Friday, October 24, 2008

Boston Retinal Implant Prosthesis

Hey guys! We talked a little about the retina last week, so here's a bit on an interesting project discussed in my bioengineering class. The goal is to create a prosthesis to restore vision for visually impaired patients. Simply put, your visual system involves capturing light and focusing it onto the back surface of the eye called the retina. Light detecting cells in the retina processes this information and sends it to the visual cortex of the brain, which in turn interprets what we see.


The group designed a retinal implant that functions for the lost photoreceptors by electrically stimulating the remaining healty cells of the retina. These cells will create discrete points of light, leading to the perception of a shape.








This is a pair of glasses that captures an image with a camera, which is then converted into a pattern of electrical stimulations. There is a transmitting coil on the arm of the glasses that uses radiofrequency transmission to send information and power to the retinal implant. No need to have battery implants or wires going through body!



There is an array of stimulation electrodes in the implant that send current to appropriate areas of the retina corresponding to image.




Excerpt from site on progress of project... very cool stuff =]

"We have performed a total of six experiments on humans. These experiments were relatively brief (i.e. they lasted hours) and involved the surgical placement of an electrode array on to the surface of the retina. Very small electrical currents were delivered to the retina. Some of our patients who had been legally-blind for decades were able to see relatively small spots of light (i.e. like a "pea" as if viewed at arm's length) and occasionally were able to distinguish two spots of light from one another and "see" a line."
For more info! --> http://www.bostonretinalimplant.org

Wednesday, October 15, 2008

Monkeys move paralysed muscles with their minds

there is an article posted on Nature about scientists being able to move paralyzed limbs of monkeys by sending brain signals through the electrodes to the paralyzed wrist. they artificially routed the signals from the brain, and were able to restore movement in the paralyzed muscle.


Nature

Tuesday, October 14, 2008

Brain's reaction to hand transplant

There was a cool posting on science news today about a man who lost his hand, and received a replacement hand 35 years later. Scientists were surprised at how quickly the associated brain region began receiving signals from the transplanted hand, because so much research has documented that neural reorganization begins within hours of limb loss or debilitation.
Source: Science News

Sunday, October 12, 2008

Raising Awareness of ALS

Brief Overview of Amoyotropic Lateral Sclerosis

Also known as "Lou Gehrig's Disease," it is a fatal neurodegenerative disease that causes nerve cells in the brain and spinal cord to degenerate.

Patients affected with this disorder progressively lose their ability to control voluntary muscles, and in the later stages, become completely paralyzed. For most people, the muscles start to atrophy from their arms or legs, so there is difficulty performing everyday activities. Muscle atrophy causes the limbs to become thin and weak. The senses are not affected since this disease only attacks motor neurons, and there has been no proven effect on cognition. In later stages, paralysis spreads to the muscles affecting swallowing and breathing, eventually leading to death. 1



It still has not been found what the definitive cause of ALS is, and there is currently no cure.

Some factors researches suspect can be a cause of ALS are viruses, neurotoxins, DNA defects, immune system and enzyme abnormalities. There have also been links to patients who were exposed to heavy metal for prolonged periods of time.2
Nothing has been found to reverse the effects of ALS, but there has been one federally approved drug (Riluzole)
that can slow down the progression.



How bioelectricity helps us diagnose and understand ALS

  • Detecting that a neuromuscular disease is Amyotrophic Lateral Sclerosis is hard, since many of its symptoms are found in other disorders. It is sometimes confused with Multiple Sclerosis, since both are neurological diseases usually affected the spinal cord. As mentioned in class, MS is a disease of myelin, not primarily of nerve cells. However, the principle characteristic in the pathology of ALS is loss of motor nerve cells. There is loss of large myelinated axons, but this is consequent to the loss of motorneurons, as compared to primary demyelination in MS.
  • The Normal Diagnosis-Nerve conduction velocity (NCV) and electromyography (EMG) helps to diagnoses these disorders. With NCV, electrodes are placed on the skin over a nerve supplying a specific muscle. An electrical stimulus goes through the electrodes and the response of the muscle is measured and amplified. With ALS, the speed of the nerves is usually slowed, but compound muscle action potentials decreased. EMG measures the nerve impulses by placing electrodes in the muscles and observing electrical responses. Tracking of the electrical signals show that these responses are abnormal in cases of ALS.3
  • But... As I mentioned earlier in this post, the senses are not affected. It is common to find normal sensory potentials, however a recent study (Mar. 4, 2008) showed that 6 patients had a reduced sensory nerve action potential (SNAP) amplitude or reduced conduction velocity (CV) or both. This first standardised multicentre study on sensory potentials show that mild sensory abnormalities should possibly be part of the diagnosis of ALS.
  • What we know so far- ALS Mice with mutated human gene SOD1 - To test electrophysiological properties of motorneurons in mice, a wide range of electrical properties influencing motorneruon excitability was measured during current clamp. There weren't any differences in the resting potential, input conductance, action potential shape, or afterhyperpolarization between mutated genes and control motoneurons. The relationship between firing frequency and injected current was changed, and the slope of the relation was much greater. This shows that the hyperexcitability observed is induced by an aberration in the process of generating an action potential.7
This study shows that motor neurons with this mutant SOD1 will survive when implanted with a minimum number of cells surrounded by glial cells and normal SOD1. Gene or stem cell therapy implanting these cells may be a way to repair motorneurons in the spinal cord. But there is still the question if muscles are doing part of the destruction.
___________________________________________________________________

HOPE for a cure!
For those who read until the end, sorry I had not intended for this post to be lengthy. I just want to shed some light on a rare disease that affects only one to two people out of 100,000, so you can imagine the difficult fight for the ALS community to raise funding for research. Especially in America, patients who are diagnosed with ALS are told by their doctors to live the years they have left and are discouraged from trying to stop the disease. But, families never want to give up on their loved ones and are always fighting for a way. I strongly believe one day we will find a cure, and in fact just recently we have hit two big milestones in ALS history. On October 2, 2008, a $5 Million ALS Research Bill was signed by President Bush, which will fund ALS reserachers across the country. The ALS Registry Act was also signed on Wednesday, October 8, which will establish the first national patient registry of people with ALS. This gives us a new tool and hopes that one day a cure will be found.

[1] http://www.alsa.org
[2] http://www.ninds.nih.gov/disorders/amyotrophiclateralsclerosis
[3] http://www.neurologychannel.com/als/diagnosis.shtml
[4]
Clinical Neurophysiology , Volume 119 , Issue 5 , Pages 1106 - 1110
[5] Andrew Eisen, Charles Krieger.
Amyotrophic Lateral Sclerosis: A Synthesis of Research and Clinical Practice. Cambridge University Press.1998
[6] http://www.cnsonline.org/www/archive/ms/ms-04.html
[7] http://jn.physiology.org/cgi/content/abstract/91/1/571

Thursday, October 9, 2008

William Thompson = Lord Kelvin!

Kelvin argued that the key issue in the interpretation of the Second Law of Thermodynamics was the explanation of irreversible processes. He noted that if entropy always increased, the universe would eventually reach a state of uniform temperature and maximum entropy from which it would not be possible to extract any work. He called this the Heat Death of the Universe. With Rankine he proposed a thermodynamical theory based on the primacy of the energy concept, on which he believed all physics should be based. He said the two laws of thermodynamics expressed the indestructibility and dissipation of energy. He also tried to demonstrate that the equipartition theorem was invalid.

Thomson also calculated the age of the earth from its cooling rate and concluded that it was too short to fit with Lyell's theory of gradual geological change or Charles Darwin's theory of the evolution of animals though natural selection. He used the field concept to explain electromagnetic interactions. He speculated that electromagnetic forces were propagated as linear and rotational strains in an elastic solid, producing "vortex atoms" which generated the field. He proposed that these atoms consisted of tiny knotted strings, and the type of knot determined the type of atom. This led Tait to study the properties of knots. Kelvin's theory said ether behaved like an elastic solid when light waves propagated through it. He equated ether with the cellular structure of minute gyrostats. With Tait, Kelvin published Treatise on Natural Philosophy (1867), which was important for establishing energy within the structure of the theory of mechanics. (It was later republished under the title Principles of Mechanics and Dynamics by Dover Publications).


http://scienceworld.wolfram.com/biography/Kelvin.html

Sunday, September 28, 2008

Potassium channel - Selectivity filter

Just by hunting down the Wiki-page and reading the article that the page refers to I was able to find some insight into how the channel works, at least to some degree. (For the record the wiki-page is a much easier read than the journal-article.)
The gist of it - Because water binds differently (more strongly) to Sodium than to Potassium and "The selectivity filter (which)is formed by five residues (TVGYG-in prokaryotic species) in the P loop from each subunit which have their electro-negative carbonyl oxygen atoms aligned towards the centre of the filter pore and form an anti-prism similar to a water solvating shell around each potassium binding site" So it is more energetically favorable to pull off water from a Potassium ion and let the channel's binding site collapse on the Potassium ion and let it pass through the channel. But since Sodium binds more strongly to water it is unfavorable for the binding site to collapse on the ion and let it pass.
Well that's the short of it. So it is the P loop that does the selectivity based on the ion's affinity for water.
http://en.wikipedia.org/wiki/Potassium_channel#cite_note-pmid16253415-10

Monday, September 22, 2008

Some cool ways of harnessing human power..

I came across this link where they have a number of ways where people have come up with very innovative ways to harness human power. While this is not exactly what we are studying in class right now..it is very interesting nonetheless..

http://www.core77.com/challenge/humanpower/