“Looking at recent, natural climate anomalies helps to understand the processes and mechanisms that human-induced global warming may trigger,” says Dr Anastasia Zhuravleva, lead author of the study. She was a PhD student at GEOMAR and received the Annette Barthelt Prize for her dissertation in 2019. She then worked as a post-doctoral researcher at GEOMAR and Dalhousie University, where the study was completed.

“Researchers often consider an increase in sea ice extent and desalination in the subpolar North Atlantic as possible triggers for past cold periods, but processes in the tropical Atlantic appear to be equally important,” says Dr Zhuravleva. “In fact, in contrast to the northern and mid-latitudes, there is little information on these recent climate events from the subtropical-tropical Atlantic and their impact on regions in the Northern Hemisphere,” adds Dr Henning Bauch, paleoclimatologist at AWI and GEOMAR, co-initiator and co-author of the study. “This is where our research comes in.”

So, what happened in the tropical Atlantic during historical climate anomalies, and how might potential changes there have affected ocean circulation and climate much further north? To answer these questions, the team worked on a sediment profile from the southern Caribbean and reconstructed the salinity and temperature of the surface water over the last 1700 years. Among other things, the researchers determined the isotopic and elemental composition of the calcareous shells of plankton.

The results show a cooling of about 1°C during the Little Ice Age. “It is a significant temperature change for this region,” says Dr Mahyar Mohtadi, co-author of the study and head of the Low Latitude Climate Variability group at MARUM. “Particularly noteworthy is the occurrence of another pronounced cooling for the 8th-9th centuries. Colder temperatures in the otherwise warm tropical ocean led to lower regional rainfall, which coincided with severe droughts in the Yucatan Peninsula and the decline of the Classic Maya culture.”

In addition, the researchers found that the cold climate anomalies in the subpolar North Atlantic and Europe were accompanied by weaker ocean circulation and increased salinity in the Caribbean. “Advection, or the movement of tropical salt to high northern latitudes, is essential for maintaining high surface densities in the subpolar North Atlantic. This is a prerequisite for the overall stability of the large-scale ocean circulation, including the transfer of warm Gulf Stream water, which is responsible for our mild temperatures in Europe,” says Dr Bauch.

The data on the historical past thus allow a reconstruction of the connection across the North Atlantic. Initial cooling can be caused by volcanic eruptions, low solar activity and feedbacks between sea ice and the ocean in the north. The new study provides evidence that a decrease in salt movement to high northern latitudes will amplify and prolong these climate events. Conversely, the slow movement of positive salinity anomalies from the tropics will eventually increase the density at the surface of the subpolar North Atlantic. This may favour the northward transport of heat by ocean currents, resulting in milder temperatures over Europe and North America.

“Such a salinity feedback is known from models and has been assumed for the Little Ice Age. However, in the absence of tropical ocean data, these assumptions have been based on less direct precipitation records,” says Dr Zhuravleva.

There is evidence that the Gulf Stream is weakening and that human-induced warming is a likely cause. What is certain is that the consequences of this change will be global. The extent to which the different climate mechanisms interact has been an open question. This study now confirms that the south-north transport of salt is a key factor in the processes involved.

Now, a new Harvard Medical School study published Nov. 3 in Science Immunology may offer a molecular explanation behind this century-old observation.

The study, done in mice, suggests that the beneficial effects of exercise may be driven, at least partly, by the immune system. It shows that muscle inflammation caused by exertion mobilizes inflammation-countering T cells, or Tregs, which enhance the muscles’ ability to use energy as fuel and improve overall exercise endurance.

Long known for their role in countering the aberrant inflammation linked to autoimmune diseases, Tregs now also emerge as key players in the body’s immune responses during exercise, the research team said.

“The immune system, and the T cell arm in particular, has a broad impact on tissue health that goes beyond protection against pathogens and controlling cancer. Our study demonstrates that the immune system exerts powerful effects inside the muscle during exercise,” said study senior investigator Diane Mathis, Morton Grove-Rasmussen Professor of Immunology in the Blavatnik Institute at HMS.

Mice are not people, and the findings remain to be replicated in further studies, the researchers cautioned. However, the study is an important step toward detailing the cellular and molecular changes that occur during exercise and confer health benefits.

Understanding the molecular underpinnings of exercise

Protecting from cardiovascular disease, reducing the risk of diabetes, shielding against dementia. The salutary effects of exercise are well established. But exactly how does exercise make us healthy? The question has intrigued researchers for a long time.

The new findings come amid intensifying efforts to understand the molecular underpinnings of exercises. Untangling the immune system’s involvement in this process is but one aspect of these research efforts.

“We’ve known for a long time that physical exertion causes inflammation, but we don’t fully understand the immune processes involved,” said study first author Kent Langston, a postdoctoral researcher in the Mathis lab. “Our study shows, at very high resolution, what T cells do at the site where exercise occurs, in the muscle.”

Most previous research on exercise physiology has focused on the role of various hormones released during exercise and their effects on different organs such as the heart and the lungs. The new study unravels the immunological cascade that unfolds inside the actual site of exertion — the muscle.

T cell heroes and inflammation-fueling villains

Exercise is known to cause temporary damage to the muscles, unleashing a cascade of inflammatory responses. It boosts the expression of genes that regulate muscle structure, metabolism, and the activity of mitochondria, the tiny powerhouses that fuel cell function. Mitochondria play a key role in exercise adaptation by helping cells meet the greater energy demand of exercise.

In the new study, the team analyzed what happens in cells taken from the hind-leg muscles of mice that ran on a treadmill once and animals that ran regularly. Then, the researchers compared them with muscle cells obtained from sedentary mice.

The muscle cells of the mice that ran on treadmills, whether once or regularly, showed classic signs of inflammation — greater activity in genes that regulate various metabolic processes and higher levels of chemicals that promote inflammation, including interferon.

Both groups had elevated levels of Treg cells in their muscles. Further analyses showed that in both groups, Tregs lowered exercise-induced inflammation. None of those changes were seen in the muscle cells of sedentary mice.

However, the metabolic and performance benefits of exercise were apparent only in the regular exercisers — the mice that had repeated bouts of running. In that group, Tregs not only subdued exertion-induced inflammation and muscle damage, but also altered muscle metabolism and muscle performance, the experiments showed. This finding aligns with well-established observations in humans that a single bout of exercise does not lead to significant improvements in performance and that regular activity over time is needed to yield benefits.

Further analyses confirmed that Tregs were, indeed, responsible for the broader benefits seen in regular exercisers. Animals that lacked Tregs had unrestrained muscle inflammation, marked by the rapid accumulation of inflammation-promoting cells in their hindleg muscles. Their muscle cells also had strikingly swollen mitochondria, a sign of metabolic abnormality.

More importantly, animals lacking Tregs did not adapt to increasing demands of exercise over time the way mice with intact Tregs did. They did not derive the same whole-body benefits from exercise and had diminished aerobic fitness.

These animals’ muscles also had excessive amounts of interferon, a known driver of inflammation. Further analyses revealed that interferon acts directly on muscle fibers to alter mitochondrial function and limit energy production. Blocking interferon prevented metabolic abnormalities and improved aerobic fitness in mice lacking Tregs.

“The villain here is interferon,” Langston said. “In the absence of guardian Tregs to counter it, interferon went on to cause uncontrolled damage.”

Interferon is known to promote chronic inflammation, a process that underlies many chronic diseases and age-related conditions and has become a tantalizing target for therapies aimed at reducing inflammation. Tregs have also captured the attention of scientists and industry as treatments for a range of immunologic conditions marked by abnormal inflammation.

The study findings provide a glimpse into the cellular innerworkings behind exercise’s anti-inflammatory effects and underscore its importance in harnessing the body’s own immune defenses, the researchers said.

There are efforts afoot to design interventions targeting Tregs in the context of specific immune-mediated diseases. And while immunologic conditions driven by aberrant inflammation require carefully calibrated therapies, exercise is yet another way to counter inflammation, the researchers said.

“Our research suggests that with exercise, we have a natural way to boost the body’s immune responses to reduce inflammation,” Mathis said. “We’ve only looked in the muscle, but it’s possible that exercise is boosting Treg activity elsewhere in the body as well.”

Inspired by the enhanced visual system of the Papilio xuthus butterfly, a team of researchers have developed an imaging sensor capable of “seeing” into the UV range inaccessible to human eyes. The design of the sensor uses stacked photodiodes and perovskite nanocrystals (PNCs) capable of imaging different wavelengths in the UV range. Using the spectral signatures of biomedical markers, such as amino acids, this new imaging technology is even capable of differentiating between cancer cells and normal cells with 99% confidence.

This new research, led by University of Illinois Urbana-Champaign electrical and computer engineering professor Viktor Gruev and bioengineering professor Shuming Nie, was recently published in the journal Science Advances.

Small Variations

“We’ve taken inspiration from the visual system of butterflies, who are able to perceive multiple regions in the UV spectrum, and designed a camera that replicates that functionality,” Gruev says. “We did this by using novel perovskite nanocrystals, combined with silicon imaging technology, and this new camera technology can detect multiple UV regions.”

UV light is electromagnetic radiation with wavelengths shorter than that of visible light (but longer than x-rays). We are most familiar with UV radiation from the sun and the dangers it poses to human health. UV light is categorized into three different regions — UVA, UVB and UVC — based on different wavelength ranges. Because humans cannot see UV light, it is challenging to capture UV information, especially discerning the small differences between each region.

Butterflies, however, can see these small variations in the UV spectrum, like humans can see shades of blue and green. Gruev notes, “It is intriguing to me how they are able to see those small variations. UV light is incredibly difficult to capture, it just gets absorbed by everything, and butterflies have managed to do it extremely well.”

The Imitation Game

Humans have trichromatic vision with three photoreceptors, where every color perceived can be made from a combination of red, green and blue. Butterflies, however, have compound eyes, with six (or more) photoreceptor classes with distinct spectral sensitivities. In particular, the Papilio xuthus, a yellow, Asian swallowtail butterfly, has not only blue, green and red, but also violet, ultraviolet and broadband receptors. Further, butterflies have fluorescent pigments that allow them to convert UV light into visible light which can then be easily sensed by their photoreceptors. This allows them to perceive a broader range of colors and details in their environment.

Beyond the increased number of photoreceptors, butterflies also exhibit a unique tiered structure in their photoreceptors. To replicate the UV sensing mechanism of the Papilio xuthus butterfly, the UIUC team has emulated the process by combining a thin layer of PNCs with a tiered array of silicon photodiodes.

PNCs are a class of semiconductor nanocrystals that display unique properties similar to that of quantum dots — changing the size and composition of the particle changes the absorption and emission properties of the material. In the last few years, PNCs have emerged as an interesting material for different sensing applications, such as solar cells and LEDs. PNCs are extremely good at detecting UV (and even lower) wavelengths that traditional silicon detectors are not. In the new imaging sensor, the PNC layer is able to absorb UV photons and re-emit light in the visible (green) spectrum which is then detected by the tiered silicon photodiodes. Processing of these signals allows for mapping and identification of UV signatures.

Healthcare and Beyond

There are various biomedical markers present in cancerous tissues at higher concentrations than in healthy tissues — amino acids (building blocks of proteins), proteins, and enzymes. When excited with UV light, these markers light up and fluoresce in the UV and part of the visible spectrum, in a process called autofluorescence. “Imaging in the UV region has been limited and I would say that has been the biggest roadblock for making scientific progress,” explains Nie. “Now we have come up with this technology where we can image UV light with high sensitivity and can also distinguish small wavelength differences.”

Because cancer and healthy cells have different concentrations of markers and therefore different spectral signatures, the two classes of cells can be differentiated based on their fluorescence in the UV spectrum. The team evaluated their imaging device on its ability to discriminate cancer-related markers and found that is capable of differentiating between cancer and healthy cells with 99% confidence.

Gruev, Nie and their collaborative research team envision being able to use this sensor during surgery. One of the biggest challenges is knowing how much tissue to remove to ensure clear margins and such a sensor can help facilitate the decision-making process when a surgeon is removing a cancerous tumor.

“This new imaging technology is enabling us to differentiate cancerous versus healthy cells and is opening up new and exciting applications beyond just health,” Nie says. There are many other species besides butterflies capable of seeing in the UV, and having a way to detect that light will provide interesting opportunities for biologists to learn more about these species, such as their hunting and mating habits. Bringing the sensor underwater can help bring a greater understanding of that environment as well. While a lot of UV is absorbed by water, there is still enough that makes it through to have an impact and there are many animals underwater that also see and use UV light.