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 roundworms. Show all posts
Showing posts with label roundworms. Show all posts

Saturday, December 3, 2016

How fast you move can predict how healthy you'll be - If you are a roundworm

We'll never know if this applies to stroke survivors.
https://www.mdlinx.com/endocrinology/medical-news-article/2015/11/24/6428485?
Institute for Basic Science News, 11/23/2015
As humans have begun to live longer it has become clear that the quality of our lives is equally as important as the duration. In the lab, a dramatic extension of lifespan isn’t difficult to achieve. In previous experiments using several types of mutated Caenorhabditis elegans roundworms (C. elegans), researchers were able to significantly extend the worm’s lifespan. The lengthened life that the worms experienced was not necessarily a good one, as many of the mutated varieties were less healthy than wild–type worms, especially during the segment of life that was extended beyond normal. Instead of focusing on drawing out the length of life, South Korea’s IBS Center for Plant Aging Research and the research group led by Coleen Murphy, a professor at Princeton University have created a tool that can be used for accurately predicting lifespan as well as assessing the current health state, and discovered the regulatory mechanism that extends “healthspan”, the time in which an organism is at its optimal health. The researchers concluded that maximum velocity (MV) of wild–type worms at day 9 of adulthood is a reliable predictor of longevity. Another factor they observed was the state of C. elegans mitochondria. Elderly humans have weaker muscles and less strength resulted from mitochondrial defects which occur later in life. C. elegans with lower MV exhibit similar defects by midlife but there are far fewer defects in worms with higher MV at the same age. These observations indicate that MV correlates with mitochondrial health expression, suggesting that MV can be a reliable indicator of the actual physical state. The findings show that MV of C. elegans is a reliable indicator of age–related physical decline, accurately reports movement ability and if measured in mid–adulthood, is predictive of future longevity. According to Hong Gil Nam, “our analysis takes into account the length of time an individual can expect to live, and how healthy that individual can expect to be with age.” Many parts of the insulin/IGF–1 signaling (IIS) pathway that enable these functions have been identified, and many of these genes and the underlying mechanisms are conserved in mammals, which mean that the extended abilities that insulin/IGF–1 signaling (IIS) exhibits could offer therapeutic target possibilities for humans in the future. The IBS Center isn’t just looking at push the limits for long life; instead they are unraveling the mechanisms in our cells to maximize our health as we age.
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Monday, November 28, 2016

Substance with the potential to postpone aging

It will be a long time before this is proven in humans. Roundworms and mice that don't have the same inflammatory system as humans don't seem like good prospects. But I won't have to worry about this because NOTHING will be done for followup since we have fucking failures of stroke associations doing nothing useful. No database of research and protocols, no strategy, no leadership, no acknowledgement of any problems in stroke. NOTHING!!!
https://www.mdlinx.com/neurology/medical-news-article/2016/11/07/aging-process-coenzyme-nad/6907659? 
University of Copenhagen Faculty of Health and Medical Sciences News, 11/07/2016
The coenzyme NAD+ plays a main role in aging processes. In mice and roundworm adding the substance can both extend life and postpone the onset of aging processes. New research conducted at the Center for Healthy Aging and the American National Institute of Health shows that this new knowledge will eventually be able to help patients with Alzheimer’s and Parkinson’s disease.

Previous research has shown that a main process in aging is the capacity of the cells to keep our genes, our DNA, more or less intact. However, changes in the cells’ power stations, the mitochondria, also affect aging processes. An international team of researchers from the Center for Healthy Aging at the University of Copenhagen and the National Institute of Health in the United States has shown that the substance NAD+ bridges the gap between two main aging theories – repairs to the DNA and poor functioning mitochondria.

The results were published in the journal Cell Metabolism.

"Our new study shows an age–dependent decrease in the level of NAD+, and this decrease is far greater for organisms with early aging and a lack of DNA repairs. We were surprised to see that adding NAD+ postponed both the aging processes of the cells and extended life in worms and in a mouse model", says Professor Vilhelm Bohr from the Center for Healthy Aging and the National Institute of Health.
Go to Abstract Print Article Summary Cat 2 CME Report