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.

Thursday, September 1, 2016

One more reason to swear off tobacco: The inflammatory trap induced by nicotine

So is this because of smoking it? Because if I ever get dementia/Alzheimers or another stroke I'm doing the nicotine patch. We'll never know because we have no one with brains in the stroke medical world.

Nicotine Holds Promise for Stronger Stroke Recovery

Nicotine Patch Appears To Help Mild Cognitive Loss

One more reason to swear off tobacco: The inflammatory trap induced by nicotine 

An Umeå-based team in collaboration with US researchers reveals a new link between nicotine and inflammation. They report that nicotine strongly activates immune cells to release DNA fibres decorated with pro-inflammatory molecules, so called neutrophil extracellular traps (NETs). The continuous exposure to these NETs can harm the tissue and could explain the hazardous consequences of tobacco consumption for human health.
Tobacco use causes death of nearly six million people annually according to WHO. Nicotine is the major addictive and toxic component in tobacco products. In cells, signals via nicotine acetylcholine receptors to mediate dangerous effects on the consumer's body. Nicotine is a major cause of inflammatory diseases among smokers and also non-smokers by passive inhalation, such as for instance chronic obstructive lung disease (COPD). COPD is widely spread and affects more than 10 percent of the adult population in westernised countries. The molecular mechanisms underlying this inflammatory activity of nicotine are not well understood.
In a recently published article in the Journal of Leukocyte Biology, researchers at the Laboratory for Molecular Infection Medicine Sweden (MIMS) at Umeå University reveal a novel link between nicotine and inflammation. They found that nicotine activates neutrophils, in an undesirable fashion.
Neutrophils are the most abundant type of that circulate in the blood stream ready to attack invading microbes with an arsenal of antimicrobial compounds. Neutrophils are essential to prevent infection by engulfing invading microbes, or by releasing reactive oxygen species as well as DNA fibres from their own nuclei, termed neutrophil extracellular traps (NETs). NET release is a mixed blessing. Loaded with antimicrobial enzymes and pro-inflammatory molecules NETs are harmful to invading microbes, however, they can also potently harm the host's own tissue, if not controlled in the right manner. In recent years, NETs have been attributed to be mediators of tissue damage in several , such as for instance small vessel vasculitis, arthritis and cancer.
For the first time, Ava Hosseinzadeh and colleagues at MIMS show that nicotine triggers NET release. The signal to trigger NETs is mediated by a specific acetylcholine receptor found on neutrophils and further signalled into the cell via a protein kinase known as Akt.
"This particular finding explains the missing piece of the puzzle of tobacco usage and inflammation," says Ava Hosseinzadeh, who worked on this project during her doctoral dissertation. "This novel finding opens new avenues to understand the consequences of tobacco usage for and should be seen as one more convincing argument to quit nicotine usage in any form."
"The next evident step is to demonstrate the NET-inducing capacity of nicotine in animal models and human samples," says Constantin Urban, associate professor and project leader at Umeå University. "Such 'in vivo' studies will enable us to attract new funders and potentially interest of the pharma industry. Our finding could hopefully lead to novel anti-inflammatory therapies of tobacco usage related diseases."
More information: A. Hosseinzadeh et al, Nicotine induces neutrophil extracellular traps, Journal of Leukocyte Biology (2016). DOI: 10.1189/jlb.3AB0815-379RR

Journal reference: Journal of Leukocyte Biology search and more info website
Provided by: Umea University search and more info website

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