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 neuronsthatDIEeach day because there areNOeffective 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.
Please comment here, you have til June 5th. They need to hear from survivors that they are complete failures. Write again even if you already commented, they need to hear from us in full throated roar.
My comment is below, make sure you mention 100% recovery and that this is all guidelines NOT PROTOCOLS.
Clinical Performance Measures for Healthcare Professionals
From the American Heart Association/American Stroke Association
Public Comment Period Friday May 8 – Friday June 5, 2020
We would like to invite you to participate in the review of the draft 2020 AHA/ASA Measurement Set Specifications for Adult Stroke Rehabilitation and Recovery.
This initiative aims to provide a standardized set of performance
measures specific to adult stroke rehabilitation while helping to
accomplish AHA/ASA’s mission of being a relentless force for a world of
longer, healthier lives.
My comment, I put it in the last box.
If you are the one of the 1 in 4 that the WHO suggests will have a stroke, is there anything in here that will guarantee that you will 100% recover? I see nothing here that suggests that anything is being done to stop the neuronal cascade of death in the first week. Neuroprotection doesn't convey any sense of urgency. Rockefeller University in January 2009 named it the cascade of death. That sounds urgent, especially if your doctor tells you they can do nothing to stop that cascade of death.
With only 10% getting to full recovery thru rehab something new needs to be tried and all this is old and barely works. At what point will you acknowledge than 10% full recovery is appalling failure and work on solving the neuronal cascade of death? By fixing at least these five known causes:
1. Not 100% recovered, some weakness and a little bit of short-term memory loss. So the medical team was excellent at promoting the tyranny of low expectations. Not the excellence I want.
2. tPA in 31 minutes is still not fast enough to get fully recovered. WHAT THE HELL IS THE NEEDED TIMEFRAME? Until we know that we don't even know the goal to be shooting for.
3. He was lucky. Strokes while in the hospital don't always have a good outcome.
Roughly 795,000 people suffer a stroke each year in the United States, according to the Stroke Awareness Foundation.
Among those already this year to suffer a stroke is Hardin County resident Mitch Hill.
On
Jan. 14, Hill was at Hardin Memorial Health Vascular Surgery, located
behind Hardin Memorial Hospital, to get an ultrasound of his carotid
arteries. While there, the staff noticed Hill was exhibiting left side
facial drooping. He was asked to speak and realized his left side was
paralyzed.
Hill’s doctor had him go straight to the HMH emergency department. Once he arrived he said the stroke team did their thing.
“They took excellent care of me,” he said. “Everything was super fast. I got the clot buster drug at 31 minutes.”
Stroke
Program Coordinator Rosa Vittitoe, MSN, SCRN, said the goal is to get
that drug administered as quickly as possible. The American Heart
Association and American Stroke Association recommend to have it
administered within 60 minutes.
“You lose 1.9 million neurons
every minute that drug is delayed,” she said, noting the quicker it is
administered, the lower risk for disability as well.
Other than some weakness and a little bit of short-term memory loss, Hill said he is doing excellent.
“I have very high praise for the stroke team. They did an excellent job,” he said.
HMH
received the Stroke Elite Honor Roll award for quality measures met in
2019, and is on target to maintain the award for measures being met in
2020, despite COVID-19.
“We have such a commitment from our stroke
team care at Hardin Memorial and our partnerships with EMS that we are
able to achieve some high quality measures that we are very proud of,”
Vittitoe said.
“Everybody has a designated role. To hear these kinds of stories, it’s so promising to our community.”
When
Hill arrived at the hospital in January, another stroke patient already
was at the designated CT Scan. Instead of waiting, he said Dr. Scott
Dishaw grabbed a wheelchair and quickly escorted him to another.
“It was super fast, excellent care, everybody knew what they were doing,” Hill said.
In
addition to care, Vittitoe said stroke patients and their families are
provided a stroke education, informed of stroke symptoms, risk factors,
recovery and more.
“A stroke not only affects the patient it impacts the entire family,” she said.
The acronym to identify a stroke is Be Fast: balance, eyes, face, arm, speech and time.
According
to the Stroke Awareness Foundation, signs of a stroke include sudden
numbness or weakness in the face, arm, or leg, especially on one side of
the body; sudden confusion, trouble speaking, or difficulty
understanding speech; sudden trouble seeing in one or both eyes; sudden
trouble walking, dizziness, loss of balance or lack of coordination; and
sudden severe headache with no known cause.
Hill said people need to be aware of stroke symptoms.
“In my case, I wasn’t even aware I was having it,” he said.
May is National Stroke Awareness Month.
IEEE TRANSACTIONS ON NEURAL SYSTEMS AND REHABILITATION ENGINEERING, VOL. 15, NO. 3, SEPTEMBER 2007
Sunil K. Agrawal, Sai K. Banala, Abbas Fattah, Vivek Sangwan, Vijaya Krishnamoorthy, John P. Scholz, and Wei-Li Hsu
Abstract—
The gravity balancing exoskeleton, designed at University of Delaware, Newark, consists of rigid links, joints and springs, which are adjustable to the geometry and inertia of the leg of a human subject wearing it. This passive exoskeleton does not use any motors but is designed to unload the human leg joints from the gravity load over its range-of-motion. The underlying principle of gravity balancing is to make the potential energy of the combined leg–machine system invariant with configuration of the leg. Additionally, parameters of the exoskeleton can be changed to achieve a prescribed level of gravity assistance, from 0% to 100%. The goal of the results reported in this paper is to provide preliminary quantitative assessment of the changes in kinematics and kinetics of the walking gait when a human subject wears such an exoskeleton. The data on kinematics and kinetics were collected on four healthy and three stroke patients who wore this exoskeleton. These data were computed from the joint encoders and interface torque sensors mounted on the exoskeleton. This exoskeleton was also recently used for a six-week training of a chronic stroke patient, where the gravity assistance was progressively reduced from 100% to 0%. The results show a significant improvement in gait of the stroke patient in terms of range-of-motion of the hip and knee, weight bearing on the hemiparetic leg, and speed of walking. Currently, training studies are underway to assess the long-term effects of such a device on gait rehabilitation of hemiparetic stroke patients.
Pathologists
at The Mount Sinai Hospital, at the epicenter of the COVID-19 global
pandemic, have prepared one of the largest, most comprehensive analysis
of autopsies of COVID-19 victims to date, revealing many complex new
details about the disease. The analysis was released on the preprint
server MedRxiv.
"An essential
contribution of pathology is the understanding of the biology of the
disease and the range of organ damage, and for this reason, we decided
to uncompromisingly perform as many autopsies as possible," said Carlos
Cordon-Cardo, MD, PhD, Irene Heinz Given and John LaPorte Given
Professor and Chair of the Lillian and Henry M. Stratton-Hans Popper
Department of Pathology, Molecular and Cell-Based Medicine, and
co-author of the study.
"Post-mortem
examinations (autopsies) are the gold standard for the elucidation of
the underlying pathophysiology of disease. Despite a rapidly growing
body of literature focusing on the clinical impact and molecular
microbiology of SARS-CoV-2, autopsy
studies have comparatively been few and far between," said Mary Fowkes,
MD, PhD, Director of the Autopsy Service, and senior author of the
paper. SARS-CoV-2 is the virus that causes COVID-19.
To
date, the team has performed more than 90 autopsies on deceased
COVID-19 patients at The Mount Sinai Hospital. The published work
analyzes the first 67. Gross anatomical findings were combined with the
clinical history and laboratory data for all 67 patients. Microscopic
examinations were carried out by the team, using special stains,
immunochemistry, electron microscopy, and molecular pathology assays.
COVID-19
was initially conceptualized as a primarily respiratory illness, but
the Mount Sinai analysis laid out in detail that it also causes damage
to the thin layer of cells that line blood vessels (endothelium), which
underlies the clotting abnormalities and hypoxia observed in severely
ill patients who develop multi-organ failure that leads to death in some
patients.
"The physical evidence
we ascertained through our postmortem analyses helps elucidate the
mechanisms behind some of the clinical symptoms observed by physicians
treating COVID-19 patients, including thromboembolisms and neuropsychiatric disorders," says Clare Bryce, MBChB, Associate Professor of Pathology, Molecular and Cell Based Medicine, and, first author of the study.
The
lungs in nearly all cases showed diffuse damage to the alveoli, the
small sacs where oxygen and carbon dioxide are exchanged with the blood.
This damage is the typical microscopic evidence of clinical acute
respiratory distress syndrome (ARDS), with most cases showing fibrin (a
fibrous, non-globular protein involved in the clotting of blood) and/or
platelet thrombi, or clots, to varying extents. This same pathology is
found in most cases of ARDS, including those related to other
coronoaviruses. However, the totality of findings in the autopsy series
as a whole, with blood clots in multiple other organ systems—most
notably the brain, kidney, and liver—reflects endothelial damage as an
underlying process, which would also correlate with the activation of
the coagulation cascade and persistent elevation of blood markers of
inflammation.
The examined brains showed a
surprising scarcity of inflammation, with only a few cases showing small
foci of chronic inflammation. However, a surprising number of cases
showed microthrombi with small and patchy evidence of tissue death
caused by blockage of blood vessels in both peripheral and deep parts of
the brain. These small microinfarcts may explain some of the
psychological changes seen in some COVID-19 positive patients.
This
study brings new light into the pathophysiology of COVID-19, offering
justification for novel treatment plans, including the anticoagulation
strategies being put into effect by clinical leaders including Valentin
Fuster, MD, PhD, Director of Mount Sinai Heart and Physician-in-Chief at
The Mount Sinai Hospital.
Still just guidelines, we do need EXACT DIET PROTOCOLS for all these needs. WHEN THE HELL WILL YOUR DOCTOR PROVIDE THEM?
With all the needs out there for diet protocols has your doctor asked the nutritionist to create these? I don't care how difficult this will be. Leaders tackle difficult problems, they don't leave them hanging to fester.
For stroke
prevention; for dementia prevention; for cognitive improvement; for
cholesterol reduction; for plaque removal; for Parkinsons prevention; for
inflammation reduction; for blood pressure reduction.
It’s been known for years that a healthy diet may benefit the brain, but
researchers are now finding that the foods you eat together may also be
associated with the risk of dementia. Find out why.
It's no secret that a healthy diet may benefit the brain. However, it
may not only be what foods you eat, but what foods you eat together that
may be associated with your risk of dementia, according to a new study
published in the April 22, 2020, online issue of Neurology®, the medical journal of the American Academy of Neurology.
The study looked at "food networks" and found that people whose diets
consisted mostly of highly processed meats, starchy foods like potatoes,
and snacks like cookies and cakes, were more likely to have dementia
years later compared to people who ate a wider variety of healthy foods.
Study explores food 'networks'
"There is a complex inter-connectedness of foods in a person's diet, and
it is important to understand how these different connections, or food
networks, may affect the brain because diet could be a promising way to
prevent dementia," said study author Cécilia Samieri, PhD, of the
University of Bordeaux in France.
"A number of studies have shown that eating a healthier diet, for
example a diet rich in green leafy vegetables, berries, nuts, whole
grains and fish, may lower a person's risk of dementia. Many of those
studies focused on quantity and frequency of foods. Our study went one
step further to look at food networks and found important differences in
the ways in which food items were co-consumed in people who went on to
develop dementia and those who did not."
The study involved 209 people with an average age of 78 who had dementia
and 418 people, matched for age, sex and educational level, who did not
have dementia.
Participants had completed a food questionnaire five years previously
describing what types of food they ate over the year, and how
frequently, from less than once a month to more than four times a day.
They also had medical checkups every two to three years. Researchers
used the data from the food questionnaire to compare what foods were
often eaten together by the patients with and without dementia.
Findings show importance in diet diversity
Researchers found while there were few differences in the amount of
individual foods that people ate, overall food groups or networks
differed substantially between people who had dementia and those who did
not have dementia.
"Processed meats were a 'hub' in the food networks of people with
dementia," said Samieri. "People who developed dementia were more likely
to combine highly processed meats such as sausages, cured meats and
patés with starchy foods like potatoes, alcohol, and snacks like cookies
and cakes. This may suggest that frequency with which processed meat is
combined with other unhealthy foods, rather than average quantity, may
be important for dementia risk.
"For example, people with dementia were more likely, when they ate
processed meat, to accompany it with potatoes and people without
dementia were more likely to accompany meat with more diverse foods,
including fruit and vegetables and seafood."
Overall, people who did not have dementia were more likely to have a lot
of diversity in their diet, demonstrated by many small food networks
that usually included healthier foods, such as fruit and vegetables,
seafood, poultry or meats.
Some findings seen years in advance
"We found that more diversity in diet, and greater inclusion of a
variety of healthy foods, is related to less dementia," said Samieri.
"In fact, we found differences in food networks that could be seen years
before people with dementia were diagnosed.
Our findings suggest that studying diet by looking at food networks may
help untangle the complexity of diet and biology in health and disease."
One limitation of the study was that participants completed a food
questionnaire that relied on their ability to accurately recall diet
rather than having researchers monitor their diets. Another limitation
was that diets were only recorded once, years before the onset of
dementia, so any changes in diet over time were unknown.
MORE INFO:
This research was funded by the Alzheimer's Association. The overall
study was funded by the INSERM Research Center at the University of
Bordeaux, Sanofi-Aventis, and the French Foundation for Medical
Research, as well as other French organizations including the French
National Research Agency and the Plan Alzheimer Foundation.
This particular jacket I have never been able to get zipped on my own, friends have always been around to help out. But today I needed it shut so I used one of my woodworking clamps to hold the left side. I can then hook my thumb into it to hold it down while attaching the pull. Not that I'm doing any woodworking right now, it is all in a friend's garage.
Or this latest one only tested in mice and probably decades away from common usage? Assuming of course that your doctor and stroke hospital have enough competence/responsibility to get this research going in humans. Can you wait that long? I'll be doing the wine thing.
Even if this works you will then need a SPECIFIC SLEEP PROTOCOL so your glymphatic system can clear the waste from your brain while you sleep.
Nanodevices are the newest weapon in medicine’s growing arsenal to fight
Alzheimer’s. They capture dangerous peptides before they can assemble
to form Alzheimer’s plaques in the brain. Find out how.
Alzheimer's disease is the sixth leading cause of death in the United
States, affecting one in 10 people over the age of 65. Scientists are
engineering nanodevices to disrupt processes in the brain that lead to
the disease.
People who are affected by Alzheimer's disease have a specific type of
plaque, made of self-assembled molecules called β-amyloid (Aβ) peptides,
that build up in the brain over time. This buildup is thought to
contribute to loss of neural connectivity and cell death. Researchers
are studying ways to prevent the peptides from forming these dangerous
plaques in order to halt development of Alzheimer's disease in the
brain.
How it works
In a multidisciplinary study, scientists at the U.S. Department of
Energy's (DOE) Argonne National Laboratory, along with collaborators
from the Korean Institute of Science and Technology (KIST) and the Korea
Advanced Institute of Science and Technology (KAIST), have developed an
approach to prevent plaque formation by engineering a nano-sized device
that captures the dangerous peptides before they can self-assemble.
The β-amyloid peptides arise from the breakdown of an amyloid precursor
protein, a normal component of brain cells," said Rosemarie Wilton, a
molecular biologist in Argonne's Biosciences division. "In a healthy
brain, these discarded peptides are eliminated."
In brains prone to the development of Alzheimer's, however, the brain
does not eliminate the peptides, leaving them to conglomerate into the
destructive plaques.
"The idea is that, eventually, a slurry of our nanodevices could collect
the peptides as they fall away from the cells -- before they get a
chance to aggregate," added Elena Rozhkova, a scientist at Argonne's
Center for Nanoscale Materials (CNM), a DOE Office of Science User
Facility.
Decorating the surface
The researchers covered the surface of the new nanodevice with fragments
of an antibody -- a type of protein -- that recognizes and binds to the
Aβ peptides. The surface of the nanodevice is spherical and porous, and
its craters maximize the available surface area for the antibodies to
cover. More surface area means more capacity for capturing the sticky
peptides.
To find the optimal coating, the scientists first searched previous
literature to identify antibodies that have high affinity to Aβ
peptides. It was important to choose an antibody that attracts the
peptides but doesn't bind to other molecules in the brain. Then the
team, led by Wilton, produced the antibodies in bacteria and tested
their performance.
A full antibody molecule can be up to a few dozen nanometers long, which
is big in the realm of nanotechnology. However, only a fraction of this
antibody is involved in attracting the peptides. To maximize the
effectiveness and capacity of the nanodevices, Wilton's group produced
tiny fragments of the antibodies to decorate the nanodevice's surface.
Engineering and testing the nanodevice
The scientists at CNM constructed the base of the porous, spherical
nanodevices out of silica, a material that has long been used in
biomedical applications due to its flexibility in synthesis and its
nontoxicity in the body. Coated with the antibody fragments, the
nanodevices capture and trap the Aβ peptides with high selectivity and
strength.
"Many attempts to prevent Alzheimer's have focused on inhibiting enzymes
from cutting β-amyloid peptides off of the cell's surface," said
Rozhkova, who led the project at CNM. "Our elimination approach is more
direct. We've taken building blocks from nanotechnology and biology to
engineer a high-capacity 'cage' that traps the peptides and clears them
from the brain."
At CNM, the scientists tested the effectiveness of the devices by
comparing how the peptides behaved in the absence and presence of the
nanodevices. Using in vitro transmission electron microscopy (TEM), they
observed a notable decline in peptide aggregation in the presence of
the nanodevices. They further analyzed the interactions using confocal
laser scanning microscopy and microscale thermophoresis measurement, two
additional techniques for characterizing interactions at the nanoscale.
The scientists also performed small-angle X-ray scattering to study the
processes that make the nanodevices porous during synthesis. The
researchers performed the X-ray characterization, led by Byeongdu Lee, a
group leader in Argonne's X-ray Science division, at beamline 12-ID-B
of the lab's Advanced Photon Source (APS), a DOE Office of Science User
Facility.
These studies supported the case that the nanodevices sequester the
peptides from the pathway to aggregation by more than 90 percent
compared to the control silica particles without the antibody fragments.
However, the devices still needed to demonstrate their effectiveness
and safety within cells and brains.
Joonseok Lee -- who originally proposed this experiment at Argonne as a
Director's Postdoctoral Appointee and pioneered the design for the
nanodevice -- continued the study of the therapeutic potential of this
device at KIST and KAIST.
"The Director's Postdoctoral Position is a rare opportunity offered at
Argonne that allows for unique research projects and cross-field
collaborations that might not otherwise be possible," said Rozhkova. "We
have incredible minds at the lab who want to explore topics that don't
fall under a predefined area of research, and this program encourages
this creativity and innovation."
Models Demonstrated Safety, Efficacy
The in vivo experiments -- experiments that took place in living cells
-- performed by Lee and his collaborators showed that the nanodevices
are nontoxic to cells. They also tested the effectiveness of the devices
in the brains of mice with Alzheimer's, demonstrating around 30 percent
suppression of plaque formation in brains containing the nanodevices
compared to control brains. The research on mice was conducted at KIST
and KAIST in South Korea with appropriate government approvals.
This study combined the strengths of antibody engineering and
nanotechnology, the power of two DOE User Facilities at Argonne and
innovative collaboration resulting from the laboratory's postdoctoral
program to explore a technological approach to preventing Alzheimer's.
Using a similar approach, scientists may also be able to pair the silica
nanoparticles with different antibodies that target molecules related
to other neurodegenerative diseases, such as Huntington's disease and
Parkinson's disease, which also involve abnormal protein aggregation.
The porous nanoparticles may be further upgraded for use in imaging
applications including fluorescent imaging and magnetic resonance
imaging. SOURCE:
GuruprasadRaghavan Caltech Pasadena, CA 91106 graghava@caltech.edu
JiayiLi UCLA Los Angeles, CA 90095 jiayi.li@g.ucla.edu
MattThomson Caltech Pasadena, CA 91106 mthomson@caltech.edu
Abstract
Biological neural networks have evolved to maintain performance despite significant circuit damage. To survive damage, biological network architectures have both intrinsic resilience to component loss and also activate recovery programs that adjust network weights through plasticity to stabilize performance. Despite the importance of resilience in technology applications, the resilience of artificial neural networks is poorly understood, and autonomous recovery algorithms have yet to be developed. In this paper, we establish a mathematical framework to analyze the resilience of artificial neural networks through the lens of differential geometry. Our geometric language provides natural algorithms that identify local vulnerabilities in trained networks as well as recovery algorithms that dynamically adjust networks to compensate for damage. We reveal striking vulnerabilities in commonly used image analysis networks, like MLP’s and CNN’s trained on MNIST and CIFAR10 respectively. We also uncover high-performance recovery paths that enable the same networks to dynamically re-adjust their parameters to compensate for damage. Broadly, our work provides procedures that endow artificial systems with resilience and rapid recovery routines to enhance the irintegration with IoT devices as well as enable their deployment for critical applications.
1 Introduction
Brains are remarkable machines whose computational capabilities have inspired many breakthroughs in machine learning [1, 2, 3, 4]. However, the resilience of the brain, its ability to maintain computational capabilities in harsh conditions and following circuit damage, remains poorly developed in current artificial intelligence paradigms [5] . Biological neural networks are known to implement redundancy and other architectural features that allow circuits to maintain performance following loss of neurons or lesion to sub-circuits [6, 7, 8, 9, 10]. In addition to architectural resilience, biological neural networks across species execute recovery programs that allow circuits to repair themselves through the activation of network plasticity following damage [11, 12, 13]. For example, recovery algorithms reestablish olfactory and visual behaviors in mammals following sensory specific cortical circuit lesions [14, 15]. Through resilience and recovery mechanisms, biological neural networks can function over the life of an animal, in difficult environments and maintain performance following seemingly catastrophic injuries like the loss of the entire visual cortex or hippocampus [16, 17, 18, 19]. Like brains, artificial neural networks also face difficult operating conditions that can induce component damage at different scales. Hardware failures in modern compute clusters due to accumulation of errors in Dynamic random access memory (DRAM) devices that occur at surprising rates, could be a disaster [20] for networks being used for critical applications, such as (i) decision-making in the healthcare industry, (ii) self-driving cars and (iii) for robots deployed in extreme environments.
Further the rising implementation of neural networks on physical hardware (like neuromorphic, edge devices) [21, 22] where networks can be disconnected from the internet and are under control of an end user necessitates the need for damage-resilient and dynamically recovering artificial neural networks. Yet, the resilience and recovery properties of biological neural networks are currently absent in the design of artificial neural networks. The resilience of living neural networks motivates theoretical and practical efforts to understand the resilience of artificial neural networks and to design new algorithms that reverse engineer resilience and recovery into artificial systems [23]. Recent studies [24, 25] have demonstrated that MLP and CNN architectures can be surprisingly robust to large scale node deletion. However, little is known about what induces network robustness, how do networks ultimately fail, or how to define recovery procedures that can maintain network performance during damage. We propose a mathematical framework grounded in differential geometry to study the resilience and the recovery of artificial neural nets. Globally, we formalize damage/response behavior as dynamic movement on a curved pseudo Riemannian manifold. Our geometric language provides new procedures for identifying network vulnerabilities by predicting local perturbations that adversely impact the functional performance of the network, and for uncovering high performance recovery paths that the network can traverse to maintain performance while it is being damaged. Our algorithms allow networks to maintain high performance during rounds of damage and repair through computationally efficient update algorithms that do not require conventional retraining. Broadly, our work provides procedures that will endow artificial systems with resilience and autonomous recovery policies to emulate the properties of biological neural networks and to enhance their deployment in critical technology applications.
Research led by Dr. Wendy Hall, Reader in Nutritional Sciences at King's College London and published in the American Journal of Clinical Nutrition
found that replacing popular snacks such as biscuits and crisps with
almonds can improve endothelial function, a key indicator of vascular
health, and lower 'bad' LDL-cholesterol.
In April, blood clots
emerged as one of the many mysterious symptoms attributed to Covid-19, a
disease that had initially been thought to largely affect the lungs in
the form of pneumonia. Quickly after came reports of young people dying
due to coronavirus-related strokes. Next it was Covid toes — painful red
or purple digits.
What do all of these symptoms have in common? An impairment in blood circulation. Add in the fact that 40% of deaths
from Covid-19 are related to cardiovascular complications, and the
disease starts to look like a vascular infection instead of a purely
respiratory one.
Months
into the pandemic, there is now a growing body of evidence to support
the theory that the novel coronavirus can infect blood vessels, which
could explain not only the high prevalence of blood clots, strokes, and
heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged.
“All
these Covid-associated complications were a mystery. We see blood
clotting, we see kidney damage, we see inflammation of the heart, we see
stroke, we see encephalitis [swelling of the brain],” says William Li,
MD, president of the Angiogenesis Foundation. “A whole myriad of
seemingly unconnected phenomena that you do not normally see with SARS
or H1N1 or, frankly, most infectious diseases.”
“If
you start to put all of the data together that’s emerging, it turns out
that this virus is probably a vasculotropic virus, meaning that it
affects the [blood vessels],” says Mandeep Mehra, MD, medical director
of the Brigham and Women’s Hospital Heart and Vascular Center.
In a paper published in April in the scientific journal The Lancet,
Mehra and a team of scientists discovered that the SARS-CoV-2 virus can
infect the endothelial cells that line the inside of blood vessels.
Endothelial cells protect the cardiovascular system, and they release
proteins that influence everything from blood clotting to the immune
response. In the paper, the scientists showed damage to endothelial
cells in the lungs, heart, kidneys, liver, and intestines in people with
Covid-19.
“The
concept that’s emerging is that this is not a respiratory illness
alone, this is a respiratory illness to start with, but it is actually a
vascular illness that kills people through its involvement of the
vasculature,” says Mehra.
A respiratory virus infecting blood cells and circulating through the body is virtually unheard of.
A one-of-a-kind respiratory virus
SARS-CoV-2
is thought to enter the body through ACE2 receptors present on the
surface of cells that line the respiratory tract in the nose and throat.
Once in the lungs, the virus appears to move from the alveoli, the air
sacs in the lung, into the blood vessels, which are also rich in ACE2
receptors.
“[The
virus] enters the lung, it destroys the lung tissue, and people start
coughing. The destruction of the lung tissue breaks open some blood
vessels,” Mehra explains. “Then it starts to infect endothelial cell
after endothelial cell, creates a local immune response, and inflames
the endothelium.”
A
respiratory virus infecting blood cells and circulating through the
body is virtually unheard of. Influenza viruses like H1N1 are not known
to do this, and the original SARS virus, a sister coronavirus to the
current infection, did not spread past the lung. Other types of viruses,
such as Ebola or Dengue, can damage endothelial cells, but they are
very different from viruses that typically infect the lungs.
Benhur
Lee, MD, a professor of microbiology at the Icahn School of Medicine at
Mount Sinai, says the difference between SARS and SARS-CoV-2 likely
stems from an extra protein each of the viruses requires to activate and
spread. Although both viruses dock onto cells through ACE2 receptors,
another protein is needed to crack open the virus so its genetic
material can get into the infected cell. The additional protein the
original SARS virus requires is only present in lung tissue, but the
protein for SARS-CoV-2 to activate is present in all cells, especially
endothelial cells.
“In
SARS1, the protein that’s required to cleave it is likely present only
in the lung environment, so that’s where it can replicate. To my
knowledge, it doesn’t really go systemic,” Lee says. “[SARS-CoV-2] is
cleaved by a protein called furin, and that’s a big danger because furin
is present in all our cells, it’s ubiquitous.”
Endothelial damage could explain the virus’ weird symptoms
An
infection of the blood vessels would explain many of the weird
tendencies of the novel coronavirus, like the high rates of blood clots.
Endothelial cells help regulate clot formation by sending out proteins
that turn the coagulation system on or off. The cells also help ensure
that blood flows smoothly and doesn’t get caught on any rough edges on
the blood vessel walls.
“The
endothelial cell layer is in part responsible for [clot] regulation, it
inhibits clot formation through a variety of ways,” says Sanjum Sethi,
MD, MPH, an interventional cardiologist at Columbia University Irving
Medical Center. “If that’s disrupted, you could see why that may
potentially promote clot formation.”
Endothelial
damage might account for the high rates of cardiovascular damage and
seemingly spontaneous heart attacks in people with Covid-19, too. Damage
to endothelial cells causes inflammation in the blood vessels, and that
can cause any plaque that’s accumulated to rupture, causing a heart
attack. This means anyone who has plaque in their blood vessels that
might normally have remained stable or been controlled with medication
is suddenly at a much higher risk for a heart attack.
“Inflammation
and endothelial dysfunction promote plaque rupture,” Sethi says.
“Endothelial dysfunction is linked towards worse heart outcomes, in
particular myocardial infarction or heart attack.”
Blood
vessel damage could also explain why people with pre-existing
conditions like high blood pressure, high cholesterol, diabetes, and
heart disease are at a higher risk for severe complications from a virus
that’s supposed to just infect the lungs. All of those diseases cause
endothelial cell dysfunction, and the additional damage and inflammation
in the blood vessels caused by the infection could push them over the
edge and cause serious problems.
The
theory could even solve the mystery of why ventilation often isn’t
enough to help many Covid-19 patients breathe better. Moving air into
the lungs, which ventilators help with, is only one part of the
equation. The exchange of oxygen and carbon dioxide in the blood is just
as important to provide the rest of the body with oxygen, and that
process relies on functioning blood vessels in the lungs.
“If
you have blood clots within the blood vessels that are required for
complete oxygen exchange, even if you’re moving air in and out of the
airways, [if] the circulation is blocked, the full benefits of
mechanical ventilatory support are somewhat thwarted,” says Li.
A new paper published last week in the New England Journal of Medicine,
on which Li is a co-author, found widespread evidence of blood clots
and infection in the endothelial cells in the lungs of people who died
from Covid-19. This was in stark contrast to people who died from H1N1,
who had nine times fewer blood clots in the lungs. Even the structure of
the blood vessels was different in the Covid-19 lungs, with many more
new branches that likely formed after the original blood vessels were
damaged.
“We
saw blood clots everywhere,” Li says. “We were observing virus
particles filling up the endothelial cell like filling up a gumball
machine. The endothelial cell swells and the cell membrane starts to
break down, and now you have a layer of injured endothelium.”
Finally,
infection of the blood vessels may be how the virus travels through the
body and infects other organs — something that’s atypical of
respiratory infections.
“Endothelial
cells connect the entire circulation [system], 60,000 miles worth of
blood vessels throughout our body,” says Li. “Is this one way that
Covid-19 can impact the brain, the heart, the Covid toe? Does SARS-CoV-2
traffic itself through the endothelial cells or get into the
bloodstream this way? We don’t know the answer to that.”
In
another paper that looked at nearly 9,000 people with Covid-19, Mehra
showed that the use of statins and ACE inhibitors were linked to higher
rates of survival.
If Covid-19 is a vascular disease, the best antiviral therapy might not be antiviral therapy
An
alternative theory is that the blood clotting and symptoms in other
organs are caused by inflammation in the body due to an over-reactive
immune response — the so-called cytokine storm. This inflammatory
reaction can occur in other respiratory illnesses and severe cases of
pneumonia, which is why the initial reports of blood clots, heart
complications, and neurological symptoms didn’t sound the alarm bells.
However, the magnitude of the problems seen with Covid-19 appear to go
beyond the inflammation experienced in other respiratory infections.
“There
is some increased propensity, we think, of clotting happening with
these [other] viruses. I think inflammation in general promotes that,”
Sethi says. “Is this over and above or unique for SARS-CoV-2, or is that
just because [the infection] is just that much more severe? I think
those are all really good questions that unfortunately we don’t have the
answer to yet.”
Anecdotally,
Sethi says the number of requests he received as the director of the
pulmonary embolism response team, which deals with blood clots in the
lungs, in April 2020 was two to three times the number in April 2019.
The question he’s now trying to answer is whether that’s because there
were simply more patients at the hospital during that month, the peak of
the pandemic, or if Covid-19 patients really do have a higher risk for
blood clots.
“I
suspect from what we see and what our preliminary data show is that
this virus has an additional risk factor for blood clots, but I can’t
prove that yet,” Sethi says.
The
good news is that if Covid-19 is a vascular disease, there are existing
drugs that can help protect against endothelial cell damage. In another
New England Journal of Medicine
paper that looked at nearly 9,000 people with Covid-19, Mehra showed
that the use of statins and ACE inhibitors were linked to higher rates
of survival. Statins reduce the risk of heart attacks not only by
lowering cholesterol or preventing plaque, they also stabilize existing
plaque, meaning they’re less likely to rupture if someone is on the
drugs.
“It
turns out that both statins and ACE inhibitors are extremely protective
on vascular dysfunction,” Mehra says. “Most of their benefit in the
continuum of cardiovascular illness — be it high blood pressure, be it
stroke, be it heart attack, be it arrhythmia, be it heart failure — in
any situation the mechanism by which they protect the cardiovascular
system starts with their ability to stabilize the endothelial cells.”
Mehra
continues, “What we’re saying is that maybe the best antiviral therapy
is not actually an antiviral therapy. The best therapy might actually be
a drug that stabilizes the vascular endothelial. We’re building a
drastically different concept.”
'May' is not good enough. WE NEED EXACT STROKE PROTOCOLS. GET THERE! If you can do aerobic exercise at two months you are an outlier and this is extreme cherry picking of participants. Bad research, I blame the mentors and senior researchers on not setting this up properly. None of this would be able to be extrapolated to the average stroke survivor. No mention of any dropouts being unable to do the exercise.
Mohamed Salah Khlif1, Emilio Werden1, Laura Bird1, Stanley Hung1, Rosalind Hutchings1, Matthew Pase1, Natalia Egorova1, and Amy Brodtmann1, 2 1 The Florey Institute of Neuroscience and Mental Health, Heidelberg, Victoria, Australia 2 Department of Neurology, Austin Health, Heidelberg, Victoria, Australia
Introduction • Stroke survivors have a high risk of developing cognitive impairment or dementia [1]. • Total and regional brain atrophy precedes such cognitive impairment, especially the reduction in hippocampal volume which is known to be more accelerated in the ipsilateral side to the stroke infarct [2]. • Exercise is a known neuroprotective factor. We present the preliminary findings comparing total brain volume (TBV) and hippocampal volume (HV) between two stroke groups sampled from the Cognition and Neocortical Volume after Stroke (CANVAS) cohort study [3] and the Post Ischaemic Stroke Cardiovascular Exercise (PISCES) study pilot data [4].
Methods
CANVAS CANVAS is an observational longitudinal study of 135 ischaemic stroke patients and 40 age-matched healthy controls over five years. Stroke patients were recruited from the Acute Stroke Units of the Austin, Box Hill, and Royal Melbourne, hospitals in Victoria, Australia. Inclusion criteria included age over 18 years, ischaemic stroke of any type confirmed on clinical imaging, and no history of dementia or any other neurodegenerative condition. Ethical approval was granted by each hospital’s Human Research Ethics Committee.
PISCES
PISCES is a Phase-2b randomised controlled trial investigating the effects of aerobic exercise on brain volume and cognitive function after ischaemic stroke. Patients who have suffered an ischaemic stroke are enrolled in one of two 8-week exercise programmes, beginning at two months post-stroke. The exercise programme involves either combined aerobic exercise and resistance training (intervention group) or balance and stretching (control group). Cognitive function and brain volumes are assessed at two, four, and 12 months post-stroke.
MRI acquisition T1-weighted MPRAGE sequences were obtained using 3T Siemens scanner (Siemens, Erlangen, Germany): 160 slices; repetition time, TR = 1900 ms; echo time, TE = 2.6 ms; inversion time, TI = 900 ms; flip angle = 9°; field of view: 256 × 256 pixels; voxel size = 1 mm3.
MRI segmentation We used the longitudinal pipeline [5] in FreeSurfer v6.0 to estimate total brain volume (TBV) and hippocampal volume (HV) in 125 CANVAS and 16 PISCES participants at two and 12 months post-stroke.
Statistical analysis We used repeated measures ANOVA (fitrm, ranova, and multcompare in MATLAB 2018a) to estimate volumetric changes between time points. Age, sex, years-ofeducation, and total intracranial volume (TIV) were used as covariates.
Results
Demographic characteristics There was no statistical difference in age, sex, education level, or TIV between the CANVAS and PISCES stroke groups.
Covariates Age, education, and TIV were associated with TBV and HV; sex was not.
Total brain volume • TBV was numerically, but not significantly, higher in the PISCES group at both time points (see Fig. 1). • There were no significant reductions in TBV between time points (PISCES: 2.16%, p = 0.079; CANVAS: 0.69%, p = 0.15).
Hippocampal volume • Contralesionally, HV was reduced by 0.26% (p = 0.62) in the PISCES group and 0.66% (p = 0.0007) in the CANVAS group. • Ipsilesionally, HV was also significantly reduced between time points for CANVAS (1.47%, p = 0.002). However, for PISCES, HV has increased by 2.15%, though not significant (p = 0.10).
Figure 1: TBV and HV at two and 12-month time points (volumes are in mm3, error bars = standard error)
Conclusions
In this small pilot PISCES sample, we observed a trend for reduced hippocampal atrophy in our stroke group. These data are still blinded (both exercise programs were analysed as one group), but the exercise interventions may have played a role in the reduction of hippocampal atrophy on the contralesional side, while possibly leading to hippocampal neurogenesis on the ipsilesional side
Is 6 years enough time and recent enough for your stroke hospital to know about and implement this? You want to make sure you aren't pushing the envelope on their ability to actually keep up-to-date on stroke research. No pressure on them, please.
Mohd Azuwan Mat Dzahir 1,2,* and Shin-ichiroh Yamamoto 1 1 Shibaura Institute of Technology, Department of Bio-Science Engineering, 307 Fukasaku, Minuma-ku, Saitama City, Saitama 337-8570, Japan; E-Mail: yamashin@se.shibaura-it.ac.jp 2 Universiti Teknologi Malaysia, Faculty of Mechanical Engineering, UTM Skudai, Johor Bahru 81310, Malaysia
* Author to whom correspondence should be addressed; E-Mail: nb11503@shibaura-it.ac.jp or azuwan@fkm.utm.my; Tel.: +80-80-4094-8009.
Received: 10 January 2014; in revised form: 17 March 2014 / Accepted: 21 March 2014 / Published: 14 April 2014
Abstract:
It is a general assumption that pneumatic muscle-type actuators will play an important role in the development of an assistive rehabilitation robotics system. In the last decade, the development of a pneumatic muscle actuated lower-limb leg orthosis has been rather slow compared to other types of actuated leg orthoses that use AC motors, DC motors, pneumatic cylinders, linear actuators, series elastic actuators (SEA) and brushless servomotors. However, recent years have shown that the interest in this field has grown exponentially, mainly due to the demand for a more compliant and interactive human-robotics system. This paper presents a survey of existing lower-limb leg orthoses for rehabilitation, which implement pneumatic muscle-type actuators, such as McKibben artificial muscles, rubbertuators, air muscles, pneumatic artificial muscles (PAM) or pneumatic muscle actuators (PMA). It reviews all the currently existing lower-limb rehabilitation orthosis systems in terms of comparison and evaluation of the design, as well as the control scheme and strategy, with the aim of clarifying the current and on-going research in the lower-limb robotic rehabilitation field.
The
Modified Intracerebral Hemorrhage (MICH) score is a simple tool created
to provide prognostication in basal ganglia hemorrhages. Current
prognostic scores, including the MICH, are based on the assessment of
baseline patient characteristics, failing to account for significant
developments, such as intraventricular extension and clinical
deterioration, which may occur over the first 72 hours. We propose to
validate the MICH in all hemorrhage locations and hypothesize that its
calculation at 72 hours will outperform its baseline counterpart with
respect to predicting mortality and functional outcome. We performed a
retrospective analysis of collated data from the Virtual International
Stroke Trials Archive database. Primary outcome was 90-day mortality.
Secondary outcome was poor outcome (modified Rankin Scale 4-6) at 90
days. Receiver operating characteristic curves were generated looking at
the predictive ability of the MICH score for mortality and poor
outcome, at baseline and at 72 hours. Competing curves were assessed
with nonparametric methods. A total of 226 patients were included, with a
90-day mortality of 22.5%. The MICH scores calculated at 72 hours were
more predictive of mortality than at baseline (area under the curve
[AUC]: 0.89 [95% confidence interval [CI]: 0.83-0.94] vs 0.78 [95% CI:
0.70-0.85]), P < .01. The MICH scores at 72 hours similarly
better predicted functional outcome (AUC: 0.78 [95% CI: 0.72-0.84] vs
AUC: 0.72 [95% CI: 0.66-0.78]), P = .047. The MICH score has
positive prognostic value for mortality and poor functional outcome in
all hemorrhage locations. Delaying its calculation resulted in higher
predictive values for both and suggests that delaying discussions around
withdrawal of care may result in more accurate prognostication in acute
intracerebral hemorrhage.
Not sure what use this research was for. I see nothing that suggests that these vascular neurologists are doing anything to get patients 100% recovered. Evaluations mean nothing if there is no followup with EXACT STROKE PROTOCOLS LEADING TO 100% RECOVERY.
We sought to determine the proportion of patients with ischemic stroke evaluated by vascular neurologists in the United States.
Methods:
Using
2009 to 2015 claims from a 5% nationally representative sample of
Medicare beneficiaries, we identified patients ≥65 years of age who were
hospitalized for ischemic stroke. We ascertained the proportion of
patients evaluated during the hospitalization or within 90 days of
discharge by nonvascular and vascular neurologists. We assessed the
relationship between county-level socioeconomic status and the
likelihood of neurologist evaluation and between neurologist evaluation
and diagnostic testing.
Results:
Among
66 989 patients with ischemic stroke, 37 820 (56.5%) were evaluated by a
nonvascular neurologist and 11 700 (17.5%) by a board-certified
vascular neurologist. Across increasing quartiles of county
socioeconomic advantage, the proportion of patients evaluated by a
vascular neurologist was 12.2%, 16.5%, 19.8%, and 23.0%. Relative to
evaluation by a nonvascular neurologist, evaluation by a vascular
neurologist was associated with a higher likelihood of postdischarge
heart rhythm monitoring (odds ratio [OR], 1.8; 95% confidence interval
[CI], 1.6-1.9), echocardiography (OR, 1.4; 95% CI, 1.3-1.4), cervical
vessel imaging (OR, 1.3; 95% CI, 1.2-1.3), and intracranial vessel
imaging (OR, 2.1; 95% CI, 2.0-2.2).
Conclusions:
In
a nationally representative cohort of Medicare beneficiaries, we found
that about three quarters of patients with ischemic stroke were
evaluated by a neurologist, and about one-sixth were evaluated by a
vascular neurologist. Patients who were evaluated by a vascular
neurologist were significantly more likely to undergo diagnostic
testing.
I include only one paragraph from here; hopefully our stroke medical professionals take it to heart and stop using the irritatingly stupid quote' All strokes are different, all stroke recoveries are different'. I did see nothing in here that suggested that patients were involved as part of that interdisciplinary team.
“We cannot conduct large, adequately powered trials of rehabilitation interventions.”
After working as a mental health clinician and researcher in the
Department of Veterans Affairs, where psychotherapeutic interventions
were randomized, tested, implemented, revised, and evaluated [9],
there is no question that rehabilitation could mirror this approach.
What interferes with progress in this area are two commonly accompanying
statements: “Each patient is different, you can’t have a standard approach,” and “There is no way to blind or control for exposure to the treatment.”Work currently ongoing in the field rebuts these contentions [10].
There is a glaring need for standardization of approaches to support
the rigor and reproducibility of the science. Standardization does not
ignore the individual, it allows for broader application of techniques
supported by evidence. New approaches to clinical trials, such as
adaptive trials, pragmatic trials, and other methodologic approaches,
may allow for more flexibility in clinical trial design and can be used
to evaluate whether an intervention or approach is effective in the real
world.
When this becomes available you will want this test so you can monitor how effectively your doctor is getting you to the correct level of exercise and if you are getting enough exercise to prevent dementia.
A
simple blood test may be able to determine how physically fit you are,
according to a new study conducted by scientists at the Stanford
University School of Medicine.
The
test could complement treadmill tests, a more traditional clinical
evaluation of fitness, and provide individuals with far more nuanced
information about their body's molecular response to exercise.
The
blood test is an offshoot of a complex study conducted by a team of
researchers that took hundreds of thousands of molecular measurements
from a group of individuals before and after exercising.
"Everybody
knows exercise is good for you, but we really don't know what drives
that at a molecular level," said Michael Snyder, PhD, professor and
chair of genetics. "Our goal at the outset was to conduct a highly
comprehensive analysis of what's happening in the body just after
exercising."
The team tracked molecular
markers of a wide array of biological processes, such as metabolism,
immunity, oxidative stress, and cardiovascular function. Hundreds of
thousands of measurements from 36 study participants provided a window
into the sea of chemical fluctuations the body experiences during
intense exercise. To the scientists' knowledge, such comprehensive
measurements of post-exercise molecular fluctuations have never been
performed. What's more, the team saw that the participants who were most
physically fit shared similar molecular signatures in their resting
blood samples captured before exercise.
"It
gave us the idea that we could develop a test to predict someone's level
of fitness," said Kévin Contrepois, PhD, director of metabolomics and
lipidomics in the Department of Genetics. "Aerobic fitness is one of the
best measures of longevity, so a simple blood test that can provide that information would be valuable to personal health monitoring."
With
the preliminary data, the team has created a proof-of-principle test,
for which they've filed a patent application. The test is not currently
available to the public.
A paper describing the study will be published May 28 in Cell.
Snyder, who holds the Stanford W. Ascherman, MD, FACS, Professorship in
Genetics, and Francois Haddad, MD, clinical professor of medicine, are
co-senior authors of the study. Contrepois shares lead authorship with
postdoctoral scholars Si Wu, PhD, and Daniel Hornburg, PhD, and with
clinical assistant professor Kegan Moneghetti, MD, PhD.
A flurry of change
Snyder's
team set out to better understand the molecular shifts that underlie
changes in physical fitness. The gold standard of medical fitness
assessments is a peak VO2 test, which measures a person's peak oxygen
consumption during intense exercise and uses the score as a proxy for
aerobic fitness. But Snyder and his team wanted more
detail—specifically, about the ways in which exercise initiates change
at the molecular level.
They
performed VO2 testing for 36 individuals, including Snyder, on a
treadmill. Participants, both male and female, had an average body mass
index of 29 kilograms/meter squared, and their age range was from 40 to
75 years old. Before the treadmill test, the researchers drew a baseline
blood sample. Participants then donned an oxygen-measuring mask and ran
at a slight incline until they reached peak oxygen consumption, at
which point they stopped and got off the treadmill. The researchers took
blood samples from participants 2 minutes, 15 minutes, 30 minutes and
60 minutes after they had reached their peaks.
"All
of these measurements allow us to describe a choreography of molecular
events that occur after physical exercise," Snyder said. "We know that
exercise causes an array of physiological responses, such as
inflammation, metabolism, and hormone fluctuation, but these
measurements allowed us to characterize those changes in unprecedented
detail."
It turns out that in the first 2
minutes post-exercise, the body experiences an intense flurry of
molecular activity. In most participants, molecular markers of
inflammation, tissue healing and oxidative stress, a natural byproduct
of metabolism, spiked sharply shortly after hopping off the treadmill,
as their bodies began to recover. Molecular markers of metabolism
varied, Snyder said. At 2 minutes, blood samples revealed evidence that
the body was metabolizing certain amino acids for energy, but it
switched to metabolizing glucose, a type of sugar, around 15 minutes.
"The body breaks down glycogen as part of its exercise recovery
response, so that's why we see that spike a little later," Snyder said.
Glycogen is a form of stored glucose.
As part
of the study, Snyder also compared the molecular response in individuals
who were insulin resistant, meaning they're unable to process glucose
properly, with the response in individuals who could process glucose
normally. "The main difference we see is that insulin resistant
individuals have a dampened immune response post-exercise," he said.
Blood test for fitness
Although
it wasn't the team's original intent, they noticed some consistencies
in the baseline measurements of the participants who performed better on
the peak VO2 test. In these individuals, the researchers saw a strong
correlation between a set of molecules and an individual's level of
aerobic fitness. They discovered a collection of thousands of
molecules—including markers of immunity, metabolism and muscle
activity—that correlate with a person's aerobic fitness. "At this point,
we don't fully understand the connection between some of these markers
and how they are related to better fitness," Snyder said. The
researchers hope to unravel those connections in a future investigation.
Snyder
said that because the molecular profiling done in the study was so
thorough, it wouldn't be practical for doctors to use in their clinics;
it would be expensive and provide more information than necessary. But
his team is working on whittling down the biomarkers to those that are
most representative of a person's fitness level in an effort to make the
test practical for broader use. Already, the team is developing an
algorithm to select a subset of these molecules that are highly
correlative to peak VO2 results, Contrepois said. As the researchers
continue to optimize the fitness test, they hope it can one day be a faster, cheaper and more convenient way for people to objectively measure aerobic fitness.
