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.

Showing posts with label Arteriosclerosis. Show all posts
Showing posts with label Arteriosclerosis. Show all posts

Wednesday, November 8, 2017

New software program allows early detection of arterial calcification

I can't imagine your insurance allowing expensive CT scans to test for this unless your doctor has another factor pointing to this high risk possibility. My Dads doctor upon seeing 80% blockage in one of his carotid arteries should have had him warn me to get tested.  Definition here: Arteriosclerosis is the stiffening or hardening of the artery walls. Atherosclerosis is the narrowing of the artery because of plaque build-up. Atherosclerosis is a specific type of arteriosclerosis.
https://www.news-medical.net/news/20171106/New-software-program-allows-early-detection-of-arterial-calcification.aspx
Little exercise, fatty food and too many cigarettes - factors like these aid the onset of arterial calcification, also known as arteriosclerosis. If blood can no longer be pumped through arteries properly, this can lead to a heart attack or stroke. Doctors are typically only able to diagnose the disease once it reaches an advanced stage. Computer scientists at the University of Kaiserslautern are developing a software program that will allow doctors to detect calcification earlier. To do so, they use image data from computer tomography (CT). They will present the technology at the medical technology exhibition, Medica, from 13 to 16 November in Dusseldorf, at the research stand (Hall 7a, Stand B06) of Rhineland-Palatinate.
According to the German Vascular League, around four million people in Germany suffer from arteriosclerosis. It is even responsible for half of all fatalities in industrialized countries. "Often, the disease is only discovered at an advanced stage," says Christina Gillmann, doctoral student at the chair for 'Computer Graphics and Human Computer Interaction' of Professor Dr Hans Hagen. "For example, doctors are only able to detect deposits in blood vessels on CT images once thicker layers are already present on the vessel walls." At that point, an operation is typically the only option available for treating patients. However, it is possible to detect the disease early enough in those who eat healthily and exercise regularly.
The computer scientists in Gillmann's team are currently developing a computer program that seeks to help doctors give an early diagnosis. To do so, they use existing CT images. This x-ray technology provides physicians layered patient images that are usually shown in greyscale. "The resolution of the images is not very high," the researcher continues. "The data has to be prepared differently in order to detect arteriosclerosis at an early stage." Although there are already techniques that can allow such values to be obtained from CT data, they are simply far too complicated and unsuitable for routine medical practice.
For their program, the computer scientists filter out the additional information from the CT scans. This makes it possible, for example, to depict the branches of the arteries accurately. The researchers at Kaiserslautern are cooperating closely with physicians from Dayton in the United States, led by Professor Dr Thomas Wischgoll, and from Colombia under Professor Dr José Tiberio Hernández Peñaloza. The procedure is not only interesting for doctors, but also industrial companies. They could use the technology, for example, to screen their products more precisely and thereby identify any areas of damage.
However, it will take a few more years of development work before the system may one day be used in hospitals. At Medica, the researchers are presenting their technology at the research stand of Rhineland-Palatinate.
The Working Group for Computer Graphics and Human Computer Interaction has already been conducting research for a long time on preparing data from imaging processes for medicine, such that it can be used simply and reliably in routine clinical practice. They have thereby succeeded, for instance, in using their procedure to separate tumors more distinctly from healthy tissue in images. The computer scientists are working closely with various partners in their projects, including the University of Leipzig Medical Center and the Premier Health Clinic in the US state of Ohio.

Tuesday, January 10, 2017

Hitherto unknown risk factor for arteriosclerosis identified

Just in case you have this your doctor may need to come up with different solutions to prevent arteriosclerosis. Interesting that atherosclerosis is in the research title but arteriosclerosis is in the writeup title. Ask your doctor for what is the difference.
Arteriosclerosis is the stiffening or hardening of the artery walls. Atherosclerosis is the narrowing of the artery because of plaque build-up. 

Hitherto unknown risk factor for arteriosclerosis identified 


Following a blood infection, the first class of antibodies produced by the immune system are IgM antibodies. They form the "vanguard" of the immune response, before other cells are activated to fight the infection. Some people are deficient or completely lack these antibodies, so that they develop congenital immune deficiency. Together with the CeMM (the Austrian Academy of Sciences Research Center for Molecular Medicine), researchers from MedUni Vienna's Division of Medical-Chemical Laboratory Diagnostics have now discovered how this deficiency can also lead to an increased risk of arteriosclerosis and consequently even to serious cardiovascular diseases.
In the human immune system, IgM antibodies (immunoglobulin M) not only play a primary role in the immune response but also maintain an important balance: they control the physiological development of B cells, which are responsible for producing and disposing of antibodies. They therefore also regulate the blood concentration of IgE antibodies and make sure that this is kept in check and always restored to the correct level to keep the immune system in balance. However, if there is a lack of IgM antibodies, this balance cannot be maintained. The uncontrolled IgE antibodies, which also play a significant role in the development of allergic reactions, lead to the increased formation of plaques, activation of mast cells and inflammatory processes and constrict and damage blood vessels. This was proven by the team headed up by Christoph Binder and lead author of the study, Dimitrios Tsiantoulas, in an animal model.
"For the first time, we were able to show that IgE antibodies can themselves provoke inflammatory reactions in vessels and that inhibition of these IgE antibodies prevents damage to the vessels," explains Binder. In future, this knowledge could open up new treatment options by restoring the balance of the immune system. "We were able to identify a completely new function of IgM antibodies, which also probably plays a major role in the development of allergies," adds Tsiantoulas, lead author of the study.
Deficiency in or total absence of IgM antibodies is very rare. However, reduced IgM antibody levels are found in up to 2.5% of the total population.
http://www.meduniwien.ac.at

Attached files

  • Hitherto unknown risk factor for arteriosclerosis identified

Full bibliographic informationCirculation Research
„Increased Plasma IgE Accelerate Atherosclerosis in Secreted IgM Deficiency.“ Dimitrios Tsiantoulas, Ilze Bot, Maria Ozsvar-Kozma, Laura Göderle, Thomas Perkmann,
Karsten Hartvigsen, Daniel H. Conrad, Johan Kuiper, Ziad Mallat, Christoph J. Binder. Circ Res. 2017;120:00-00.
DOI: 10.1161/CIRCRESAHA.116.309606

Thursday, April 7, 2016

Immunology: An alternative route to inflammation

We should be following this up to see if this might be useful in stopping the inflammation of atherosclerosis/arteriosclerosis. 

Immunology: An alternative route to inflammation


Using a combination of newly developed methods, researchers led by Ludwig-Maximilians-Universitaet (LMU) in Munich immunologist Veit Hornung have defined a previously unknown pathway that triggers inflammation.
The immune system in vertebrates is capable of distinguishing “self” from “non-self” components, which enables recognition and destruction of invasive pathogens and aberrant cell types such as tumor cells. Adaptive immune reactions, e.g. based on antibodies, are powerful and highly specific, yet require tedious and time-consuming gene rearrangements. For effective immediate defense, intruders must be detected rapidly, and this task is performed by the so-called innate immune system. Innate immune cells express a relatively small set of receptors on their surfaces, which recognize molecular structures that are uniquely associated with pathogens. Binding of these structures triggers an inflammatory response that kills the pathogen or the infected cell. In order to analyze the signal pathways that mediate these processes, researchers led by Veit Hornung, who holds the Chair of Immunobiochemistry at LMU’s Gene Center, combined two different methodologies. They first utilized a novel cell culture system that mimics the function of monocytes, a class of immune cells involved in regulating inflammation. Then they systematically deleted single genes to determine their role in initiation of the inflammatory response – and uncovered a previously unknown signaling pathway. The findings appear in the journal “Immunity”.
Hornung and his group began their study of a protein complex called the NLRP3 inflammasome at Bonn University Hospital before he moved to the LMU in October 2015. This complex is found in monocytes, and plays a key role in inducing inflammation, as well as being implicated in diseases associated with chronic inflammatory reactions, such as gout, Type 2 diabetes and arteriosclerosis. However, our knowledge of its mode of action is primarily based on studies carried out in mouse cells. In mouse monocytes, two stimuli are required to cause the NLRP3 inflammasome to trigger secretion of the pro-inflammatory signal protein interleukin 1beta (IL-1), while freshly isolated human monocytes were found to produce IL-1 in response to a single signal, which acts via a receptor called TLR4. However, no established human monocyte-like cell lines react to this signal. This is why Hornung and his colleagues had to employ the new human monocyte-like cell line in order to understand the basis for the species difference.
“We developed a procedure which allowed us to specifically delete single genes in cultured human immune cells that closely resemble human monocytes. Using this system, we were able to identify, at the genetic level, the components responsible for signal transmission to, and activation of the NLRP3 inflammasome,” explains Moritz Gaidt, a doctoral student in Hornung’s group and first author of the new study. In this way, the team was able to analyze the secretion of IL-1 by human monocytes in unprecedented detail – and to define the mechanism that enables human NLRP3 to be activated in response to a single signal.
The researchers activated the TLR4 receptor by exposing their monocytes to bacterial lipopolysaccharide (LPS) – a complex molecule made up of sugars and fats, which is found on the surface of many pathogenic bacteria. They then showed that binding of LPS triggers the secretion of IL-1 via a previously unrecognized signal relay. “The activation of this new pathway explains why human monocytes do not need a second signal to secrete IL-1. Conversely, in mouse monocytes this particular pathway is not activated, so a second stimulus is required,” Veit Hornung explains. Moreover, while inflammasome activation in the mouse induces programmed inflammatory cell death, the pathway used in human monocytes does not. “We refer to this signal pathway as the alternative inflammasome, in order to distinguish it from previously described pathways,” says Hornung. “We believe that this signal pathway plays a critical role in inflammatory processes in humans.”
The new study underlines the fact that results obtained in mice are not always translatable to humans. So far, only human monocytes have been found to react directly to contact with LPS by releasing interleukin 1, without the need for a second signal. The researchers now intend to analyze the in-vivo function of the TLR4 receptor in other model organisms. Using Hornung’s monocyte-like cells, it should be possible to identify further signal pathways in vitro. “Our results refute some of the classical tenets of inflammasome research. We hope that our new method will also enhance our understanding of the cell biological basis of immune disorders,” Hornung concludes.
http://www.en.uni-muenchen.de/news/newsarchiv/2016/hornung_inflammasome.html

Friday, April 3, 2015

Targeting dangerous inflammation inside artery plaque

I would think that this would be vastly more important for prevention of strokes than statins.  But since we don't have an effective stroke association this will not be followed up to make a translational stroke protocol out of this. Unless you are willing to wait 50 years and your grandchildren have strokes before doing anything about this. Screaming in your doctors face would be a good start.
http://medicalxpress.com/news/2015-04-dangerous-inflammation-artery-plaque.html
A research team showed that a nanotherapeutic medicine can halt the growth of artery plaque cells resulting in the fast reduction of the inflammation that may cause a heart attack, according to a study led by researchers from Icahn School of Medicine at Mount Sinai and published April 3 in Science Advances.
In just one week our novel cell proliferation-specific approach successfully suppressed atherosclerotic plaque growth and inflammation in mice engineered to mimic human vascular disease," says lead study author Jun Tang, MS, a PhD student at Icahn School of Medicine at Mount Sinai. "Atherosclerosis is a major cause of death around the globe, and our nanomedicine strategy promises to offer a new way to reduce the number of heart attacks and strokes."
Building upon a recent discovery by their Massachusetts General Hospital research collaborators that macrophage proliferation dictates atherosclerosis-related vessel wall inflammation, the Mount Sinai research team applied a nanomedicine strategy with a molecule of "good cholesterol," or high-density lipoprotein (HDL), a naturally occurring shuttle that travels from the liver to arteries. The research team took advantage of HDL's natural travel routes, loading it with the widely-used cholesterol-lowering medication called simvastatin (Zocor), which it shuttles into arterial walls.
The simvastatin-loaded nanoparticles, named S-HDL, work by targeting inflamed immune cells called macrophages within high-risk arterial plaques. These macrophages become laden with cholesterol and start proliferating in plaques, thereby increasing inflammation. This lipid-driven inflammatory process drives atherosclerotic plaque buildup and rupture leading to a heart attack or stroke.
Since patients hospitalized after heart attack or stroke have a high recurrence rate of up to 20 percent within three years, the researchers also tested the possible benefits of adding an eight-week regimen of oral statins after the one-week S-HDL nanotherapy. Mice study results showed superior long-term therapeutic benefits of a combined total nine-week S-HDL and oral statins regimen, by first rapidly reducing plaque inflammation and then continuously keeping it suppressed.
"We envision our S-HDL nanomedicine therapy could be translated quickly to human clinical trials as a short-term infusion therapy for and stroke patients to rapidly suppress plaque inflammation, which can be sustained using current standard of care oral statin medication," says Zahi Fayad, PhD, Professor of Radiology and Director of the Translational and Molecular Imaging Institute at Icahn School of Medicine at Mount Sinai.
"Nanotherapeutically inhibiting local macrophage proliferation is possible and we can effectively apply it to treat inflammation inside arteries. Collectively, our results demonstrate that the two-step regimen not only reduces macrophage accumulation but also reduces the expression of key genes linked to in this cell type," says senior study author Willem Mulder, PhD, Associate Professor of Radiology in the Translational and Molecular Imaging Institute at the Icahn School of Medicine at Mount Sinai.
Researchers look forward to translating their promising mice study findings to larger animal models and human clinical trials in the near future.
More information: Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation, Science Advances, advances.sciencemag.org/content/1/3/e1400223.

Tuesday, February 18, 2014

What to do if you have plaque in your arteries?

Well first you talk to your doctor, then you ask which of these options she knows about and has worked with. But don't do anything about this on your own.
Some reading for you; No idea how close any of these are to real world use.
http://oc1dean.blogspot.com/2011/11/treatments-for-clogged-arteries.html                                     lawnmower, drano or conventional?
 Ask your doctor about this one.
http://oc1dean.blogspot.com/2011/08/beets-brain-health.html