Image credit: David McClenaghan, CSIRO, via Wikimedia Commons
Bees have long impressed behavioral scientist Lars Chittka. In his lab at Queen Mary University of London, the pollinators have proven themselves capable of counting, using simple tools, and learning from nestmates. What really surprised Chittka, however, were the nuances of the insects’ behavior.
In 2008, for instance, a study from Chittka’s lab looked at how bumblebees reacted to a simulated attack by a fake spider on a flower. The bumblebees later approached suspect flowers cautiously and sometimes left even spider-less flowers quickly “as if they were seeing ghosts,” Chittka recalled. By contrast, the bees were seemingly more upbeat after receiving a sugar treat.
To Chittka, these observations defy a long-held view that insects are robot-like, controlled by hard-wired cognitive programs. Rather, the bees’ behavior seemed to be influenced by subjective experience — a perception of pleasant and unpleasant. Chittka said he increasingly suspects “there’s quite a rich world inside their minds.”
Early in his career, Chittka never protested when his colleagues opened bees’ skulls and inserted electrodes to study their nervous system. But he now wonders whether such procedures might create “potentially very unpleasant situations” for the insects. Like most invertebrates — any animal without an internal skeleton — insects tend to be legally unprotected in research. Regulations intended to minimize suffering in vertebrates like rodents largely don’t apply.
Some countries have already improved the welfare of select invertebrates, such as octopus, squid, crabs, and lobster. But there’s disagreement over whether other invertebrate species — a kaleidoscopically diverse cast of animals — also deserve protection. Some scientists believe species with relatively simple brains, like insects, or perhaps even those with no central nervous system at all, also deserve ethical consideration, although the details are under debate.
None of the experts who spoke with Undark argued that research on these invertebrate species should stop. Some organisms, including widely used species of fruit flies or nematode worms, have long led to breakthroughs in genetics, cell development, and other biological processes, and have played important roles in roughly a fifth of Nobel Prizes for Physiology or Medicine that were based on animal research. Many scientists are also shifting their research from vertebrates to invertebrates to avoid ethical bureaucracy associated with animal welfare regulation.
Still, recent research is prompting some scientists to rethink traditional research ethics. As Adam Hart, an entomologist at the University of Gloucestershire, put it: “I think we are at a point where people are willing to entertain the idea that perhaps ethics isn’t just something for animals with backbones.”
I recently started asking scientists I interview if they have any questions about the journalistic process. It turns out that they have a lot! So I wrote about common issues scientists have with journalists and how to improve this vital relationship; read my story in The Scientist.
Image: A view inside the department of zoology and animal ecology at Kharkiv National University. The institution’s main building lost many of its windows due to a shockwave following a rocket attack on nearby official infrastructure. Credit: Glib Mazepa
My latest is about the impact of Russia’s invasion on Ukraine’s scientific community, and efforts to keep science going amid the horror that’s unfolded since. I’m so grateful to everyone who shared their story – from universities providing humanitarian aid, scientists scrambling to rescue years’ worth of research, and clinical trial leaders finding other ways for patients to get needed treatments. Please read, at The Scientist!
Image: Martin Picard
Mitochondria have shelflike internal membrane folds called cristae. Picard’s research group observed that when mitochondria touch, their cristae can line up on either side of the membrane.
During his doctoral research on the ties between aging and mitochondria, Martin Picard frequently saw micrographs of those energy-producing organelles. Yet it wasn’t until fairly late in his graduate work that he first watched sped-up video of mitochondria moving inside live human cells, and the sight came as a revelation.
Tagged with fluorescent dye, the mitochondria were neon squiggles crawling through the soupy interior of the cells — stretching and contracting, fusing together and splitting up again, sidling up to one another and parting ways. Their apparent eagerness to network reminded Picard of the social exchanges among complex creatures like fish and ants. “They just look a little more primitive,” he said.
Now, after years of work in his own laboratory and others that has underscored the importance of those dynamic mitochondrial interactions, he is pressing that comparison more literally. Recently, in Neuroscience & Biobehavioral Reviews, Picard, a mitochondrial psychobiologist at Columbia University, and the neuroscientist Carmen Sandi of the Swiss Federal Institute of Technology Lausanne argued that mitochondria need to be understood as the first known social organelles.
As evidence, they cite a long line of discoveries showing that mitochondria are surprisingly interdependent and that their functions go far beyond their familiar role as cellular powerhouses: Mitochondria also make certain types of hormones, help drive immune responses, and shape the developmental fate of cells. To these diverse ends, like ants in a colony, mitochondria divide up tasks, form groups, synchronize activities and respond to both their environment and each other. A “social lens,” Picard and Sandi wrote, may be essential not only for explaining the behavior of individual mitochondria, but for revealing the mitochondrial collectives that influence human health.
Despite some reservations about the label “social,” other scientists generally agree that understanding the bustling signaling networks that mitochondria establish within and between cells could help unlock secrets about health and disease. “If we understand how the mitochondria are acting together, and we learn how to manipulate it,” said James Eberwine, a molecular neurobiologist at the University of Pennsylvania, “we’re going to gain so much more insight into biology.”
Read the whole story in Quanta Magazine
Conceptual Photograph: The Voorhes
Re-creating everything that happens inside the womb belongs firmly in the realm of science fiction. There’s still too much that scientists don’t know about the early stages of development, when fetal cells grow into organs, limbs, and tissues. But George Mychaliska thinks that creating an artificial version of the placenta, or at least replicating its most important function, is in reach. As a fetal and pediatric surgeon at the University of Michigan’s C.S. Mott Children’s Hospital, in Ann Arbor, he often sees premature babies who have left the womb too soon. Although modern medicine can save many of them, the chances of survival for extremely small preemies—those younger than 28 weeks, barely in their third trimester—remain slim. Of the survivors, many are left with long-term health problems. Lungs simply aren’t designed to breathe until the baby is close to full term, which is currently defined as 39 weeks, and even the gentlest techniques to assist breathing can damage the tissue.
“We’re in a catch-22 as baby doctors,” Mychaliska says. “If we don’t do anything, they die. If we want to save them… they may survive, but they likely will have varying degrees of lung disease from the treatment itself.”
For more than a decade, Mychaliska has been working on a solution: an artificial placenta to keep extremely young preemies alive until they can breathe on their own. Already, he’s proven that it can sustain premature lambs for several weeks. Building a breathing apparatus for a premature infant is not trivial, as the baby’s tiny size and fragile physiology pose both medical and engineering challenges. Mychaliska’s team has been adapting existing technology to work reliably with the skinniest of blood vessels and developing materials compatible with the unique biology of fetuses. Now, after several recent breakthroughs, Mychaliska thinks his team’s artificial placenta is only five years away from human trials.
Read my April 2021 cover story for IEEE Spectrum
The image above shows a slice of a deceased COVID-19 patient’s olfactory bulb, illustrating an area (the blotch on the left) with significant leakage of the protein fibrinogen (fluorescent green) into the tissue, which researchers think is likely the result of damage to small blood vessels. Courtesy of Dragan Meric
Neurological symptoms are not unheard of during pandemics. A British throat specialist observed in the late 1800s that influenza seemed to “run up and down the nervous keyboard stirring up disorder and pain in different parts of the body with what almost seems malicious caprice.” In fact, many patients during the 1889–92 pandemic at the time became afflicted with psychoses, paranoia, stabbing pains, and nerve damage. Scholars have also linked the 1918 flu pandemic to parkinsonism, neuropsychiatric disorders, and other symptoms, although there is some debate around whether some of them were actually caused by the pandemic.
The fact that SARS-CoV-2 is also associated with neurological symptoms isn’t entirely surprising, although the sheer numbers of patients developing such symptoms has alarmed some scientists. The list now includes a range of symptoms, from delirium, strokes, peripheral nerve damage, inflammation of the brain, as well as long-term symptoms like headaches, fatigue, and cognitive difficulties.
Researchers are hard at work trying to figure out how SARS-CoV-2 causes such symptoms. The results so far are a bit puzzling. Though a handful of autopsy studies have found signs of damage in the brains of some COVID-19 patients, it’s still not clear if the virus directly infects the brain. This has pushed researchers to come up with other explanations via which it could affect the human brain.
“I think all of us probably . . . would agree that there is no overwhelming infection of the brain,” Avindra Nath, a neurovirologist at the National Institute of Neurological Disorders and Stroke, told me. “If there is, it’s a very, very miniscule amount. That cannot explain the pathology that we see. It has to be something more than that.”
Read the whole story at The Scientist!
Why some people die while others recover is thought to depend in large part on the human immune response, which spirals out of control in severe disease. Over the past few months, researchers have developed a better understanding of this dysfunctional immune response. By comparing patients with varying degrees of disease severity, they’ve catalogued a number of dramatic changes across the human immune arsenal that are often apparent when patients first come into the hospital—from signaling cytokine proteins and first-responder cells of the innate immune system, to the B cells and T cells that confer pathogen-specific adaptive immunity.
The factors that trigger this immune dysregulation have so far remained elusive due to the complexity of the immune system, which consists of seemingly endless biological pathways that twist and turn and feed back on one another like a ball of spaghetti. But researchers—drawing on knowledge from other conditions such as sepsis, cancer, and autoimmune disease—are gradually building coherent theories of what puts patients en route to severe disease. Along the way, they’re also uncovering signals that clinicians could use to predict disease prognosis and identify potential new treatment avenues.
“We don’t have the clearest picture yet. Nor do we know why there’s variability in this immune response,” says Nuala Meyer, a critical care physician at the Hospital of the University of Pennsylvania who researches sepsis. While it’s well-established that underlying conditions increase the risk for developing severe COVID-19, “I definitely see patients with diabetes, obesity, and high lipids that did not become severe [cases],” she says. “I think we have a lot of work to do to understand precisely what accounts for this differential response.”
Read the story at The Scientist
In recent years, a field that has traditionally relied on fossil discoveries has acquired helpful new tools: genomics and ancient DNA techniques. Armed with this combination of approaches, researchers have begun to excavate our species’ early evolution, hinting at a far more complex past than was previously appreciated—one rich in diversity, migration, and possibly even interbreeding with other hominin species in Africa.
“To piece together that story, we need information from multiple different fields of study,” remarks Eleanor Scerri, an archaeologist at the Max Planck Institute for the Science of Human History in Jena, Germany. “No single one is really going to have all the answers—not genetics, not archaeology, not the fossils, because all of these areas have challenges and limitations.”
Read the full story here or in The Scientist‘s September magazine issue
Image: © ISTOCK.COM, PONOMARIOVA_MARIA
Despite uncertainties around whether some cases are in fact SARS-CoV-2 infections, “long-haulers” such as those in the online group point to the possibility that COVID-19 is not just a transient respiratory disease, but could manifest as neurological and physical symptoms that persist even months after people fall ill. Although many of them may yet recover in the coming months, some scientists are becoming increasingly worried that some may end up with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a debilitating and poorly understood condition associated with some viral infections. In a press conference last week, for instance, National Institute of Allergy and Infectious Diseases Director Anthony Fauci noted that some of the long-haulers’ symptoms resemble those of ME/CFS. Studies are now underway to track whether some long-haulers develop the disease, and if so, to investigate its underlying mechanisms and possible avenues for treatment quickly.
“This is a massive infection of millions and millions of people. I think one has to be really concerned about the long-term consequences,” notes Avindra Nath, a neurovirologist at the National Institute of Neurological Disorders and Stroke. “A lot of emphasis early on has been on providing treatments and vaccines and antibodies and all that kind of stuff, but the long-term consequences have not received the attention that they deserve.”
Read the whole story at The Scientist
“Fast forward a month, and the world did have a pandemic on its hands. Modelers around the world scrambled to forecast the spread of SARS-CoV-2 and the COVID-19 disease it causes in their own countries and communities. Many epidemiologists were then and still are tasked by policymakers with answering urgent questions: How fast will it spread? How many hospital beds and ventilators will we need? When can we lift lockdowns and restart our economies again? Will we see a second wave? Will it be worse than the first?
Getting good estimates for R0—a key epidemiological metric that reflects the transmissibility of a virus—is key to answering such questions with accuracy. But R0 is notoriously tricky to nail down. It depends not only on the biological characteristics of a virus—which are a mystery at the beginning of an outbreak—but also on understanding how often people come into contact with one another. Faced with uncertainty, modelers have to make assumptions about the factors that determine human movement, which can limit the precision of their models and the accuracy of the predictions they generate.
“R0 is a metric that is, first of all, poorly measured. And secondly, it’s informing models that result in public health action,” says Juan B. Gutiérrez, a mathematician at the University of Texas at San Antonio. “If we get it wrong, the public health action will be misplaced.”
Read The Scientist’s most popular feature in 2020!