“The use of an AED is the single most important factor in saving lives. We have been deploying drones equipped with AED since the summer of 2020 and show in this follow-up study that drones can arrive at the scene before an ambulance by several minutes. This lead time has meant that the AED could be used by people at the scene in several cases,” says Andreas Claesson, Associate Professor at the Center for Cardiac Arrest Research at the Department of Clinical Research and Education, Södersjukhuset, Karolinska Institutet, and principal investigator of the study.

Every year, around 6000 people in Sweden suffer a sudden cardiac arrest, but only a tenth of those affected survive. Although an early shock with a AED can dramatically increase the chance of survival and there are tens of thousands of AED in the community, they are not available in people’s homes where most cardiac arrests occur.

To shorten the time to defibrillation with an AED, Karolinska Institutet, together with Region Västra Götaland, SOS Alarm and the drone operator Everdrone, has since 2020 tested the possibility of sending out a drone with a AED at the same time as an ambulance is alerted. The project covered an area of approximately 200,000 people in western Sweden. An initial study conducted in the summer of 2020 in Gothenburg and Kungälv showed that the idea was feasible and safe.

“This more comprehensive and follow-up study now shows in a larger material that the methodology works throughout the year, summer and winter, in daylight and darkness. Drones can be alerted, arrive, deliver AED, and people on site have time to use the AED before the ambulance arrives,” says Sofia Schierbeck, PhD student at the same department and first author of the study.

In the study, drones delivered a AED in 55 cases of suspected cardiac arrest. In 37 of these cases, the delivery took place before an ambulance, corresponding to 67 percent, with a median lead of 3 minutes and 14 seconds. In the 18 cases of actual cardiac arrest, the caller managed to use the AED in six cases, representing 33 percent. A shock was recommended by the device in two cases and in one case the patient survived.

“Our study now shows once and for all that it is possible to deliver AED with drones and that this can be done several minutes before the arrival of the ambulance in connection with acute cardiac arrest,” says Andreas Claesson. “This time saving meant that the healthcare emergency center could instruct the person who called the ambulance to retrieve and use the AED in several cases before the ambulance arrived.”

The research was mainly funded by the Swedish Heart-Lung Foundation.

Hikikomori is a condition characterized by sustained physical isolation or social withdrawal for a period exceeding six months. It was first defined in Japan in 1998, and while thought to be a Japan specific ‘culture-bound’ syndrome, recent evidence has shown a marked growth of it worldwide. Researchers and medical professionals also fear that the recent COVID-19 pandemic has compounded the increase of hikikomori patients across the globe.

However, there is yet to be a standardized tool to identify the hikikomori pathology. The new HiDE assessment tool, developed by Associate Professor Takahiro A. Kato of the Graduate School of Medical Sciences published in World Psychiatry, is intended to be the next step in a transcultural tool to help identify and assess hikikomori individuals.

In 2013, the Kyushu University hospital established the world’s first outpatient clinic for hikikomori in the hopes to research the pathology and find better methods of treatment. Over the years, Kato and his team have developed different methods for early detection of hikikomori and has even been investigating possible biomarkers of the pathology.

“HiDE is a questionnaire we’ve been developing at our clinic at the University Hospital. We’ve refined it over the years, and today it takes roughly 5-20 minutes to complete depending on the answers,” explains Kato. “It’s primarily divided into two sections. The first section looks at the features of the patient’s behavior to see if they exhibit hikikomori. The second section is used to help us gain context to the patient’s extent of social withdrawal.”

The team has also added a screening form to the HiDE in case clinicians lack the time to administer the entire tool. They suggest that the full questionnaire be administered to patients who respond that they ‘spend one hour or less per day out of their home, at least three days a week’ and that ‘their family, others, or are personally bothered by this.’

“The HiDE has proven to be an indispensable tool for the structured assessment of pathological social withdrawal in our clinical practice and research. But more empirical studies must be done to assess its validity beyond our practice,” concludes Kato. “We would like to see this used by our colleagues around the world, so we can work to refine the tool. Hikikomori is becoming a global phenomenon, and a collective effort in recognizing and treating hikikomori is going to be vital.”

It is well known that patients with rheumatoid arthritis are at increased risk of autoimmune thyroid diseases such as Hashimoto’s disease and Graves’ disease. While patients with RA are usually treated with immunomodulatory drugs that affect the immune system, such drugs are rarely used in autoimmune thyroid diseases. Instead, such patients are treated with thyroid hormone to compensate for the changes in normal thyroid function that accompany autoimmune thyroid disease.

The researchers in the current study wanted to investigate whether immunomodulatory drugs that reduce inflammation in the joints of patients with RA might also reduce the risk of these patients developing autoimmune thyroid disease. Previous studies in mice suggest that so-called DMARDs, a type of immune-modulatory drugs used to treat rheumatoid arthritis, can reduce inflammation in the thyroid gland. Still, knowledge of whether this effect also applies to humans is limited, according to the research team.

The researchers used data between 2006 and 2018 on over 13,000 patients with rheumatoid arthritis and their treatment, as well as data from over 63,000 individuals in a matched control group without rheumatoid arthritis.

The researchers found that the risk of developing an autoimmune thyroid disease among RA patients was lower after their onset of the rheumatic disease than before diagnosis.

The most pronounced reduction in the risk of autoimmune thyroid disease was seen in patients with rheumatoid arthritis treated with immunomodulatory drugs or ‘biological DMARDs’. In these patients, the risk of autoimmune thyroid disease was 46 percent lower than in the control group without rheumatoid arthritis.

“These results support the hypothesis that certain types of immunomodulatory drugs could have a preventive effect on autoimmune thyroid disease,” says Kristin Waldenlind, researcher at the Department of Medicine, Solna, Division of Clinical Epidemiology, Karolinska Institutet, specialist in rheumatology at Karolinska University Hospital and first author of the study. She continues:

“Our results do not prove that it is the treatment with immunomodulatory drugs that led to the reduced risk of autoimmune thyroid disease, but provide support for this hypothesis. The results, if they can be replicated in further studies, open up the possibility of studying more directly in clinical trials whether the immunomodulatory drugs currently used for rheumatoid arthritis could also be used for the early treatment of autoimmune thyroid disease, i.e. for new areas of use of these drugs, known as drug repurposing.

The Swedish Research Council, the Swedish Heart-Lung Foundation and Vinnova mainly financed the study.

There’s a popular saying in some circles that “a calorie is a calorie,” but science shows that it may not be true. In fact, it may be possible to eat more of some kinds of calories while also improving your health.

“We like to say a calorie is not just a calorie,” says Dudley Lamming, a professor and metabolism researcher at the University of Wisconsin School of Medicine and Public Health. “Different components of your diet have value and impact beyond their function as a calorie, and we’ve been digging in on one component that many people may be eating too much of.”

Lamming is the lead author of a new study in mice, published recently in the journal Cell Metabolism, showing that cutting down the amount of a single amino acid called isoleucine can, among other benefits, extend their lifespan, make them leaner and less frail as they age and reduce cancer and prostate problems, all while the mice ate more calories.

Amino acids are the molecular building blocks of proteins, and Lamming and his colleagues are interested in their connection to healthy aging.

In earlier research, data from UW-Madison’s Survey of the Health of Wisconsin showed the scientists that Wisconsinites with higher body mass index measurements (higher is more overweight or obese) tend to consume more isoleucine, an essential amino acid everyone needs to eat. Isoleucine is plentiful in foods including eggs, dairy, soy protein and many kinds of meat.

To better understand its health effects, Lamming and collaborators from across disciplines at UW-Madison fed genetically diverse mice either a balanced control diet, a version of the balanced diet that was low in a group of about 20 amino acids, or a diet formulated to cut out two-thirds of the diet’s isoleucine. The mice, which began the study at about 6 months of age (equivalent to a 30-year-old person) got to eat as much as they wanted.

“Very quickly, we saw the mice on the reduced isoleucine diet lose adiposity — their bodies got leaner, they lost fat,” says Lamming, while the bodies of the mice on the low-amino-acid diet also got leaner to start, but eventually regained weight and fat.

Mice on the low-isoleucine diet lived longer — on average 33% longer for males and 7% longer for females. And, based on 26 measures of health, including assessments ranging from muscle strength and endurance to tail use and even hair loss, the low-isoleucine mice were in much better shape during their extended lives.

“Previous research has shown lifespan increase with low-calorie and low-protein or low-amino-acid diets starting in very young mice,” says Lamming, whose work is supported by the National Institutes of Health. “We started with mice that were already getting older. It’s interesting and encouraging to think a dietary change could still make such a big difference in lifespan and what we call ‘healthspan,’ even when it started closer to mid-life.”

The mice on the low-isoleucine diets chowed down, eating significantly more calories than their study counterparts — probably to try to make up for getting less isoleucine, according to Lamming. But they also burned far more calories, losing and then maintaining leaner body weights simply through adjustments in metabolism, not by getting more exercise.

At the same time, Lamming says, they maintained steadier blood sugar levels and male mice experienced less age-related prostate enlargement. And while cancer is the leading cause of death for the diverse strain of mice in the study, the low-isoleucine males were less likely to develop a tumor.

Dietary amino acids are linked to a gene called mTOR that appears to be a lever on the aging process in mice and other animals as well as to a hormone that manages the body’s response to cold and has been considered a potential diabetes drug candidate for human patients. But the mechanism behind the stark benefits of low-isoleucine intake is not well understood. Lamming thinks the new study’s results may help future research pick apart causes.

“That we see less benefit for female mice than male mice is something we may be able to use to get to that mechanism,” he says.

While the results are promising, humans do need isoleucine to live. And winnowing a significant amount of isoleucine out of a diet that hasn’t been preformulated by a mouse chow company is not an easy task.

“We can’t just switch everyone to a low-isoleucine diet,” Lamming says. “But narrowing these benefits down to a single amino acid gets us closer to understanding the biological processes and maybe potential interventions for humans, like an isoleucine-blocking drug.”

The Survey of the Health of Wisconsin showed that people vary in isoleucine intake, with leaner participants tending to eat a diet lower in isoleucine. Other data from Lamming’s lab suggest that overweight and obese Americans may be eating significantly more isoleucine than they need.

“It could be that by choosing healthier foods and healthier eating in general, we might be able to lower isoleucine enough to make a difference,” Lamming says.

This research was funded in part by grants from the National Institutes of Health (AG056771, AG062328, AG081482, AG084156, DK125859, F31AG066311, R01AG062328-03S1, F31AG081115, F31AG082504, T32AG000213, F32AG077916, RF1AG056771-06S1, K01AG059899, R01DK133479, P30DK020579, K12HD101368, R01AA029124, P30 CA014520, P50DE026787, U54DK104310, R01DK131175 and P30CA014520) and the U.S. Department of Veterans Affairs (I01-BX004031).

The picture, it turns out, is a little different.

The team, led by Zachary Knight, PhD, a UCSF professor of physiology in the Kavli Institute for Fundamental Neuroscience, discovered that it’s our sense of taste that pulls us back from the brink of food inhalation on a hungry day. Stimulated by the perception of flavor, a set of neurons — a type of brain cell — leaps to attention almost immediately to curtail our food intake.

“We’ve uncovered a logic the brainstem uses to control how fast and how much we eat, using two different kinds of signals, one coming from the mouth, and one coming much later from the gut,” said Knight, who is also an investigator with the Howard Hughes Medical Institute and a member of the UCSF Weill Institute for Neurosciences. “This discovery gives us a new framework to understand how we control our eating.”

The study, which appears Nov. 22, 2023 in Nature, could help reveal exactly how weight-loss drugs like Ozempic work, and how to make them more effective.

New views into the brainstem

Pavlov proposed over a century ago that the sight, smell and taste of food are important for regulating digestion. More recent studies in the 1970s and 1980s have also suggested that the taste of food may restrain how fast we eat, but it’s been impossible to study the relevant brain activity during eating because the brain cells that control this process are located deep in the brainstem, making them hard to access or record in an animal that’s awake.

Over the years, the idea had been forgotten, Knight said.

New techniques developed by lead author Truong Ly, PhD, a graduate student in Knight’s lab, allowed for the first-ever imaging and recording of a brainstem structure critical for feeling full, called the nucleus of the solitary tract, or NTS, in an awake, active mouse. He used those techniques to look at two types of neurons that have been known for decades to have a role in food intake.

The team found that when they put food directly into the mouse’s stomach, brain cells called PRLH (for prolactin-releasing hormone) were activated by nutrient signals sent from the GI tract, in line with traditional thinking and the results of prior studies.

However, when they allowed the mice to eat the food as they normally would, those signals from the gut didn’t show up. Instead, the PRLH brain cells switched to a new activity pattern that was entirely controlled by signals from the mouth.

“It was a total surprise that these cells were activated by the perception of taste,” said Ly. “It shows that there are other components of the appetite-control system that we should be thinking about.”

While it may seem counterintuitive for our brains to slow eating when we’re hungry, the brain is actually using the taste of food in two different ways at the same time. One part is saying, “This tastes good, eat more,” and another part is watching how fast you’re eating and saying, “Slow down or you’re going to be sick.”

“The balance between those is how fast you eat,” said Knight.

The activity of the PRLH neurons seems to affect how palatable the mice found the food, Ly said. That meshes with our human experience that food is less appetizing once you’ve had your fill of it.

Brain cells that inspire weight-loss drugs

The PRLH-neuron-induced slowdown also makes sense in terms of timing. The taste of food triggers these neurons to switch their activity in seconds, from keeping tabs on the gut to responding to signals from the mouth.

Meanwhile, it takes many minutes for a different group of brain cells, called CGC neurons, to begin responding to signals from the stomach and intestines. These cells act over much slower time scales — tens of minutes — and can hold back hunger for a much longer period of time.

“Together, these two sets of neurons create a feed-forward, feed-back loop,” said Knight. “One is using taste to slow things down and anticipate what’s coming. The other is using a gut signal to say, ‘This is how much I really ate. Ok, I’m full now!'”

The CGC brain cells’ response to stretch signals from the gut is to release GLP-1, the hormone mimicked by Ozempic, Wegovy and other new weight-loss drugs.

These drugs act on the same region of the brainstem that Ly’s technology has finally allowed researchers to study. “Now we have a way of teasing apart what’s happening in the brain that makes these drugs work,” he said.

A deeper understanding of how signals from different parts of the body control appetite would open doors to designing weight-loss regimens designed for the individual ways people eat by optimizing how the signals from the two sets of brain cells interact, the researchers said.

The team plans to investigate those interactions, seeking to better understand how taste signals from food interact with feedback from the gut to suppress our appetite during a meal.

When the French archaeologist Jean-Claude Marquet entered the La Roche-Cotard cave in the Loire Valley for the first time back in 1974, he suspected that the fine lines on the wall could be of human origin. He also found scrapers and other retouched pieces known as Mousterian stone artifacts that suggested the cave had been used by Neanderthals. Were the marks on the wall evidence of early Neanderthal artistic activity?

Posing this question raised the possibility of breaking with the consensus of the time, which largely assumed that Homo neanderthalensis lacked any higher cognitive abilities. Fearing he would be unable to provide sufficient scientific evidence to prove his hypothesis, Marquet left the cave untouched for almost 40 years.

Marks on the wall produced by human hands

Together with an international team, he made another attempt in 2016. This time he was accompanied by Dr. Dorota Wojtczak from Integrative Prehistoric and Archaeological Science (IPAS) at the Department of Environmental Sciences of the University of Basel, who specializes in archaeological use-wear analysis. “Our task was to use modern methods to prove the human origin of these wall engravings,” explains Wojtczak in her office at IPAS. The researchers recently published their findings in the journal PLoS ONE.

First with photos and drawings and later with a 3D scanner, the marks in the tuff rock of the cave wall were meticulously recorded. In her laboratory in Basel, Wojtczak compared these samples from the cave with tuff she had worked on experimentally with wood, bone and stone tools, as well as with her hands. “This research clearly showed that the cave marks were not made with tools, but by scratching with human fingers,” says Wojtczak.

Cave sealed for over 50,000 years

At the same time, examination of cave sediment by researchers from Denmark showed that the cave must have been sealed off by mud residues from the Loire and soil sediments for over 50,000 years before being rediscovered. This makes the La Roche-Cotard cave system a very special location — a veritable “time capsule.” “At this time, 50,000 years ago, there were no modern humans in Europe, only Neanderthals,” says Wojtczak. The wall marks and artifacts can therefore only come from these early humans.

While the clear geometric shapes with parallel and triangular lines suggest that these marks were not scribbled on the wall by chance, the researcher does not know what they represent. “But they could only have been made by someone who proceeded with planning and understanding,” she says. And whether it was “art” as such, or a form of recording-keeping, is a matter of interpretation.

La Roche-Cotard promises further findings

The cave holds many other archaeological secrets. Jean-Claude Marquet also found an object that resembles the face of a human or animal back in 1976, and Wojtczak’s use-wear analysis suggests that this object is also man-made. Another object from the cave appears to be a small oil lamp. “Specialists are currently investigating whether the object bears any pigments or soot substances that could help to identify the type of fuel used at the time,” explains Wojtczak.

The chamber of La Roche-Cotard that has been explored so far is just one part of an entire cave system. The researcher hopes to gain further insight into the Neanderthals’ activities, particularly from Chamber 4, which is still largely covered by sediment. Wojtczak is convinced that every investigation will help to further the dismantle traditional consensus of Neanderthals as mentally inferior humans, and reinforce the perception of them as more like the cousins of modern humans. “They could speak, and probably even sang,” she adds, grinning.

Dorota Wojtczak will continue her research into Neanderthal life in La Roche-Cotard together with her students from the Prehistory and Archaeological Science degree program.

“There’s never been any infrared data on this region with the level of resolution and sensitivity we get with Webb, so we are seeing lots of features here for the first time,” said the observation team’s principal investigator Samuel Crowe, an undergraduate student at the University of Virginia in Charlottesville. “Webb reveals an incredible amount of detail, allowing us to study star formation in this sort of environment in a way that wasn’t possible previously.”

“The galactic center is the most extreme environment in our Milky Way galaxy, where current theories of star formation can be put to their most rigorous test,” added professor Jonathan Tan, one of Crowe’s advisors at the University of Virginia.

Protostars

Amid the estimated 500,000 stars in the image is a cluster of protostars — stars that are still forming and gaining mass — producing outflows that glow like a bonfire in the midst of an infrared-dark cloud. At the heart of this young cluster is a previously known, massive protostar over 30 times the mass of our Sun. The cloud the protostars are emerging from is so dense that the light from stars behind it cannot reach Webb, making it appear less crowded when in fact it is one of the most densely packed areas of the image. Smaller infrared-dark clouds dot the image, looking like holes in the starfield. That’s where future stars are forming.

Webb’s NIRCam (Near-Infrared Camera) instrument also captured large-scale emission from ionized hydrogen surrounding the lower side of the dark cloud, shown cyan-colored in the image. Typically, Crowe says, this is the result of energetic photons being emitted by young massive stars, but the vast extent of the region shown by Webb is something of a surprise that bears further investigation. Another feature of the region that Crowe plans to examine further is the needle-like structures in the ionized hydrogen, which appear oriented chaotically in many directions.

“The galactic center is a crowded, tumultuous place. There are turbulent, magnetized gas clouds that are forming stars, which then impact the surrounding gas with their outflowing winds, jets, and radiation,” said Rubén Fedriani, a co-investigator of the project at the Instituto Astrofísica de Andalucía in Spain. “Webb has provided us with a ton of data on this extreme environment, and we are just starting to dig into it.”

Around 25,000 light-years from Earth, the galactic center is close enough to study individual stars with the Webb telescope, allowing astronomers to gather unprecedented information on how stars form, and how this process may depend on the cosmic environment, especially compared to other regions of the galaxy. For example, are more massive stars formed in the center of the Milky Way, as opposed to the edges of its spiral arms?

“The image from Webb is stunning, and the science we will get from it is even better,” Crowe said. “Massive stars are factories that produce heavy elements in their nuclear cores, so understanding them better is like learning the origin story of much of the universe.”