Lab Notes

Netflix recently released a medical reality series called Diagnosis.  The show is based on Dr. Lisa Sanders' column in the New York Times, in which she uses the NYT's unparalleled readership and reach to crowdsource diagnoses for patients needing answers.

The first episode follows Angel Parker, a young woman dealing with excruciating pain that keeps her from working and even walking. Her pain is severe and intermittent, and comes with dark “Coca-Cola” colored urine. After years of hospital visits, Parker still had no answers.

Dr. Sanders wrote a description of the case and turned it over to the masses, collecting over 1000 responses from doctors, patients, veterinarians, and hobbyists ⁠— anyone who read the article was free to submit their opinion about what was ailing Parker. Among the possible diagnosis was a disease that stuck out to both women:  carnitine palmitoyltransferase 2 deficiency, or CPT2 deficiency.

CPT2 is a metabolic disorder in which patients can’t break down certain fatty acids, leading to muscle damage. To fuel a typical human day, the body relies on two sources of energy: carbohydrates and fats. Carboydrates are easier to burn, so those usually get used up first. But, what happens when the body needs more energy than expected?

If a person is exercising, or fasting, their cells turn to stored fats for a boost of energy. But in CPT2 deficiency, that system is broken and the body's cells are incapable of transporting fatty acids. Without this source of energy, muscle cells break down. That breakdown overwhelms the kidneys, darkens urine, and triggers  excruciating pain.

This is exactly what Parker had, but she had to travel to Italy to find out. A team of doctors in Turin ran a gamut of metabolic and genetic tests to conclusively diagnose her with CPT2, giving her a satisfying ending to a long and painful medical struggle. And luckily, CPT2 can be fairly easily controlled by reducing fats in the diet. 

But to me, the most striking detail about Diagnosis was not the metabolic disorder, but rather the show's subtext about healthcare in America. Parker suffered for years with no clear diagnosis. Even worse, she apparently had no screens for metabolic disorders at all (CPT2 is rare, but common enough that I originally learned about it from an undergraduate biochemistry class). Worse still, she says that she is deep in debt, being sued by doctors, and considering bankruptcy. 

I’m not a doctor. I’m also not an economist. But when it makes more sense to fly halfway across the globe for a diagnostic test, it shouldn’t take either to see the underlying problem.   

Normally when we think of viruses, we think of how they make us sick and miserable. But what if we could make viruses work for us, instead of against us? That’s exactly what John Hales and his team did at University College London: They took viruses and turned them into lasers.

While this sounds like a sci-fi villain’s dream, it promises to be a force for good. Hales’ group works on bacteriophages, a type of virus that only infects bacteria. They have engineered a specific type of bacteriophage to express a fluorescent dye on their protein coat: in other words, they literally glow, allowing scientists to track them. These phages can be programmed to attach to a broad array of targets such as proteins and DNA. 

The florescent dye is what makes the virus a laser. Once inside the target, the virus can emit a detectable pulse of light, making it really easy to find the protein or DNA region of interest. 

An important application of this technology is in blood and urine  diagnostics. When tested, the viral lasers could clearly detect clinically relevant concentrations of antibodies. This exciting marriage of synthetic biology and physics is still being optimized in the lab, but it may one day replace the current diagnostic tools in clinics and doctors’ offices. 

The National Cancer Institute (NCI), part of the prominent National  Institutes of Health (NIH) funding agency, has now joined the movement towards open access publishing.

The open access model for publishing research is a simple idea: anyone should be able to access free peer-reviewed scientific publications, as opposed to research articles being hidden behind a paywall. Many advocates for open access argue that the taxpayers who contribute the tax money that supports the federal grants funding research should have access to the information.  Opponents say that the business model of open access journals isn’t sustainable and can hinder publishing by putting too much financial burden on the researchers doing the science, who have to pay to get their manuscripts published. While the open access movement has gained many supporters, some of the most  prestigious “brand name” journals still place their publications behind an extremely profitable paywall.

But institutions and funding agencies are making changes to their policies that may have the power to tip the scales towards supporting open access publishing. Back in November of 2018, Science Europe launched their Plan S initiative, backed by a coalition of 18 funding bodies, which will require every scientific publication originating from research they’ve funded to be publicly available. Earlier this year, the University of California system, one of the largest public research institutions in the world, broke their agreements for access to paywalled publications with the powerhouse publisher Elsevier.

Now NCI, a $1.8-billion research initiative, has also decided that they will require any research funded by them to be immediately accessible upon publication. Beyond NCI, the NIH (a $5.7 billion institute with substantial funding power) doesn’t require this of any other program, but maybe it’s finally not too crazy or hopeful to expect this in the future. While it’s hard to predict what lasting cultural changes these events might trigger, I believe these bold decisions reflect the fundamental belief that knowledge should be shared openly and transparently for scientific discoveries to achieve their greatest impact. 

More than 84 million Americans are at an increased risk of developing type 2 diabetes in adulthood. During recent years, low blood levels of vitamin D have surfaced as a potential risk factor for type 2 diabetes. However, until recently it was unclear whether vitamin D supplementation could help prevent type 2 diabetes. A group of researchers in the United States, working on the D2d (Vitamin D and Type 2 Diabetes) study, just published the results of a randomized placebo-controlled clinical trial that helps answer this question.

As part of the D2d study, researchers tracked 2,423 pre-diabetic patients, who received either 4000 IU (International Units) per day of vitamin D3 or a placebo for approximately 2.5 years. They found that vitamin D3 supplementation at the administered dose did not result in a significantly lower risk of a participant developing diabetes, compared to those participants who took the placebo. 

So while type 2 diabetes actually may not be prevented by vitamin D supplementation, persons at high risk for type 2 diabetes who are overweight or obese can still prevent or slow the progression to diabetes by incorporating lifestyle changes such as weight loss and physical activity. 

All dog owners know how difficult it is to stay upset with their beloved pets, even if Rover is behaving badly. Something about those puppy dog eyes just melt away the anger. Researchers at Duke University have now worked out a potential explanation for why we fall for “those” looks from dogs but less so from wolves, their close relatives.  

The domestication of dogs took place around 33,000 years ago.  The Duke researchers identified a muscle in dogs' facial anatomies that is used to raise the inner eyebrow. Wolves do not have this muscle, which suggests that humans selected for it during domestication.  

When dogs use this facial muscle, it actually makes them appear more relatable and sympathetic to our emotions. This phenomenon where the dogs mimic human behaviors is called “paedomorphism," and it gives animals that have it a selective advantage over their counterparts. This means that, over thousands and thousands of years, we humans preferentially bred dogs that had the muscle, and today all of them do. 

Unlike some forms of artificial selection, like farmers purposely creating varieties of corn that are adapted to very wet or dry soils, humans probably didn't select animals specifically because they had a strong inner eyebrow muscle. But, according to the Duke researchers, this feature triggers a subconscious impulse in us to nurture them, making them cuter and more snuggable in our eyes, which is likely why it exists only in today's dogs and not in wolves. 

Your roommate bursts through the door, throws her bag down onto the kitchen table, and storms into her room. How do you think she's feeling?

We can generally guess people's emotions based on their facial expressions and body language. Your roommate's body language  provides pretty clear clues that she's probably feeling angry. But in some situations, physical cues could be ambiguous, like if you smile nervously or cry because you're happy. That's why people can't rely on facial expressions or body language alone — they consider the context too. But can people accurately guess the emotions of someone they can't see, based only on the setting the person is in?

In this new study by UC Berkeley scientists, they set out to figure out how context helps people identify others' emotions. They showed videos in which one person's face and body were masked to study participants. The researchers then asked the participants to predict the invisible person's feelings based solely on the context of the visual scene they were in. Context clues included factors such as the spatial configuration of the people in the video, the behavior of other people in the scene, or the type of interactions other people have with the invisible character.

They discovered that people can infer and track an invisible person's emotions based only on context. These results suggest that we need to update emotional intelligence tests to include context clues, not just static pictures of faces with no background or movement. The researchers also suggest that we could  improve computer vision, a technology that, among other features, allows machines to infer people's emotions in social profiles or security footage. 

Every day, 20 people in need of an organ transplant die because there are no viable organs available for them. One idea to mitigate this shortage is to manufacture organs in the laboratory. In an exciting advancement, a research team at Carnegie Mellon University printed 3D beating heart tissues.

3D bioprinters allow scientists to control the exact placement of multiple cells and proteins in a defined architecture which could be ideal for copying the complicated structures of organs. In practice, bioprinting organs has been limited, partially because creating holes in a tissue (such as a channel for a blood vessel or the chambers of the heart) requires a removable scaffold to hold the cells in a particular shape during printing, but that can also be removed without disrupting the tissue structure. 

Published in Science, the researchers developed a method that uses gelatin microparticles as a scaffold during bioprinting. The gelatin bath is a semi-solid jelly that melts away at body temperature. Using this scaffold, the scientists precisely print pre-defined shapes with collagen, a structural protein that surrounds cells within body, then melt the gelatin, leaving a collagen structure behind. The precision of this technique allowed the researchers to print a full-sized replica of an infant heart with the collagen, demonstrating the accuracy of the technique to print delicate, complicated structures.

While this scaffolding method may solve structural limitations of bioprinting, the organs must also be functional. Heart muscle cells must contract rhythmically to pump blood. In living hearts, an electrical pulse moves through the heart cells, causing the entire heart to contract and making blood flow through the body. 

In this study, the scientists printed a millimeter wide cup-shaped heart ventricle. Heart muscle cells added within the walls of the printed ventricle began to contract within a few days, and by pulsing the tissue with an electrical signal, the scientists got it to beat like a real heart. 

To print a heart, you need blood vessels, heart shaped structures, and a beating tissue. Now we just need to bring these pieces together into functional organs that integrate heart muscle and the other cells of the heart. This advancement in printing collagen into physiological structures serves as an exciting tool for the field moving forward, bringing us one step closer to making organs in the lab.

Patients in need of life-saving organ transplants can spend years waiting for a suitable donor. The ultimate solution to the organ shortage crisis may be the development of processes to grow healthy transplant-able organs in the lab – and for some, this means growing human organs inside animal hosts.

Chimeras, creatures containing parts from multiple animals, are not a new concept in biology. Chimeras can even arise naturally: on occasion, two fertilized eggs occupying the same womb can fuse and eventually develop into a single organism. However, the creation of hybrid chimeras with cells from two different species tends to give us pause, especially when the hybrid is part human. Such experiments blur the boundaries between human and animal that we use to justify animal experimentation in the first place, raising difficult ethical and philosophical questions.  

Earlier this year, Japan lifted its ban on bringing human-animal hybrid embryos to term (scientists had previously been required to abort such embryos after 14 days), and Japanese scientists are taking advantage of the new legality of hybrid experiments to attempt to grow human organs. The strategy is to deprive the host animal embryo of its ability to form a specific organ of its own, instead providing it with human cells, with the hope that the host animal will then use the human cells to build the organ it lacks. 

Time will tell whether this approach will be successful, but there's so much to consider here ethically. For instance, it is possible that the human cells get integrated into other organs inside of the host animal. We need to somehow reconcile our cultural concepts of humanity with our views on other animals before biotechnology forces us to take positions on fraught ethical issues.    

Is the peer review system broken? Many scientists, reporters, and even editors of peer-reviewed journals have weighed in extensively on this question, so I’ll let their words speak for themselves. I did, however, think of a slight permutation to  the question after seeing a recent Tweet from virologist John Schoggins about his inability to recruit a peer reviewer over the summer.

It made me wonder: Do peer-reviewed journals go through a summer slump just like we do? In other words, does it take longer for a study to be accepted, edited and published when it’s submitted in the summer?

Unfortunately, I wasn’t able to find a peer-reviewed study on this topic, but I did find several discussions in fora for scientists that supported my hypothesis that summer slump for the peer review process is indeed a real thing. One article proposed that many potential reviewers are on vacation during the summer. Another poster on the topic posited that the delays may actually be caused by journal editors who are away. 

I also discovered a couple of blog posts published by the peer-reviewed journal conglomerates PLOS and Cell Press that explicitly mentioned summer delays. Both journals observed that  submissions tend to be highest in summer months — a trend that Emilie Marcus for Cell Press guessed was a combination of theses defended in the spring, professors with newfound free time, and “inspiration/competitive angst” from the science presented at summer conferences.

All this is to say that you, the scientist, can take back some control of the process of getting a paper published. And if your paper is already stuck in the peer review summer slump, know that you’re not alone! It’ll get better in September after reviewers and editors get back in the swing of things. 

 A recent Massive Science article by Adriana Romero-Olivares  highlighted the fact that many fungal and protist species are missed in microbiome studies, which tend to focus heavily on just bacteria. If this doesn't change, we might miss out on a lot of important discoveries. But now, a new paper in Nature, led by Marcus de Goffau and Gordon Smith of the University of Cambridge, U.K., shows that the opposite is also true: some microbiome studies are finding microbes that aren't actually there at all! 

Ed Yong explained this finding in his excellent piece for The Atlantic. A 2014 study claimed to find a defined microbiome in the human placenta, an environment previously thought to be sterile. This surprised scientists, who had long thought that we are colonized by our microbial friends soon after birth, based on the fact that babies delivered by C-section take a lot longer to develop a stable and healthy microbiome than babies born vaginally. The paper made waves back then because, if the placenta itself were also colonized, this would certainly change our view on when and how the human body becomes host to a complex microbial ecosystem.

But the recent Nature paper by de Goffau and colleagues strongly challenges the published observation of a placental microbiome. They showed that there were reproducible microbial contaminants in the equipment and reagents used in the 2014 study, a nightmare scenario for lab-based scientists. Knowing that this type and scale of microbial contamination is possible in microbiome studies is hugely important, and encourages a healthy level of skepticism among readers of such studies. 

Although the whole thing might seem like an embarrassing oversight to some, rest assured that this is how science should work: we test our colleagues' work and refine our findings based on the data. Mistakes and misinterpretations happen, but we are always in search of the truth.

The last major Zika virus outbreak began in 2015, which was also the year that Brazil identified a link between the virus and brain damage in developing fetuses. Zika is a mosquito-borne disease that usually causes minor illness in infected patients, but transmission of the virus from an infected mother can cause her growing fetus to be born with an abnormally small head and brain damage, a condition called microcephaly. There is currently no treatment for Zika, nor is there a way to prevent fetal infection.  

Now, a team of researchers from Johns Hopkins University has found that Kineret, an anti-inflammatory drug used to treat rheumatoid arthritis, may protect infected fetuses from brain damage. We previously knew that inflammation in the fetal brain can cause lasting damage, and that Kineret had been found to prevent fetal brain damage after other kinds of infections.  So the researchers infected pregnant mice with the Zika virus, then treated some of them with Kineret. At five days old, the pups of untreated mice had impaired motor and cognitive skills while pups whose mothers had received Kineret showed normal development. Unsurprisingly, the treated pups also had less inflammation in their brains. Kineret also reduced inflammation in and promoted normal developing of the placenta. 

Kineret is a well-characterized drug that appears to be safe to use during pregnancy, which smooths the path toward its potential use in Zika patients. Thanks to the Johns Hopkins researchers and some pregnant mice, we just may be more prepared for the next  outbreak.  

After Democratic presidential candidate Marianne Williamson’s controversial claims about medicine and healthcare, individuals with chronic illnesses took to Twitter under the hashtag #iNeedMyMedsMarianne to raise awareness of how medication improves their health and quality of life. One meme circulated by some of these Twitter users, many of whom suffer from  psychiatric illnesses, contains the following slogan: “If you can’t make your own neurotransmitters store bought is fine.” The well-intentioned meme was meant to reduce the stigma against psychiatric drugs. However, this assertion is false: these medications are not “store-bought neurotransmitters.”

Neurotransmitters are chemicals that help signals travel between nerve cells, helping to regulate thoughts and emotions. Many mental illnesses occur when levels of neurotransmitters in our brains get out of balance. No current psychiatric drug produces new neurotransmitters, but they can change how much or how little is available at any one time. 

For instance, depressed patients have too little of the neurotransmitter serotonin in the brain. Selective serotonin reuptake inhibitors (SSRIs) prevent serotonin from being reabsorbed back into the cells, while the older antidepressant drugs, called monoamine oxidase inhibitors (MAOIs), block the enzyme that helps break down serotonin. 

Some psychiatric illnesses, like schizophrenia, result from too much serotonin and dopamine rather than too little.  Antipsychotics work by blocking the receptors of these chemicals on the nerve cells, preventing the cells from being overloaded.

This misunderstanding of psychiatric drugs as “store-bought neurotransmitters” or otherwise made of the same "stuff"  as neurotransmitters may seem minor, but it isn’t. People who claim to be on the side of science and medicine need to demonstrate that they know what they’re talking about, or they (and the rest of us scientists) won’t be taken seriously. And the reality is that, because the brain is so complex, scientists simply don’t yet know the best way to treat psychiatric illnesses. The drugs available today were discovered through serendipity and don’t work for every person. Unfortunately, no patient can simply buy neurotransmitters off the shelf, the way a diabetic can take insulin. Anyone who uses psychiatric drugs should know what they actually do and why. 

Did you know that the brine used to make pickles is saltier than seawater? While this gives pickles their delicious taste, it also creates concerns about the water waste – the salt concentration in pickle brine exceeds the EPA’s maximum limit by about four orders of magnitude.

Most commercial vendors recycle their brine to reduce their waste, but this is only a short-term solution. Eventually, the brine loses enough salt in the pickling process to be unusable, but is still salty enough to be bad for the environment. And considering that a  2018 Forbes article reported that an estimated 245 million Americans will be consuming pickles by 2020, the salinity and environmental impact of pickle juice will become a growing concern.

Enter North Carolina State University-affiliated food scientist Erin McMurtrie and her colleagues. Based on a fermentation process proposed by another research team in 2010, they have now used a calcium chloride brine containing acetic acid (the same acid that is in vinegar) to pickle cucumbers. The resulting pickles had firm skin and high rates of sugar conversion to lactic acid, making them flavorful. The firm skin of these pickles was thanks to relatively low abundances of yeasts, molds, and bacteria, microbes which produce cucumber skin-softening enzymes during the traditional fermentation process.  

Using this new brine, commercial retailers can completely eliminate sodium waste and cut the chloride in their fermentation broth by a fifth without sacrificing the flavor or quality of their pickled products. So rest easy, and enjoy a dill pickle – one made in a calcium brine, that is. 

You might think that magnetism is as simple as a north pole and a south pole attracting each other. Yet this phenomenon, silently omnipresent in our daily life, still isn't completely understood, as evidenced by a new study from physicists at the University of Illinois at Urbana-Champaign.

Magnetic fields are created whenever electric charges move, most commonly when electrons spin around themselves. But electrons also orbit around the nucleus of an atom, much like the Earth orbits around the sun. This creates another magnetic field. The combination of the magnetic field from the spin with the magnetic field from the orbiting creates and effect called the spin-orbit  torque. This causes electrons in a current to shear off to opposite sides of a film depending on their spins. Electrons spinning clockwise might move to the top of the sheet, and those spinning anticlockwise to the bottom. 

Scientists previously thought that to create the spin-orbit torque, another metal touching the magnetic film was needed, but this new study suggests otherwise. To show this, the researchers passed a  current from one edge of a magnetic film to the other and measured the spin of the electrons on both sides by shining light onto the film. Since the magnetic surface actually changes the direction of light's vibrations, they could then measure the reflected light to infer the direction of magnetization. It sounds complicated, but the press release for the paper makes it clear that this is "indisputable evidence" in favor of the phenomenon observed, which is called "anomalous spin-orbit torque."

It is exciting that even for something as well-studied as magnetism, we still have discoveries to make. And this research could lead to advances in magnetic-memory technology, which will make computer memory storage faster and more energy-efficient.  

Up to one million species are at risk of extinction, including some 40% of invertebrate pollinators, including bees and butterflies. There have been some biodiversity conservation success stories here in the United States, including the healthy return of the iconic bald eagle and the recovery of the American crocodile. Such stories are largely thanks to the Endangered Species Act (ESA). Originally signed in 1973 under President Nixon’s administration, the ESA has been called one of the most successful pieces of environmental legislation ever. 

We’re still in the middle of a major biodiversity crisis, but now the Trump administration wants to take the cynical and counterproductive step of considering economic concerns when categorizing species — even though prioritizing the economy over nature is what jeopardizes many species in this country. The edits to the ESA would allow for removing species from the endangered list, as well as limiting protections for threatened species. This could accelerate habit degradation and the demise of our country's wildlife. 

I’m studying forest ecology and I worry about the future of forestry in this country. The ESA encouraged sustainable forest management, forcing industry, land managers, and conservationists to work together. The logging industry was able to adapt to these changes and continues to be productive while preserving species’  habitat. But now, if economic assessments predict lost revenue from restricted logging in habitats with endangered species, ESA protections might be overlooked.

Changes to the law are set to go into effect in 30 days. If you are worried like I am, consider calling or writing to your senators and representatives! Endangered species are counting on us.
 

The human brain is hugely complex. There is still much that scientists don't understand about this incredible organ — and the things that we do know can often be hard to visualize and communicate. For the last nine years, the Netherlands Institute for Neuroscience in Amsterdam has run a competition called the Art of Neuroscience, celebrating artwork that powerfully and beautifully illustrates the intricacies of brain biology. This year's winners include a striking installation representing the  neurological links between depression and loneliness, and veins depicted in ways you've never seen them before. Have a look at 2019's top entries, and be both captivated and educated at the same time. 

You can see images like these year-round by following Art of Neuroscience on Twitter.

A largely overlooked area of modern medicine is preventative medicine. In medical schools and rehabilitation fields, we are trained to fix problems, a skill which is hard to apply if the problem is still in the future. However, that is not the way that medicine used to be. Historically, the town doctor took time to know their patients and understand their lifestyle, which was possible because they interacted with their patients more frequently, both personally and professionally, than doctors do today. And while (or, perhaps, because) we see the doctor less than ever before, the collective health of the U.S. population is consistently poor. In fact, every year since 2004, the U.S. has come in last place in terms of life expectancy among the top 11 industrialized countries in the world.

Preventative medicine often results in better personal and financial health for patients. For example, as detailed in the Scientific American article linked above, an otherwise healthy man was repeatedly admitted to the hospital for breathing problems during a scorching Texas summer, spending $60,000 on repeated hospital stays and medical exams. When someone finally stepped back to question why a relatively healthy individual suddenly developed poor lung health and sent a team member to visit the man’s home, they discovered that he lived without an air conditioner, which was damaging his lungs. The fix for this simple problem costed $400. 

Preventative medicine could also help relieve the health and economic challenges that people with obesity-related illnesses face. Routine check-ups with a doctor could catch heart disease or cancer before they become life-threatening. Regular dental cleanings can even be considered preventative medicine! Stopping diseases before they start is the best outcome for patients, and should be the goal of modern medicine.

In the face of constant reports regarding the rapid and rising impacts of pollution and climate change, a call to action can often seem overwhelming. While there is a lot to be said about federal, global, and industry action, the power to incite mass changes isn’t always in our hands. However, there are things that we can do in our everyday lives that can add up.

Swapping a coffee cup with a reusable mug may not seem like a large impact if  you do it once, but what about bringing your own mug every day? If you’re one to drink two to three cups of coffee per day, that’s nearly a thousand coffee cups a year! That will surely cut down on your landfill contributions. According to David McLagan of Ecoffee Cup, "If two million people chose to reuse their cup just once a week, it would save 104 million cups a year." 

Clearly small swaps can add up over time. More importantly, they are stepping stones to larger changes. Setting and meeting achievable green goals can make way for a sustainable lifestyle. If you are understandably overwhelmed and unsure where to start, here are some swaps you can incorporate today:

1. Invest in a reusable coffee mug and water bottle. This can be a real money-saver if you normally drink bottled water.
2. Buy bigger tubs of yogurt and other snacks instead of to-go containers. This requires a few minutes to portion out your food into a reusable snack container, but has the added benefits of saving money and reducing plastic.
3. Carry your own utensils. Having a handy set of travel utensils (and potentially, straws) can reduce plastic waste. Some examples can be found here.
4. Cut down on take-out meals. Those styrofoam containers they are packaged in are bad for the environment and our health, and are hopefully going extinct: Earlier this year, Maine became the first U.S. state to ban styrofoam containers.

While seemingly insignificant in the short term, just a few months of sustainable changes can make an impact. However, research suggests that people often feel satisfied with the small changes they make and forget to support the larger-scale policy and economic solutions that are necessary to save the planet. Congratulations on doing what you have thus far, and at the same time, let's keep our eyes on the prize!

On April 11 this year, the Israeli spacecraft Beresheet was about to land on the moon when it lost contact with Earth and crashed into the moon. Its precious cargo included a DVD-sized archive of 30 million pages of information… and thousands of tardigrades. Tardigrades, also known as “water bears,” are microscopic organisms that can survive under harsh conditions like radiation, extreme temperatures, and dehydration.

So should we be worried?

Without water, the moon is unlikely to support extraterrestrial life. The tardigrades spilled on the moon were dehydrated, meaning that for them to come back from dormancy, they need water - something they can’t get on the moon. (Another source of contamination: Apollo astronauts left 96 bags of human feces on the moon. It’s debated whether the microbes in there are alive or dead.

But for planets like Mars that has potential for supporting life, contamination is more worrisome. A tardigrade spill on Mars could endanger any possible life. This is why space missions to Mars and other moons, such as Europa, undergo sterilization precautions to reduce the chance of microbes from Earth hitching a ride to another celestial body and vice versa. 

Yet, can we actually safeguard against interplanetary contamination? Meteorites have bombarded planets for billions of years potentially transferring microbes from one planet to another. Some scientists think that interplanetary contamination has already happened. But it doesn’t hurt to be careful just in case. 

Bumblebees (Bombus spp.) are the chunky black and yellow insects that dwell in our gardens. Their buzzy nature attracts children, home gardeners, naturalists, and scientists to take a closer look. Bumblebees do not produce large amounts of honey like the other types of bees do, but they are excellent pollinators of crops including cucumbers, tomatoes, squash, and a variety of berries. Unfortunately, bumblebees are in decline, and may eventually disappear all together.

Many European and North American cities have planted linden trees (Tilia spp., which can also go by the common name of basswood) in parks and along roads. These trees have lovely flowers and an "intoxicating" fragrance that attracts insects. However, a new study published last month in PLOS ONE suggests that, despite their appealing flowers, linden trees are killing bumblebees. 

I've observed this myself walking around my campus at the Institute for Insect Biotechnology at Justus Liebig University Giessen in Germany. In the last few days I have seen either crawling and dead bumblebees on the ground around the bases of linden trees. Bee mortality has previously been linked with mannose (a type of sugar) toxicity from the nectar. Bees that depend entirely on these trees are also at risk of starvation, because linden flowers bloom relatively late in the season and so nectar is only available at specific times of year.

The PLOS ONE study ties the story together. The researchers found that the mass death of bumblebees is due partly to ineffective metabolism of linden nectar and partly to a toxin in the nectar that impairs the bees' nervous systems. Specifically, in cool morning temperatures, the energy that the bees get from nectar isn't enough for constant flight, so the bees are forced to crawl on the ground and may not be able to regulate their body temperatures. Also, the linden nectar is loaded with toxic chemicals, so bees that continue feeding on it eventually die. 

The linden trees are just a small piece of the larger puzzle of what is causing bumblebee declines all over the world, but may point researchers working on other causes in new directions. Hopefully we can find a way to save the bumblebees, because they are responsible for much of the nutritious food we humans rely on each day.

Drugs can be incredibly effective or complete duds in different people: One that works for me may not do anything for you. Researchers at Yale have now pinpointed the genetic and metabolic processes of our gut microbes that cause these differences. 

Gut microbes perform a variety of natural functions in the human body, from digesting the carbohydrates in your lunch to producing essential vitamins. In addition, gut microbes also interact with pharmeceuticals – sometimes irreversibly changing the active component and inhibiting its intended function. 

Evaluating how these microbes modify drugs in vivo during product development is difficult, most notably because we have not identified all the microbes, and consequentially active in our intestinal tracts. Drugs treating everything from cancer to Parkinson’s disease show strong evidence of modification or inactivation from gut microbes, and until recently the "how" and "why" of this process was unclear.

Andrew Goodman’s team at Yale University tackled this problem by developing a “gain-of-function” assay. They introduced genes from one well-known bacterial species into E. coli cells and observed which cells degraded or changed a range of chemical compounds, functions that they were not able to perform before the bacterial gene was introduced. They tested a large variety of genes from our gut bacterial microbiome to see which genes encoded enzymes that affected 271 different drugs. 

This experiment and the data they produced offer exciting potential for drug development and disease treatment. For instance, drug developers could use the data to avoid using chemical compounds that are easily digested by common gut microbes. And doctors may eventually be able to cultivate a patient's microbiome and identify the exact reason why some presciption is not working as expected, and then identify drugs that might work more effectively.  

A warmer world with more extreme weather events is here, and things will almost certainly get worse. Scientists are currently working to understand how animals may respond to these new environmental stressors, and particularly want to understand the effects of combined stressors that will likely co-occur in the real world. 

Two commonly occurring stressors that occur in aquatic environments and are often individually studied are high water temperatures and low water oxygen content (hypoxia). A new study by researchers at Canada's University of Guelph looks at the effects of these two stressors in concert on zebrafish embryos and larvae. Specifically, the researchers wondered whether zebrafish had increased tolerance to hypoxia when exposed to high temperature early in life. This could happen through a phenomenon known as "cross-talk," which occurs at the cellular level.

First, they needed to identify if exposure to just high temperature or just hypoxia would elicit similar responses from zebrafish embryos. They measured the average expression of genes from each stress pathway for each group to determine if there were differences in expression between embryos exposed to high temperatures and those exposed to hypoxic environments. They found that either stressor caused an increase in gene expression in the other stress pathway as well, suggesting that there was cellular cross-talk!

Next, to determine if the gene expression differences caused physiological changes for the fish themselves (not just within their cells), embryos from each treatment group were reared until the larval stage and then exposed to hypoxia. The researchers were looking for differences in larval tolerance to low-oxygen environments between larvae that had experienced the high-temperature environments as embryos and those that had already been exposed to hypoxic environments as embryos. They expected that more tolerant larvae would be able to maintain normal levels of activity (e.g. swimming) and have better survival rates than their counterparts at lower water oxygen levels. But contrary to their expectations, there was no significant increase in either tolerance or survival regardless of what conditions the larvae had been exposed to as embryos.

So although there was cross-talk at the cellular level, this did not translate into higher-level differences in zebrafish stress responses. Still, this research opens interesting avenues for better understanding whether animals will be able to increase their physiological tolerances to the warmer and less oxygenated environments that may develop as the climate changes. 

For years, people have been following doctor’s orders of taking a daily dose of aspirin for the primary prevention of cardiovascular disease (CVD). However, three randomized controlled trials published last year set out to determine the efficacy of a daily low dose of aspirin for this indication in adults, and they found surprising results. The associated health risks observed with daily aspirin were higher than expected, with few benefits overall. One such risk is major bleeding. Guidelines from the American Heart Association and the American College of Cardiology were re-evaluated and as of March 2019, they advise against daily aspirin use as a primary prevention of CVD for many adults.

To figure out how many U.S. adults might be affected by the changes, a group from Harvard and Beth Israel Deaconess Medical Center set out to characterize aspirin use for CVD prevention among this population. Based on data from the 2017 National Health Interview Survey, they project that nearly 30 million U.S. adults 40 years old and older used aspirin to prevent CVD despite having no known heart disease. A large proportion of these were self-medicating, which can be dangerous, even with an over-the-counter drug. While patients who have experienced a previous heart attack may still be advised by their doctors to take some aspirin, those with no history of CVD who do are potentially causing themselves harm. 

[Editor's note: This article does not constitute medical advice. If you have questions about using aspirin or CVD, please speak to a medical professional.]

Editor's note: as part of our Massive training, we ask authors to write about one concept for a few different audiences. It's inspired by one of our favorite science storytelling series: Wired's One Concept in 5 Levels of Difficulty video series. Here's one example of the result of this exercise!

Audience: a five year-old

Has your dog ever come home with a seed stuck to its fur, or have you ever thrown out an apple core because you don’t want to eat the seeds? These are both forms of seed dispersal, the movement of seeds to new homes away from their parents. Because seeds can’t walk on their own, sometimes they’re moved by the wind, sometimes by big animals, and sometimes by tiny animals, like ants. Some seeds have a gooey attachment that smells like yummy dead insects to hungry ants. Ants take their new food home to their nest, and the seed goes along for the ride, ending up in a new location where it has a higher chance of surviving and growing into a big plant.

Audience: a college student studying your field

Across the world, different plants have evolved seeds that rely on small but strong ants for movement. The distances ants transport these seeds are often small, under a meter or so, but the benefits can be quite large, as ant nests are often rich in nutrients and safe from predators. However, not all ant species provide obvious benefits to these plants, and some actually exploit the system, eating the juicy bits of the seed without dispersing it, or even worse, eating and killing the entire seed. This variation provides scientists with plenty of questions about seed dispersal, mutualism, and ecology.

Audience: someone with a PhD in your field

Seed dispersal is an important step in most plants’ life cycles, profoundly affecting fitness by determining many of the conditions in which new generations will germinate and grow. Different plants have evolved different strategies for seed dispersal, but one is particularly striking for its specificity of syndrome yet ubiquity across plant families, continents, and habitats. Seeds of around 11,000 species exhibit the same suite of traits that attract ants, which then disperse them with varying degrees of faithfulness. For something so common, we still have much to learn about the different evolutionary pressures that led to such convergent evolution.

In 1990 a Danish Biologist noticed an odd narwhal skull in West  Greenland. The man who had hunted the animal described it as a mix between a narwhal and a beluga. These two types of whales were known to have synchronous mating seasons and close evolutionary history, which added up to a plausible story, but the origin of this hybrid creature could not be confirmed with the technology available.

Flash forward almost 30 years later and we finally have the technology to figure out whether narwhal-beluga whale hybrids really exist. Scientists from the Natural History of Denmark used Next Generation Sequencing (NGS), the results of which were recently published in Nature Scientific Reports. NGS allows researchers to sequence genomes in parallel, instead of one base at a time. This comes in handy when you’re working with a 31 million base-pair genome! But the authors didn’t just sequence the potential hybrid's genome, they also sequenced eight belugas and eight narwhals from West Greenland for comparison. 

Collecting DNA from the 30-year-old hybrid skull was a task in and of itself: bone and teeth contain much less DNA then tissues do, and so the researchers had to collect 0.5 g of bone dust for each  sample. Even from that, they were only able to cover 5% of the total  narwhal-beluga genome. Five percent of 31 million is still over 1 million base pairs. When the researchers compared these sequences to the two whale species, they observed similarities to both narwhals and  belugas. They also used NGS to determine which of the whale species - narwhal or beluga - contributed mitocondrial DNA, which is only passed down by mothers. Their final determination was that the hybrid was indeed a narwhal-beluga mix, with a narwhal mother. Some have even dubbed the animal a "narluga."

There are still so many mysteries about the world's biodiversity to be solved, and NGS will be key in unlocking them!