Brain shock therapy that actually works!

Justin Williams ’13

Just today, April 18th, 2010, researchers from various universities (University of Pennsylvania School of Medicine, Tufts University, and The University of Illinois in Urbana-Champaign) published that they have developed a new and improved way to implant electrodes into the brain in order to monitor and react to different patterns of brain activity.

As of now, the most advanced methods we have for measuring brain activity are either thin needle-like electrodes that can be inserted deep within the brain or micro-electrode arrays (made up on dozens of electrodes attached to a silicon base or grid). Although both of these methods are useful, they each have drawbacks. The needle-like electrodes are very vulnerable and can be moved or broken when the brain changes position and the silicon base of the micro-electrode arrays do not allow for much flexibility when attaching to the surface of the brain.

An example of an electrode array set up on a model of the brains surface.

However, now researcher Dr. Brian Litt M.D. from University of Pennsylvania School of Medicine and colleagues have developed a new and improved method that uses a silk base instead of silicon. Dr. Litt, when explaining their reasoning behind their micro-electrode array design, said that “the implants contain metal electrodes that are 500 microns thick, or about five times the thickness of a human hair. The absence of sharp electrodes and rigid surfaces should improve safety, with less damage to brain tissue. Also, the implants’ ability to mold to the brain’s surface could provide better stability; the brain sometimes shifts in the skull and the implant could move with it. Finally, by spreading across the brain, the implants have the potential to capture the activity of large networks of brain cells.” In addition to these advantages, the silk base can also be dissolved at a controlled time point which would provide for even better stability for the electrodes.

The potential impact of this new method for measuring and altering brain activity is enormous.This design has promising implications for treatment of epilepsy, spinal cord injuries, and other neurological disorders. For example, the arrays could be read the start of epileptic activity and deliver a shock that would calm the brain down and prevent the seizure. Although these results are a step in the right direction, researchers are still experimenting with varying numbers and arrangements of arrays in order to maximize the clarity of the measurements the electrodes read.


Live long and prosper

Justin Williams ’13

On April 1, 2010, scientists funded by the Biotechnology and Biological Sciences Research Council at the University of Birmingham uncovered a gene that is strongly related to the lifespan in Caenorhabditis elegans (C. elegans) and three of its close relatives. Scientists used longevity of life, immunity, and resistance to stress as the main determinants of the worms lifespan.

Activation of DAF-16 gene promoting increased resistance to stress.

Head researcher Dr. Robin May explains the purpose of their research: “We wanted to find out how normal ageing is being governed by genes and what effect these genes have on other traits, such as immunity.” To do this,  they looked at a gene that has been known to play an important role in the ‘dauer’ stage of development and influence the longevity of life in worms, gene DAF-16.

To figure out the exact role this gene plays in the worms lifespan, researchers sought out the relationship between the worms lifespan/resistance to stress and that its expression of the DAF-16 gene. To induce stress in worms scientists exposed “them to high temperature, heavy metals and a range of bacterial and fungal diseases.”

Their results were very promising. As they expected, the DAF-16 gene and it’s expression in worms positively correlated to their lifespan, and, in general, “higher levels of DAF-16 activity correlated with longer life, increased stress resistance and better immunity against some infections.”

Although this study was performed on worms, scientists have high expectations for the implications in humans. Researchers say that “it is possible that this knowledge could open up new avenues for altering ageing, immunity and resistance to stresses in humans.”


TB or not TB?

Justin Williams ’13

Ever since doctor Robert Koch discovered the bacteria responsible for tuberculous, there has been many hours poured into researching everything about the disease. Through the years, researchers have unearthed almost everything, but one area that is notably lacking is determining any kinds or risk factors. However, on March 4, 2010, researchers at the University of Washington have discovered a gene that may be a major determining factor in susceptibility to TB.

Researchers conducted experiments on zebrafish, in which the severity of the TB could be easily identified due to their clear bodies. The scientists genetically altered the genetic makeup of the zebrafish before injecting them with the tuberculous bacteria and then observing the severity of their TB symptoms.

X-ray of a person with tuberculous.

Their experimentation and subsequent results turned out to be very interesting. They found that the lta4h gene, and it’s genotype (what two particular copies of it you have) are very important in determining how susceptible a person is to contracting TB.

For those of you who are not familiar with genetics, the majority of genes come in two differentforms. You get one copy from each of your  parents. It is possible to get both of one kind, one of each, or one of  the other kind. In this particular lta4h gene, the two different types  are inflammatory and anti-inflammatory. Researchers found that  when zebrafish have one copy of each of the genes, their response to  TB is much better than if they only have copies of one or the other  (i.e. the response of zebrafish with one inflammatory and one anti-inflammatory copy was much better than those who had two copies of the inflammatory or two copies of the anti-inflammatory).

Comic illustration of the lta4h gene.

While this research was conducted on zebrafish, the scientists did look into the structure of the gene in humans to determine its relevance. Their investigations proved fruitful and the implications of this for humans are promising.Also, their newfound knowledge that an over inflammatory response can be hurtful for the fight against TB provides some hope “that corticosteroids and other anti-inflammatory agents can be useful as adjuvants in some cases of TB where antibiotics alone are failing.” Whichever way you look at it, the results are exciting and promising for people involved with tuberculous.


How heart malfunctions function

By Justin Williams ’13

Calcineurin Enzyme

Heart disease is among the deadliest diseases in the world. Last year it was responsible for  631,636 deaths in the United States alone. For many years it has been known that the enzyme calcineurin plays a major role in heart function, but what exactly it did was not known until now. Just this week (February 19th), researchers at the Cincinnati Children’s Hospital Medical Center and the Howard Hughes Medical Institute published the results of their study, which shows that calcineurin plays a major role in regulating many vital functions of the heart.

In this study, the researchers observed the hearts of mice, manipulating the level of calcineurin in their systems. Their data shows that “calcineurin in hearts of mice is directly linked to proper cardiac muscle contraction, rhythm and maintenance of heart activity.” When mice were almost completely stripped of calcineurin they displayed major heart problems which included “heart arrhythmia, failure and death” said Dr. Marjorie Maillet, one of the leading investigators in the study.

Prior to this, calcium has also been identified as necessary for a healthy heart. In this study, in addition to the aforementioned results, researchers found that the mice who were bred with a calcineurin deficiency displayed a severe reduction in the expression of these calcium related genes. Using this newfound link they have proposed a “feed-forward” mechanism, hypothesizing that when the calcineurin is activated by calcium, the effects of calcineurin on the heart will be increased.

While there are some drawbacks to this study, mainly that it is the first of it’s kind and was performed on mice, the results are still promising. Dr. Maillet certainly thinks so, saying that it “offers important insights for future studies that could lead to new approaches in diagnosis and treatment of heart patients.” It is still a little early to call, but things are starting to look up in the world of heart disease.

The original article can be found here.

Diabetic Blindness, a Light at the End of the Tunnel?


Susanne Mohr

Many of you, like me, may know some one close to you that has diabetes. Diabetic retinopathy is very prevalent, not only in the diabetic community but in the population as a whole. Roughly forty-five percent of diabetics are affected by diabetic retinopathy and it is among the leading causes of blindness among American adults. In this particular disease, existing blood vessels may swell, or new ones may form, both of which result in the obstruction of the retina. It is this obstruction of the retina, which is vital for human sight, that causes the  blindness associated with diabetic retinopathy.

Until now, this disease has gone untreated for the most part. That is until Susanne Mohr, a researcher at Michigan State University, made a major breakthrough in identifying the primary cause of diabetic retinopathy. In her research, she has found that a protein, siah-1, is produced in the body when blood sugar levels are correspondingly high, as you would find in a diabetic. She found that the siah-1 protein could be used to indicate the levels of a different protein, glyceraldehyde-3-phosphate dehydrogenase (GAPDH). 

This second protein, GAPDH, is the real culprit in diabetic retinopathy. When the levels of this protein are high in the blood, they accumulate in special cells in the eyes called Müller cells. Müller cells live on the blood vessels in the retina and when these cells die, it causes the blood vessel damage in the eyes that is associated with diabetic retinopathy. 

GAPDH is necessary throughout the body for energy among other things, so regulating the production of that is not possible. However, siah-1 is only produced when the blood sugar levels are high, so the regulation of that protein may be possible. Although this is one of the first studies with these results, and subsequent research is not yet known concerning the regulation of siah-1, the news is promising. This may have enormous impact in the scientific community and American society as a whole.

Justin Williams ’13