Improbable Science: The Ig® Nobel Prize

https://www.improbable.com/ig/ (Permission granted by Marc Abrahams - editer and founder of Ig Nobel Prizes)

“The Stinker”: The official mascot of the Ig Nobel Prizes

When you think of scientific research that is worthy of international recognition, 10 trillion dollars, and a prize handed out by Nobel laureates, you are probably envisioning high-impact research that helped revolutionize its field. Unfortunately, the international recognition is not for the right reasons, the 10 trillion dollars is from Zimbabwe and is worth roughly 30 US dollars, and the Nobel laureates might be laughing as they hand out the prizes. The Ig® Nobel Prize is awarded annually to ten different people in ten different categories. The prize is intended to honor achievements in scientific research that first make people laugh, and then make them think.

Started in 1991 by Marc Abrahams, the Ig® Nobel Prizes are awarded every September at Harvard University. The winners are kept secret until the ceremony, where 1200 spectators cheer on the recipients for their discoveries. Looking back at previous winners can help one get a sense of what kind of research fits the criteria for this prize. The 2017 Ig® Nobel Prize in Medicine focused on using brain-scanning technology (fMRI) to measure how disgusted people are by cheese, while the 2015 Mathematics prize was awarded for mathematically determining whether and how Moulay Ismael the Bloodthirsty, an emperor who reigned Morocco from 1697 to 1727, was able to father 888 children. My personal favorite was the 2005 Chemistry Prize, which attempted to settle the debate of whether people can swim faster in syrup or in water. For more laughs, check out previous winners!

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A live frog levitates in a magnetic field (2000 Ig Nobel Prize in Physics)

With 2017 behind us, we can all look forward to the announcement of the 2018 winners later this year. The event is broadcast live on the internet, with additional coverage provided by NPR’s Science Friday. If you believe your research is worthy of an Ig® Nobel (hopefully it isn’t!), you can send nominations to marc@improbable.com (10-20% of the 9000 nominations every year come from self-nominations). If you happen to be nominated, you will be invited to attend the ceremony, but at your own expense! Don’t feel too self-conscious if you find yourself in this scenario. You can take comfort in knowing that Sir Andre Geim, the winner of the 2000 Physics Ig® Nobel (which he won for using magnets to levitate a frog), also won the Nobel Prize in 2010. Regardless of who wins, it is fun to follow the motto of the Ig® Nobels’, “celebrate the unusual, honor the imaginative, and spur people’s interest in science.”

Peer edited by Bailey DeBarmore.

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Epigenetics: The Software of the DNA Hardware

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Scientists identified the genes of the human genome to understand how the genes influences the function and physical characteristics of human beings.

The Human Genome Project (HGP) was an amazing endeavor to map the full human genome, and so intense an effort that it required an international collaborative research team. One of the ultimate goals of this project was to shed light on human diseases and find the underlying genes causing these health issues. However, the HGP ended up creating more questions than answering them. One thing we found out is that most diseases are complex diseases, meaning that more than one gene causes the disease. Obesity is one such example of a complex disease. This is in contrast to cystic fibrosis which is a disease caused by a mutation in a single gene. To further complicate diseases, there are gene and environment interactions to consider. A gene-environment interaction is a situation in which environmental factors affect individuals differently, depending on their genotype or genetic information. The possible number of gene-environment interactions involved in complex diseases is daunting, but the HGP has given us the information necessary to start better understanding these interaction.

Although the HGP did not end up giving us the answers we were looking for, it pointed us in the direction we needed to take. We needed to consider the role of environmental factors on human health and disease. For not only are complex diseases not fully explained by genetics alone, but another aspect of these diseases remains unexplained by genetics: the health disparities seen within diseases like obesity, diabetes, cancer, etc. The HGP showed us that not all diseases are caused by single mutations and that genetic diversity does not explain the differences in health outcomes. The environment plays a big part.

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Epigenome  is the software that controls gene expression to make the different cells that make up the human body.

Gene-environment interactions begin to answer why genetics alone cannot explain  varying health outcomes by considering that the environment may have varying effects on our genetic data. However, there is another dimension to our genetic background that could better answer why genes often can’t be mapped directly to a disease. Imagine that our genome is our computer hardware, with all the information necessary to create the cells we are composed of. However, something needs to configure the genome to differentially express genes so as to make skin and heart cells from the same DNA. Skin and heart cells have the same information (DNA) in their nucleus but only express what’s necessary to function as a skin or heart cell. In other words, software is needed for the hardware. For us, that software is the epigenome. The epigenome consists of a collection of chemical compounds, or marks, that tell the genome what to do; how to make skin and heart cells from the same information. The epigenome, unlike the genome, is flexible. It can change at key points in development and even during the course of one’s lifetime. This flexibility makes the epigenome susceptible to environmental factors and could explain: (1) Why our genome alone cannot explain the incidences of diseases such as obesity, (2) the health disparities within these complex diseases, and (3) the transgenerational inheritance of complex diseases like metabolic syndrome, defined as a cluster of conditions such as high blood pressure and high blood sugar that increase your risk for heart disease and diabetes.

Now of course, the more we find out the more questions are left unanswered. As stated before, the epigenome can change due to lifestyle and environmental factors which can prompt chemical responses. However, the mechanisms by which things like diet and smoking induce these chemical responses is unclear. But researchers have started to fill in the gap. For example, certain types of fats, like polyunsaturated fatty acids (corn oil is high in these), can generate highly reactive molecules and oxidative stress, which can cause epigenetic alterations. Tobacco smoke contains a mixture of chemicals that have been independently investigated with mixed results on the epigenetic effects. Psychological stress, more specifically child abuse, has been seen to cause increased methylation (a sort of mark on the genome) of a receptor for hormones responsible for metabolism (glucocorticoid receptor) in suicide victims. This has also been seen in mouse models where higher maternal care of pups decreased methylation of the glucocorticoid receptor. Increased methylation usually decreases the expression of the glucocorticoid receptor, and decreased methylation would increase the glucocorticoid receptor’s expression.

The HGP was an amazing endeavor of science and has given us amazing insight into the structure, organization, and function of the complete set of human genes. It has also helped point us in a new direction to better understand chronic diseases and seek to find the solutions to address the burden of disease.

Peer edited by Mejs Hasan and Emma Hinkle.

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The Perfect Storm

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Hurricane Maria caused significant damage to Puerto Rico in September 2017. Image by Antti Lipponen.

There is a trend with recent natural disasters: out of the media, out of mind. Hurricanes Harvey, Irma and Maria all had major impacts on the US in 2017 (and yet I could only remember 1 of 3 names off the top of my head!). Once the non-stop media coverage ceases and calls for donations lose steam, we continue on with our lives without a second thought. However, these storms have lasting impacts which can radiate far beyond the directly affected areas.

When Hurricane Maria hammered the island of Puerto Rico, nearly all the territory lost power (see image). The outages affected both residents and businesses, including all 3 manufacturing facilities operated by Baxter, a critical provider of hospital products for the mainland US. Baxter is the major source of several heavily used products including sterile saline (sodium chloride 0.9%), and IV tubing and bags. Saline bags are used for patient rehydration as well as dilution of many IV drugs.

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Comparison of lights at night in Puerto Rico before (top) and after (bottom) Hurricane Maria

In the wake of Hurricane Maria’s destruction last September, production at the Baxter plants was at a stand-still. The FDA released a statement regarding the potential impact of the shortage, and even worked to get critical Baxter facilities priority for re-establishing electric power. Drug shortages are nothing new, and the FDA acknowledged in their press release that saline bags have been in shortage since 2014. But the drop in availability of basic supplies such as saline has many hospitals, including those in the Triangle, scrambling to adapt.

Exacerbating the situation, the shortages have coincided with an unusually vigorous flu outbreak and a spike in hospitalizations. As population densities increase, disease epidemics are more likely to occur, so issues such as drug shortages and over-filled hospitals will continue to occur (also see David Abraham’s post for more on the challenges of flu season). For example, the severity of the current flu season has also led to shortages of flu medication for children.

Kendra Connelly

A pharmacy technician prepares drugs in a sterile hood

Pharmacies do their best to cope, and behind the scenes are talented pharmacists, nurses and administrators working to keep operations running as normal as possible, with little impact on real-time patient care. To reduce saline bag usage, normal pharmacy protocols can sometimes be modified. This may include manually injecting drugs normally administrated by drip, switching to oral medications, and preparing drugs in different types of bags. Fortunately, all 3 Baxter plants are back online and will soon catch up with production.

In the absence of a familiar “Made in China” sticker, most people don’t consider the origin of many products in their life. And while the current drug and supply shortage cannot be compared to the ongoing suffering of those living in hurricane affected areas, the perfect storm came together to cause lasting and far-reaching effects of the latest hurricane season. Communities directly affected by Maria are still dealing with the challenges of rebuilding and likely will be for some time, but hopefully highlighting these situations will serve as a reminder to the rest of us of the lasting impact of natural disasters.

Peer edited by Hannah Perrin.

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Space Travel is Possible with the Sound of Light

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Optical communication devices may be the first step in space travel.

Technology moguls dream of human colonies on other planets. For this dream to become reality, science needs to develop new spacecraft capable of transporting people and cargo to the outer reaches of our galaxy. Another challenge is how to find a route to these other planets.  We can’t just use Google Maps. Space travelers would have to navigate around comets, space debris, or orbiting planets.  Complex models and communications developments would be needed to move through galaxies safely and quickly.

Light-based communication is desirable because it can transmit more data per second while producing significantly less heat. This means that less energy is spent cooling equipment, making the it more efficient to run compared to conventional electron-based communication.

Similar to how electronic devices maneuver electrons through a computer chip, photonic devices maneuver light for optical communication. Normally, a magnetic field is required to produce a change in optical properties necessary for one-way light propagation. However, the size of magnets are too large to be incorporated efficiently into nanoscale devices. To address this problem, University of Illinois researchers created a nanoscale photonic device called an optical isolator, using sound waves instead of magnets for one-way light guidance.

Erika Van Goethem

Cartoon of optical device

The optical isolator device is made from aluminum nitride. A radio frequency driver (RF driver) generates a radio frequency signal that is used to create a sound wave. The RF signal is applied to an IDT, consisting of two interlocking comb-shaped arrays of metallic electrodes that convert electrical signals into surface sound waves. The grating couplers allow the light, generated by a laser, to enter into the device from one direction.  The light travels along the optical waveguides and is transferred from one optical band to another, interacting with the previously converted sound waves. Light is able to pass through the device when the shape of the light wave matches the shape of the sound wave going in the same direction. However, light waves going in the opposite direction of sound waves are absorbed by the device and are unable to pass through, thus maintaining the one-way propagation of light.

This new device allows for a more reliable and sensitive transfer of information that can be used in devices such as atomic clocks and GPS.  Such innovations may be the first step toward developing deep space navigation and travel.

Peer edited by Portia Flowers.

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New Year, New Discoveries in Alzheimer’s Research

 Alzheimer’s disease is both debilitating and fatal. Its associated memory loss is more than a sign of normal aging, and Alzheimer’s is a leading cause of death in the United States. While the pace of Alzheimer’s treatment research is impressive, it is mirrored by a monumental projected increase in prevalence over the next 30 years.

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Image shows a beta-amyloid protein (orange) and tau protein (blue). Image courtesy of the National Institute on Aging/National Institutes of Health.

A key aspect of developing effective treatments for Alzheimer’s, and for any disease, is to understand how the disease progresses. One of the causes of Alzheimer’s is believed to correlated with malfunctioning tau proteins in our nerve cells, or neurons. Tau proteins, when under a normal function, stabilize neuron’s microtubules serving as information carriers. When tau proteins malfunction, the nerve cells reject the accumulated debris of tau and spit it out. Another small section of protein, beta-amyloid peptides, are involved in neuronal structure as well as in Alzheimer’s disease. Scientists believe the nasty feedback loop in which beta-amyloid’s failure would trigger tau protein malfunction and that tau tangles, in turn, enhance beta-amyloid toxicity. These extracellular proteins stick together in bundles, forming strands of tangles and clusters of plaques around the dying neurons. 

Research  out of the University of Cambridge, published in Brain this month, combined functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) scans to visualize the location and extent of tau proteins in the brains of 17 Alzheimer’s patients and 12 controls. They also included 17 patients with progressive supranucelar palsy (PSP), a brain disorder sometimes mistaken for Parkinson’s disease.

The Cambridge researchers wanted to test the theory of “transneuronal spread” – that tau tangles from one neuron pass to other neurons, rather than simultaneously occur at multiple locations. The imaging from their research study showed that abnormal tau proteins seemed to accumulate along heavily connected regions of the brain, where neurons are densely connected to one another. This theory supports the progressive nature of Alzheimer’s with an increasing loss of functional connectivity, and the researchers are planning additional studies to follow these patients over time and document the spread of these proteins. Animal research has previously shown tau propagation via synaptic connectivity in rodent models.

https://www.nia.nih.gov/

Image shows abnormal tau proteins in neuronal bodies (blue) and amyloid plaques (orange) in a diseased Alzheimer’s brain. Image courtesy of the National Institute on Aging/National Institutes of Health.

Interestingly, the Cambridge researchers found evidence of a different tau propagation in progressive supranucelar palsy (PSP) patients. The spread of tau tangles seemed to follow increased metabolic demand, not functional neuronal connectivity. This different mechanism may explain the different symptoms seen in Alzheimer’s, often presenting as memory loss, and PSP, often presenting as weakness.

Want to learn more about Alzheimer’s disease? Take an interactive tour of the brain and learn how the disease occurs and progresses at the physiological level.

 

Peer edited by Chiung-Wei Huang and Kate Newns.

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Heart to Heart

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Hearts and heart health are front and center throughout the month of February.

The month of February is a big month for hearts. Between Valentine’s Day and American Heart Month, you cannot escape heart-shaped decorations and reminders to exercise daily. And while many of us are fortunate that our heart health can be maintained through diet and exercise, there are some cases where that is not enough. Individuals with certain congenital heart defects, weakened heart muscles, or other types of heart disease may need a totally new heart. In the United States, about 2,300 heart transplants occur each year with over 70% of those patients surviving for five years afterwards. This high survival rate is in stark contrast to the early days of heart transplants in the late 1960s and 1970s, and it is largely due to advances not in heart physiology, but the immune system.

Our immune systems are exceptionally good at identifying foreign invaders and attacking them. In the cases of bacterial or viral infections, the immune system’s voracious assault on foreigners keeps us healthy. However, in the case of a heart transplant, where foreign tissue is introduced to the body to save the patient’s life, such voracity is detrimental to survival. A distressing catch-22 emerged as early heart transplants were performed – doctors gave patients powerful immunosuppressants to prevent rejection of the heart, but these drugs left the immune system so weakened that it could not fight off post-surgical infections. Eventually, a breakthrough came from an unexpected place – a Norwegian soil fungus.

https://www.flickr.com/photos/usdagov/38151055715

Sometimes medical breakthroughs come from unlikely places – like a Norwegian soil fungus.

While on vacation in Norway, a scientist collected a soil sample that would change the fate of organ transplants forever. The soil sample was taken to Sandoz Pharmaceutical Ltd. where Jean-Francois Borel worked diligently with a team of scientists to characterize an interesting compound found in the Norwegian soil: cyclosporine, which was made from a fungus.

Sandoz Pharmaceutical was interested in developing new antibiotics, but, cyclosporine did not prove to be an effective antibiotic. Luckily for future recipients of heart transplants, cyclosporine  did show promise as an immunosuppressant. Cyclosporine specifically inhibited white blood cells and T cells instead of killing them, thus preventing organ rejection while still allowing the immune system to fight off infections. Dr. Borel and his team faced several setbacks while studying cyclosporine, including pressure from Sandoz to discontinue the studies. However, they persisted until 1983 when the Food and Drug Administration approved cyclosporine as an immunosuppressant for all organ transplants. Many healthy hearts are beating today due to cyclosporine, and a heartfelt thanks goes out to the countless individuals who worked so hard to make these survival stories a reality.

Peer edited by Kaylee Helfrich.

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Cloned Monkeys: Another Human Creation

http://english.cas.cn/head/201801/t20180123_189488.shtml Image credited to Qiang Sun and Mu-ming Poo, Institute of Neuroscience of the Chinese Academy of Sciences

First cloned none-human primates: Zhong Zhong and Hua Hua (Image credited to Qiang Sun and Mu-ming Poo, Institute of Neuroscience of the Chinese Academy of Sciences)

Cloned primates are here! Over three decades have passed since the birth of Dolly, the sheep, scientists have now tackled cloning mammals that are even closer to us on the evolutionary tree: macaque monkeys. What does this mean for a society that witnesses dramatic changes day by day: computers are outperforming doctors in calling out heart abnormalities in patients; 3D-printed organs are bringing us one step closer to tissue restoration; genome sequencing has become an online product easily available for anyone curious about their ancestry, bodybuilding, or just simply wine tastes. Breakthroughs in science and technologies are so prevalent in our life that by now, we probably shouldn’t be surprised by any new discovery. Yet when the two cute, little, cloned monkeys were born, the whole world was, once again, shaken.

Published in Cell on January 24th, 2018, a study from a group of scientists in China reported their methods in generating two non-human primates that are genetically identical. To clone the two identical macaque monkeys, the scientists applied Somatic Cell Nuclear Transfer, the same method that generated Dolly in 1996. The key idea behind cloning is that a new organism, be it sheep or monkey, is generated without sexual reproduction. Asexual reproduction is not as uncommon as one would think, plenty of plants do so. For example, Bryophyllum shed plantlets from the edge of the leaves to produce new plants. Some insects, such as ants and bees, also exploit asexual reproduction to clone a huge working class army. Since asexual reproduction is essentially an organism duplicating itself, the offsprings are all genetically identical. Evolution, however, doesn’t favor asexual reproduction as identical offsprings don’t prevail in a fast changing environment. On the other hand, sexual reproduction combines different sperms and eggs to create diverse offsprings, of which some may survive. To combat challenges from the mother nature, higher organisms, such as mammals, almost exclusively reproduce sexually. This is why a cloned monkey, an anti-evolution human creation, is mind blowing.

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The succulent, genus Kalanchoe, uses asexual reproduction to produce plantlets.

To clone mammals, scientists came up with the idea of transferring the nucleus of a somatic cell to an enucleated egg (an egg that lacks nucleus). Unlike  germ cells (sperm and eggs), somatic cells refer to any cells that don’t get passed onto the next generation. These cells have the full genome of an organism that is split equally in germ cells during sexual reproduction. Carrying half of the genome, sperm and egg need to fuse their genetic materials to make one viable embryo. Technically, the nucleus of a somatic cell holds all the genetic information an organism needs. Thus, by inserting the somatic cell nucleus into an egg, scientists could generate a functional embryo. But why not into a sperm? Evolution has trimmed mammalian sperm tremendously so that it can accomplish its only job better: swim faster to fertilize the egg. As a result, not much other than the sperm’s genetic information is incorporated into the fertilized egg and the embryo relies on the cellular machinery from the egg to finish development. Using this technology, the scientists generated over 300 “fertilized” embryos. Of these embryos, 260 were transferred to 63 surrogate mothers to finish developing. 28 surrogate mothers became pregnant, and from those pregnancies, only 2 healthy monkey babies were born. Although they were carried by different surrogate mothers, every single piece of their genetic code is the same as the the somatic nucleus provider, a real-life demonstration of primate-cloning. Followed by millions of people since their debut to the world, these two macaque superstars are the living samples of a revolutionary breakthrough in our science and technologies.

 

Despite the extremely low success rate, this technology erects another monument in the history of mankind’s creations. Carrying identical genetic information, cloned monkeys like these two can be a very powerful tool in biomedical research and diseases studies. Co-author Mu-ming Poo, director of the Chinese Academy of Sciences’ Institute of Neuroscience in Shanghai, said that these monkeys could be used to study complicated genetic diseases where environmental factors also play a significant role, such as Alzheimer’s and Parkinson’s diseases. While there are ethical concerns on this technology and its easy application to human cloning, it is worth noting that almost all human creations (explosives, GMO food, the internet, etc.) are double-sided swords. It is up to the hand that wields this sword to decide whether to do good or bad. It is wise to be cautious with the development of new technologies, but it’s also important not to constrain our creativity. After all, it is our creative minds that drive us toward creating a better life for everyone.

Peer edited by Cherise Glodowski.

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Why is the Flu such a Big Deal?

With each flu season comes a bombardment of new advertisements reminding people to get a flu vaccine. The vaccine is free to most and widely available, yet almost half of the United States chooses to forgo the vaccine.

When Ebola emerged, there was 24 hour news coverage and widespread panic, but the influenza virus (the flu) feels more familiar and much less fear inducing. This familiarity with the flu makes its threat easy to brush aside. Yet, every flu season is met with stern resolve from the medical community. What’s the big deal with the flu?

What makes the flu such a threat?

Influenza is a globetrotting virus: flu season in the northern hemisphere occurs from October to March and April to September in the southern hemisphere. This seasonality makes the flu a year round battle. The virus also evolves at a blistering pace, making it difficult to handle.

To understand why the flu is able to evolve so rapidly, its structure must be understood.The graphic to the right shows an illustration of the ball-shaped flu virus.

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Illustration of flu structure

On the outside of the ball are molecules that let the virus slip into a person’s cells. These molecules are called hemagglutinin and neuraminidase, simply referred to as HA and NA. HA and NA are also used by our body’s immune system to identify and attack the virus, similar to how a license plate identifies a car.

These HA and NA molecules on the surface can chanAntigenic shift in the fluge through two processes. One such process is like changing one license plate number; this is known as antigenic drift. When the flu makes more of itself inside a person’s cells, the instructions for making the HA and NA molecules slightly change over time due to random mutations. When the instructions change, the way the molecules are constructed also changes. This allows the flu to sneak past our immune systems more easily by mixing up its license plate over time.

Another way the virus can evolve is known as antigenic shift. This type of evolution would be more like the virus license plate changing the state it’s from in addition to a majority of its numbers and letters, making the virus completely unidentifiable to our immune systems. Unlike antigenic drift, antigenic shift requires a few improbable factors to coalesce.  

Antigenic shift happens more regularly in the flu when compared to other viruses.For instance, one type of flu virus is able to jump from birds, to pigs, and then to people without the need for substantial change. This ability to jump between different animals enables antigenic shift to occur.

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How antigenic shift occur in the flu

This cross species jumping raises the odds of two types of the virus to infect the same animal and then infect the same cell. When both types of the flu virus are in that cell, they mix-and-match parts, as can be seen in the picture to the right. When the new mixed-up flu virus bursts out of the cell, it has completely scrambled it’s HA and NA molecules,generating a new strain of flu.

Antigenic shift is rare, but in the case of the swine flu outbreak in 2009, this mixing-and-matching occured within a pig and gave rise to a new flu virus strain.

This rapid evolution enables many different types of the flu to be circulating at the same time and that they are all constantly changing. This persistent evolution results in the previous year’s flu vaccine losing efficacy against the current viruses in circulation. This is why new flu vaccines are needed yearly. Sometimes the flu changes and becomes particularly tough to prevent as was the case with swine flu. At its peak, the swine flu was classified by the World Health Organization (WHO) as a class 6 pandemic, which refers  to how far it had spread rather than its severity. Swine flu was able to easily infect people, fortunately it was not deadly. The constant concern of what the next flu mutation may hold keeps public health officials vigilant.

Why is there a flu season?

A paper by Eric Lofgren and colleagues from Tufts University grapples with the question “Why does a flu season happen?”. The authors highlight several prevailing theories that are believed to contribute to the ebb and flow of the flu.

One contributing factor to the existence of flu seasons is our reliance on air travel. When flu season in the Australia is coming to an end in September, an infected person can fly to Canada and infect several people there, kickstarting the flu season in Canada. This raises the question: why is flu season tied with winter?

The authors touch on this question. During the winter months, people tend to gather in close proximity allowing the flu access to many potential targets and limiting the distance the virus need to cover before infect another person. This gathering in confined areas likely contributes to the spread of flu during the winter, but another theory proposed in this paper is less obvious and centers around the impact of indoor heating.

Heating and recirculating dry air in homes and workplaces creates an ideal environment for viruses. The air is circulated throughout  a building without removing the virus particles from the air, improving the chances of the virus infecting someone. The flu virus is so miniscule that air filters are unable to effectively remove it from the air. The authors come to the conclusion that the seasonality of the flu is dependent on many factors and no single cause explains the complete picture.

What are people doing to fight the flu?

The flu is a global fight, fortunately the WHO tracks the active versions of the flu across the world. This monitoring system relies on coordination from physicians worldwide. When a patient with the flu visits a health clinic, a medical provider, performs a panel of tests to detect the type and subtype of flu present. This data is then submitted to the WHO flu database, which is publicly accessible.

This worldwide collaboration and data is invaluable to the WHO; it allows for flu tracking and informed decision making when formulating a vaccine. Factor in the rapidly evolving nature of the flu and making an effective vaccine seems like a monumental task. Yet, because of this worldwide collaboration twice a year, the WHO is able to issue changes to the formulation of the vaccine as an effort to best defend people from the flu that year.

Peer edited by Rachel Cherney and Blaide Woodburn.

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Finding Power in Discomfort: 5 Ways to Advocate for Yourself and Others in Science

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Share your experiences, it might just empower others. Image: Parliamentary Copyright/Jessica Taylor

Three years ago, I moved from California to North Carolina for graduate school, an experience that pushed me out of my comfort zone in more ways than I expected. The most discomforting was feeling very different from my colleagues. For example, my identity as a woman of color became more salient when I realized there were fewer people who looked like me in the classes and meetings I attended. It wasn’t until recently that I found a community of like-minded, underrepresented students who told stories similar to mine. I felt empowered through this shared struggle to learn how to advocate for myself and others in order to increase visibility for underrepresented groups in science. Not sure how to do it (like me)? Try these tips!

Bring your personal identity into your work. Increase the visibility of your personal identity in the workplace so that you are not left out of the conversation. It can be uncomfortable to bring up your experiences and challenges related to gender, race, sexual orientation, socioeconomic status, etc., but doing so may provide the opportunity for others to exhibit empathy. Regardless of the differences between people, everyone shares the mutual need for kindness and respect. It’s important and necessary to stay true to who you are in order to create more of a dialogue, so don’t hide it.

Empower others by sharing your story. Share your own stories of success or hardship because not only does it feel intrinsically rewarding to communicate your thoughts and feelings with others, but it can also validate the range of experiences that other underrepresented students face and often in silence. If you’re shy or nervous, try sharing your story on Akin, an anonymous digital storytelling platform created by my friend, Cassandra Lam, to empower people to connect through stories of shared experiences.

Step into a world you don’t know much about. Equally important is the ability to listen to others’ stories, as it can provide insight into the privileges you might not even realize you have. Be mindful that some people will face certain challenges that you might never have to face (e.g., gender identity, sexual orientation). Be open-minded, ask questions, and acknowledge others’ perspectives (try to avoid phrases like “at least you don’t have to deal with…” which might undercut what they’re sharing).

Express your intellectual humility. It can be hard to say “I don’t know” to anything, but learning how to articulate exactly what you don’t know can be the engine for establishing new learning and networking opportunities. Seek knowledge from teachers and experts about topics you’re unfamiliar with, but are interested in learning. It’s also okay to ask for support from mentors and colleagues. You’ll be surprised at how many people want you to succeed and are willing to help.

Dive into more uncomfortable conversations about uncomfortable topics. When discussion of uncomfortable topics (e.g., lack of visibility for underrepresented groups) arises, I challenge you to speak up, even when it’s easier to stay silent to avoid causing rifts in conversation. Advocating for the importance of your/others’ needs lifts up the voices of those who are unable or are afraid to so themselves.

Peer edited by Mikayla Armstrong.

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Bonnethead Shark: The Newest Veggie Lovers of the Sea

Vegetarian sharks.

If you love a cheesy sci-fi movie as much as I do, the word shark probably brings a few images to mind; swimmers rushing to shore, a huge, hungry, Great white, ready to devour anything in its sights. You may have even started humming the iconic Jaws theme. But you might be surprised to hear that off the big screen, not all sharks are out for blood. In fact, one shark prefers a leafy, green, salad.

We often think of sharks as strict meat eaters, but researchers at the University of California-Irvine are turning the meat hungry shark stereotype on its head with their (mostly) vegetarian Bonnethead sharks. The Bonnethead shark is a small type of hammerhead shark often found in warm, shallow waters of the Northern hemisphere. Bonnetheads get their name from their distinct shovel-like head shape.

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The Bonnethead shark’s unique head shape distinguishes it from its hammerhead cousins.

 

Though distinct in appearance, the characteristic that makes the Bonnethead shark truly unique is its diet. Sharks are infamous meat-eaters. The Bonnethead, however, prefers its meat with a side of veggies. Studies on the diet of the Bonnethead began in 2007 when large amounts of seagrass were found in the stomach of a shark in the Gulf of Mexico. For many years, it was thought the seagrass was indigestible and eaten on accident while the sharks were hunting for shrimp, mollusks, and small fish in the seagrass ridden waters. Recent research now suggests Bonnethead sharks can digest the seagrass they eat and could use it as a source of nutrients.

As the first seagrass-eating shark be discovered, there are still many questions surrounding this veggie-loving shark. Does the Bonnethead eat seagrass on purpose? Or is it accidentally consumed while hunting for creatures on the ocean floor? Perhaps the most puzzling question is how  the Bonnetheads are able to digest seagrass? Because Bonnethead sharks have short intestines that are typical of a strict meat eater, scientists suspect bacteria living in the gut give the Bonnethead the ability to digest seagrass. More research is needed to discover which, if any, bacteria help the Bonnethead digest its dinner.

Although questions remain, one thing is certain; the Bonnethead shark is a unique and remarkable creature with much to teach their human neighbors about what constitutes a five-star meal under the sea.

Peer edited by Zhiyuan Liu.

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