Lab Notes

Black holes are mysterious objects in space that physicists use as a tool to learn about gravity. On the experimental side, physicists use data from large telescopes to further understand how our universe works. On the theoretical side, the mathematics behind how black holes work have become our main guide towards a more fundamental interpretation of our universe.

Currently, physicists, including myself, are trying to explain the properties of black holes. This turns out to be quite a challenge! One way to tackle this is to use a principle that relates the gravitational theory of black holes to another physical theory called quantum field theory. This principle has become a dictionary of sorts, allowing us to translate ideas about black holes, such as entropy and temperature, between gravitational theory and quantum field theory. 

Recently, a group of scientists has predicted the entropy of black holes on the quantum side using a unique method, called the Cardy limit. The Cardy limit is a limit on the angular momentum of the black hole and corresponds to highly spinning black holes. No one has yet confirmed this method on the gravity side.

My collaborators and I have taken on this challenge to verify that the Cardy limit is valid on the gravity side and reproduces the expected entropy. It turns out this method works best when we zoom towards the event horizon of a black hole — a region of spacetime that acts a bit strange. If we get too close to the event horizon, nothing — not even light — can escape and we are destined to fall into the black hole! Yet, this region of spacetime along with the Cardy limit lead us to the same entropy and other properties of the black hole that were computed on the quantum side.

Our paper is one of many recent results that aim to solve the riddles behind black holes. It is a step towards getting closer to a full understanding our of universe.

In light of rising antimicrobial resistance, scientists have turned to metallic compounds to fight bacterial infections. By sculpting metallic compounds of silver, copper, and zinc into tiny spikes called nanowires, one can essentially stab the bacteria and and prevent them from growing. The design of nanowires was originally inspired by nature: cicadas and dragonflies have similar structures on their wings, helping them curb the spread of harmful bacteria.

Not all bacteria easily fall prey to nanowires, though. A recent study has found that, among Gram negative bacteria, antibiotic resistant and susceptible strains have different mechanical properties. The researchers used atomic force microscopy to determine the stiffness of a host of different types of bacteria. Across the board, they saw that antibiotic-susceptible bacteria were “tougher” and stiffer, able to withstand more poking and prodding. Antibiotic-resistant bacteria, on the other hand, were “softer" and thus more likely to be impaled by nanowires. But what is the reason for this difference?

Beta-lactams, the most widely used class of antibiotics, kill bacteria by preventing them from adding peptidoglycan, a key component for mechanical strength, to their cell walls. When the scientists looked at how strains resistant or susceptible to antibiotics made their cell walls, they found that the softer resistant strains make and use less peptidoglycan. This likely stems from generations of exposure to sub-lethal concentrations of beta-lactams, making the cell walls of antibiotic-resistant strains progressively thinner and softer.

Based on theoretical analysis, the researchers then crafted some nickel-cobalt-based nanowires of different tip diameters. They found that a tip diameter of 5 nanometers — about 20,000 times thinner than a human hair — penetrated the soft antibiotic-resistant bacteria best, but had little effect on the tough, antibiotic-susceptible bacteria. This is a promising development toward a potential solution to the pesky problem of antimicrobial resistance.

It’s this time of the year when those of us in northern temperate zones are spectators of a fascinating natural phenomenon – the appearance of autumn leaf colors.

The leaves start to change colors as they age, or senesce. During this period a cluster of enzymes in the leaves start chewing up their green pigment, called chlorophyll. As the leaves become less green, their red, yellow, and orange pigments (known as anthocyanins and carotenes) begin to shine. However, exactly how chlorophyll breakdown works is still only partially understood.

While autumn leaves are a great example of chlorophyll breakdown, evergreen plants (those that remain green all year long), vegetables, and fruits also experience chlorophyll decay. However, this happens only under special conditions such when fruit ripen or when evergreen plants are deprived of nutrients and water. 

Banana skin is one of the few fruits where chlorophyll degradation can be mapped under ultraviolet (UV) light. As bananas ripen, their skins lose their green color – a sign of chlorophyll breakdown – and form new pigments that fluoresce blue under the UV light. Scientists know that this new pigment, known as hypermodified fluorescent chlorophyll catabolite (hmFCC), is produced very briefly in most plants. Banana skins and grapevine leaves are known to produce hmFCCs for a longer period.

Recently scientists at Instituto de la Grasa, Spain analyzed devil’s ivy, an evergreen plant, in their quest to find signs of this fluorescent compound. They activated the aging process by starving the plant, and voila! Exposure to UV light produced the blue, fluorescent pigment hmFCC. The team also observed two other newly identified compounds that will provide more insights into the evergreen chlorophyll breakdown puzzle.

Although the actual benefit of producing this blue, fluorescent compound is still a mystery, scientists think that it could provide protection against radiation or function in communication between animals and plants.

The trillions of microbes in our guts connect the food we eat to the rest of our body, playing crucial roles in stress and health. Some dietary fibers in our food are digested by these microbes to generate signaling molecules.

Millions of people worldwide struggle from stress and associated burdens. A group of researchers from the Translational Research Center in Gastrointestinal Disorders in Belgium tested whether dietary fiber could modify our stress responses. These fibers are converted to signaling molecules called short-chain fatty acids (SCFAs), that may attenuate stress.

For one week, 66 healthy male subjects were given a pill containing the amount of fatty acids found in either 10 or 20 grams of fiber, or a placebo. Before they received their treatment or placebo, participants were stressed to get a baseline measurement.  To stress out these subjects, researchers used a common experimental paradigm that combined social and physical aspects of stress. Participants kept their hand submerged in cold water for two minutes, while being closely watched. They were told that their facial expressions were monitored. Afterwards, the researchers took blood samples to look at the stress hormone cortisol, as well as SCFAs at different points after the stress.

They discovered that the greater the dose of fatty acids a person received, the smaller the cortisol-stress response (meaning, that person had less cortisol in their blood in response to the stressful event), and the more SCFAs in their blood.

This study shows that eating more fiber could attenuate the acute stress response. Future studies on this topic could establish a dietary intervention that doctors could prescribe to lower high blood pressure associated with stress.

Most mammals stop being able to digest lactose — the main sugar in milk — past infancy. But an estimated 35 percent of the world's population retains lactose tolerance, or lactase persistence, past childhood. During infancy all mammals produce lactase, an enzyme that breaks lactose down into simpler sugars and allows its digestion, but around weaning time they stop producing it.

This lactase persistence is due to genetic mutations that keep bodies producing lactase well past childhood. There are several mutations known to have arisen independently in human populations the last 10,000 years. Today the trait is unevenly distributed in the world and can be more or less frequent in the populations depending on their ancestry. Previous studies have found that the evolution of lactase tolerance shows signs of positive selection — indicating it must have conferred an advantage to its bearers. 

A new study published in Current Biology using genetic analyses and bones from Bronze Age archeological sites dated from 5980 to 3200 years ago brings new information about the evolution of this trait.

Northern Europeans show a high frequency of a specific mutation, called rs4988235-A, that confers lactase tolerance. An international team led by Joachim Burger from Johannes Gutenberg University in Germany, studied gene variants from DNA extracted from bones of warriors found in the Tollense battlefield archeological site in Germany dated to 3200 years ago. The analysis revealed they belonged to Central/Northern European individuals. They also analyzed bones from an archeological site in Serbia dated 4100 to 3700 years before present, and from sites from the Eastern Europe Pontic-Caspian Steppe dating back 5980 to 3980 years.

Lactose tolerance in the Central/Northern European samples was low (7.1 percent), contrasting with present-day levels of 90 percent lactose tolerance in the same region, and it was also low in the South Eastern samples (4.6 percent). The trait was absent in the samples from the 37 individuals studied from the Eastern Europe steppes. This does not support an existing hypothesis that proposes that this mutation, rs4988235-A, originated at the Eastern European steppes. Although the sample sizes were small, the results indicate an big increase of lactose tolerance frequency in just the past 120 generations. 

You may have heard that President Donald Trump is sick with COVID-19. He immediately received an experimental "polyclonal antibody" cocktail made by the large biopharma company Regeneron. This treatment has not yet been evaluated by the FDA. 

When our immune systems begin generating antibodies to a foreign object, they don't generate just one kind of antibody. They generate many, many different kinds, that have different structures and also target different individual pieces of the thing it's attacking (through a genetic mechanism unique to the immune system, immune cells can shuffle the genes that code for a "variable" region of an antibody like a deck of cards, generating antibodies of variable shape and targeting). So, in the case of SARS-CoV-2, our immune systems might generate one antibody that attacks the spike protein, while another antibody that attacks a part of the viral envelope. Or, they might generate multiple antibodies that all attack different parts of the spike protein. 

To create this antibody cocktail, Regeneron created "humanized" mice, which had immune systems more closely related to the human version than their natural mouse immune system. Sifting through antibodies from these mice after infection with SARS-CoV-2 and antibodies from humans who'd recovered from infection, they isolated two antibodies that targeted two different parts of the virus. 

It's called "polyclonal" because it's a mix of genetically distinct antibodies (with different targets). A collection of genetically identical antibodies that all attacked the same thing would be called "monoclonal." Whether this truly "polyclonal" or "two monoclonal antibodies mixed together" is a somewhat academic debate, in my mind.

The idea is that the antibodies shouldn't block each other out (imagine two people reaching for the same doorknob) and will hopefully have a combinatorial effect. The cocktail is still in trials but has some positive data. 

Until recently people believed pancreatic ductal adenocarcinoma (PDAC), the most common and lethal pancreatic cancer, to be a single cancer type. In the last few years, subtypes of PDAC have been discovered, providing potential for treating each subtype as a different disease. This is important in PDAC as most patients don’t respond to current treatments.

Unfortunately, the PDAC subtyping methods were not useful in the clinic as they have been developed in a group dependent manner, where subtype is determined based on groups of samples. The addition or removal of a single sample to the overall group could change any other sample’s subtype.

One study set about to change that and develop a method to subtype a single patient. The researchers first determined they would try to create a single sample method to break patients into classical or basal-like subtypes, because classical patients respond better to therapy. Therefore, if doctors could tell if a patient was classical or basal-like, they could choose different treatment option.

Researchers created a system of gene pairs, where one first gene is present in classical patients, and the second gene is present in basal-like patients. Think of these pairs as light switches. Depending on which way the light switch points, a sample can be classified as one subtype or the other. With just 16 genes, they method is inexpensive and easily applied in a clinical setting.

Overall, researchers managed to create a clinically actionable subtyping system which has recently been adopted into the PanCAN Know Your Tumor Program and the Precision Promise clinical trial. The hope is that trials will be able to identify which patients will respond to their therapies as well as to create subtype specific therapies, similar to breast cancer where treatment is specialized by subtype.

Ostracods are tiny crustaceans that have existed for almost 500 million years. Also known as seed shrimp, these organisms are covered by a hard shell that tends to fossilize easily, allowing scientists to piece together a detailed picture of their exceptionally long history.

While hard parts of animals like bones and shells generally preserve well, softer components like organs and fluids are much more rare, making it difficult to learn about aspects of life that we can’t see. But a team of scientists recently uncovered a cache of ancient ostracods with many of these soft physical elements intact.

These ostracods were found in a village in Myanmar, nestled within a small chunk of amber estimated to be 100 million years old. Of the 39 ostracods present in the amber, 31 belong to a new species, which the team named Myanmarcypris hui.

To peer inside these tiny organisms without damaging them, the team left the ostracods inside the amber and X-rayed them at a high resolution. When they analyzed the images of an adult female M. hui, they found something shocking: coiled threads of sperm.

The previous record holder for oldest ostracod sperm was a 17 million year old individual from Australia, while the oldest sperm ever discovered was from a 50 million year old worm. But this 100 million year old sperm surpasses both records.

And this sperm isn’t just old — it's giant. The team found that when uncoiled, it would have been almost half as long as the animal itself. These megasperm would have had an advantage as they raced through the long coils to the female’s eggs, a strategy that is also found in fruit flies.

Finding such ancient, giant sperm shows just how successful this reproductive strategy has been over the last 100 million years. It also provides a snapshot of a singular moment deep in the past — one that occurred in a world that looked very different from our own, and is still occurring among ostracods today.

In a paper recently accepted in Nature, a team spanning several departments at Yale University and from Howard Hughes Medical Institute investigated differences in immune responses between men and women diagnosed with COVID-19. 

Different immune responses between males and females have been documented previously, but whether and how these immunological differences influence people's responses to COVID-19 have yet to be well-documented. Such distinctions may offer unique opportunities to better predict and monitor patient outcome and tailor therapeutic intervention. 

This team of researchers collected blood, nasal swab samples, saliva, urine, and stool from people recently admitted to the hospital who had tested positive for COVID-19. They determined the types and population sizes of specific immune cells, such as B cells, T cells, and monocytes in the samples. They also investigated the amount of molecules responsible for inflammation and cell recruitment, called cytokines and chemokines, respectively, detected in patient serum. These were compared between male and female patients as well as male and female health care workers, who served as non-infected controls. Finally, they evaluated how these factors were correlated the severity of each patient's COVID-19 symptoms.

They concluded that male patients developed lower T cell responses, specifically in a subset of T cell responsible for killing infected cells. Disease severity was greater over the course of infection in male patients who exhibited lower responses of this cell type. In female patients, disease severity was more determined by elevated inflammatory cytokines and chemokines. 

Furthermore, older males had worse disease outcomes, correlating with the less robust T cell responses in this population, while this trend did not hold true for females. 

This study provides important preliminary understandings of the difference of responses between males and females during COVID-19 infection. 

On top of Volcán Llullaillaco in northern Chile, scientists captured the yellow-rumped leaf-eared mouse at 6,739 meters above sea level (22,000 feet). The small creature, whose identity was verified through DNA sequence analysis, holds a big record: highest dwelling mammal in the world. It was found far above the hypothesized altitudinal limit for mammals of 5800 m (19,000 feet). 

Life at such high elevations is physiologically taxing, so these mice raise big questions. Have they evolved adaptations to low-oxygen compared to their lower dwelling relatives? And perhaps more puzzling, what are they eating at an elevation over 2000 m higher than green plants survive? This discovery highlights how much we still don’t know about high-elevation ecosystems and the organisms that live in them. 

Host-plant interactions have long been a topic that intrigues scientists. However, for smaller species, like insects and their larvae, it has not always been possible to conclusively identify interactions. Just because you find a larva in a certain tree, doesn’t necessarily mean that tree is itself the larva's meal of choice. It could very well be eating lichens, mosses, fungi or other much smaller species associated with the larger plants. 

But now, thanks to advances in DNA sequencing and the vast DNA reference library datasets, scientists now can turn to genetics to confirm associations and make new insights into the world of insect-plant interactions.

That is what three research groups in Germany (Bavarian State Collection of Zoology, University of Würzburg, and Advanced Identification Methods Gmbh [disclosure: I work for AIMG]) are piloting on a large sample of caterpillars from Peru. They sequenced a specific gene in each of 119 individual caterpillars that matched to 92 species in the database. DNA from the caterpillars' guts revealed that these caterpillars feed on many plant species, including lianas (a type of climbing vine) and mosses. Around 80% of them did not have the DNA of the trees where they were found in their gut content. 

Scientists are still trying to optimize the whole protocol, but this methodology shows a new way of looking into host-plant and food web interactions, and informing species diversity for conservation efforts. Now that they know this system works, their future plans include identifying much bigger datasets of arthropod groups and their hosts.

New memories undergo a period of consolidation to become stable and long-lasting in our brains. However, when we recall a new memory, it becomes unstable and susceptible to change. To persist, a memory undergoes a process called reconsolidation thought to make it stable again.

Memories from stressful situations do not become unstable after recall, and changes during the consolidation of these memories may influence this resistance to instability and reconsolidation. The neurotransmitter noradrenaline could have a role in this, as it is released during the consolidation of emotional memories.  

Researchers from McGill University assessed if noradrenaline released into the amygdala, a brain region important for consolidation of emotional memories, was essential for the resistance to instability and reconsolidation after recall. To do this, they taught rats to associate a tone to a mild foot shock. To form “weak” or “strong” memories, animals were exposed to either 1 or 10 tone-shock presentations, respectively. Memory instability and reconsolidation were evaluated by treating animals with anisomycin, an antibiotic that interferes with memory reconsolidation by blocking protein production. Anisomycin blocks reconsolidation on animals that formed a “weak” memory but has no effect on animals that formed a “strong” memory. 

Animals that formed a “strong” memory have lower levels of proteins associated with neural plasticity changes, which are important to the brain to change and adapt, in the amygdala. Decreasing the noradrenergic signaling in the amygdala by either blocking its receptors or reducing noradrenaline release from the locus coeruleus (the major source of noradrenaline in the brain) before a “strong” memory is formed lead to memory susceptibility after recall. This susceptibility is related to neural plasticity changes in a “strong” memory that are similar to the ones observed in a “weak” memory.    

These findings may help to better understand why memories from highly stressful events, like traumatic situations, persist in the brain, and are resistant to manipulations after recall. This, in turn, may help developing new treatment strategies for people affected by stress-related disorders such as post-traumatic stress disorder.

Like SARS-CoV-2, human cytomegalovirus (HCMV) is a virus that causes only mild symptoms in most people it infects, but has the ability to cause severe problems in certain cases.

Most people around the world encounter HCMV as children. Infection is lifelong, and the virus usually remains latent. However, HCMV infection is a major cause of illness in organ transplant recipients, whose immune systems must be suppressed for transplants to be accepted. And children born with HCMV infection may also develop related congenital disorders, including childhood hearing loss and neurological problems. Development of new treatment strategies is still needed to address these complications.

Vaccines that stimulate an immune response against HCMV are one strategy to protect against infection by the virus. Potent virus-neutralizing antibodies are part of another strategy to treat HCMV infection. But the development of these strategies depends on our ability to answer questions about how the virus infects cells and how the immune system responds.

In a paper published in PLOS Pathogens, Xiaohua Ye and colleagues clarified answers to some questions about HCMV infections. They isolated antibodies that are part of a human donor’s response to a natural HCMV infection. Among these antibodies, they found one that was especially powerful at neutralizing the virus.

Other antibodies targeting the same region of the virus as the powerful antibody they discovered have been associated with protective immunity against HCMV disease in transplant recipients and infants at risk for congenital HCMV infection — two populations most affected by severe consequences from HCMV. This work advances our understanding of how antibodies neutralize HCMV, which will be helpful for the development of vaccines and antibody drugs against HCMV infection. 

Laterality — or hemispheric specializations within the brain, the thing that makes us right- or left-handed — was once thought to be a human-only trait. Research has found, however, that this trait is shown by many nonhuman species, too! A multitude of organisms demonstrate differential brain hemisphere control for behaviors like vocalization, escape reactions, and feeding.

Knowing that nonhuman animals exhibit laterality in their behavior raises several questions: how far back in history does laterality go? How many extinct organisms may have had lateral hemisphere control of their behaviors? And, is it even possible to figure out whether prehistoric animals did display laterality?

Much of the present research into lateralization in living organisms uses non-invasive observations of behavior. Since we can’t do that with extinct organisms, we have to turn to fossil records to see what clues we might find about their behavior. 

A recent study cleverly used the fossilized dental records of an extinct reptile, Captorhinus aguti, in an effort to determine if this reptilian ancestor showed a lateralized feeding preference. Investigations of 89 intact jaws of Captorhinus resulted in a clear pattern: there was much greater wear on the teeth of the right side of the jaw, suggesting a clear right side preference for feeding. That is, Captorhinus reptiles were ripping, tearing, and chewing food with and on the right side of the jaw significantly more often than with the left side of their jaw. This preference for right side control of feeding behavior has been maintained in present-day species like toads and domestic chickens. 

The Captorhinus fossil records demonstrate that this reptilian ancestor showed lateralized responses with the crucial-to-survival behavior of feeding. But this finding raises further questions. What other functionally relevant lateralized behaviors may have existed in the lives of extinct organisms, and what might such lateralized behaviors tell us about the evolution of hemispheric specializations of vertebrate species alive today?

How do we hear? When noise is produced, sound waves travel through the air and reach our inner ear, causing a mechanical perturbation in specialized rod-shaped cells — known as hair cell bundles. These auditory receptor cells transform the mechanical force from the sound waves into an electrical signal sent to our brains, which then reads it as sound.

But how does this mechano-electric transduction work? Auditory scientists have long believed that this signal transduction occurs through two adaptation processes. One is the opening of pore-like channels on the surface of cells that allow ions to enter. The other process, a “motor model,” involves the movement of a fiber-like protein known as myosin. This protein connects the upper sides of each hair cell in the bundle, and upon a mechanical stimulus, it slides, slightly pulling the connected hair cells down. Or so it was thought.

After more than 30 years of research, researchers at the University of Colorado Anschutz Medical Campus reported in Science that the motor model hypothesis was incorrect and, therefore, scientists still do not fully understand the underlying mechanisms by which our auditory cells work.

In brief, the team mechanically perturbated mammalian hair cell bundle samples, taking high-speed videos to test cell movement as hypothesized in the motor model. To resemble perturbations generated by sound, they splashed hair cells with a small stream of water or pushed them down using flexible glass fiber. Video analysis then showed that regardless of the stimulus used — water or glass fiber — the hair cells didn't move during the adaptation process, ruling out the decades-old motor model hypothesis.

Because the adaptation process is considered a critical factor in the high sensitivity and range of the mammalian auditory system, the authors foresee that their findings will lead to future technological improvements in sound processing and treatment of hearing loss.

If you’ve ever eaten sushi, you’ve probably scrolled through a list of different raw fish on the menu, in addition to all the spider rolls and dragon rolls. Salmon, tuna, and shrimp are some of the most common, but what about other, commonly eaten fish, such as catfish or trout? Why don’t we see these in any Western sushi restaurants? 

The big difference is in where the fish were caught. The science behind freshwater or ocean fish consumption is fairly simple: freshwater fish, at least in the United States, tend to have more parasites. 

Scientists are calling for caution when selecting raw fish for consumption as our demand for it expands across the globe. In a review published earlier this year, researchers updated the current understanding of food safety hazards of raw fish. 

Microscopic creatures such as Diphyllobothriidae (a type of tapeworm) can cause horrible illness when consumed, leading to diarrhea and intestinal issues in humans. One of the best ways to get rid of these parasites is by cooking the fish, whether by frying or baking at a certain temperature. If you’ve ever caught food poisoning from seafood, you’ll know it is perhaps the most painful version of a stomach bug. There are exceptions to this need for ocean caught fish rule for raw consumption in other countries. Namely, that is the eel, which is smoked and then prepared with a sugar-based sauce. Other problematic fish, such as mackerel, are pickled.

How fish is prepared is another reason why sushi is often ocean fish. Most ocean caught fish are frozen immediately after catching and butchering. This kills most of their potential parasites. Once the fish is frozen, it can be safely transported to a wide variety of destinations, including places far from local coasts, and inspected for parasites. 

On September 17th, the 30th Ceremony of the Ig Nobel Prize took place virtually. Although the ceremony might seem like a joke, it is actually a real prize ceremony with real scientists to recognize overlooked research that "makes you laugh, then think". But how do you deliver a prize virtually? 

The answer is that you make the winner build it! Unlike the Nobel Prize, which is honored with a medal, a diploma, and 9 million Swedish kronas (over $1 million USD), the Ig Nobel usually gives out a certificate, a crafty trophy, and a $10 trillion Zimbabwean bill. But in the virtual reality of 2020, the prizes were all self-assembled by the winners following the instructions sent out in a PDF.

This year's winners did research on a crocodile’s voice before and after inhaling helium, how people from countries with more income inequality kiss more often, "poop knives", and arachnophobic entomologists. A very well-deserved prize for Medical Education was also awarded to several political leaders for their mishandling of the COVID-19 pandemic.

If you think this is mocking the "real" Nobel prize, you'd be surprised to know that actual Nobel Laureates deliver the Ig-Nobel prizes to the winners. During the ceremony, former winners, Nobel laureates, and other invited scientists deliver 24/7 lectures. They have 24 seconds to explain their research, and then they explain it again in a way that anyone can understand in just 7 words. Dr. Elena Bodnar made an appearance again this year with the invention that made her win the Ig-Nobel back in 2009: a bra that turns into protective face masks.

I'd highly recommend watching the ceremony, which demonstrates just how ingenious, sometimes disgusting, and very funny scientists can be. 

Parkinson’s Disease (PD) is characterized by resting tremor, slow movements, and rigid muscles. For decades we have known it involves dopamine-releasing neurons in the middle of the brain dying. However, in recent years scientists have suggested its origin could be in the gut rather than the brain.

For example, people with PD have been shown to experience symptoms in the gut, such as abnormal bacteria populations, and gut “leakiness”, which lets bacteria and toxins pass easily from the gut into the blood. Exactly how this relates to PD is a mystery.

In a paper published in Neurobiology of Disease in February, researchers used mice with PD-like features to investigate gut leakiness and fecal bacteria populations. Some of the mice were also chronically stressed, and the researchers compared their gut features to unstressed mice. The researchers examined their intestines under a microscope and measured their gut inflammation levels.

They found that the stressed mice had damaged, leaky intestines. Additionally, stress activated the microglia, small cells in the brain known for their role in inflammation and immunity. Chemical markers of inflammation were increased in these mice, and the types of bacteria found in their feces were also different than in unstressed mice: stress reduced the “anti-inflammatory” bacteria. Stressed mice with PD-like features had severe gut hyperpermeability.

This increase in gut inflammation could lead to increased inflammation in the brain too. These findings support the gut-brain axis hypothesis of PD, showing a role of chronic stress in driving this. Understanding what occurs in the gut, and what causes this gut disruption, would allow a whole new therapeutic strategy for treating PD.

A mother jaguar and her 8-month old male cub climb further up the tree, trying to avoid a swarming mob below. Unable to carry up the capybara she recently killed, the female jaguar drops it as the cats make their rapid upward escape, ultimately spending the next 10 hours up the tree.

The jaguars’ adversaries were not what you might think. They were white-lipped peccaries, pig-like animals that often serve as prey for the majestic spotted cats. These ungulates (hoofed animals) are found from Mexico to Argentina and often occur in groups of 150-200, while jaguars are usually solitary predators, except for mothers with cubs.

This amazing scenario is one of several similar events recently published in the journal Acta Ethologica which demonstrate the complexities of what were once thought to be simple predator/prey interactions. 

In this case, the researchers have video proof that the peccaries (prey) engage in mobbing behavior toward a predator. Mobbing is when individuals or a group of prey attack or harass a predator until the predator leaves the area or stops pursuing them. Anti-predator behaviors, including alarm calls and guarding young, as well as mobbing have previously been reported in primates, birds and ungulates. 

Although scientists had heard anecdotal reports of this behavior in the past, these researchers were able to catch the mobbing peccaries on video camera traps. In one video, a group of 15 peccaries were seen at the base of a tree with a jaguar in it, clacking their canines with their hackles raised. Later they chased the jaguar into the Brazilian forest. In other videos, the peccaries were not deterred even though the jaguar they were mobbing snarled, hissed and fake-charged them. 

Prey spend time and energy and put themselves at risk through anti-predation behaviors like mobbing, but they aren’t the only ones incurring a cost. This video showed direct evidence that the peccary prey actually disrupted the predator's ability to successfully catch or consume prey. Far from the simple “eat or be eaten,” scientists are continuing to discover more complexities of predator-prey interactions.

The thought of seabirds might evoke memories of a perfect beach day ruined by a flock of noisy gulls stealing your lunch and defecating on you or your belongings. While you were shooing away the unwelcome visitors, you probably thought “What good are gulls anyway?” 

Researchers from the Universidade Federal de Goiás in Brazil now have an answer to your question. Seabirds like your annoying beach companions produce incredibly important and valuable excrement that is rich in nutrients such as nitrogen and phosphorus. This excrement (called guano) has been used as organic fertilizer since ancient times and is still collected and used in countries like Peru and Chile. Those two countries alone collected 27,000 tons of guano in 2018, which sold for $12.2 million USD. 

But bird guano isn’t just an important fertilizer for humans, it also fuels ocean ecosystems. To estimate just how important seabird excrement is, the researchers calculated how much it would cost to replace the nutrients excreted by seabirds with man-made versions, and found that seabird poop could be worth over $473 million per year. 

And that value does not even take other ecosystem benefits into consideration. For instance, a lot of reef fish rely on bird guano. The researchers valued the impact of bird guano on commercial reef fisheries at $650 million per year, increasing the total value of seabird guano to over $1 billion per year!

It may seem silly to put a dollar value on bird poop, but doing so is critical for improving conservation of these highly threatened species. So next time you find yourself cursing while wiping the bird poop off your favorite beach blanket, remember how valuable that bird and its poop can be. 

In a report published September 10th, researchers at ACEEE, the American Council for an Energy-Efficient Economy, found that “low-income households spend three times (8.1 percent) more of their income on energy costs compared to the median spending (2.3 percent) of non-low-income households.” 

The team of researchers measured energy burdens from 2017 in communities from 25 metro areas, places such as Atlanta, Chicago, New York City. By comparing households regionally and nationally, this team discovered that 25 percent (about 30 million) American households experience high energy burdens, spending more than 6 percent of their income on home energy. Half of those households (so about 15 million) experience what they call "severe burdens"  — where 10 percent of income is used on energy cost.

Black, Hispanic, Indigenous, and elderly households experienced disproportionate higher energy burdens. The researchers recommended further research on race, ethnicity, age and other factors affect affect energy burdens.

As rising temperatures affect portions of the US, energy usage will increase. Already high energy burdens for low-income communities will too. Identifying communities, increasing funding for energy efficiency, and weatherization are just some of the policy changes that can be implemented for a more energy security.

Coral reefs all over the world are suffering the effects of climate change. Coral restoration has become a popular conservation strategy to replenish coral coverage lost to bleaching, disease, and other factors. Restoration efforts could maintain genetic diversity and improve coral reef resilience, but how effective are these programs?

Studies on the success of such programs have found high costs and low long-term success. A paper recently published in PLOS ONE found that survivorship of outplanted colonies of staghorn corals in the Florida Keys was initially high but decreased after two years, when growth rates plateaued. After seven years, at least 90% of the planted corals had died. 

Overall, these outplanting efforts preserve genetic diversity in the wild and keep extinction of endangered species in check, but significant human intervention will still be required until external stressors are reduced. Outplanting requires huge amounts of proactive human effort, and provides only temporary relief to the suite of problems facing corals, namely, climate change and the associated issues of warming temperatures, acidification, and disease. The results show that these stressors are the problems we should be targeting if we want to save coral reefs.

New data released Monday described the discovery of phosphine in the atmosphere of Venus. The poorly kept secret has been making the rounds since last week but were officially announced in a video from the Royal Astronomical Society.

Phosphine can be made in natural, non-living processes, industrially on Earth, and can also be made by anaerobic bacteria (living in the absence of oxygen). 

However, the scientists suggested that life "would struggle...in the incredibly acid atmosphere of Venus." 

"On Venus, the clouds are about 90% acid," said Jane Greaves at Cardiff University, who led the study. The results were published in Nature Astronomy on September 14th. 

"So is there really life on Venus? I really hope so, but we can't really tell with the results so far," said Greaves in the video.

Other scientists were cautious. Jessie Christiansen, a research scientist at the NASA Exoplanet Science Institute, tweeted:

Life is not the only explanation for the presence of phosphine, since there are geological and chemical events that can also produce it. However, the Cardiff group claims that they examined and ruled out all known possibilities that don't involve life. Phosphine was also discovered on Jupiter and Saturn as far back as 1975.

Just as scientists are rapidly learning how SARS-CoV-2 affects humans, they are also quickly working to understand how it affects other animals.  House cats, tigers, golden hamsters, and rhesus monkeys are all susceptible to SARS-CoV-2 infection. And while avian species such as duck and chicken are not, dogs, pigs, and ferrets have shown intermediate susceptibility. 

The critical entry point for the virus into our cells is a protein called ACE2, which bonds with the spike protein of SARS-CoV-2. Animals and humans both expressing ACE2 in their cells, so scientists have been wondering why different species have different SARS-CoV-2 susceptibility, and if it is possible to predict which animals might be at risk.

In a preprint posted on bioRxiv in July, researchers at Vanderbilt University approached this question by comparing the amino acid sequence of ACE2 from different animal species. Amino acids are compounds that combine to form proteins. Inside cells, this amino acid chain folds into a three-dimensional shape. And as a result, some amino acids become hidden, and others exposed. Exposed ACE2 amino acids are of great interest because they determine whether SARS-CoV-2 can attach to the cell. 

Using computer models, researchers identified amino acids in ACE2 that showed strong interactions with SARS-CoV-2. They observed that in non-susceptible animal species, these amino acids were often different, ultimately disrupting the attachment between the ACE2 protein and the spike protein of SARS-CoV-2. This allowed the researchers to make predictions about which animals species are possibly at risk of infection. They estimated that while horses and camels would be vulnerable to infection, cows, goats, and Malayan pangolins would present intermediate susceptibility.

In August, another preprint from researchers at Dalhousie University in Nova Scotia examined whether marine wildlife are susceptible to the virus. Using similar modeling methods, these researchers concluded that whales, dolphins, seals, and otters would be susceptible to SARS-CoV-2. They suggest that exposure could happen through contaminated sewage entering the sea.

"To comb gray hairs" is a Spanish expression used to indicate that someone has reached a certain age, and they are not young anymore. It is an accurate idiom since, as we humans get old, our head hair generally becomes more gray. While little gray hair appears in the first half of our lives, once we reach midlife the color of our hair may totally disappear. But, is this the case in our closest evolutionary relatives? Can you tell a chimpanzee's age looking at the grey hair on their heads? 

To find out, a group of anthropologists took pictures of the faces of chimpanzees of different ages. They recruited 152 human observers, who were unfamiliar with these chimpanzees, and asked them to score the number of gray hairs they saw. 

The researchers discovered that hair graying in chimpanzees occurs at different times than it does in humans. Chimpanzees' hair becomes more gray from the time they are young up until the middle of their lives, but then the graying tends to stop. The opposite is true for humans, where graying is more striking from midlife on. They also found that a lot of variation between individuals, meaning that a 5-year-old chimp might have grayer hair than a 50-year-old ape. So, you cannot tell a chimp's age by the gray hairs on their heads!

It is unclear what the purpose of this difference might be, but it does indicate that going gray is not a reliable measure of age in mammals.