Deans' stroke musings: Training Monocytes by Physical Exercise

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, July 23, 2015

Training Monocytes by Physical Exercise

I'm sure your doctor knows how to train monocytes.

Training Monocytes by Physical Exercise

+ Author Affiliations

From the Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, United Kingdom (E.A., P.M.); and MultiMedica Research Institute, Milan, Italy (G.S.).

Correspondence to Paolo Madeddu, MD, Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Upper Maudlin St, Bristol BS2 8HW, United Kingdom. E-mail mdprm@bristol.ac.uk

Peripheral artery disease is caused by obstructing atherosclerotic plaques that critically reduce blood flow during exercise. The disease affects ≈4% of people >40 years and 15% to 20% of subjects above 65 years of age. Critical limb ischemia, the most severe manifestation of peripheral artery disease, describes patients with chronic ischemic rest pain, or patients with ischemic skin lesions, either ulcers or gangrene. It requires foot amputation in 25% of cases within 1 year from the diagnosis. Revascularization therapies are indicated in critical limb ischemia patients, but they are often ineffective or unfeasible; and in the latter case, the reported amputation and mortality rates exceed 50%. Therefore, new therapeutic approaches are urgently needed.

See accompanying article on page 1862

Promotion of arteriogenesis, which refers to the enlargement and functionalization of preformed collateral arterioles, represents a promising therapeutic approach in critical limb ischemia patients. Several clinical studies have used the administration of growth factors (mostly basic fibroblast growth factor or vascular endothelial growth factor, either as protein or gene therapy) or stem and progenitor cells.¹ In addition, exercise rehabilitation programs have been shown to improve symptoms of claudication.^2,3 Mechanistic understanding of how physical exercise increases collateral artery formation is inadequate.

The new study from Schirmer et al⁴ shows that voluntary training confers mice with an improved capacity to recover from operatively induced limb ischemia when compared with sedentary controls. The positive outcome is associated with homing of inducible nitric oxide synthase (iNOS)-expressing mononuclear cells. The importance …

[Full Text of this Article]