Texarkana and the Affordable Care Act

When the Obama administration set out to provide health insurance for millions of uninsured, impoverished Americans, it was under the assumption that all states would expand Medicaid to cover more low-income residents. However, when the Supreme Court ruled that states could not be coerced into expanding Medicaid, 20 states declined to do so, leaving millions of Americans still without health insurance.

This particularly affects citizens of towns that border state lines, such as the Texarkana metropolitan community. In the Arkansas side of Texarkana, homeless shelters are about $6 a night, and on the Texas side they are generally free. When the Affordable Care Act was set into motion, many citizens were dangerously uninformed about its implications, which ultimately meant that those who slept on the Arkansas side of Texarkana were eligible for Medicaid, and those who slept on the Texas side of Texarkana were not.


This brings up the question: will American citizens in border towns begin moving to acquire such health benefits? It seems that the answer is “no.” As of now, about half of surveyed Americans admit that they don’t understand how the ACA will affect their own families (Kaiser, 2013). It seems as though the public has had a long-standing tradition of not understanding – and, ultimately, not trusting – government aid. When the ACA was introduced, it promised millions of Americans health coverage, but the decisions of many states against the ACA have broken such promises and left many citizens confused and uninsured. Only time will tell how the Obama administration plans to care for such citizens and to eliminate the ridiculousness of such border constraints; hopefully, such a plan will boost their confidence in a government that has accepted their underprivileged, uninsured status quo for so many years.

Lindsey Rogers, Summer Research Intern


Kaiser, H. J. (2013). Kaiser health tracking poll: August 2013. Kaiser Health Tracing Poll, Retrieved from


More SEX!

Got your attention? Well, so can you! You can steal the attention of your seductive partner if you’re a male rat infected with this virus called Toxoplasma Gondii. Apparently, this sexually and vertically transmitted parasite makes its host more attractive to the opposite sex. Uninfected estrous rats spent more time and gave more mating opportunities to the infected males than the other, healthier choice. This study was done in Singapore but it seems like some people at Stanford were interested enough to confirm this study with a different strain of rats.  Can’t blame them. Who isn’t interested in sex?

Seriously, who doesn't like talking about sex?

Anyway, this phenomenon, as crazy as it may sound, makes perfect sense. Everything in nature is under evolutionary pressure to pass on their genes and it would be extremely beneficial for a STI to promote the sexual activity of their infected host. Many human STI are asymptomatic, unlike other viral infection that would make the host sick and less attractive. The scientist on NPR said this might be an adaptation for these viruses to pass on their genes. The radio show also claims that many other species have similar STIs such as beetle, ladybugs and crickets. Currently there is no evidence that suggest human STIs having this sort of effect, but who knows? Someday you might actually be attracted to someone’s parasite more than the actual person…

-Ryoe Will Takakura


The Y Chromosome and Somatic Cells

We may have finished sequencing the human genome, but we still have a lot to learn about our genetic makeup and how it controls our physiology. Scientists have long known that genes on the Y chromosome are responsible for sexually differentiating males from females, but according to a recent New York Times article, research has shown that key regulatory genes expressed in all cells have evolved to be slightly different on the human Y chromosome than on its X counterpart. Though the X and Y chromosomes are typically associated with reproduction and sex determination, they are present in every somatic (non-sex) cell and also contain genes responsible for producing proteins that are not gender-specific. A recent study by Daniel W. Bellott, David Page et al. has identified a dozen such genes on the Y chromosome that have become distinct from their originally identical X chromosome counterparts since the origin of the Y chromosome some 180 million years ago.

Since these twelve genes have crucial roles in switching other genes on and off, they control a large number of cellular processes and have a disproportionately high impact across the body. Dr. Page, one of the authors of the study, states that the differences in these genes are responsible for “the cells of males and females being biochemically different.” He believes that the differential incidence rates of many diseases between men and women, which have been largely attributed to the influence of sex hormones, may in fact be at least partially a result of this evolution of Y chromosome genes. If this is the case, it could redefine how we treat the underlying causes of many diseases.  

For the New York Times article, follow this link: or dive into the research itself here:

Andrew Wilson, Summer Research Intern


A New Take on Electric Shock Therapy

Over the past several decades, health care has benefited from the development of pharmaceutical drugs. The rise in the use of these drugs has greatly contributed to the higher standard of care and longer life expectancy that our society now enjoys. However, these drugs are not always without flaws. Some times, unintended and possibly harmful side effects arise as the result of the drug interacting with areas of the body that it was not supposed to interfere with, as molecules can't find their targets with 100% accuracy. Fortunately, as described in the New York Times article "Can the Nervous System Be Hacked," by Michael Behar, alternative treatments that avoid some of these side effects might not be far away. 

Behar, in his article, introduces us to the exciting world of bioelectronics. He begins with the origins of the movement in the lab of Kevin Tracey, and describes the recent successes of the field, as well as where the field can one day lead us. The idea that he chronicles of a world where people walk around with networked computers hooked up to their nervous systems and treating physiological irregularities sounds like something straight out of a science fiction novel, but he shows us the science that backs it up. He tells of how chronic inflammation related diseases like rheumatoid arthritis and Crohn's disease can be treated by shocking the vagus nerve with a specific intensity at specific intervals using a small implant. These treatments are said to have the same positive results as pharmaceuticals while avoiding the side-effects associated with pharmaceutical drug use, not to mention the debilitating financial burden that patients take on to pay for their drugs. Aside from chronic inflammation related conditions, scientists believe that bioelectronics will one day be able to treat a range of conditions including hypertension, diabetes, and even cancer. 
The article also points out an important weakness of these implants. While the idea that we can harness the incredible power of our own nervous system to treat diseases is alluring, the same technologies could be electronically hacked to gain control of the systems that keep us alive. It is terrifying to imagine a world where hackers are not limited to stealing our credit card information and social security number, but able to change the regulation of our nervous systems. 
Jack Kent. Summer Research Intern
Read more about the exciting field of bioelectronics from the original article at




The Common Basis of Addictive Behaviors: Over-Eating and Drug Abuse

I will never forget the first time my naive idealization of the Punnett square as the sole descriptor of human genetics was shattered. I was 15 y ears old attending my first conference on genetics when a Harvard-educated geneticist, Dr. Sam Rhine, gave his analogy of genetics as a world of "three boxes." The first two, labeled cytogenetics and monogenetics, contained all the diseases that my freshman-year biology course explained so easily with the story of Mendel and his plants, simple gene dominance and recessiveness, and nondisjunction of chromosomes. Such diseases included Down syndrome, Klinefelter syndrome, Cystic Fibrosis, and Muscular Dystrophy. I smiled with delight as I recalled the karyotypes and Punnett squares I had so often seen for these diseases. It was then that Dr. Rhine pointed out how rare such diseases were. “So why not study the most common human diseases, like Type 2 Diabetes, Hypertension, ADD, or Bipolar Disorder?” he asked. This is when he presented the third box, which he labeled “multifactorial.” It was then that I realized so many common illnesses afflicting the modern world were much more complex in origin than I could have ever imagined.

This brings me to an article I read recently in Nature Magazine’s web focus on addiction. This study ultimately points out that there are common biological mechanisms relating drug addiction and obesity; just as genetic factors play a role in vulnerability to drug addiction, they do so as well in vulnerability to obesity. Just as environmental cues that predict the delivery of drugs increase dopamine transmission in certain brain areas, they do so as well when predicting the delivery of palatable food, which can help explain the often addictive nature of delicious food – something we have all experienced at some point. This study remains constant with the theme that genetics are increasingly complex and not easily explained with a simple Punnett square. Our genes make some of us more likely to over eat, abuse drugs, etc., a fact that can serve as a reminder as to why being aware of one’s own addictive tendencies can be important in preventing over-eating and other harmful and excessive behaviors.

Lindsey Rogers, Summer Research Intern


Kenny, P. J. (2011, NOVEMBER). Common cellular and molecular mechanisms in obesity and drug addiction.Nature, 12, 638-651. Retrieved from