
“Natural food products such as green tea, red wine, berries, and pomegranates continue to be studied for their potential benefits in combating Alzheimer's disease," said lead researcher Dr. Navindra P. Seeram, a scientist at Texas State University, in the statement. “And now, in preliminary laboratory-based Alzheimer's disease studies, phenolic-enriched extracts of maple syrup from Canada showed neuroprotective effects, similar to resveratrol, a compound found in red wine.”
Alzheimer’s disease is a progressive condition that gradually worsens over time and causes memory loss, difficulty with language, concentrating, planning, and organizing. According to the Alzheimer’s Association, current treatments cannot stop the disease progression, but they can temporarily slow the worsening of symptoms to improve the quality of life. Using diet to prevent or delay the onset of the neurodegenerative disease may be an effective and inexpensive intervention, however researchers plan to continue their investigation to confirm the benefits.
Source: Weaver D and Seeram NP, et al. American Chemical Society National Meeting & Exposition. 2016.
Dabigatran Versus Warfarin for Atrial Fibrillation in Real-World Clinical Practice
In case you need to be informed on this.
http://circoutcomes.ahajournals.org/content/9/2/126.abstract?etoc
http://circoutcomes.ahajournals.org/content/9/2/126.abstract?etoc
A Systematic Review and Meta-Analysis
- Robert J. Romanelli, PhD, MPH,
- Laura Nolting, BS,
- Marina Dolginsky, BS,
- Eunice Kym, PharmD and
- Kathleen B. Orrico, PharmD
+ Author Affiliations
- From the Palo Alto Medical Foundation Research Institute, Palo Alto, CA (R.J.R., L.N., M.D.); and Department of Clinical Pharmacy, University of California, San Francisco (E.K., K.B.O.).
- Correspondence to Robert J. Romanelli, PhD, MPH, Palo Alto Medical Foundation Research Institute, 795 El Camino Real Ames Bldg, Palo Alto, CA 94301. E-mail romanellir@pamfri.org
Abstract
Background—Trial
data for the benefits and risks of dabigatran versus warfarin in the
treatment of nonvalvular atrial fibrillation are
lacking. We sought to review real-world
observational evidence for the comparative effectiveness and safety of
these agents.
Methods and Results—A
systematic search of multiple databases was conducted from first
available date to March 10, 2015 for longitudinal, observational
studies comparing dabigatran with warfarin.
Two reviewers evaluated studies for eligibility and extracted hazard
ratios for
ischemic stroke and gastrointestinal and
intracranial bleeding. hazard ratios were pooled using random-effects
meta-analysis.
Metaregression was performed to assess
treatment-effect heterogeneity. We identified 232 unique citations.
Seven retrospective
cohort studies met study eligibility
criteria, with 348 750 patients and a mean follow-up of 2.2 years. In
pooled analyses,
dabigatran-150 mg was not superior to
warfarin in preventing stroke (hazard ratio, 0.92; 95% confidence
interval, 0.84–1.01;
P=0.066), but had a significantly lower hazard of intracranial bleeding (0.44; 0.34–0.59; P<0.001). Dabigatran-150 mg had a significantly greater hazard of gastrointestinal bleeding than warfarin (1.23; 1.01–1.50;
P=0.041), which was potentiated in
studies of older (elderly) versus younger populations (median/mean age,
≥75 versus <75 years;
β=1.53; 95% confidence interval, 1.10–2.14; P=0.020).
Conclusions—In
real-world clinical practice, dabigatran is comparable with warfarin in
preventing ischemic stroke among patients with
nonvalvular atrial fibrillation. However,
dabigatran is associated with a lower risk for intracranial bleeding
relative to
warfarin, but—particularly among the
elderly—a greater risk for gastrointestinal bleeding. Bleeding outcomes
from observational
studies are consistent with those from the
pivotal Randomized Evaluation of Long-Term Anticoagulation Therapy
trial.
Abstract TP143: Effects of Aerobic Exercise Intensity on Novel Blood Biomarkers of Neuroplasticity After Stroke
How many years and more research is needed before a stroke protocol is put together on the levels of exercise needed to assist neuroplasticity and stroke recovery? This won't occur with our fucking lack of stroke leadership. Writeups like this are totally worthless without making translational protocols on how this can be used by survivors.
http://stroke.ahajournals.org/content/47/Suppl_1/ATP143.short
http://stroke.ahajournals.org/content/47/Suppl_1/ATP143.short
Abstract TP143: Effects of Aerobic Exercise Intensity on Novel Blood Biomarkers of Neuroplasticity After Stroke
- Dustyn Whitesel1;
- Pierce Boyne1;
- Daniel Carl1;
- Jennifer Westover1;
- Colleen Meyrose1;
- Johnny Wilkerson1;
- Jane C Khoury2;
- Myron Gerson3;
- Kim Seroogy4;
- Kristal Hatter5;
- Darcy Reisman6;
- Brett Kissela4;
- Kari Dunning1
+ Author Affiliations
- 1Dept of Rehabilitation Sciences, Univ of Cincinnati, Cincinnati, OH
- 2Div of Biostatistics and Epidemiology, Cincinnati Children's Hosp Med Cntr, Cincinnati, OH
- 3Depts of Internal Medicine and Cardiology, Univ of Cincinnati, Cincinnati, OH
- 4Dept of Neurology and Rehabilitation Medicine, Univ of Cincinnati, Cincinnati, OH
- 5Clinical Translational Rsch Cntr, Cincinnati Children's Hosp Med Cntr, Cincinnati, OH
- 6Dept of Physical Therapy, Univ of Delaware, Newark, DE
Abstract
Introduction: Aerobic
exercise (AEX) may facilitate neurologic stroke recovery. Among healthy
adults, intense AEX is known to upregulate
brain-derived neurotrophic factor (BDNF), a
critical facilitator of neuroplasticity, motor learning and cognition.
Increased
blood lactate during AEX appears to be a key
mechanism underlying this effect. Intense AEX also increases blood
ionized calcium
(Ca++). In animal studies, some of this
increased Ca++ has been shown to be transported to the brain and enhance
synthesis
of monoamine neurotransmitters (e.g. dopamine)
that are associated with neuroplasticity and motor learning. Thus,
increased
blood lactate and Ca++ during AEX represent
potentially important biomarkers of central neurologic benefits, but
neither has
been previously studied in persons with stroke.
Hypothesis: High intensity AEX will elicit significantly larger lactate and Ca++ responses than moderate intensity in chronic stroke.
Methods: Using a
crossover design, eight subjects (mean ± SD age, 57 ± 8 years; years
post stroke, 8.7 ± 2.7) performed one 20 minute
session each of moderate and high intensity
treadmill AEX in random order. Blood lactate and Ca++ were measured at
baseline
and multiple time points during and after AEX.
Mixed effects models were used to examine changes within and between
protocols
using an alpha of 0.05.
Results: Blood lactate
response was significantly greater for high vs moderate intensity AEX
(p<<0.0001). While moderate intensity
showed no significant changes with time
(p=0.60), high intensity showed significant increases during and
immediately after
AEX (all p<0.0001). Blood Ca++ showed no
significant protocol by time interaction (p=0.08) but did show a
significant time
effect (p<0.0001) with increases during
(p<0.0001) and immediately after (p=0.01) AEX.
Conclusions: Unlike
moderate intensity AEX, high intensity elicited a robust lactate
response. This has promising implications for the
effects of high-intensity AEX on BDNF
post-stroke. Both protocols combined showed an increase in Ca++, which
has promising
implications for the effects of AEX on monoamine
neurotransmitter synthesis after stroke.
Astrocyte-Derived Pentraxin 3 Supports Blood–Brain Barrier Integrity Under Acute Phase of Stroke
So we just need researchers to follow up this to see if it possibly fixes this problem in the neuronal cascade of death. But that won't occur because we have NO strategy or stroke leadership.
Problem needing fixing:
Inflammatory action leaking through the blood brain barrier.
Astrocyte-Derived Pentraxin 3 Supports Blood–Brain Barrier Integrity Under Acute Phase of Stroke
Problem needing fixing:
Inflammatory action leaking through the blood brain barrier.
Astrocyte-Derived Pentraxin 3 Supports Blood–Brain Barrier Integrity Under Acute Phase of Stroke
- Akihiro Shindo, MD, PhD,
- Takakuni Maki, MD, PhD,
- Emiri T. Mandeville, MD, PhD,
- Anna C. Liang, MPS,
- Naohiro Egawa, MD, PhD,
- Kanako Itoh, MD, PhD,
- Naoki Itoh, MD,
- Mia Borlongan,
- Julie C. Holder, PhD,
- Tsu Tshen Chuang, PhD,
- John D. McNeish, PhD†,
- Hidekazu Tomimoto, MD, PhD,
- Josephine Lok, MD,
- Eng H. Lo, PhD and
- Ken Arai, PhD
+ Author Affiliations
- From the Neuroprotection Research Laboratory, Departments of Radiology and Neurology (A.S., T.M., E.T.M., A.C.L., N.E., K.I., N.I., M.B., J.L., E.H.L., K.A.) and Pediatrics (J.L.), Massachusetts General Hospital, Harvard Medical School, Charlestown, Boston; Department of Vascular Biology, GlaxoSmithKline, Harlow, United Kingdom (J.C.H., T.T.C., J.D.M.); and Department of Neurology, Mie University Graduate School of Medicine, Mie, Japan (A.S., H.T.).
- Correspondence to Ken Arai, PhD, Neuroprotection Research Laboratory, MGH East 149–2401, Charlestown, MA 02129. E-mail karai@partners.org
Abstract
Background and Purpose—Pentraxin
3 (PTX3) is released on inflammatory responses in many organs. However,
roles of PTX3 in brain are still mostly
unknown. Here we asked whether and how PTX3
contributes to blood–brain barrier dysfunction during the acute phase of
ischemic
stroke.
Methods—In vivo,
spontaneously hypertensive rats were subjected to focal cerebral
ischemia by transient middle cerebral artery occlusion.
At day 3, brains were analyzed to evaluate
the cellular origin of PTX3 expression. Correlations with blood–brain
barrier breakdown
were assessed by IgG staining. In vitro, rat
primary astrocytes and rat brain endothelial RBE.4 cells were cultured
to study
the role of astrocyte-derived PTX3 on
vascular endothelial growth factor–mediated endothelial permeability.
Results—During the
acute phase of stroke, reactive astrocytes in the peri-infarct area
expressed PTX3. There was negative correlation
between gradients of IgG leakage and
PTX3-positive astrocytes. Cell culture experiments showed that
astrocyte-conditioned
media increased levels of tight junction
proteins and reduced endothelial permeability under normal conditions.
Removing PTX3
from astrocyte-conditioned media by
immunoprecipitation increased endothelial permeability. PTX3 strongly
bound vascular endothelial
growth factor in vitro and was able to
decrease vascular endothelial growth factor–induced endothelial
permeability.
Conclusions—Astrocytes
in peri-infarct areas upregulate PTX3, which may support blood–brain
barrier integrity by regulating vascular endothelial
growth factor–related mechanisms. This
response in astrocytes may comprise a compensatory mechanism for
maintaining blood–brain
barrier function after ischemic stroke.
The Up- and Downside of Caloric Restriction for Aging and Health
So maybe the partial fasting diets aren't all that great. So go ask your doctor for guidance.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=162124&CultureCode=en
It’s already well known that a diet may have a life-extending effect. Researchers from Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, now showed that besides improving the functionality of stem cells in mice, a caloric restriction also leads to a fatale weakening of their immune system – counteracting the life-lengthening effect of a diet. The results are published in the Journal of Experimental Medicine on March, 14. 2016.
Only few years ago, researchers succeeded in prolonging the lifespan of worm C. elegans, fruit fly D. melongaster and rats by almost 50% through a simple caloric restriction – which immediately fueled hopes for having found one key to a longer life also for humans. However, transferring these results to long-lived primates short after was not equally successful and cooled down enthusiasms quite quickly. Now, aging researcher Karl Lenhard Rudolph, Scientific Director at the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, and his team showed that caloric restriction even has a severe downside. In feeding experiments, the stem cells of mice, which were set on a diet, were found to age slower – but the murine immune system was almost completely cut down. Outside of optimal, sterile laboratory conditions, this could lead to severe live-shortening infections. The results of the study are published in the Journal of Experimental Medicine’s current issue.
Caloric restriction slows down the aging of blood stem cells
The study focused on the effects of caloric restriction on blood stem cells (so-called hematopoietic stem cells, HSC) that are responsible for building red blood cells or lymphocytes (immune cells). Like for any other adult stem cell, HSC functionality decreases with every single cell division – the stem cells age. This is why they stay in a resting phase (quiescence) most of the time and are only activated when a massive cell reproduction is required (e.g. after acute blood loss). In their study, the researchers from Jena investigated how a 30% food restriction effects stem cell aging in mice. One main result was that the HSC stayed in a quiescent state even if simulated stress would have required their activation. This effect was found regardless of how long the diet lasted. Thus, during diet, the blood stem cells did not age at all and their functionality to build new blood cells remained increased even one year after diet.
Caloric restriction weakens the immune system
But the long-term diet had a downside, as well: The mice’s immune system almost completely was cut down. Although the diet had no strong effect on the overall cell number of blood cells, the production of lymphocytes – needed for immune defense – was decreased by up to 75%. As a consequence, mice were particularly prone to bacterial infections.
Slowing down aging under laboratory conditions is not yet transferable to humans
“The study provides the first experimental evidence that long-term caloric restriction – as intervention to slow down aging – increases stem cell functionality, but results in immune defects in the context of prolonged bacterial infection, too. Thus, positive effects of a diet are not transferable to humans one to one”, Rudolph sums up the study results. Even if – under laboratory conditions – aging of single cells or tissues may be slowed down through a diet, the immune suppression may have fatal consequences in real life. To benefit from caloric restriction or medicinal mimetika aiming at increasing health in the elderly, possible risks of such interventions to come down with life-threatening infections remain to be elucidated. „In sepsis patients, we see a higher survival rate for those with a higher body weight than for patients who are very lean“, Prof. Dr. Michael Bauer, Director of the Center for Sepsis Control and Care at University Hospital Jena (UKJ), concurs.
http://www.leibniz-fli.de/nc/institute/public-relations/press-releases/research/detailpage/?tx_news_pi1%5Bnews%5D=2510&cHash=7d5cbe951317dc513959534631b4def2
http://www.alphagalileo.org/ViewItem.aspx?ItemId=162124&CultureCode=en
It’s already well known that a diet may have a life-extending effect. Researchers from Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, now showed that besides improving the functionality of stem cells in mice, a caloric restriction also leads to a fatale weakening of their immune system – counteracting the life-lengthening effect of a diet. The results are published in the Journal of Experimental Medicine on March, 14. 2016.
Only few years ago, researchers succeeded in prolonging the lifespan of worm C. elegans, fruit fly D. melongaster and rats by almost 50% through a simple caloric restriction – which immediately fueled hopes for having found one key to a longer life also for humans. However, transferring these results to long-lived primates short after was not equally successful and cooled down enthusiasms quite quickly. Now, aging researcher Karl Lenhard Rudolph, Scientific Director at the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, and his team showed that caloric restriction even has a severe downside. In feeding experiments, the stem cells of mice, which were set on a diet, were found to age slower – but the murine immune system was almost completely cut down. Outside of optimal, sterile laboratory conditions, this could lead to severe live-shortening infections. The results of the study are published in the Journal of Experimental Medicine’s current issue.
Caloric restriction slows down the aging of blood stem cells
The study focused on the effects of caloric restriction on blood stem cells (so-called hematopoietic stem cells, HSC) that are responsible for building red blood cells or lymphocytes (immune cells). Like for any other adult stem cell, HSC functionality decreases with every single cell division – the stem cells age. This is why they stay in a resting phase (quiescence) most of the time and are only activated when a massive cell reproduction is required (e.g. after acute blood loss). In their study, the researchers from Jena investigated how a 30% food restriction effects stem cell aging in mice. One main result was that the HSC stayed in a quiescent state even if simulated stress would have required their activation. This effect was found regardless of how long the diet lasted. Thus, during diet, the blood stem cells did not age at all and their functionality to build new blood cells remained increased even one year after diet.
Caloric restriction weakens the immune system
But the long-term diet had a downside, as well: The mice’s immune system almost completely was cut down. Although the diet had no strong effect on the overall cell number of blood cells, the production of lymphocytes – needed for immune defense – was decreased by up to 75%. As a consequence, mice were particularly prone to bacterial infections.
Slowing down aging under laboratory conditions is not yet transferable to humans
“The study provides the first experimental evidence that long-term caloric restriction – as intervention to slow down aging – increases stem cell functionality, but results in immune defects in the context of prolonged bacterial infection, too. Thus, positive effects of a diet are not transferable to humans one to one”, Rudolph sums up the study results. Even if – under laboratory conditions – aging of single cells or tissues may be slowed down through a diet, the immune suppression may have fatal consequences in real life. To benefit from caloric restriction or medicinal mimetika aiming at increasing health in the elderly, possible risks of such interventions to come down with life-threatening infections remain to be elucidated. „In sepsis patients, we see a higher survival rate for those with a higher body weight than for patients who are very lean“, Prof. Dr. Michael Bauer, Director of the Center for Sepsis Control and Care at University Hospital Jena (UKJ), concurs.
http://www.leibniz-fli.de/nc/institute/public-relations/press-releases/research/detailpage/?tx_news_pi1%5Bnews%5D=2510&cHash=7d5cbe951317dc513959534631b4def2
- Full bibliographic informationTang D, Tao S, Chen Z, Koliesnik IO, Gebert N, Calmes PG, Hörr V, Löffler B, Morita Y, Rudolph KL.
"Long-term dietary restriction improves repopulation but impairs lymphoid differentiation capacity of aging hematopoietic stem cells."
Journal of Experimental Medicine 2016, 13 (4). doi: 10.1084/jem.20151100
Top researchers advocate united actions to fight Alzheimer’s disease
If we had any leadership at all in stroke that leader would pull together top researchers and publicize the actions needed for stroke. There are hundreds if not thousands of research possibilities needing some final investigations and translation to stroke protocols that could easily make stroke a much less damaging prospect. But almost everyone in stroke puts out the 'Happy talk' that everything in stroke is fine because of all the prevention information out there and the F.A.S.T. campaign. Well everything in stroke is a complete fucking failure and will be until heads are pulled out of asses. By 2050 there will be another 350 million stroke survivors(10 million yearly stroke survivors), vastly more than Alzheimers.
Top researchers advocate united actions to fight Alzheimer’s disease
To meet the challenge of Alzheimer's disease and other dementias, a concerted effort and long-term economic commitment is needed, according to a new expert report by internationally leading researchers in the field. The journal Lancet Neurology devotes its entire April issue to a detailed overview and recommendations about how patient care, as well as basic and clinical research on Alzheimer's disease and other dementias should be organised in the future. The report will be presented at a workshop hosted by the European Parliament in Brussels on March 15, during the Brain Awareness Week 2016
The comprehensive report is the work of the Lancet Neurology Commission led by Professor Bengt Winblad, Centre for Alzheimer Research at Karolinska Institutet in Sweden. This commission was initiated by Lancet editors and formed with the aim to provide expert recommendations and information to politicians and policy makers about Alzheimer’s disease and related dementias. More than 30 internationally leading researchers collaborated on the 78 pages long report, which identified a range of challenges that need to be addressed to reduce the burden of dementia.
“What we need now is for the politicians to realise that this is a growing problem that already costs society tremendous amounts of money”, says Professor Bengt Winblad. “We need investments of resources in research in all areas involved in this disease, to find better drugs, but also to improve compassionate care and prevention.”
Alzheimer's disease is the most common form of dementia and accounts for approximately 60 percent of the cases. The most important risk factor is high age and as life expectancy increases, the number of persons with dementia is expected to rise. In 2015, almost 47 million persons around the world were estimated to be affected. By 2030, the number is expected to reach 75 million. By 2050, up to 131 million persons are expected to be burdened by the disease. So far no treatment is available that can effectively halt or reverse the disease.
The Lancet Neurology Commission report discusses health economics, epidemiology, prevention, genetics, biology, diagnosis, treatment, care and ethics. The commission advocates that public governmental agencies form large multinational partnerships with academic centres and pharmaceutical companies to deploy capital resources and share risk.
“To defeat Alzheimer's disease and other dementias, united actions are needed, not only within research, but also within the political arena on all levels”, says Professor Winblad. “My hope is that our work will stimulate increased national and international collaboration.”
The authors of this report are researchers from Sweden, France, UK, Australia, Denmark, Canada, Switzerland, Italy, Luxembourg, the United States, Germany and the Netherlands. The report will be presented at a workshop hosted by the Science and Technology Options Assessment (STOA) panel of the European Parliament in Brussels, Belgium, during the international Brain Awareness Week 2016.
http://ki.se/pressroom
- Full bibliographic information'Defeating Alzheimer’s disease and other dementias: a priority for European science and society', Bengt Winblad, Philippe Amouyel, Sandrine Andrieu et al, Lancet Neurology, 2016;15:455-532, online 14 March 2016.
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