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Interested in direct-to-consumer (DTC) genetic tests? Interested in learning and teaching others about genetics? Interested in your family history? Interested in public outreach? The Personal Genome Learning Center is looking for student participants in public outreach events focused on navigating, interpreting and using results provided by DTC genetic testing companies such as 23andMe and AncestryDNA.

The DTC market is estimated to now have reached over 15 million customers. These numbers reflect wide public interest in using personal genetic tests for exploration of ancestry composition, genealogical relationships, and the genetic basis of physical and behavioral traits. However, the reality for many consumers is that the results provided by these tests are often daunting and difficult to interpret due to an insufficient understanding of genetics. Through participation in the Personal Genome Learning Center, you will gain experience interpreting and using the results provided by DTC genetic tests. Your knowledge of these results, coupled with an understanding the underlying genetic principles and methods applied, will enable you to help others understand their own results.

DTC test kits will be available at no cost to participants in the Personal Genome Learning Center. Participants will be expected to build understanding of the results provided by these tests and their uses through weekly meetings and engagement with their own results. Students of the Personal Genome Learning Center will host public outreach events scheduled throughout the year.


Informational Workshop (flyer)

Sept. 12, 5:30pm, B20 Biology Building

Weekly Meetings:  Wednesdays, 5:30-6:30 pm, B20 Biology Building


Participants in the PGLC contribute programming for the monthly meetings of the DNA Interest Group - Iowa City - a forum bringing together individuals in the Iowa City area interested in learning about and supporting others in the use and interpretation of commercial DNA test results. Meetings are scheduled the 4th Tuesday of each month, 6:00-7:00 pm in Meeting Room A of the Iowa City Public Library. Programming of these monthly meetings addresses a variety of different topical areas, including applications in genealogy, inferences of traits, exploration of human genetic variation, and the societal impact of these services. A designated organizer/presenter focuses each meeting on a topic of interest to the group. Meetings will also include time for interaction and discussion among participants. The group is open to all members of the community.

 

For more information, contact Bryant McAllister

I posted a few times in the summer of 2015 when 23andMe and AncestryDNA both reached the threshold of genotyping their first million customers. I'm consistently amazed at how popular these commercial DNA tests have become. In this year, 23andMe has grown to 2 million customers in the 10 years since launching the first version of their DNA testing service. AncestryDNA now has 5 million customers in their database, adding over 2 million so far this year. The graph below plots the growth of 23andMe and AncestryDNA customers. The graph includes press releases of customer numbers, and also includes customer numbers and test dates from the #Powerof1Million social media campaign that shows a more detailed picture of early growth of the 23andMe database than represented by the press releases. It would be nice to have a similarly fine-grained view of the growth from 1 to 2 million, because the 23andMe product has undergone a lot of changes during this period (e.g. website redesign, carrier status reports, FDA approved health reports). While the addition of the 2nd million 23andMe customers over about a year and a half is remarkable, growth of the AncestryDNA customer database is truly astounding.


To get a better view of growth in the AncestryDNA database, I've dropped the start date in May 2012 and the first reported size of the database (120,000 customers) the following year and plotted customer numbers on a logarithmic scale over about a 3-year period. This does a good job linearizing the exponential growth experienced by the AncestryDNA database since the spring of 2014, which is about the time when I gave tests to my parents. Growth of customer numbers in the first year after introducing the product was a bit lower than it has been over the past 3 years, so the April 2013 number is a bit of an outlier. Remarkably, there does not appear to be any slowdown in the recent growth rate. The time it takes for the database to double in size has been about 10.5 months over this period, so if this trend continues, anticipate that the database will reach a size of 10 million customers in the summer of 2018! 

23andMe and AncestryDNA are by far the two largest and well known direct-to-consumer (DTC) genetic testing services, and the sustained growth of the customer bases at both continues against ever increasing competition. MyHeritage recently launched a DNA service to accompany their genealogical platform. Many companies are entering into the health and trait prediction market and working hard to compete. At the Baltimore Ravens football game this weekend, for example, Orig3n is giving away DNA test kits. American, and increasingly international, consumers are clearly interested in the interpretations of DTC genetic testing services. An article by Andelka Phillips that reviewed over 200 DTC genetic services astutely pointed out, "there is also a continuing need for educational initiatives that will allow consumers to understand what test results will mean for them in order to make informed decisions about whether to use such services."


A recent article from Nature reports the Chinese scientists have been the first to inject humans with genes edited by the CRISPR-Cas9 technique. On October 28th a team of oncologists at Sichuan University injected the modified cells into a patient with aggressive lung cancer as a part of a clinical trial. Though this is not the first time oncology clinical trials have used edited cells it is the first time with the new and significantly more efficient CRISPR technique This new method will hopeful speed up the race to get gene-edited cells in to clinics across the world. One scientist has predicted a sort of "Sputnik 2.0" with the race being a biomedical duel between the United States and China. With competitive research occurring these studies usually come to marked quicker and the end product is better than had the field been less competitive. The U.S. will soon be using the new technology in a cancer trial that is predicted to start in early 2017. Another Chinese trial is expected to begin in March 2017 specifically focusing on bladder, renal, and prostate cancers. Neither of these trials have approval or funding yet. Specifics about the trial in China were included and began with researchers removing immune cells from a cancer infected patient. They would then use CRISPR, which combines a DNA-cutting enzyme with a molecular guide that can be programmed to tell the enzyme precisely where to cut, to disable a gene in the immune cell. The specific gene they were disabling usually puts a stop to the immune response, a trait cancers can take advantage of to continue proliferating. After the gene splicing the cells were cultivated and injected back into patient. The hope is that with that specific gene blacked that the cells will be able to fight off and defeat the cancer. The Chinese team plans on treating ten people with this method who will each receive two, three, or four injections. For six months these patients will be monitored for any adverse effects and to see if they are benefiting from the treatment. Oncologists across the world are excited for this study and are looking froward in hopes of bettering and saving more lives.

-Elizabeth Struyk

http://www.nature.com/news/crispr-gene-editing-tested-in-a-person-for-the-first-time-1.20988

An article in The Atlantic from September 2015 explores the history of feline modification and asks the question is there a future of genetically improved house cats. The article begins with an excerpt from a Times article from 1885 explaining the genetic research of Francis Galton and his quest to make the perfect house cat, who in Galton's mind should be deaf. The Times went on to say that Galton was impractical and useless when there were so many other things to fix about a cat like it's voice, teeth, and paws. Later in 1981 a task force called the Human Interference Task Force was set up to keep curious humans away from radioactive-waste sights, specifically Yucca Mountain. Some of the philosophers came up with the idea to create cats who's fur would change color when exposed to radiation and create a sort of folklore that insisted cats with colored fur were a bad omen. Obviously this never occurred but the idea of genetically engineered animals was not dead. In 2004 a biotech company Allerca announced their plans to create the first hypoallergenic cat. The cats were on sale for $4,000 but the potential buyers were put through a screening process much like adoption of a child. The company eventually pulled the plug with rumors that the cats were not really hypoallergenic. The most recent genetic expirament occurred in 2011 when a photo of a glowing green cat was released to the public. This cad had been used for feline AIDS testing in hopes of finding a cure for human AIDS. This cat had been injected with monkey genes which prevented the strand of feline AIDS from entering the feline eggs prior to fertilization. As for the green color, the geneticists used jellyfish genes that cause the infected cells to glow an eerie green color. Though this may look like some sort of genetic experiment gone wrong, the researcher assured that their goals were to help take another step in curing AIDS, no creating a generation of glowing, disease-resistant cats. With advancing technology felines may be a part of the future to help find cures for genetic diseases. On the domestic side no current research is being done on "improving" the modern house cat. Along with the lack of research genetic engineering on animals for mass production and consumption comes with a large moral and political debate that may take years to sort out. This may put a damper on those who wish to have hypoalergenic glowing cats but hopeful many research breakthroughs will make up for it on the other side. 

-Elizabeth Struyk

http://www.theatlantic.com/science/archive/2015/09/theres-more-than-one-way-to-breed-a-mutant-cat/405814/

While exploring your 23andMe account, you may have come across a report relaying how many Neanderthal variants you have in your DNA. The report, after providing a brief history of Neanderthal origins on planet Earth, advances to explain which of these variants may be associated with four specific traits: hair straightness, height, back hair, and likeliness to sneeze after eating dark chocolate. This may appear to be a very limited (and oddly specific) amount of traits which appear to be related to Neanderthal ancestors. However, as an article by The Scientist explains, researchers from outside of 23andMe's lab have reason to believe that Neanderthals have more of an impact on the human genome than previously believed. 

Neanderthals bred with modern humans before becoming extinct nearly 40,000 years ago. As a result of this interbreeding, the genomes of European and Asian individuals contain around 2% Neanderthal DNA. Individuals of Melanesian decent have an additional 2-4%. These statements have been widely accepted and published in the field of anthropology for years, but a group of genomicists, who published their findings in a recent issue of Current Biology, are declaring that the Neanderthal variants present in the genomes of humans contain alleles which hold evolutionary advantages such as increased immunization and uncommon skin pigmentation attributes. The findings were discovered by analyzing the sequences of both human genomes and genomes of Neanderthals. Maps of nearly one million Neanderthal sequences (previously found in the genomes of modern humans) were constructed and then compared with human sequences that contained prevalent amounts of Neanderthal variants. The genomes of 1,523 individuals of European, Asian, and Melanesian decent were compared. In the end, 126 gene positions were discovered where ancient hominin DNA appeared to persist at a high frequency. 

 Of the 126 gene positions that were discovered, 7 genes were associated with skin pigmentation and 31 genes were associated with immunity. The researchers concluded that these specific variants were the ones that assisted modern humans in their adaptation to geography outside of Africa. The study supports the theory that modern humans increased their abilities to survive and adapt to new environments because of the traits they inherited from Neanderthal interbreeding. These traits of skin pigmentation adaptation and immunity most-likely helped early humans accommodate themselves to changing climates and new infectious organisms in their various treks out of Africa. 

 Not all of the variants adopted from Neanderthals appear to be advantageous, however. Another article published by The Scientist examines the correlation between prevalent Neanderthal variants and forms of clinical depression. A study of over 28,000 individuals discovered that a statistically significant amount of individuals with increased numbers of Neanderthal variants in their genomes tended to also be more susceptible to major depressive disorder. Other clinical conditions present included skin lesions and excessive blood clotting. So the presence of Neanderthal variants seems to present an ambiguous sense of whether or not more variants should be celebrated or bemoaned. Either way, the link between the longevity of modern humans and our relationship with ancient Neanderthals has become a little clearer upon analyzing our own genomic identities.

 

http://www.the-scientist.com/?articles.view/articleNo/47474/title/Advantages-of-Neanderthal-DNA-in-the-Human-Genome/

http://www.the-scientist.com/?articles.view/articleNo/45309/title/Neanderthals--Genetic-Legacy/

A team of researchers from IST Australia have recently discovered a new genetic link to autism spectrum disorders, along with the method that this newfound mutation uses to cause autism. These particular discoveries led the scientists to find that mutations in many other autism-linked genes behave the same way, showing that they may have also discovered an autism spectrum disorder subgroup. However, the scientists stated that the process to finding all of these mutations was long and difficult. 

Through a group effort, scientists discovered a mutation in gene SLC7A5, a gene that transports branched-chain amino acids to the brain, in people who had syndromic autism. To further study this, the researchers removed the SLC7A5 gene from a group of mice, lowering the amount of branched-chain amino acids in their brains. They then observed their behavior, and found that these mice showed classic signs of autism such as reduced social interaction. The scientists wanted to see if these effects could be changed somehow, so they introduced branched-chain amino acids directly into the brains of the mice without the SLC7A5 gene. After roughly three weeks the mice started to participate in more social interaction and had an overall improvement in behavior, showing that autism spectrum disorders caused by an amino acid deficiency could possibly be reversed or at least treated. Dora Tarlungeanu, one of the researchers, supports that their findings here could be extremely beneficial, but changing the delivery method of the amino acids for humans would be tricky. However despite the difficulties, the researchers of this study have a positive outlook on the treatment for the future. 

This article interested me at first glance because as a child I grew up attending school with numerous kids who had autism, and my dad's cousin was also severely autistic just recently passed around the age of 45 due to complications. My whole life I've been surrounded by people with autism and have seen the effects the disorder can have on not just the individuals' lives, but their families' as well. I think it's amazing and important that research is being done on the topic and that scientists are getting closer and closer to breakthroughs for treatments everyday. 

Institute of Science and Technology Austria. (2016, December 1). Autism spectrum disorders: New genetic cause of identified. ScienceDaily. Retrieved December 7, 2016 from www.sciencedaily.com/releases/2016/12/161201121502.htm

              Since finishing the sequencing of the human genome in 2003, millions of individuals around the globe have been curious as to what story their DNA tells. Recently, thousands upon thousands of individuals are being tested for athletic performance. Some wish to know if they possess variants on particular genes associated with elite athletes while others wish to know if they should focus on endurance or strength athletic events. Either way, there has been much controversy over the legitimacy of these tests.

              More than 200 genes have been linked to physical performance, and 20 variants have been associated with the status of elite athlete. Two mutations in particular have received much attention: the ACE gene and the ACTN3 gene. The ACE gene helps to regulate blood pressure and cardiac and respiratory efficiency. This is important information to an athlete. One variant of the gene suggests that the individual is predisposed for endurance events while the other suggests that the individual should focus on power and strength events. The ACTN3 gene codes for a protein that regulates fast-twitch muscle fibers. The variant ACTN3 R577X has been associated with Olympic-caliber sprinters.

              Though many studies have been conducted, there is still much to learn about these genes. For example, almost one-third of those living in the United Kingdom carry the ACTN3 variant, but only a small percentage are elite sprinters. Other factors come into play regarding one’s athletic performance. These include diet, training, and determination. Genes alone do not determine if one becomes an elite athlete.

              I found this article particularly fascinating because 23andme has a report that tells users if they are likely endurance or power types. According to my report, I am likely a sprinter. Interestingly enough, over past summer, I began running longer distances. This certainly makes me question how much the variants in our genes affect our physical performance and how much is due to other environmental factors.

Salamon, Maureen. "Genetic Testing for Athletic Ability." Genome Magazine. Genome, 23 June 2016. Web. 06 Dec. 2016.

An article from the Genetic Literacy Project states that our genes may play a part in whether we may develop cancer from smoking cigarettes. Over 30% of cancer-related deaths each year are caused by smoking. These are not just cancers of organs that are exposed to cigarette smoke, such as lung, throat, and larynx cancers. Smoking can also be responsible for several cancers in other parts of the body, including the kidney, cervix, and colon. A study published in Science on November 4th stated that “for each year a person smoked a pack a day there were 150 new genetic mutations in each of his or her lung cells”. However, other recent studies also prove that genetic mutations occur in organs that have no direct contact with tobacco smoke. The LA Times reported that for every “pack year”, a smoker will have about 18 new bladder cell mutations and 6 new liver cell mutations (per cell).

Several studies performed on cancerous tissues have resulted in the identification of several consistent DNA mutations. Scientists have identified 20 genomic signatures that are caused by tobacco carcinogens, including mutations such as base-pair swaps and other more complicated issues. These signatures have been proven to effect the person’s susceptibility to various different cancers. One of these issues that is currently being researched is called signature 5, which so far seems to accelerate the amount of mutations depending on how heavily the person smokes. While signature 5 has proven to be related to age in non-smokers, it has only shown to be caused by tobacco intake for smokers. Signature 5 is also much more common in smokers, ranging from 30 to 500 percent more likely.

These genetic mutations caused by smoking have surprisingly only been found within actual genomes, as opposed to the out packaging of the genome that alters gene expression. However, cancer research has shown that environmental exposures to the carcinogens found in tobacco can alter the expression of cancer-causing genes without resulting in a mutation of the gene’s sequence. This research also supports why smoking during pregnancy has devastating effects on the development of the fetus.

While smoking is a dying trend in the United States, there are still 1 billion people in the world who frequently smoke cigarettes. This topic and the continuation of this research are important to me because of the amount of people in developing nations who smoke. They are much less likely to have access to the healthcare, information, or necessary tools that they need to quit smoking. Therefore, continued research on how tobacco carcinogens cause genetic mutations may help us to better understand smoking-related cancer and how to prevent it from taking so many lives.

 

Knight, Meredith. "Cancer and Genetics: How Your Whole Body Smokes a Cigarette | Genetic Literacy Project." Genetic Literacy Project. N.p., 29 Nov. 2016. Web. 05 Dec. 2016.

Obesity is currently seen as one of the world's biggest health problems, as it affects millions of people of all ages, ethnicities, and environments. One's risk to becoming obese is primarily determined by their genetics, lifestyle, and diet, and much research is being done to better understand how these affect the problem on a deeper level. An article written for Science Daily discusses scientists' recent finding of a genetic receptor that plays a role in developing obesity. 

Scientists at King's College London and Imperial College London have been looking at how the FFAR2 (Free Fatty Acid Receptor 2) receptor affects the role of fermentable carbohydrates in the body. Fermentable carbohydrates are found in things such as bread, fruits, and vegetables, and are called fermentable carbohydrates because they are fermented easily in the digestive system. To test how these and the FFAR2 receptor combined affect the body, the scientists fed mice, with and without the FFAR2 receptor, foods high in fat containing fermentable carbohydrates and compared the results from these tests to a control group. It was found that mice with the FFAR2 receptor did not become obese despite the high fat diet, but the mice without the FFAR2 receptor did suffer from obesity.The mice with the FFAR2 receptor showed an increase in hormones that made them feel fuller faster, ultimately preventing the obesity. Because of this study, scientists can better understand how diet can affect appetite regulation, and they can now look into the possibility of changing the gut with diet or pharmaceuticals to treat obesity and many other gastrointestinal disorders. Professor Gary Frost, one of the leaders of the study made the comment that, "the fact it actually has a major impact on cells that help control appetite regulation in the colon is amazing." Because of this their next step is applying the knowledge from this study to humans and eventually create food systems to help people suffering from obesity. 

This article intrigued me as I know a vast number of people in the world suffer from obesity, including members of my family and friends. The impact of obesity is huge, and as a nursing major I know in my future I will likely be faced with patients who suffer from obesity every single day. I want to be able to offer these patients the best advice that I can, so I'm glad research is being done on treating the problem.

King's College London. (2016, November 25). New target receptor discovered in the fight against obesity. ScienceDaily. Retrieved December 5, 2016 from www.sciencedaily.com/releases/2016/11/161125104749.htm

A team in the United Kingdom concluded that there is a hormone link between the liver and the brain that may affect alcohol consumption. The team made this observation after compiling data from large scale genome studies which included more than 105,000 participants that also completed surveys about their alcohol usage. 

The researchers discovered that the β-Klotho gene appeared to be partially responsible for the amount of alcohol the research participants drank. They made this observation after noticing that those with a certain variant of the β-Klotho gene (about 40% of the participants of the study) drank less alcohol than those with the other variant.

Next the researchers observed the genes in mice and found the same thing - that those with the β-Klotho gene consumed less alcohol than their counterparts. Researchers then examined the hormone FGF21 - a hormone in the liver that has been known to hinder the desire for alcohol in mice. What they noticed was that this hormone did not have that same effect in mice without the β-Klotho gene present. In fact they reported that the hormone had no effect on the consumption of alcohol at all in the non-carriers, meaning that the effects of FGF21 were directly related to whether the mice had the gene or not.

The researchers also stated that the results of this study may indicate that there is a "feedback loop" related to FGF21 and the brain. Consuming alcohol causes FGF21 to be produced, which would lead to a self-limiting response in those with the less common β-Klotho gene variant. They believe further studies need to be conducted before it is known whether the gene directly causes this effect or if it affects other related genes instead. The study also only surveyed those without an addiction to alcohol, so they remain unsure whether this gene has the same effect on those suffering from alcoholism.

Paul Elliott, one of the heads of this research, said that their "findings may eventually lead to new treatments for people whose health is being harmed by drinking". If new treatments were developed it would be fantastic, as irresponsible use of alcohol is a huge issue worldwide. In just 2012 alone, alcohol was responsible for 5.9% of all deaths worldwide. More research investigating the relationship between the body and alcohol will hopefully lead to less deaths as a result.

 

http://www.medicalnewstoday.com/articles/314419.php

 

 

 

 

I came across this article posted on Science Daily that discussed scientists' newly discovered design of a 3D model for the protein responsible for cystic fibrosis.

Cystic Fibrosis is an inherited disease that has no cure. It is caused by mutation in the protein, cystic fibrosis transmembrane conductance regulator (CFTCR). CFTCR forms a channel on a cell's surface and allows chloride particles (a salt component) to pass through the cell membrane. Since the distribution of salt affects the movement of water, an interruption to the channel dehydrates the mucus that lines certain organs (particularly the lungs) which in result can lead to life threatening health complications. Dehydration can cause a build up of thick mucus in the lungs, which leads to breathing problems or other respiratory infections. 

Scientists at Rockefeller University have been looking into the CFTCR protein and how it specifically mutates in patients. There are hundreds of mutations in CFTCR's gene that can cause cystic fibrosis, and thus far it is hard to see how these channels in cell membranes are being affected because scientists lack the ability to see in depth the structure of the CFTCR gene. Scientists at Rockefeller have just recently discovered that by using advanced technology, when taking pictures of almost a million CFTCR molecules frozen in a thin layer of ice, they can compile layers of 2D pictures to build a first ever 3D structural depiction of the cystic fibrosis protein. With this new 3D structure, scientists can now study the mechanics behind the opening and closing of the cell membrane channels. Through this they have located 46 sites on the protein that are altered by mutation that causes diseases, and found a location on the protein that is weaker and more vulnerable to disruption. With this recent discovery, biochemists now have the opportunity to develop drugs that function as some sort of glue that could strengthen these weak parts of the CFTCR protein. 

I found this particularly interesting because I am majoring in biochemistry and I think it is beyond cool to hear about the different advancements biochemists have in progress that can greatly benefit public health. With such vast technological developments, biochemists are able to study new things each and every day that they previously could not because they lacked the equipment. I have a strong interest in medicine, and seeing how closely linked it is to genetics has been a very eye opening experience to me in this class, as I can now look at how limitless the application of genetics and biochemistry are to pharmaceutical sciences. 

 

Rockefeller University. (2016, December 1). First structural map of cystic fibrosis protein sheds light on how mutations cause disease. ScienceDaily. Retrieved December 4, 2016 from www.sciencedaily.com/releases/2016/12/161201121401.htm

Many people undergo stressful or traumatic events during their lifetime, some more frequently than others. While there are a multitude of different stressors and everyone reacts in their own way, evidence shows that it is possible for two people to experience the same trauma that results in only one of them developing post-traumatic stress disorder (PTSD). An article from McClean Hospital states that one of the main explanations for this circumstance relies on genetics.

 

Scientists have discovered that individual risk for PTSD is highly influenced by genetic variation. Research is still being done to determine which genes are involved with this risk and how they interact with environmental responses. The gene FKBP5 is one of the genes most commonly known to interact with environmental factors to instigate the development of PTSD. FKBP5 is responsible for regulating the brain’s response to stress (affecting the hypothalamus-pituitary-adrenal axis) and causes the release of cortisol, also known as the “stress hormone”. The body is designed to release cortisol in order to help us cope with stressful situations. However, genetic variants to the FKBP5 gene can disrupt the system, causing either unrestrained or inadequate activation of cortisol release. Problems like these can also inhibit the ability to turn off the release of cortisol when the stressful situation is over. This type of dysfunction puts people at a much higher risk for developing PTSD.

 

While FKBP5 is a major gene that affects a person’s predisposition to PTSD, scientists have yet to discover the entire complex system of genes and environmental factors that can impact individual risk. One of the biological concepts that helps explain how both genetics and outside experiences affect this predisposition on the molecular level is known as environmental epigenetics, which is “the idea that we are not simply a product of our genes but also our experience”. While the genes we inherit from our parents play crucial roles, external factors and how they affect us are just as important.

Having family in the military makes this topic very important to me, as PTSD is most common in police officers, firefighters, and soldiers. I am thankful that researchers are continuing to study the development of PTSD as well as finding new methods of treating it.


Klengel, Torsten. "PTSD: How Does Genetics Affect Your Risk?" McClean Hospital. Harvard Medical School, 3 Dec. 2016. Web. 04 Dec. 2016.

The Zika Virus has become a growing concern worldwide. It not only affects the people who contract it, it also affects the future lives of unborn children. Offspring of mothers infected during the time of the pregnancy often have severe birth defects: microcephaly and mental impairment. It is because of these health consequences that government officials and those of the scientific community are looking for a way to eradicate the mosquitos that carry the virus. Our own country is researching potential answers to this crisis. Florida has had over 1,200 cases of the Zika Virus with over 200 of them being locally acquired. This means that mosquitoes carrying the virus can be found in the area.

Scientists believe that they may have found a way to get rid of the disease-carrying creatures, though their methods have been controversial. They want to introduce genetically modified males that possess a gene for sterility into the local population of mosquitoes. These males will mate with wild females, creating eggs that contain the sterile gene. Upon hatching, the larva will die before developing into a pupa. This method ends the reproductive cycle. More genetically modified males are created in laboratories by having wild females mate with the sterile males. After the eggs hatch, the larva is treated with tetracycline. This allows them to develop into pupa and then adults. These adults mate with wild females, and the cycle continues.

A field test is scheduled to happen in Key Haven, Florida, though this may be delayed. Many citizens believe that the genetically modified males pose a threat to the local environment. Hopefully, should a lawsuit ensue, the government will realize the benefits of such a trial and that agencies governing environmental laws have been properly contacted to ensure that regulations have been followed. Should the trial be a success, there are global implications. Other viruses transmitted by a vector, such as malaria, dengue fever, yellow fever, and encephalitis can be brought to a halt.

I found that article particularly fascinating because I hope to one day become a pediatrician. Viruses, the spread of viruses, the consequences of viruses, and ways to stop the spread of viruses are intriguing. This method of introducing genetically modified males has several potential applications that could change the future of the field of medicine.

Giddings, Val. "Why Genetic Engineering Is Blocked from Eradicating 'world's Deadliest Killer'-disease-carrying Mosquitoes | Genetic Literacy Project." Genetic Literacy Project. Genetic Literacy Project, 01 Dec. 2016. Web. 04 Dec. 2016.

An article in Live Science last week discussed a study led by Jennifer Smith, a doctoral student in nursing at the University of Kentucky.  The study was presented at a Scientific Sessions Meeting of the American Heart Association.  The study indicates that people with a variation of their TAS2R48 gene were more likely to consume too much sodium than people without the variation.  The American Heart Association suggests that people limit their sodium intake to 2300 mg per day.  Those with the variant on their gene were almost twice as likely to exceed this amount.  The study was conducted on over 400 people living in rural Kentucky who were trying to keep lower their risk of heart disease.  The participants kept food diaries and had their genes analyzed.  The researchers found no additional correlation between other risk factors like sugar or saturated fat intake.  The TAS2R48 gene is linked to another taste factor, sensitivity to bitterness.  Those with the variant are more sensitive to bitter flavors.  This has lead to theories that those with the variant can possibly taste saltiness more so they enjoy it more and use more salt or that because they taste bitter flavors more intensely they add salt to try and mask the flavors.  Being conscious of the variation of the gene is helpful because it allows individuals with the variant to recognize that they need to keep an eye on their sodium intake because they could overindulge without realizing it.  Being aware of their genes can help people make intelligent life style choices and healthy habits.

I was particularly interested in this study because it related a report from 23andMe to possibly a new discovery.  23andMe reports on the bitter taste trait and I know that I have it so I'll be sure to monitor my sodium intake from now on!

Miller, Sara G. "More Over Sweet Tooth: Introducing the Salt Tooth." Live Science. Purch, 13 Nov. 2016. Web.