Tuesday, December 1, 2009

Ricochet Science is Moving!!

As of January 1, 2010, this blog is moving to a new location - ricochetscience.com . In the process we will be evolving to include both pod and video casts, and coverage of sciences other than just genetics.

Please come visit us at our new site after the start of 2010!

Wednesday, July 29, 2009

Sunbeds as Carcinogens

Finally some sense has been made about the use of tanning beds. A study by cancer researchers supported by the World Health Organization have determined that the use of tanning beds before the age of 30 increases the risk of developing skin cancer, specifically the deadly form melanoma, by 75%. Although the tanning bed industry has for the most part denied any link between tanning beds and increased rates of skin cancer - from a genetic point of view, it was only a matter of time until the evidence supported what we already knew: Lying inside a metal coffin and being bombarded by radiation is bad for your health.

The bottom line is that UV radiation, in all wavelengths, damages DNA to some degree. Some forms of UV are worse than others, but no wavelength is DNA "friendly". To put it bluntly, UV radiation fries DNA. More scientifically, UV radiation causes small breaks in the DNA molecule and the formation of a chemical structure called a thymine dimer. Thymine dimers represent a special challenge for our DNA repair mechanisms, and although our cells have evolved mechanisms to repair these structures, the changes that the repair generates an unintended detrimental mutation is high. If this mutation occurs in a gene that is responsible for regulating cell growth (or maybe even mitochondria now?), the result can be an out-of-control cell - commonly called cancer.

Of course, the head of the The Sunbed Association disputes the claim, stating that there is no link between responsible use of sunbeds and cancer. Seems like similar statements were made in the 1970s and 1980s with regards to cigarettes. I imagine that the debate will now focus on what constitutes "responsible". But according to this study, the only responsible use would be to lie down in the tanning bed and not turn on the UV light. Anything else is simply inviting an increased risk of death.

For more info - see this article in USAToday

Friday, July 24, 2009

A New Twist in Understanding Cell Division.

Pop Quiz: What is the role of the mitochondria in a cell?
  1. digest incoming food particles
  2. store DNA
  3. produce ATP
  4. regulate the cell cycle
Until just a few days ago, the only correct answer to this question would have been #3. The mitochondria of a cell are well recognized as the powerhouses of the cell. They are the location where energy-rich nutrients such as carbohydrates and fats are brought in and "burned"in the presence of oxygen to produce the energy (in the form of ATP) to power our cells. It is one of the earliest lessons of any introductory biology course.

However, in a development that is sure to change the way we look at cell biology, it now appears that answer #4 also may be correct. A group of researchers at the National Institutes of Health reported in the July 21, 2009 issue of PNAS that the fusion of the the mitochondria in a cell influences the buildup of a protein called cyclin. This in turn, acts as a control mechanism for the cell to bypass an important checkpoint (G1/S), allowing the cell to divide.

Cyclin is a form of protein "clock" within a cell. Its job is relatively simple, as cyclin levels accumulate in the cell, it overcomes a series of thresholds that tell the cell to undergo important activities. One of these activities is the cell cycle. The cell cycle is a type of cell "day". At specific points in the cycle the cell undergoes DNA replication and specific activities to prepare for cell division. These activities are regulated by special proteins called checkpoint proteins. You should be very interested in these checkpoint proteins - their job is to ensure that the cell does not divide unless it needs to, since unrestricted cell growth is called cancer. There are two specific classes of these proteins, proto-oncogenes and tumor supressor genes. Until earlier this week, they were the primary focus of most research dedicated to understanding the cell cycle.

What the NIH team reported is that just prior to one of these checkpoints (G1/S) is that the mitochondria form an unusual tubular network in the cell. The images from their paper show a network of mitochodnria that is reminiscent of a map of a subway line in a major city. The authors then show that the presence of this network is correlated to a increase in a form of cyclin that is known to be a major key in overcoming the G1/S checkpoint, allowing the cell to duplicate its DNA in preparation for cell division.

Why should we be interested in this? First of all, because it demonstrates that by looking in unconventional areas, we can find new clues as to how cell function. Until earlier this week, no one would have answered #4 in the above quiz. But more importantly, scientists who study cancer genetics and biochemistry can now look for relationships between these mitochondria and unregulated cell growth, which should, eventually, lead to new insights on how to battle some forms of cancer.

Click here to access the article in PNAS

Friday, May 29, 2009

Solutions for the Higher Education Financial Quagmire

This has not been a good year for higher education. Economic downturns traditionally benefit the educational community by providing a surge of displaced workers to fill the classrooms, but the severity of the current economic situation actually has had a negative effect on campuses across the U.S. While people are returning to higher education, the financial mess on Wall Street has crippled the financial backbone of academia. Across the country, state budgets are in crisis.

In my own backyard, for example, the University System of North Carolina experienced a 5.8 percent reduction in funding in 2008-2009, and the North Carolina state budget is facing a $3.4 billion shortfall for 2009-2010. In addition to budget cuts, the General Assembly enacted a 7 percent reversion in the budgets of higher education — the new name for supplemental budget cuts.

On a more individual basis, since this recession directly involves the financial sector, people are having a hard time securing the funding to return to school, and scholarships and grants are reducing their support as their endowments struggle. Somehow, we have become accustomed to this type of news, with many wondering how any good can come out of this situation.

The Bright Side of Budget Woes
The budgetary quagmire facing academia often is viewed as an obstacle to program and curriculum development. But this actually may be the event that finally catalyzes the blending of higher education and industry.

Across academia there always has been a rather small minority that actively has promoted and fostered direct interactions with the corporate world, not just in the form of grants, but in direct collaborations in research activities and the training of skilled workers to satisfy the needs of industry. Even though the current economic woes also are influencing the private sector, the time may be ideal for a revolution in the way that academia and industry (including big pharma) interact.

We are beginning to see that happen already. At Appalachian State, my home institution, the faculty is actively encouraged to develop partnerships with both the private and government sectors. Within the past few years, long-standing ultra-conservative policies regarding copyrights and ownership of patents have been discarded in favor of more liberal policies that promote technology transfer and cooperative agreements with industry.

The Ethics of Industry-Academic Collaborations
We do, however, need to get a handle on the ethics of these new relationships. In countless committees on college campuses, faculty and administrators are questioning whether these new relationships are in the best interests of the students. As is always the case, a few bad cases can upset years of progress. An excellent example of how ethical problems can cause havoc in an academic program is at Harvard Medical School. A March 2 article in The New York Times outlines Harvard's problems with both faculty and administrative personnel receiving financial support for their research from the pharmaceutical industry. In this case, individuals at Harvard are accused of placing their personal interests over those of professional interests. Even though the faculty and administration at Harvard had disclosed that they were working as consultants to private industry, the students' perception was that the faculty was using these relationships to influence the students' views on certain drugs. While the matter is still being debated at Harvard, it does show that potential problems exist.

Of course, the overall issue is one of transparency. Most of us recognize that transparency is the key to an effective workplace. When all issues are on the table and open to discussion, people feel more comfortable with their environment and their leaders. This type of change has been slow to develop on college campuses, where the authoritarian role of professors and administrators resembles a form of medieval caste system. Most institutions, including Harvard, fail the transparency test — but not all. As pointed out in the article, the University of Pennsylvania, Stanford and Columbia have developed more transparent reporting systems and have received high grades for their achievements.

Promoting Collaborations Through Peer Review
There is another solution, and one that is deeply embedded in the scientific process. The scientific community, both academic and private, prides itself on the peer review process. With regards to research, review by one's peers is considered to be the benchmark of ensuring academic integrity.

What is needed in order to ensure that academic-industry relationships are handled ethically is an adaptation of the peer review process in academic-biopharma partnerships. Simply put, faculty must disclose their relationships to a community of peers, including representatives from industry. Since we are dealing with finances, these peer review committees should be inter-institutional, further compelling an environment of transparency in higher education.

This process will ensure that transparency is maintained, and it will promote the interactions of academia and big pharma. Furthermore, it will help encourage the interaction of academia with the biopharma community, which may result in an influx of much-needed capital into an increasingly bankrupt educational system. These are the types of partnerships that higher education, the industry, and even more importantly, the students, desperately need.

This article was first published in BioWorld Perspectives (May 28, 2009 vol 3 #21) by AHC Media and reproduced here by permission.

Wednesday, May 20, 2009

Fighting HIV Without Traditional Vaccines

Why can't scientists just develop a universal vaccine against HIV and the swine flu? Is it because the biopharm industry wants to make money each year off of a new vaccine?

The answer to the second question is a definite "no", but the answer to the first question is far more complicated....

The problem is that HIV, and in fact many viruses, do not play fair. Viruses, although not technically "alive", evolve over time. One way that viruses evolve is by changing the protein structure of their outer protein coat. This protein coat is responsible for the majority of the properties of a virus - for example what species and types of cell in infects. In viruses, the evolutionary rate of change is higher than that of living organisms, for several reasons, including the fact that viruses lack DNA repair mechanisms. This means that they accumulate mutations faster, and often these mutations change the outer structure of the virus. Since vaccines are prepared using purified outer proteins of a virus, you can see how as viruses evolve they make previous vaccines ineffective. Such is often the case in the flu vaccine, where the yearly vaccines are prepared from the previous year's flu viruses. Vaccines for HIV has so far met limited success, and epidemiologists balk at the idea of putting a vaccine on the market which would make people think that they are safe. Furthermore, HIV belongs to a class of viruses called the retroviruses, an especially nasty sub-set of viruses that accumulate mutations faster than most.

Vaccines, when introduced into the body, cause the immune system to target specific cells and proteins for destruction. This is called the specific immune response, and one of the ways that it works is to produce antibodies against the invading virus. Unfortunately, we all do not generate the same antibodies, meaning that a vaccine in one person might not have the same result as in another. Coupled with the high mutation rates of viruses, this causes real problems in developing a population-wide vaccine for highly mutable viruses.

But what if we could bypass the whole antibody-generation step and instead introduce virus-specific antibodies into the body. These antibodies could be designed to target a specific type of virus, and would actively recruit the cells of our immune system to destroy the virus before it caused significant damage. This type of procedure has just been reported for HIV-type infections in primates, and the initial results suggest that it might hold promise. And not only for HIV, but also for viruses such as H1H1 (swine flu) and H5N1 (avian flu). Both of these are now in the human population, and the development of an effective vaccine against them both is not soon forthcoming, so adding a new technique to our anti-viral arsenal is well advised.

For more information - see Jon Cohen's article in ScienceNow
"Designer Antibodies Derail Monkey AIDS Virus"