Chemists shine a new light on safer pigments, by accident

Mankind has historically used colors to symbolize their sense of community. Of all the colors, blue is the most favored. In the Major League Baseball teams, for instance, nearly half of them feature a blue signature color. In North Carolina, the shades of Carolina blue and Duke blue can be found filling bars during basketball season. Though blue appears to be the most popular, it is not so easy for human hands to create.

Humans perceive the color of an object because it reflects a specific wavelength of light on the visible light spectrum. Color, though, is not accurately equal to pigment. A pigment is a tangible material that humans can physically utilize to provide color for uses like painting or cosmetics. Extracting pigments from nature, however, can be difficult and expensive. The quest is therefore on to find alternatives. To tackle the challenge of making the color blue, in particular, researchers take advantage of synthetic techniques. 

One of those successful at this challenge is Mas Subramanian, a materials science professor at Oregon State University at Corvallis. Subramanian and his team discovered the first new blue pigment in more than two centuries. The last invention of blue was cobalt blue, in 1802, derived from a mix of cobalt and aluminum oxides.

This ‘Bluetiful’ color came out of the blue

The birth of the brand-new blue, known as YInMn blue, turned out to be an accidental discovery. The research team was investigating novel electronics properties in hopes of revolutionizing the computer industry. They mixed oxides of three elements: yttrium (Y), indium (In) and manganese (Mn), each providing the desired electronic and magnetic properties. Surprisingly, after the mixture was baked for hours at intense heat, more than 2,000 °F, a vibrant blue powder was spit out of the oven, rather a brown or black material as the team would have expected.

YInMn blue powder. Source: Mas Subramanian, CC BY-SA 4.0

This out of the blue breakthrough has since triggered interest across industries, from Nike shoes to Chanel eye shadow, because of the safe and durable properties of the material. In 2017, Crayola created a crayon based on the YInMn blue, Bluetiful, aiming to inspire children by publicly recognizing the connection between scientific discovery and the real world. Earlier this year, YInMn made a chapter in the book “Chromatopia: An Illustrated History of Color.”

A broader palette: finding the perfect Ferrari red

The true breakthrough of YInMn blue was the structure of the crystals in the compound—the atomic arrangement in their respective lattices. This compound can not only provide blue, but is the basis to create a whole spectrum of colors. Adding titanium, zinc, copper and iron to the YInMn mix makes purple, orange and green materials. Soon, there may be bright and commercially viable pigments created by simply altering the chemical formula.

Now Subramanian’s team focuses on making a new non-toxic red pigment, especially desirable to replace the harmful cadmium-based red. The dangerous chemical elements in the pigment, similar to cobalt blue, can be poisonous if ingested in large quantities. Other red pigments, like Pigment Red 254, the characteristic Ferrari red, can fade to dullness unless treated with additional protection. Therefore, a safe and stable pigment is in demand. If the team succeeds, the new red should be a big hit and in high demand because of its attention-grabbing nature.

The search for the eye-catching red.

The search of the perfect red is, however, elusive. The challenge of these studies is that even with the most careful planning, it is hard to predict the color that will be produced. Whether Subramanian’s team will find the billion-dollar red or not, the world awaits.

Hear the story on TEDx Talks from Dr. Mas Subramanian.

Peer edited by Rita Meganck.

Fungi Join the Fight Against Malaria

SLAP. You’re sitting outside at a summer bonfire and you catch a mosquito feasting on your leg. Groaning, you realize this probably means a couple days of itching and a swollen welt. Usually in North Carolina, you’re going to be just fine and should only seek medical attention if you experience complications. However, for many, particularly in Sub-Saharan Africa, a mosquito bite can mean something particularly dangerous: the possibility of infection with malaria.

Cells infected with Plasmodium falciparum possess characteristic purple dots, often connected in a “headphones” shape. Source: Steven Glenn, Laboratory and Consultation Division, USCDCP (PIXIO)

Malaria is a parasitic infection caused by Plasmodium falciparum, a single-celled organism that lives in the salivary gland of Aedes aegypti mosquitoes and is considered the deadliest human parasite. The World Health Organization reported in 2018 that progress in reducing cases of malaria globally has stalled, with nearly 435,000 people, primarily Sub-Saharan African children, dying from the disease per year. Much of this lack of progress can be attributed to mosquitoes developing a tolerance for commonly used chemical insecticides. Recent work from scientists at the University of Maryland in collaboration with researchers in Burkina Faso has hacked biology to create a new tool to combat the problem of malaria-carrying mosquitoes. The tool? Genetically modified fungus that wipes out mosquitoes with a deadly dose of spider toxin.

To develop their tool, the researchers used a type of fungus that already occurs in malaria-affected areas and targets mosquitoes: Metarhizium pingshaense. This species of fungus is entomopathogenic, which means that the fungus is a parasite to insect hosts and kills or disables them. In the wild, this fungus can kill mosquitoes, albeit quite slowly. It takes over a week in the lab for Metarhizium to kill a mosquito, by which time the mosquito could spread malaria and reproduce. To speed up the process, the scientists used genetic engineering to give Metarhizium a deadly tool: a gene from the Australian Blue Mountains Funnel-web spider that creates a potent toxin. In the wild, the spider’s fangs deliver a neurotoxin that disrupts the way neurons send signals in the brain. This causes symptoms including dangerously elevated heart rate and blood pressure and difficulty breathing. If bitten by a funnel web spider, death can occur in humans rapidly. However, to ensure the toxin only affects mosquitos, the scientists disabled the toxin from being made by the fungus until the right moment — when the fungus reaches the bloodstream of the mosquito.

The Australian Funnel Web spider is considered to be one of the deadliest spiders on Earth. Source: Brenda Clarke (flickr)
A cockroach infected with a species of Metarhizium. Source: Chengshu Wang and Yuxian Xia, PLoS Genetics Jan. 2011 (Wikimedia Creative Commons)

The fungus was tested in a unique environment in Burkina Faso: the MosquitoSphere, an enclosure where genetically modified organisms are permitted to be tested.

To conduct the experiment, two populations of 1500 mosquitoes were released in the MosquitoSphere. To expose the insects to the fungus, the investigators mixed the Metarhizium spores with sesame oil and spread the mixture onto black cotton sheets. When mosquitoes landed on the sheets, they were exposed to the toxic fungal spores. The mosquito population exposed to the unmodified Metarhizium had no problem reproducing before the fungus proved fatal, with their population totaling nearly 2500 after 45 days. In contrast, the population of mosquitoes exposed to the genetically modified Metarhizium after 45 days shrunk to a mere 13 individuals. A population of 13 mosquitoes indicated that the mosquitoes were dying more quickly than they could breed, therefore producing an unsustainable, or collapsed population. The striking results of the experiments in the MosquitoSphere encouraged the investigators to conclude that the genetically modified Metarhizium can function as a potent mosquito-killing bio-pesticide and cause an interbreeding colony of mosquitoes to collapse in a little over a month.

Despite success in the MosquitoSphere, the fungus still needs to undergo more testing to be considered safe for humans and the environment. If it is approved, a formulation of the fungal spores could be used to protect dwellings and mosquito netting from malaria-carrying mosquitoes. This study is a promising sign for the use of genetically modified bio-pesticides to wipe out disease-causing insects, which could prove invaluable for malaria prevention. 

Peer editor: Elise Hickman

Are some of us “immune” to genome editing?

https://www.flickr.com/photos/nihgov/27669625144

Some of us may have characteristics we would like to change. We may want to be taller, skinnier, or smarter. While many traits can be changed during our lifetime, others simply cannot. There are certain ‘fates’ we cannot avoid, such as inherited diseases. For example, if you inherit two copies of a gene called CFTR that has mutations, you are likely to develop Cystic Fibrosis. Although your life choices can help accommodate the disease, there is currently no cure for Cystic Fibrosis and many other genetic disorders. However, with the development of genome editing, the potential to alter the entirety of our genetic information, there is hope in the ability to one day eradicate genetic diseases once and for all.

There are currently several genome editing methods available, but the most popular method is the CRISPR-Cas9 system, which was recently and famously used to edit the germline of babies born in China. Editing the germline means that the changes made to the genome will be inherited throughout following generations. Although this practice is still officially banned around the world, CRISPR-Cas9 was used to change two twins’ genomes. This tool allows us to edit parts of the genome by either removing, adding, or changing a given segment of DNA sequence. It is the go-to editing technique used by scientists because it can generate changes quickly, efficiently, and accurately  at a relatively low cost. There are two major components of this system – Cas9 and a guide RNA (gRNA). Cas9 is an enzyme that acts as ‘molecular scissors’ and cuts both strands of DNA at a specific location, which allows the removal, addition, or change of DNA sequence. The sequence where Cas9 cuts is determined by the gRNA, which, as its name implies, is an RNA molecule that ‘guides’ Cas9 to a specific place in the genome through complementary base pairing.

The CRISPR-Cas9 system was originally discovered in bacteria as a defense mechanism against viral infection. The most commonly used versions of Cas9 for genome editing come from two bacterial species – Staphylococcus aureus and Streptococcus pyogenes. Both species of bacteria frequently live on the body as harmless colonizers, but in some instances, they can cause disease. If you have been infected with either S. aureus or S. pyogenes, you likely developed adaptive immunity to the bacterium in order to protect yourself against future infections. A recent study from Stanford University published in the journal Nature Medicine examined this phenomenon, asking whether healthy humans possessed adaptive immunity against Cas9 from S. aureus and S. pyogenes.

First off, you may be wondering why adaptive immunity to Cas9 would matter at all. When we are exposed to ‘invaders,’ such as bacteria, our body develops adaptive immunity in the form of antibodies and T cells that target specific components (also called antigens) of the invader. For example, if you’ve eaten raw eggs (in cookie dough, let’s say), you may have suffered from an upset stomach caused by infection with Salmonella. If you are then exposed to Salmonella again in your lifetime, both antibodies and T cells that developed in response to the first infection should act quickly to suppress and clear the infection. Similarly, if you were previously infected with S. aureus, your body may negatively respond to receiving modified human cells producing Cas9 originating from S. aureus for the purpose of genome editing but the antibodies and T cells generated during the initial infection may quickly clear these cells. Our own body may think it is protecting us, although in reality it may be thwarting our efforts to make a change in our genome that is intended to have a positive effect. Even worse, this unintentional stimulation of our immune system could lead to an overwhelming response that can lead to organ failure and potentially death. Unfortunately, there is a documented case of a patient death due to an immune response to gene therapy using viruses. It may therefore be necessary to screen each patient before the start of therapy to determine whether they possess immune components that would make this form of therapy inefficient or even deadly.

The Stanford study mentioned above examined this phenomenon by testing for the presence of both antibodies and T cells against Cas9 from S. aureus and S. pyogenes in healthy donors. The authors found that ~75% of donors produced antibodies against Cas9 from S. aureus and ~60% of donors produced antibodies against Cas9 from S. pyogenes. These results come from analyzing blood from more than 125 adult donors. The scientists also used several approaches to examine T cell responses. In this case, 78% and 67% of donors were positive for antigen-specific T cells again Cas9 from S. aureus or S. pyogenes, respectively.

In summary, the authors of this study provide evidence for existing adaptive immunity to Cas9 from S. aureus and S. pyogenes in a large number of healthy adults. Two additional studies examined adaptive immunity against Cas9 with varying results. However, all three studies suggest that pre-existing immunity to Cas9 needs to be carefully considered and addressed before the CRISPR-Cas9 system moves toward clinical trials as a therapy for genetic diseases. In other words, scientists need to address whether the presence of antibodies and/or T cells against Cas9 would lead to destruction of cells carrying Cas9 for the purposes of genome editing. Other potential solutions include using Cas9 derived from bacterial species that do not cause human infections and thus should not trigger an adaptive immune response, or suppressing the immune system while administering CRISPR-Cas9.

CRISPR-Cas9 genome editing has the potential to transform our lives in many ways. While this technology certainly holds promise for the treatment of genetic disease, the Stanford study highlights the need for more research before we can conclude that CRISPR-Cas9 is effective and safe. Optimization of this system may improve its performance in clinical trials and lead to future approval for the treatment of human disease.

Peer edited by Keean Braceros and Isabel Newsome

Transforming Blood Transfusions

Blood is essential. It carries the oxygen you breathe throughout your body and to your lungs, keeping you alive and invigorated. However, our body can only produce so much blood in a day, and when we undergo serious blood loss through car accidents, genetic disorders, or surgeries, we need to replenish our body’s blood supply. People around the world donate their blood to those who are in desperate need and each year, 4.5 million lives are saved thanks to blood donations.

The transfer of one person’s blood to another person’s body is called transfusion, and in the United States alone, someone needs a transfusion every two seconds1. Currently, blood transfusions are limited by the type of blood one has – and therefore needs. Blood has four major types: ‘A’, ‘B’, ‘AB’, and ‘O’, and each of these major types has two subtypes, positive or negative. This means there are a total of eight blood types: A+, A-, B+, B-, AB+, AB-, O+, O-. These types are determined by different molecules called antigens (you can think of them as tags or signs) on the outside of the blood cell (see image below, different blood types have different molecular patterns or “tags”). 

The four major blood types are defined by the antigens, or “tags”, on their surfaces. The “H” antigen of blood type “O” is the most common, and can be converted by enzymes to “A” or “B” antigens. If you don’t have “A” or “B” blood types, it is because you don’t have the enzymes that can convert antigen “H” to the other antigen types.

Blood transfusions are limited by these specific antigens (tags) because the antigens are recognized by a person’s immune system or, the body’s defense system. If you have blood type “B”, and now have blood type “A” in your body, due to a transfusion, your immune system will recognize that “A” is not part of your body, and will trigger an immune response which attacks and destroys the blood that has been transfused.

A group from the University of British Columbia in Canada identified a bacterium in the human stomach that can convert blood type ‘A’ to the universal donor type, ‘O’2. By screening thousands of microbes in our stomachs, the scientists identified a particular obligate anaerobe (can only survive when oxygen is not present), Flavonifractor plautii. Inside F. plautii, two enzymes were found to work together to change the molecules on the surface of red blood cells of blood type ‘A’ to molecules of blood type ‘O’.

But how can blood types be changed from one blood type to another? 

Below is a diagram of blood type ‘A’ and blood type ‘O’. They have some “tags” in common (the blue squares, orange circles, and grey diamonds), and some that differ (green pentagon). The enzymes in F. plautii are able to cut off the extra molecular tag of blood type ‘A’, which then leaves blood type ‘O’! First, the enzyme FpGalNAcDeAc changes the ‘A’ blood type molecules to a slightly different molecule, which can then be recognized and cut by the second enzyme, FpGalNase, leaving blood type ‘O’. Not only can these enzymes change blood type ‘A’ to ‘O’, but they can do it fairly efficiently, which could greatly increase the blood supply for transfusions. 

Blood Type “A” to Blood Type “O” Conversion Pathway. FpGalNAcDeAc enzyme recognizes the “A” antigen, and changes it to a different molecule. This new molecule is recognized and removed by FpGalNase, leaving only the “H” antigen which characterizes blood type “O”.

The group from British Columbia are not the first to try changing blood type3. A previous study converted blood type ‘B’ to blood type ‘O’, albeit very inefficiently. So inefficiently, in fact, that the conversion would never have practical use4

Since the enzymes from F. plautii are bacterial, and only small amounts of the enzymes are needed for conversion of blood type ‘A’ to blood type ‘O’, it could be possible to mass produce the enzymes to be able to transform large quantities of blood for transfusions, increasing blood supply for medical procedures and saving more lives.

Sources:

  1. https://www.redcrossblood.org/donate-blood/blood-types.html
  2. Rahfeld, P., Sim, L., Moon, H., Constantinescu, I., Morgan-Lang, C., Hallam, S. J., Kizhakkedathu, J. N., and Withers, S. G. (2019) An enzymatic pathway in the human gut microbiome that converts A to universal O type blood. Nat. Microbiol. 10.1038/s41564-019-0469-7
  3. Goldstein, J., Siviglia, G., Hurst, R., Lenny, L. & Reich, L. Group-B erythrocytes enzymatically converted to Group-O survive normally in A, B, and O individuals. Science 215, 168–170 (1982).
  4. Kruskall, M. S. et al. Transfusion to blood group A and O patients of group B RBCs that have been enzymatically converted to group O. Transfusion 40, 1290–1298 (2000).

Peer edited by Abigail Agoglia

A glass of wine a day…does not keep the doctor away

https://www.flickr.com/photos/117025355@N05/12429334035
Wine glasses with different types of wine in them.

One day, science shows that coffee is good for you, but the next day, science finds that coffee is bad for you. One day, chocolate is bad for you, and the next, it is good for you. Studies show that red meat is both good and bad for you. As we read the latest news, science seems to contradict itself every day. With all this confusion about science and nutrition how do we know which foods are good or bad for our health? A recent study has tried to simplify the answer for the link between alcohol and health.

One of the reasons for apparent contradictions in science is due to the nature of science. There is no answer sheet to check for the right answer and no textbook to see if your conclusion is correct. Science is completely new, and each study adds a small piece to our understanding of the world. Because each study is limited in what it investigates, occasionally the conclusions drawn from different studies may be at odds with one another. However, once enough science has been conducted, it is possible to “average out” all the information on a particular topic and come to a consensus. This consensus is often a “yes” or “no” answer to a single question, such as “Does chocolate lower blood pressure?” or “Does coffee increase the risk for cancer?” (Hint: the answers are yes, chocolate lowers blood pressure and no, coffee does not increase the risk for cancer!). One way to do this is by performing what is called a metanalysis.

Metanalyses investigate the research on a specific topic (such as a possible link between processed meats and cancer) and combine it to come to a single conclusion. A recent metanalysis studied the link between alcohol consumption and disease by combining information from 592 studies that investigated the risks and benefits of  alcohol.

The most important finding from the study is that even a single standard drink of alcohol per day increases a person’s risk of health problems, such as cancer, stroke, injuries, and infections. Furthermore, two drinks per day lead to a 7% higher risk of dying from alcohol-related health problems, and five drinks per day lead to a 37% higher risk of dying. Because of the study’s design, it is unclear how long these drinking levels must be sustained to increase the risk for health problems; future research should study this question. Although the metanalysis found that moderate consumption of alcohol (1-3 standard drinks daily) reduces the risk of ischemic heart disease and diabetes moderate alcohol consumption still increases the risk of developing over twenty other health complications and diseases. This increased risk explains the finding in this study that alcohol is the 7th leading risk factor for deaths globally, with alcohol involved in 2.2% of female deaths and 6.8% of male deaths in 2016. The disparity in male vs. female deaths may be due to discrepancies in drinking rates, since in many areas of the world, men drink more alcohol than women.

This metanalysis emphasizes the importance of re-evaluating current public health recommendations. The U.S. Dietary Guidelines recommends no more than 1 drink per day for women and no more than 2 drinks per day for men, and it also suggests that people who do not drink should not start drinking. However, the metanalysis discussed above suggests that we should reconsider these guidelines and avoid recommending alcohol consumption to anyone. This recommendation is unlikely to be a popular opinion, due to the number of people who enjoy consuming alcohol on a regular basis as well as the alcoholic beverage companies who prefer to cite science showing that moderate drinking is healthy. However, the sheer number of deaths caused by alcohol consumption (2.8 million deaths globally in 2016) highlights the importance of a thorough review of alcohol recommendations. Until then, we should individually consider how much and how frequently we consume alcohol, since alcohol does not keep the doctor away.

Peer-edited by Priya Stepp

Golden Medicine: Use of Plasmons for Cancer Therapy

Cancer is an immensely complex disease to treat. The number of mutations and combinations of mutations that can lead to its development make each “cure” more of a patch to a few specific cases. Couple that with the increasing rate of mutation within cancer cells, and it becomes difficult to even diagnose the issue. Plasmon therapy offers the potential for a broadly applicable treatment, and because it couples well with the bodies immune response, offers a therapy that could decrease the chance for metastatic tumor development.

Before we discuss this topic with greater specificity, a few terms should be defined. Plasmons, from the word plasma, are a material that has electrons that flow back and forth in a wave when light shines on them. Plasmas are just gaseous ions, like lightning or neon signs, and in the case of a plasmon, this plasma is confined to the surface of a nanoparticle. You can read more about plasmon theory here.

Nanoparticles abound in modern technologies and are defined by one dimension, the so called “critical dimension”, which is around two hundred nanometers. For reference, that’s roughly one hundred thousand times smaller than a human hair. This size can afford a variety of unique properties to a molecule: distinct colors, uncharacteristic electronic activities, and even the ability to move through a cellular membrane. All these attributes will come into play in how these molecules interact with cancer cells, so they’re important to keep in mind.  Plasmons are nanoparticles that are so small, that the plasma on the surface can be manipulated by light. This rapid movement of plasma gives rise to heat as it collides with surface particles just as your hands generate heat rubbing together. The type of light that does this can be visible or even radio waves, meaning that very low-energy and harmless beams can be used to generate this rapid heat.

The second bit of background knowledge necessary for this discussion is: how is cancer treated in the first place? Many current cancer therapies come from small molecules roughly the size of glucose. Whether they use metals or strictly carbon, small molecule cancer therapies usually rely on interrupting one or a few cellular pathways, like DNA replication or a checkpoint before mitosis (cell splitting). One of the first nanoparticles approved for cancer therapy have been gold nanorods, which are thousands of times larger than a small molecule and have used physical rather than chemical mechanisms for therapy. To clarify, instead of changing some pathway in a cell, these nanorods can selectively heat cancer cells until the cell dies. If you were to think about this in terms of pest control, nanoparticle therapy is like burning a nest of cockroaches. In that same case, using small molecules like cisplatin would be like spraying the cockroaches with the latest bugkiller.

Extending this analogy, it’s fairly obvious that setting a fire inside someone’s body is not a good medicinal practice, so it would be fair to question how plasmon therapy might be helpful. There are two strategies for plasmon cancer therapy: precision lasers and radio waves which can pass through a body. The earliest use of plasmon cancer therapy used a fiber optic that was inserted under the skin to a location near the tumor. Then, beams of light would hit only the tumor. This has the advantage of targeted dosing, but can still be considered fairly invasive. Others have begun using plasmons that generate that intense heat with radio waves so that no procedure is necessary: simply an injection or ingestion of nanoparticles and then stepping into a radio transmitter This can be impractical if the tumor is not in a confined space. Common gold plasmonic nanoparticles would go inside all cells so healthy cells would be damaged just as easily as cancerous ones. Recent work shows that the surface of the nanoparticle can be changed so that the majority of uptake occurs by cancer cells. Cancer cell metabolism makes the charge of cancer cell membranes different from the charge of normal cell membranes, so these nanoparticles can exploit that difference to target only cancer cells.

With this targeted dosing, plasmons show promise as a noninvasive form of therapy that do not harm the patient and would be applicable to most forms of cancer. Even though the safest and most effective nanoparticles will use gold, treatment costs are currently around  $1000, thereby promising a treatment that will not be prohibitively expensive for the future.

Peer edited by Kasey Skinner.

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Midterm Election Ballot Amendments: What’s up with the Right to Hunt and Fish Amendment?

Do you think the right to hunt should be protected by the NC state constitution?

This election cycle, North Carolinians will be voting on six constitutional amendments, one of which is the Right to Hunt and Fish Amendment. The amendment would upgrade hunting and fishing to a constitutional right, designating “public hunting and fishing [to] be the preferred means of managing and controlling wildlife.” Restrictions on hunting and fishing would be prohibited, except to comply with wildlife conservation and management laws.

At UNC’s Science Policy Advocacy Group (SPAG), we highlighted the quoted language from the amendment, wondering: Are voters being asked to make a decision motivated by wildlife conservation science or by politics? While the U.S. Fish and Wildlife Services claims that hunting is a wildlife management tool, this largely depends on local context based on hunting regulation and the species in question.

To answer this question in North Carolina, we consulted resources at the NC Wildlife Resources Commission. While NC has a Deer Management Assistance Program, a recent publication on the Wildlife Restoration Program states that the primary contribution of hunters is financial. In addition to the state taxes we all pay, hunters contribute to conservation funds through hunting licenses and excise taxes on arms, ammunition, and equipment. The Wildlife Commission uses those funds to purchase and manage habitat lands, restore wildlife species, conduct research, and survey wildlife populations. In fact, the increase in game populations (turkey, quail, fox, black bear, etc) is desirable because it incentivizes a growth in the popularity of hunting, which would in turn maintain revenue streams for conservation. The report does not mention hunting’s impact on wildlife population control in NC, and a search of academic literature yielded no results on the topic.

So hunting is an important financial tool for wildlife management, rather than a tool for wildlife population control. However, there’s also no evidence that anyone wants to reduce hunting licenses. If anything, because of the important funds generated by hunting, NC has a Hunter Heritage program to try to reverse declines in the number of people who hunt.

Which brings us back to the ballot amendment – what are we really voting for?

A “yes” vote supports creating a state constitutional right to hunt, fish, and harvest wildlife, affording it the same protection as free speech. This would mean the NC General Assembly would have the sole power to regulate hunting and fishing. In comparison, a “no” vote opposes codifying this right in the state constitution, maintaining having a license as a privilege.

In the end, it’s unclear what exactly this amendment would accomplish besides adding another amendment. Of all the ballot amendments, this is the one toward which state legislators feel the most ambivalent. Some democratic state representatives believe the amendment is politically motivated to draw more conservative voters to the polls who may misunderstand the amendment to mean that their ability to hunt and fish is vulnerable. This would help shore up votes for Republicans across the state.

This article is not a referendum on hunting, which, it turns out, is a prime example of how recreational activities can be leveraged to support conservation and science. However, we find this amendment uses misleading language about the efficacy of hunting itself as a wildlife management tool in NC to create unnecessary legislation.

Peer edited by Izzie Newsome.

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Stop Insulting Anglerfish Sex

http://www.photolib.noaa.gov/htmls/expl5923.htm

A deep sea anglerfish called a goosefish and is a member of the Lophiidae family – Sladenia remiger.  Image Credit: NOAA Okeanos Explorer Program, INDEX-SATAL 2010

You may have seen the anglerfish sex video floating around the Internet recently, with titles like “The worst sex in the world is anglerfish sex, and now there’s finally video.” While the video is worth a watch, I think most behavioral ecologist would beg to differ with the main assertion: there’s a lot of bad sex in the animal kingdom.

Why is anglerfish sex supposedly so terrible? A male anglerfish bites a females when he finds her, and then hangs onto her for the rest of his life, essentially turning into a living sac of sperm. But hey, at least he’s alive. In contrast, some species of male widow spiders somersault into the mouths of females as they mate, impaling themselves on their mates’ fangs. It sounds like an evolutionary enigma–why would an organism ever willingly sacrifice itself?–but turns out that that self-sacrifice can increase a male’s chances of fathering the female’s offspring.

https://commons.wikimedia.org/wiki/File:Traumatic_insemination_1_edit1.jpg

The female bed bug (the larger of the two) is traumatically inseminated by the male (bottom) through her abdomen.

Traumatic insemination” is another great example of not-so-great sex. In this case, bed bug females are the ones getting royally screwed, because traumatic insemination is a nice way of saying males stabbing females through the abdomen with their penises. The sperm then travels through the female’s hemolymph (the insect equivalent of blood), until reaching the ovaries and fertilizing the eggs. Males mate with all available females, because the last male to mate with any given female has the best chance of fathering her offspring. However, females who are subjected to these multiple matings pay a high cost: they have shortened lives and reduced reproductive output, because they have to allocate energy to healing the wounds and dealing with any resulting infections.

People often assume that two organisms mating with one another have the same “goals.” After all, both males and females are presumably invested in having as many healthy offspring as possible. But this is only true up to a certain point. Female widow spiders don’t need males to remain alive after mating, and in fact gain an advantage from eating the male (a ready source of nutrients that will help her with her next clutch!). In contrast, male widow spiders obviously benefit from not being eaten, and instead living to mate another day. Similarly, mating multiple times via traumatic insemination is costly to female bed bugs, who only need enough sperm to fertilize their eggs, while male bedbugs benefit from mating as many times as possible.

These are examples of what biologists call sexual conflict. While the source of conflict is obvious in the widow spiders’ and bed bugs’ cases, sexual conflict occurs anytime male and female genetic interests don’t align. In fact, the only time there is absolutely no potential for conflict is when males and females have exactly the same lifetime reproduction, so that each is equally invested in all of their shared offspring, with no opportunities for having offspring with other partners. In contrast, conflict can arise whenever one sex has the opportunity to improve their chances of having more, or better, offspring. This can happen in many different ways, such as: eating your partner, mating multiple times with the same partner, or even mating with multiple partners.

As a result, sexual conflict isn’t likely in anglerfish, at least those species which only have one mate for their entire lives. Although there are genera of anglerfish where females can have up to 8 males hanging off of her! So there’s potential for sexual conflict there, since the males will presumably compete to father her offspring and could do so in ways that are harmful to the female. However, anglerfish are incredibly hard to study because they generally occur in the deep sea. Frankly, male anglerfish have way more going for them than you might’ve ever thought–keep that in mind next time someone’s making fun of them.

 

Peer edited by Karen Setty.

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Mimicking Electric Eels to Provide Power to Medical Devices

https://www.flickr.com/photos/ryanready/4593249712

The electric organ of eels has inspired researchers to develop biocompatible power sources that could be used to power medical devices

While the shock of an electric eel sounds like more of a medical nightmare than a fortunate asset, researchers at the University of Michigan were inspired to simulate the power of these slick creatures in hope of creating power sources for a variety of medical devices. With society’s heavy reliance on technology, it’s not surprising that medical treatments have continued to rely more and more on electrical devices including wearable and implantable sensors, pacemakers, and prosthetics. Just as with any piece of technology, these devices require an electrical power source. However, medical devices face the added requirement of being biocompatible, meaning they must function safely and effectively in the human body. Eel-inspired power sources may achieve this goal of being biocompatible while supplying medical devices with the electricity they need to function.  

The inspirational efficiency with which an eel uses its electrical shock, to help catch prey and protect itself against predators, is the result of natural selection. Electrophorus electricus, know commonly as a knifefish or an electric eel, possesses an electric organ that extends through the back 80% of its body. The organ contains parallel stacks of special cells called electrocytes. When a situation arises that warrants a shock from the eel, its nervous system generates an electric current by activating thousands of electrocytes at the exact same time. As the cells are activated, the positively charged sodium and potassium ions, in and around the cells, move toward the head of the eel. The movement of these ions allows each of the electrocytes to act like small batteries. The activated end that lost the ions has a negative charge, while the opposite side that acquired the sodium and potassium ions carries a positive charge. The battery-like cells can each generate a small, innocuous voltage (less than that of a AAA battery). But when combined, the eel’s shock can be over 600 volts! For reference, a US household outlet supplies 120 volts. While a significant portion of this voltage is lost to the water around the eel, its prey or attacker will still get a nasty shock.

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By developing this work further, researchers hope to successfully use their artificial electric organ to run medical devices like pacemakers

The University of Michigan team has successfully created an artificial electric organ that can potentially be used by humans to power devices. To make the electrical power supply biocompatible, it was necessary to efficiently mimic the features of the eel’s electric organ. This was achieved by preparing hydrogel membranes that could be layered to replicate the structure of the organ. To mimic the movement of ions in and out of the cells, the hydrogels were filled with dissolved table salt, which is made of sodium and chlorine ions. Half of the cells were designed to allow only positively charged sodium ions out and the other half would only allow negatively charged chlorine ions to exit. The gels containing the salt water were alternated on the membrane sheet with gels containing pure water, which allows the sodium and chlorine to move in opposite directions. This flow of ions generates an electric charge with an electrical potential of 110 volts. While this voltage is less than that of the inspirational eel organ, in its current state the artificial organ may be sufficient to power some low-power devices.

Though pleased with the engineering of a potentially biocompatible power source, the researchers acknowledge that there are plenty of opportunities to improve its design. By increasing the efficiency of these artificial organs, researchers believe their utility will increase, as they will become more suitable for use in combination with implantable devices.

Peer edited by Erika Van Goethem.

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Science Communication, Advocacy and the Federal Budget

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Scientific societies, such as ASBMB, provide opportunities for trainees to travel to Washington, D.C. and meet with policymakers.

Recently, the federal budget for the fiscal year (FY) 2019 (beginning October 1st, 2018) was released. Shockingly, the initial plan called for brutal cuts to basic research funding agencies—slashing the budget of the National Institutes of Health (NIH) and the National Science Foundation (NSF) by 27% and 29%, respectively. While Congress subsequently lifted spending caps to compensate for these losses, the budgets of both the NIH and NSF will now remain stagnant at levels for FY2017.

Although catastrophic funding losses have been avoided, these flat budgets are still worrisome. When adjusted for inflation, a stable budget equates to a decrease in funding.  Furthermore, three health research institutes currently located in the Agency of Healthcare and Human Services and the CDC will be terminated and their successors will be created within the NIH. The relocation of these institutes without an increase in NIH funding will further strain the budget.

Numerous scientific societies have responded with criticism to the federal government’s budget proposal. A statement from The Society for Neuroscience (SfN) highlighted the public’s support for scientific research funding and emphasized that adequate funding is critical to combat devastating diseases, such as Alzheimer’s. Likewise, a press release from the American Society for Biochemistry and Molecular Biology (ASBMB) expressed concern regarding America’s ability to lead in science and innovation amidst stagnant funding.

Educating elected officials on the importance of scientific research is a key focus of scientific societies. ASBMB sponsors an opportunity for graduate students and postdocs to travel to the capital and meet with Congress through their annual Hill Day. Societies also encourage local action. For example, the American Society for Cell Biology (ASCB) compiles an advocacy toolkit to guide members through the process of contacting local representatives, scheduling meetings and organizing lab tours. On the UNC campus, the Science Policy Advocacy Group (SPAG) is a resource for graduate students and postdocs to gain skills in science communication and advocacy through outreach events, workshops and seminars.     

At the core of science advocacy is the ability to communicate why science is necessary. While the significance of developing new cancer therapies is clear, the importance of basic science research is still often misunderstood. Basic science research is often described as “curiosity-driven” and asks fundamental questions such as: “How do cells move?” This basic research provides a thorough understanding of cellular processes that is critical for later medical innovations. In the 1990s, Yoshinori Ohsumi observed an unusual structure in yeast cells when he starved them. His work in yeast was essential for uncovering the mechanism behind autophagy, a recycling pathway in the cell. Today, researchers know that defects in autophagy result in cancer, Parkinson’s Disease and Type 2 Diabetes, and Ohsumi was awarded the Nobel Prize in Medicine in 2016.

Ohsumi’s story demonstrates that breakthroughs in basic science are critical for breakthroughs in medicine. Yet, proper funding must be secured before further innovations in either field can occur. As a result, it is critical to create a culture that both understands and values scientific research.

Peer edited by Kelsey Miller.

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