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.

https://www.cdc.gov/flu/images/virus/fluvirus-antigentic-characterization-large.jpg

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.

https://commons.wikimedia.org/wiki/File:AntigenicShift_HiRes_vector.svg

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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Superbug Super Problem: The Emerging Age of Untreatable Infections

You’ve heard of MRSA. You may even have heard of XDR-TB and CRE. The rise of antibiotic-resistant infections in our communities has been both swift and alarming. But how did these once easily treated infections become the scourges of the healthcare world, and what can we do to stop them?

Antibiotic-resistant bacteria pose an alarming threat to global public health and result in higher mortality, increased medical costs, and longer hospital stays. Disease surveillance shows that infections which were once easily cured, including tuberculosis, pneumonia, gonorrhea, and blood poisoning, are becoming harder and harder to treat. According to the CDC, we are entering the “post-antibiotic era”, where bacterial infections could once again mean a death sentence because no treatment is available. Methicillin-resistant Staphylococcus aureus, or MRSA, kills more Americans every year than emphysema, HIV/AIDS, Parkinson’s disease, and homicide combined. The most serious antibiotic-resistant infections arise in healthcare settings and put particularly vulnerable populations, such as immunosuppressed and elderly patients, at risk. Of the 99,000 Americans per year who die from hospital-acquired infections, the vast majority die due to antibiotic-resistant pathogens.

http://www.lab-initio.com

Cartoon by Nick D Kim, scienceandink.com. Used by permission

Bacteria become resistant to antibiotics through their inherent biology. Using natural selection and genetic adaptation, they can acquire select genetic mutations that make the bacteria less susceptible to antimicrobial intervention. An example of this could be a bacterium acquiring a mutation that up-regulates the expression of a membrane efflux pump, which is a transport protein that removes toxic substances from the cell. If the gene encoding the transporter is up-regulated or a repressor gene is down-regulated, the pump would then be overexpressed, allowing the bacteria to pump the antibiotic back out of the cell before it can kill the organism. Bacteria can also alter the active sites of antibacterial targets, decreasing the rate with which these drugs can effectively kill the bacteria and requiring higher and higher doses for efficacy. Much of the research on antibiotic resistance is dedicated to better understanding these mutations and developing new and better therapies that can overcome existing resistance mechanisms.

 

While bacteria naturally acquire mutations in their genome that allow them to evolve and survive, the rapid rise of antibiotic resistance in the last few decades has been accelerated by human actions. Antibiotic drugs are overprescribed, used incorrectly, and applied in the wrong context, which expose bacteria to more opportunities to acquire resistance mechanisms. This starts with healthcare professionals, who often prescribe and dispense antibiotics without ensuring they are required. This could include prescribing antibiotics to someone with a viral infection, such as rhinovirus, as well as prescribing a broad spectrum antibiotic without performing the appropriate  tests to confirm which bacterial species they are targeting. The blame is also on patients, not only for seeking out antibiotics as a “cure-all” when it’s not necessarily appropriate, but for poor patient adherence and inappropriate disposal. It’s absolutely imperative that patients follow the advice of a qualified healthcare professional and finish antibiotics as prescribed. If a patient stops dosing early, they may have only cleared out the antibiotic-susceptible bacteria and enabled the stronger, resistant bacteria to thrive in that void. Additionally, if a patient incorrectly disposes of leftover antibiotics, they may end up in the water supply and present new opportunities for bacteria to develop resistance.

 

https://www.flickr.com/photos/diethylstilbestrol/16998887238/in/photostream/

Overuse of antibiotics in the agricultural sector also aggravates this problem, because antibiotics are often obtained without veterinary supervision and used without sufficient medical reasons in livestock, crops, and aquaculture, which can spread the drugs into the environment and food supply. These contributing factors to the rise of antibiotic resistance can be mitigated by proper prescriber and patient education and by limiting unnecessary antibiotic use. Policy makers also hold the power to control the spread of resistance by implementing surveillance of treatment failures, strengthening infection prevention, incentivizing antibiotic development in industry, and promoting proper public outreach and education.

 

While the pharmaceutical industry desperately needs to research and develop new antimicrobials to combat the rising number of antibiotic-resistant infections, the onus is also on every member of society to both promote appropriate use of antibiotics as well as ensure safe practices. The World Health Organization has issued guidelines that could help prevent the spread of infection and antibiotic resistance. In addition, World Antibiotic Awareness Week is November 13-19, 2017, and could be used as an opportunity to educate others about the risks associated with antibiotic resistance. These actions could significantly slow the spread and development of resistant infections and encourage the drug development industry to develop new antibiotics, vaccines, and diagnostics that can effectively treat and reduce antibiotic-resistant bacteria.

Peer edited by Sara Musetti 

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H What N What? A Designer Protein Hits the Science Runway

Image ID: 10073 https://phil.cdc.gov/phil/details.asp

TEM Image of Influenza Virion. Content Providers: CDC/ Erskine. L. Palmer, Ph.D.; M. L. Martin, 1981.  Photo Credit: Frederick Murphy

Influenza is a virus that straddles two worlds: that of the past and that of the future. Responsible for more deaths than HIV/AIDS in the past century, the flu is one of the world’s’ most dangerous infectious diseases though it may not seem so, especially in the United States. However, the flu is responsible for millions of cases of severe illness and approximately 250,000 to 500,000 deaths worldwide each year.

Influenza Pandemics
Influenza A and B circulate each flu season, but it is the emergence of new influenza A strains that have been responsible for worldwide epidemics, or pandemics, in the past such as the 1918 ‘Spanish Flu’ pandemic and the 2009 H1N1 pandemic. There are 2 ways a new influenza virus can emerge. Every time the virus replicates, small genetic changes occur that result in non-identical but similar flu viruses: this is called “antigenic drift”. If you get infected with a certain flu virus, or get a vaccine targeting a certain flu virus, your body develops antibodies to that virus. With accumulating changes, these antibodies won’t work against the new changed virus, and the person can be infected again. The other source of change is “antigenic shift”, which results in a virus with a different type of hemagglutinin and/or neuraminidase, such as H3N2 to H1N1. The 2009 H1N1 virus is cited by some as a result of antigenic shift, because the virus was so different than previous H1N1 subtypes; however, as there was no change in the actual hemagglutinin or neuraminidase proteins, it was technically a case of antigenic drift.

Image ID: 13469 https://phil.cdc.gov/Phil/details.asp

This diagram depicts how the human cases of swine-origin H3N2 Influenza virus resulted from the reassortment of two different Influenza viruses. The diagram shows three Influenza viruses placed side by side, with eight color-coded RNA segments inside of each virus. The virus from the 2009 pandemic (right) has HA/NA proteins and RNA from Eurasian and North American swine instead of from humans like in previous years (left two viruses).
Content Provider: CDC/Douglas Jordan, M.A. 2011.

 

Challenges in Studying the Flu
Scientists and policymakers face many challenges when studying the influenza virus. For instance, the virus can be transmitted among people not showing symptoms and cough, sneeze, or handshake can spread infectious droplets from someone who doesn’t know they’re sick. Scientific study is further complicated by the virus itself: there are 3 antigenic types of influenza virus that infect humans, (A, B, C), with various subtypes and strains. Each year, government agencies work with scientists to decide which strains to target in that year’s vaccine manufacturing. The lag time between production in the spring and the flu season in the winter provides time for unexpected types to emerge.

Image ID: 17345 https://phil.cdc.gov/Phil/details.asp

This is a 3D illustration of a generic Influenza virion’s fine structure. The panel on the right identifies the virion’s surface protein constituents. Content Provider: CDC/ Douglas Jordan, Dr. Ruben Donis, Dr. James Stevens, Dr. Jerry Tokars, Influenza Division. 2014. Illustrator: Dan Higgins.

The H#N# nomenclature for influenza A subtypes refers to the hemagglutinin (H) and neuraminidase (N) proteins that sit on the surface of the virus. There are 18 types of hemagglutinin and 11 types of neuraminidase. Hemagglutinin aids the virus in fusing with host cells and emptying the virus’ contents inside. Neuraminidase is an enzyme embedded in the virus membrane that facilitates newly synthesized viruses to be released from the host cells to spread the infection from one cell to another.

Targeted Therapy
In studying ways to prevent and battle influenza, research scientists have focused their efforts on blocking the actions of neuraminidase and hemagglutinin. Antiviral drugs, such as oseltamivir (Tamiflu®) and zanamivir (Relenza®), bind neuraminidase, both interact with neuraminidase at sites crucial for its activity. The drugs act to render the virus incapable of self-propagating. A computational biologist at the University of Washington in Seattle, David Baker and his team know the hemagglutinin protein well. In 2011, they utilized nature’s design by studying antibodies that bind hemagglutinin in order to design a protein that targets the glycoprotein’s stem in H1 subtype flu viruses and prevent the virion from infecting the host cell. However, antiviral resistance contributed to by antigenic drift, is a serious issue. Researchers much constantly develop new drugs to keep up with changes in the virus.

David Baker and his team now focus their research on the hemagglutinin protein. Utilizing a computational biology approach, they designed a protein that fits snugly into hemagglutinin’s binding sites. They tested their designer protein on 10 mice and found that in mice exposed to the H3N2 influenza virus, their protein worked both as a preventative measure and as a treatment.  Though there is a long road to human testing, this binding protein shows promise for bedside influenza diagnosis as well as a model for possible treatments.

Want to know more? 

Image ID: 8675 https://phil.cdc.gov/phil/details.asp

This photograph depicts a microbiologist in what had been the Influenza Branch at the Centers for Disease Control and Prevention (CDC) while she was conducting an experiment.  Content Provider: CDC/Taronna Maines. 2006. Photo Credit: Greg Knobloch.

Learn how scientists monitor circulating influenza types and create new vaccines each year.

See flu activity and surveillance efforts with the CDC’s FluView and vaccination trends for the United States using the FluVaxView.

 

Peer edited by Richard Hodge and Tyler Farnsworth.

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Science and Ethics

So let’s say, hypothetically, that your lab receives blood samples from a group of individuals to study genetic links with diabetes.  However, these samples would also provide important insights into other diseases.  But the researchers did not get consent from the blood samples donors for the extra research.  For researchers at Arizona State University (ASU) and the University of Arizona (U of A), this was not a hypothetical situation.  

https://www.flickr.com/photos/neeta_lind/3572379084

DNA from blood samples provide the information needed to potentially cure many diseases that plague us today.  But if the proper procedure is not followed, these scientific breakthroughs may never leave the courtroom.

They collected 400 blood samples from the Havasupai Tribe around 1990 to understand if there was any connection between genes and diabetes, at the tribe’s request. This particular tribe is from an isolated area of the Grand Canyon, with a restricted gene pool contributing to genetic diseases.  This Native American tribe has a high-incidence with diabetes.  The researchers did investigate this problem with diabetes, but they also wrote a grant proposal for researching schizophrenia in the Havasupai Tribe, which the tribe was not aware of nor gave consent for.

The main issues raised in this case are:

  • What is informed consent?  In this case, the consent form stated that the samples were to be used for studies on behavioral and medical diseases. But, meetings between the researchers and tribe members indicated that only diabetes was to be studied.  Using broad or vague language in consent forms can lead to miscommunication between scientists and subjects.
  • What information in the medical records can be accessed and by who?  Some researchers gained access to medical records without permission. Files should be kept in a secured place where only the authorized users have access.
  • Who has control of the samples?  This is a question that needs to be discussed with the subjects before samples are collected.  Researchers might want to contact their university’s research center for more information on sample ownership.

 

As scientists, we have a set of standards, or ethics, that help members coordinate their actions and establish trust with the public. Below are four ethical norms (or goals) that affect graduate students:

https://upload.wikimedia.org/wikipedia/commons/d/d9/March_for_Science%2C_PDX%2C_2017_-_29.jpg

Scientists build and maintain credibility with the public by conducting research responsibly and with integrity.

  1. Promote the goals of scientific discovery, such as furthering knowledge and truth.
  2. Advocate collaboration between scientists; diversity and collaboration create new and novel discoveries that we can all benefit from.
  3. Promote accountability to the Public; it’s essential that the Public can trust the scientists to do their best work and avoid misconduct, conflicts of interest, and ensure that human/animal subjects are properly handled.
  4. Build Public support, without federal funding many of us graduate students would not be able to do our research.

For the misuse of their DNA samples, the  Havasupai Tribe filed a lawsuit against Arizona Board of Regents and ASU researchers in 2004, which eventually led to a settlement in 2010.  The tribe received $700,000 and their blood samples were returned.  The situation with ASU and U of A researchers has left an air of mistrust in Native American communities.  As scientists, it’s our responsibility to build trust with the public and maintain open and honest communication.  

 

Peer Edited by Bailey DeBarmore

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Frog Slime: The Secret to Kicking that Awful Flu

 

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Frog slime, although gross, might help combat some strains of the influenza virus.

Got the flu? Time to start looking for your frog prince.

Researchers at Emory University have identified a substance that kills influenza, the virus that causes seasonal flu. The influenza-killing substance, called urumin, is produced on the skin of the South Indian frog and stops influenza virus growth by causing the virus to burst open-think of smashing an egg with a hammer!

Researchers think urumin disrupts a structure on the outside of the virus. Influenza, like an egg, has an outer shell that protects the contents of the virus- the “yolk”- which the virus uses to grow and replicate. Unlike an egg, the outer shell of influenza is not smooth. Instead, it contains small spikes. Urumin sticks to these influenza spikes, interfering with their function and causing the virus to burst open.

The influenza virus uses the spikes to stick to human cells and cause infection. Two types of spikes are found on each influenza virus, H and N. There are multiple types of H’s and N’s, and each virus picks one H and one N to “wear” on its outer shell, similar to the way we choose a pair of pants and shirt to wear every day.

https://pixnio.com/science/microscopy-images/influenza/3d-graphical-representation-of-flu-virus

Cartoon of Influenza. The outside is covered in spikes, H in light blue and N in dark blue.  The coils in the center contain the genetic information or “yolk” that causes the virus to replicate.  From: Doug Jordan.

 

Surprisingly, urumin is only effective against viruses containing the H spike type, H1. This is because urumin can only stick to H1 spikes, not to N spikes or to other types of H spikes. H1 is one of only 3 types of H spikes known to infect humans. Shockingly, H1 viruses are responsible for some of the worst flu outbreaks in history such as the 1918 Spanish flu pandemic that caused 50 million deaths and, more recently, the swine flu pandemic of 2009.

Destroying influenza in a lab environment is great, but what about in a living animal? In the same study, urumin treatment resulted in a 250% increase in mouse survival after influenza infection. Urumin treatment also decreased disease severity by lessening weight loss and decreasing the amount of virus in the lungs.

Although these mouse experiments are promising, it is important to point out that the mice were given urumin 5 minutes before they were infected with influenza and also received urumin everyday for the rest of the infection.  Because most of us do not know the exact moment we are exposed to influenza virus – the grocery store? the breakroom? the gym? – it is difficult to treat someone at the moment they are infected with influenza. Thus, more research is needed to look at the effectiveness of urumin when it is given days after infection, which is the typical time that an infected person might visit their doctor.  

With more research, urumin could be the promising new influenza drug researchers have been looking for, to potentially reduce influenza-associated deaths and complications.

Peer edited by Kaylee Helfrich

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A Call to Guts

I’ve found that it is rather difficult to write an article when you are lying in the fetal position and afraid to move. No, I wasn’t trying to hide from a T-rex. I was having a migraine attack, and what really kept me curled up was its good friend and accomplice, nausea. According to a 2013 study, over half of migraineurs suffer from this additional punch to the stomach during the majority of their attacks. Is this collection of symptoms merely a coincidence, or are the brain and stomach in cahoots to make people miserable?

The brain “communicates” back and forth with the gastrointestinal tract via neuronal, immunological, and hormonal signals, forming what is now called the gut-brain axis. The link between the immune system and microbes within the body has already been well established, and has recently begun percolating into the mainstream media. For example, podcasts are discussing fecal transplants (yes, really) to combat gastrointestinal disease, and the hygienic hypothesis has parents thinking that maybe they should let their kids eat dirt every now and then to avoid developing allergies. Only recently has the contribution of the brain been thrown into the mix to form the microbiome-gut-brain axis.

The mutual communication between the gut (enteric nervous system) and brain (central nervous system) was discovered serendipitously, with a fascinating backstory. As scientists were attempting to form a link between the immune response, stress, and disease, they discovered that mice, when fed a bacterium that does not trigger the murine immune response but that makes humans sick, exhibited more anxious behavior. Meanwhile, animals raised in germ-free environments were less anxious. As interest in the link between behavior and biota grew, more associations between gut bacteria and emotional changes or changes in an animal’s ability to learn were discovered. This line of research has been taking off ever since.gutbrainaxis

According to PubMed, “gut-brain axis” publications per year recently nearly doubled from 75 (2014) to 146 (2016), and over 70 have already been published in 2017. Thanks to this fervor, preliminary evidence is popping up everywhere linking the microbiome, which is predominantly focused in the gut, to neurological disorders from anxiety to Alzheimer’s disease (reviewed recently in Cell). This is also jumping into the mainstream media, with such catchy headlines as, “A Yogurt a Day Could Relieve Depression.” Always remember to take such information with a grain of salt, as this information is preliminary.

So why did it take so long to find the link between this system? More often than not, scientists have been approaching the human body much like the Blind Men and the Elephant parable*: A neuroscientist grabbed a tusk and an immunologist grabbed a tail. While each scientist can make valid conclusions based on their own observations, neither can fully understand the elephant by themselves. Likewise, if scientists had continued studying the gut and the brain independently, without also considering behavior and learning, we would still be blind to their reciprocal relationship. Now, by investigating neurological health problems from a gastrointestinal point of view and vice versa, we can potentially double the chances of finding treatments for each. There is hope yet for my migraine.

*Special thanks to Dr. Keith Kelley, editor-in-chief of Brain, Behavior, and Immunity for using this in his talk at the 2016 Triangle Society for Neuroscience Spring Meeting!

Peer edited by Rachel Haake.

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The Amazing Microbiota of Brown Bears

http://www.cell.com/cell-reports/abstract/S2211-1247(16)00047-4

A brown bear’s seasonal cycle.

Image a researcher has been tasked with studying how hibernation affects a bear’s microbiota, or the collection of microorganisms residing on and in an organism. The researcher begins his day tracking brown bears until he finally finds one in a cave. His trusty veterinarian partner shoots a dart containing a potent mix of tranquilizers and narcotics at the bear. After waiting for the drugs to work, he cautiously moves towards the animal, kneels down, and collects a fecal sample straight from the bear’s rectum, sweating and praying that the bear won’t wake up to murder him.

At least that’s how I imagine the field work went for a study in Cell Reports on the gut microbiota and energy metabolism of Eurasian brown bears during hibernation. Brown bears switch between periods of heavy eating in the summer and fasting for up to half a year in the winter, during which time the bears do not eat or defecate and only urinate intermittently. Despite this extreme weight gain and obesity in the summer, bears remain metabolically healthy.

The researchers wondered how a bear’s microbiota changes throughout the seasons and how this might contribute to a bear’s healthy weight gain, and found that the bear’s gut microbiota and metabolism change with each season cycle. The researchers inserted the bears’ microbiota collected from either summer or winter into specialized mice. Soon, the mice’s own microbiota began resembling that of its summer or winter donor. Mice receiving the summer microbiota gained more fat and tended to be heavier. However, despite this increased fat mass, their glucose (sugar) tolerance was not impaired. In contrast, increased fat mass is associated with insulin resistance in humans. This suggests the bear’s microbiota plays a role in maintaining a healthy metabolism throughout its life cycle, despite extreme seasonal fluctuations in their body mass and energy metabolism. That is, the summer microbiota allow the bear to eat more without sacrificing its health. 

Studies like this one underscore the importance of studying bear biology, as it may lead to advances in how we treat disease. Imagine if we attempted to mimic a bear’s yearly cycle. We would likely suffer from kidney failure, cardiovascular disease, and muscle loss, among numerous other conditions. Yet, miraculously, brown bears avoid all these conditions, with help from their gut bacteria. This study provides a link between a bear’s healthy obesity and its gut microbiota, which suggests that the gut microbiota may be an effective target for treating obesity. So next time you see a bear, thank him…and then play dead to avoid getting killed.

Peer edited by Rachel Haake

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Are Stem Cells Just Tiny Normal Cells?

You’re at a social gathering and someone asks, “So, what do you do?” It’s meant to be a casual conversation starter, but do you ever find yourself taking a mental breath before answering? As an immunologist studying stem cells, I take that mental breath to prepare for a dialogue that usually follows about stem cell research, a field that has captured my fascination… and seemingly many of yours.

Anyone who knows me well can attest to the fact that I like questions; in fact, as a scientist, my livelihood relies on it. I enjoy asking questions, and I admire those who ask questions in return. Someone recently continued our “So, what do you do?” chat by asking, “What even is a stem cell: just a tiny normal cell?” What a great question! What exactly is a stem cell?

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Drug Resistance 1-2-3

Recently, I read an article in The Atlantic by Ed Yong, an experienced science writer whom I admire. In this article, Mr. Yong describes a study commissioned by the Wellcome Trust, designed to probe the public’s understanding of drug resistant infections. The conclusions of the study are troubling: the public does not understand the basics about antibiotics. Continue reading