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, May 28, 2014

“Virtual human” shows that stiff arteries can explain the cause of high blood pressure

Maybe you want to ask your doctor about these possible solutions to stiff arteries. Why would you listen to me? I'm a non-medical person.
You can test if you have stiff arteries here and here.
Watermelon juice reverses hardening of the arteries
Stiff arteries relax like younger blood vessels after taking alagebrium
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142222&CultureCode=en
High blood pressure is highly age-related and affects more than 1 billion people worldwide. But doctors can’t fully explain the cause of 90 per cent of all cases.  A computer model of a “virtual human” suggests that stiff arteries alone are enough to cause high blood pressure.
“Our results suggest that arterial stiffness represents a major therapeutic target. This is contrary to existing models, which typically explain high blood pressure in terms of defective kidney function,” says Klas Pettersen, a researcher at the Norwegian University of Life Sciences and first author of the study, recently published in PLOS Computational Biology.
High blood pressure is a major source of morbidity and mortality, because it makes individuals more prone to heart failure, stroke and kidney disease.
When blood pressure travels down the aorta from the heart, a special group of cells in the aortic wall, called baroreceptors, sense the pressure in this stretch of the aortic wall and send signals with this information to the nervous system.
If the blood pressure is too high, these cells send stronger signals and the body is able to lower blood pressure. However, if the aorta gets stiffer, as typically happens with age, this stretch of the aorta is not as sensitive as it once was in measuring blood pressure. Thus, although a person’s blood pressure may have increased, the baroreceptors do not signal as intensively as they should and the body does not get the message to lower blood pressure.
“With the stiffening of the wall that follows ageing, these sensors become less able to send signals that reflect the actual blood pressure. Our mathematical model predicts the quantitative effects of this process on blood pressure,” says Pettersen.
“If our hypothesis is proven right, arterial stiffness and baroreceptor signaling will become hotspot targets for the treatment of high blood pressure and the development of new medicines and medical devices,” says Stig W. Omholt from the Norwegian University of Science and Technology, who was the senior investigator of the research project.
With the use of existing experimental data and models of the aging human aorta, the researchers were able to show quantitatively how the stiffening of the aorta with age causes the baroreceptors to misinform the central nervous system about blood pressure, thus preventing the system from downregulating blood pressure. The model predictions were compared with data from the Nord-Trøndelag Health Study (HUNT2), which is comprised of information on the health history of 74,000 people, including blood sample collection from 65,000 people.
NTNU’s Omholt says that the study is a good example of how very complex human disease can be understood by use of mathematical models and thus allow for much better treatment strategies.
“If we are to succeed in developing  predictive, preventive and participatory medicine envisioned by so many, there is no substitute for building much stronger transdisciplinary ties between the life sciences, the mathematical sciences and engineering across the whole spectrum of basic, translational and applied research.  And mathematical models of the human physiology will be at the core of this development,” he says.
In September the Norwegian University of Science and Technology will host the biannual conference on the Virtual Physiological Human, where this research will be presented. http://www.ntnu.edu/vph2014

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