Monthly Archives: November 2008

Cell suicide can stave off cancer

cell!I was reading some science news, as I am prone to do, and came across this article which just so happens to deal with what we’re learning about in class right now–cell organelles and their function. The organelle this particular blog post features is the lysosome. Need to digest a food particle? The lysosome has digestive enzymes that will hydrolyze that food particle right up! Got a mitochondrion or two on their last legs? Lysosomes are right there to digest them and get rid of them. Did your cell engulf a bacterial cell or virus? The lysosome will dispose of the invaders quickly and efficiently. You get the idea…lysosomes are little sacs containing digestive enzymes that must work at a specific pH in order to perform properly.

Now what do lysosomes have to do with cancer cells? Well, quite a lot actually. When we start talking about the death of cells, lysosomes are a key player in aiding a cell’s demise. In a study conducted by researchers at M.D. Anderson Cancer Center in Houston, they found that ovarian cancer cells which express a protein known as PEA-15 have a higher rate of autophagy than those that do not. This higher level of PEA-15 causes the cancer cells to basically commit suicide (by causing the lysosomes to open and release their contents) and can lead to an increase in a woman’s survival rate from this particular type of cancer, which kills over 15,000 annually. PEA-15 causes cell death by interacting with a protein known as ERK (extracellular signal-regulated kinase, an enzyme). When PEA-15 interacts with ERK in the nucleus, it will move ERK into the cytoplasm, which prevents ERK from having an effect on the growth of the cell. When PEA-15 is in the cytoplasm, it will cause the cell to become autophagic.

It should be noted that PEA-15 is what is known as a “death effector domain” protein; in other words, it is responsible for contributing to cellular death. This leads to some interesting questions that can be asked about this protein and its role in cells. If ovarian cancer cells contain higher levels of PEA-15, would other cells affected by ovarian cancer (such as the cells of the uterus and omentum–the covering over the intestines) also have high levels of PEA-15? How could the presence of PEA-15 in other types of cells affect the survival rate of those cancers? What about ERK? What sorts of treatments could be developed to prevent ERK from doing its job? PEA-15 is also found in astrocytes (a type of brain cell), so could this research be extended to those who suffer from various cancers of the brain?

A friendly reminder

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Google slices, it dices, it juliennes, and…predicts the next flu epidemic!

fluvirusAs we enter cold and flu season, I thought I’d share this neat little web nugget with you all: Google Flu Trends. Now how amazing is this? Just when you thought Google could do it all…it pretty much DOES. In the past, state and local health departments have relied on data compiled by the Centers for Disease Control to predict when flu outbreaks will occur. The problem with this is that the data provided by the CDC is often two weeks behind the trend–not terribly helpful if you are a county health officer who is trying to ensure that the people in your county have adequate supplies of flu vaccine.

What Google has done is compiled key search terms that increase in frequency during flu season, as their programmers believe that this is a good indicator of flu activity in a particular area. Now you’re probably wondering, ‘well how the heck does Google know where I am?’ Your computer’s IP address (its address on the web) is localized to a certain geographical area, and Google searches can be traced back to certain IP addresses. Thus, if a bunch of people in Bucksnort, Tennessee are using Google to search terms such as “runny nose and cough” repeatedly over time, this may serve as an indicator that perhaps flu activity in Bucksnort is high.

Now how cool is that? Who would have thought that Google could be used as an epidemiology tool? It makes you wonder, could Google be used to predict where hotspots for certain health conditions may pop up? For example, in the early 1980’s, in South Texas, many babies were born with a condition known as anencephaly. Babies born with this condition are born without the cerebral cortex of their brain, and are often born missing the cranial cap. They do not survive more than a few hours in most cases, with a few surviving only a few days. The number of anencephalic babies born to mothers in South Texas was disproportionate compared to the normal statistic (around 1000-2000 babies total per year). Back then, no definitive cause was given for the high number of anencephalic births. To this day, it is still unknown what could have caused the mothers to give birth to these babies.

Now, flash forward to today: if the same thing occurred, do you think a tool like Google Flu Trends could be used to predict it? Should this kind of tool be used to predict relatively rare conditions such as anencephaly, or should it be used to predict chronic conditions such as diabetes, high blood pressure and heart disease? How can doctors, health officials and the public use this data?

image from the CDC Public Health Image Library:

Fantastic Plastics May Not be so Fantastic After All

Have you ever conducted an experiment that produced results that may not have turned out the way you wanted them to? Think about the things in your experimental environment that may have contributed to your “off” results. Would you ever suspect the lab equipment you use as the source of your error?

Well, scientists at the University of Alberta in Edmonton, Canada didn’t either, until the experiment they were conducting about monoamine oxidase and how drugs affected this enzyme’s activity produced some very odd results. Andrew Holt, the researcher who cast light on this issue, noticed that the enzyme was being inhibited at lower concentrations than it should have been, and began poking around to find out why this was happening.

tubeUsing common laboratory solvents such as water, DMSO and methanol, Holt cleaned out the plastic lab equipment he routinely used–things like plastic culture tubes and pipet tips. He discovered that there were several compounds that were washed out in the leachate (the resulting solution that was washed out of the equipment) that had the potential to affect the outcome of any experiment conducted with the equipment in question.

Because so much plastic labware is used in experimentation, Holt felt the need to record and share the data he’d collected with some of his colleagues to see if they’d experienced similar issues. Much to his surprise, they had.

Now, the implications for Holt’s work are far-reaching. Think about all the labs conducting research in life science, biochemistry, genomics and other sciences that are likely to use plasticware as a part of their lab equipment. Think about why they use plasticware as opposed to glassware. How do you think that the presence of these organic leachates will change the way scientists do research? How will results already reported be treated by the scientific community, based on this new knowledge? How will this study affect the way scientists do their work?

A spoonful of sugar makes the E. coli go down…

A Spoonful of sugar helps the medicine go down
The medicine go down-wown
The medicine go down
Just a spoonful of sugar helps the medicine go down
In a most delightful way

We’ve all heard the song “A Spoonful of Sugar” from the movie “Mary Poppins.” Now replace the word “medicine” with “E. coli” and you’ve got an entirely different song and idea altogether. A team of researchers from Australia and the US worked together to discover that an endogenous sugar in red meat and dairy products may promote binding of toxins produced by E. coli bacteria. Now before you go giving up your milk and meat, calm down…this study is not a cause for alarm, but it certainly provides those who shun consumption of bovine products more evidence for why eating beef isn’t quite as good for you as you think. Or does it?

sialic acidThe sugar in question is what is known as a sialic acid N-glycolylneuraminic acid (say that 3 times fast!), which is present in most mammals…except, guess who? Yep, humans. It seems that quite a long time ago, in our early evolutionary history, because of a mutation, we lost the ability to produce this sugar which resides on the outer surface of mammalian cell membranes. Instead, we produce its analog, Neu5Ac. The significance of this sugar is that it belongs to a group of compounds known as glycoproteins which serve as identifiers on the outside of our cell membranes. They are key in stimulating an immune response against foreign cells (like bacteria, viruses and cancer cells), but also in aiding our own immune system to prevent it from attacking us inadvertently. Apparently, the mutation happened right before our common ancestor with other primates appeared and so we do not produce this particular sugar. However, other mammals like cows (the source of many an ice cream shake or tasty hamburger) retained the ability to produce this sugar as the gene responsible for its production has been well-conserved over time. It should be noted that the Neu5Ac also allows for us to be resistant to a strain of Plasmodium that causes malaria in other animals, but makes us susceptible to other Plasmodium species that cause malaria in humans.

Now what does this sugar have to do with E. coli? Bear in mind that the E. coli the authors are looking at are what we call Shiga-producing E. coli; in other words, they produce Shiga toxin, which is extremely harmful to the gastrointestinal system of humans and has been known to cause death. One researcher, Andy Benson of the University of Nebraska states: “Now you’ve got a scenario where the organism — the toxin — actually needs something from the food it’s carried in — that’s truly unique.” It is rather interesting that in this particular case, the toxin produced by the bacteria requires something to activate it, rather than the bacteria requiring something to activate it to produce the toxin itself. Could this be a form of molecular coevolution? And if it is, why hasn’t it happened this way for other toxins produced by bacteria? If this is a form of molecular coevolution, how did selection occur at the molecular level so that this toxin could bind to this particular sugar and not some other?

Now does this mean you need to give up that burger and milkshake? No. But it does raise some interesting issues. Many countries around the globe consume beef products in large quantities, and many people raise cattle as a livelihood. Could this spell the end of ranching and cattle-raising as we know it? Or will it lead scientists to find ways to possibly genetically modify and then selectively breed cows so that they no longer produce this sugar on their cell membranes? What would the ethical implications be of such an action? What would the ethical implications be if no action were taken?