One of the greatest strengths of NASA’s James Webb Space Telescope is its ability to give astronomers detailed views of areas where new stars are being born. The latest example, showcased here in a new image from Webb’s Mid-Infrared Instrument (MIRI), is NGC 346 — the brightest and largest star-forming region in the Small Magellanic Cloud.

The Small Magellanic Cloud (SMC) is a satellite galaxy of the Milky Way, visible to the unaided eye in the southern constellation Tucana. This small companion galaxy is more primeval than the Milky Way in that it possesses fewer heavy elements, which are forged in stars through nuclear fusion and supernova explosions, compared to our own galaxy.

Since cosmic dust is formed from heavy elements like silicon and oxygen, scientists expected the SMC to lack significant amounts of dust. However the new MIRI image, as well as a previous image of NGC 346 from Webb’s Near-Infrared Camera released in January, show ample dust within this region.

In this representative-color image, blue tendrils trace emission from material that includes dusty silicates and sooty chemical molecules known as polycyclic aromatic hydrocarbons, or PAHs. More diffuse red emission shines from warm dust heated by the brightest and most massive stars in the heart of the region. An arc at the center left may be a reflection of light from the star near the arc’s center. (Similar, fainter arcs appear associated with stars at lower left and upper right.) Lastly, bright patches and filaments mark areas with abundant numbers of protostars. The research team looked for the reddest stars, and found 1,001 pinpoint sources of light, most of them young stars still embedded in their dusty cocoons.

By combining Webb data in both the near-infrared and mid-infrared, astronomers are able to take a fuller census of the stars and protostars within this dynamic region. The results have implications for our understanding of galaxies that existed billions of years ago, during an era in the universe known as “cosmic noon,” when star formation was at its peak and heavy element concentrations were lower, as seen in the SMC.The James Webb Space Telescope is the world’s premier space science observatory.

Scientists from Bristol and the University of Occupational and Environmental Health in Japan, sought to understand how ‘circadian misalignment’ — a phenomenon commonly associated with ‘jet-lag’ whereby the body’s biological clock is disrupted — affects the hormones responsible for regulating appetite.

Prevalent in night shift workers, in this new study, the international team reveal how circadian misalignment can profoundly alter the brain’s regulation of hormones controlling hunger to the detriment of metabolic health.

The team focused on glucocorticoid hormones in the adrenal gland which regulate many physiological functions including metabolism and appetite. Glucocorticoids are known to directly regulate a group of brain peptides controlling appetitive behaviour, with some increasing appetite (orexigenic) and some decreasing appetite (anorexigenic).

In an experiment using animal models, comprising a control group and a out-of-phase ‘jet-lagged’ group, the team found misalignment between light and dark cues led the out-of-phase group’s orexigenic hypothalamic neuropeptides (NPY) to become dysregulated, driving an increased desire to eat significantly more during the inactive phase of the day.

Strikingly, the team discovered that rats in the control group ate 88.4% of their daily intake during their active phase, and only 11.6% during their inactive phase. In contrast, the ‘jet-lagged’ group consumed 53.8% of their daily calories during their inactive phase (without an increase in activity during this time). This equated to nearly five-times more (460% more) than what the control group consumed during the inactive phase. These results show that it is timing of consumption that has been affected.

This new discovery revealed how completely, and significantly, disordered the neuropeptides become when daily glucocorticoid levels are out of synch with light and dark cues. However, the authors suggest the neuropeptides identified in this study may be promising targets for drug treatments adapted to treat eating disorders and obesity.

Dr Becky Conway-Campbell, Research Fellow in Bristol Medical School: Translational Health Sciences (THS) and the study’s senior author, said: “For people working throughout the night, a reversed body clock can play havoc with their health.

“For those who are working night shifts long-term, we recommend they try to maintain daylight exposure, cardiovascular exercise and mealtimes at regulated hours. However, internal brain messages to drive increased appetite are difficult to override with ‘discipline’ or ‘routine’ so we are currently designing studies to assess rescue strategies and pharmacological intervention drugs. We hope our findings also provide new insight into how chronic stress and sleep disruption leads to caloric overconsumption.”

Stafford Lightman, Professor of Medicine at Bristol Medical School: THS and co-senior author on the study, added: “The adrenal hormone corticosterone, which is normally secreted in a circadian manner, is a major factor in the daily control of brain peptides that regulate appetite. Furthermore when we disturb the normal relationship of corticosterone with the day to night light cycle it results in abnormal gene regulation and appetite during the period of time that the animals normally sleep.

“Our study shows that when we disturb our normal bodily rhythms this in turn disrupts normal appetite regulation in a way that is at least in part a result of desynchrony between adrenal steroid hormone production and the timing of the light and dark cycle.”

Dr Benjamin Flynn, one of the study’s co-authors who conducted the study while at Bristol but is now based at the University of Bath, added: “This is further evidence of how phase shift ‘jet-lag’ affects feeding behaviours and neuronal gene expression — data important for shift work co-morbidity research.”

This research was funded by the Medical Research Council.

As the largest member of the dolphin family, killer whales, also known as orcas, are found worldwide. Marine vessel traffic can disturb the hunting and communication of these black-and-white marine mammals. But they face another type of human threat — legacy and emerging persistent organic pollutants (POPs) in their environments. POPs include chlorinated hydrocarbons and flame retardants, and can accumulate in animals’ fat stores as the contaminants move up the food chain though a process called biomagnification.

Previous studies have shown that some Pacific orca populations can carry POP loads in their blubber that pose potential health risks, including reduced immunity, hormonal imbalances and reproductive issues. But information on orcas living in the North Atlantic are lacking. So, Anaïs Remili, Melissa McKinney and colleagues wanted to assess the contaminants present in animals spanning from Eastern Canada to Norway.

The researchers collected skin and blubber biopsies from over a hundred free-ranging killer whales, across the North Atlantic Ocean from Canada, Greenland, Iceland to Norway. They analyzed half of each tissue sample for five classes of POPs, including polychlorinated biphenyls (PCBs). The other portion was used to evaluate the animals’ diets. Multiple features stood out in the data:

• Specimens from orcas in the western North Atlantic contained substantially higher contaminant loads than ones from orcas on the eastern side — a pattern that contrasts with previously reported POP levels in other Arctic marine organisms.
• The pattern could be attributed to individuals’ diet rather than location. Specifically, killer whales foraging on fish had the lowest POP levels, and animals consuming marine mammals, such as seals or other whales, had the highest.
• PCB-associated health risks were highest for killer whales that ate primarily marine mammals, with most animals’ levels exceeding the threshold for a higher risk of female reproductive failure.
• The levels of one POP, known as α-HBCDD, were the highest reported for any marine mammal to date, despite the fact that this brominated flame retardant was banned a decade ago.

The researchers say the findings support the need for proper waste disposal to prevent contaminants from entering the oceans’ food chains and reaching the top predators. They explain that the findings of their study underscore the need for action to protect North Atlantic killer whales and their ecosystems.

PhD candidate Emily Massingham from UQ’s Faculty of Science managed a team of researchers which visited 79 villages across the Bornean orangutan range in Kalimantan, conducting face to face interviews with 431 people.

“Our study builds on previous research which indicated killing was one of the key reasons for orangutan population decline, alongside habitat loss,” Ms Massingham said.

“The aim of our project was to understand whether orangutans have been killed in recent times, to look at whether conservation projects are effectively preventing killing, and to gain insights into community perceptions and the motivations behind it.

“It has been almost 15 years since the previous study, and we did not find a clear decrease in killings despite Indonesia’s commendable efforts to reduce habitat loss.

“Thirty per cent of villages reported orangutans had been killed in the last 5 -10 years, despite the practice being both illegal and taboo — which also makes it hard to get an accurate picture of the true scale.”

Ms Massingham said Borneo’s orangutan population had decreased by 100,000 in recent decades, with current estimates suggesting fewer than 100,000 animals remain.

“Our findings did not indicate that conservation projects are reducing killing, highlighting an urgent need to improve the collective approach to orangutan conservation,” she said.

“Killing by humans needs to be addressed, as our findings suggest it may still be occurring and poses a real threat to the species.”

Ms Massingham said orangutans have long lifespans and breed slowly, so are particularly vulnerable to population declines driven by the death of adult apes.

“Our interviews revealed some of the situations which lead to the killing or displacement of individual orangutans,” she said.

“They include protecting crops and taking infant apes to keep as pets.”

The researchers outlined recommendations that could improve future conservation efforts.

“Working with communities and collaborating across disciplines and projects will be key,” Ms Massingham said.

“Conservationists need to work closely with individual villages to understand their needs and perspectives, identify the social drivers of killing of orangutans and implement solutions that reduce human-orangutan conflict.”

The research was conducted under a RISTEK permit, with the engagement of a local social development organisation to facilitate fieldwork.

A new study published today in the journal Neuron by researchers at the University of Wisconsin-Madison showed that FMRP, a protein deficient in individuals with fragile X syndrome, has a role in the function of mitochondria, part of a cell that produces energy, during prenatal development. Their results fundamentally change how scientists understand the developmental origins of fragile X syndrome and suggest a potential treatment for brain cells damaged by the dysfunction.

The study, led by four postdoctoral fellows — Minjie Shen, Carissa Sirois, Yu (Kristy) Guo and Meng Li — working in the lab of the lab of Xinyu Zhao, neuroscience professor and neurodevelopmental diseases researcher a UW-Madison’s Waisman Center, found FMRP regulating a gene called RACK1 to promote mitochondrial function. Using a drug to enhance mitochondrial function, they were able to rescue brain cells damaged by lack of FMRP.

Individuals with FXS may present developmental delays — not sitting, walking or talking at expected ages — as well as mild to severe intellectual disability, learning disabilities and social and behavioral problems. About half are also diagnosed with autism spectrum disorder.

In previous research, Zhao found that mitochondria in mice with an FMRP deficiency that imitates FXS were smaller and unhealthy. Diving deeper, they also discovered that FMRP regulates genes involved in mitochondria fission-fusion, a process into which mitochondria fuse into a bigger shape in order to produce more energy for the cell.

For the study, researchers grew brain cells called neurons grown from induced pluripotent stem cells. Because the stem cells came from people with FXS, the researchers could study the development of the disorder at a cellular level, determining whether mitochondria in human cells experienced issues similar to those in mice.

“And indeed, we found that human neurons also have fragmented (smaller) mitochondria,” Zhao says. They also found fewer mitochondria in neurons derived from FXS patients, which they did not see in the neurons of the mice modeling FXS.

“In human neurons, it’s a deficit in twofold. Not just fission-fusion, but also likely in the production of mitochondria,” Zhao says.

Although it has been long known that FMRP is deeply involved in FXS, the new discovery pinpoints a role for the protein in early development of the condition.

Symptoms of FXS present long after the baby is born. Many babies appear to be developing typically before showing slower development, autistic features or developmental deficits. Children with FXS are typically diagnosed at three years of age or older.

“Which means many scientists have been thinking that FMRP is more important for the postnatal maturation state,” Zhao says.

FMRP is protein that regulates the use of messenger RNA, sort of a of working copy of DNA used to produce the proteins that make things happen in cells. The researchers found that many of the mRNA strands that interact with FMRP are implicated in autism, providing a molecular link between FXS and autism spectrum disorder. Unexpectedly, many FMRP-bound mRNAs are expressed by genes classified as essential — genes that are very busy during prenatal development but less active after birth.

“This means that FMRP has a function in prenatal development that we have not really thought about before,” Zhao says. “The fact that we found that FMRP also regulates prenatal development is really interesting and is actually indicating that what we see in fragile X syndrome, some of the effects already happened within the prenatal development.”

One of those essential genes is RACK1, identified for the first time as playing a role in FXS.

“When RACK1 is lower in fragile X neurons, the mitochondria are suffering and the neurons exhibit mitochondrial deficit and hyperexcitability, like immature neurons. But when we reintroduce RACK1, we can rescue this,” Zhao says.

Using cultured neurons derived from individuals with FXS to screen for drugs, the researchers found a drug called leflunomide that corrected mitochondrial deficits. The treatment improved mitochondrial function and reduced the neurons’ hyperexcitability.

Next, Zhao wants to do a detailed biochemical analysis of mitochondrial dysfunction and figure out which key proteins are less present in FXS-affected neurons. She is also working on better understanding how RACK1 and leflunomide work to rescue mitochondrial function.

Other collaborators on the study include Waisman Center investigators Qiang Chang, Anita Bhattacharyya, Andre Sousa, Daifeng Wang, Donna Werling and UW-Madison neuroscience professor Jon Levine.

This research was supported by grants from the National Institutes of Health (R01MH118827, R01NS105200, R01MH116582, R01MH118827, R01HD064743, R01NS064025, R01AG067025, U01MH116492, P51 OD011106, U54HD090256, P50HD105353, R24HD000836 and T32 GM141013) and the Department of Defense (W81XWH-22-1-0621).

Though scientists have long known through observational data that the Milky Way is warped and its edges are flared like a skirt, no one could explain why.

Now, Harvard astronomers at the Center for Astrophysics | Harvard and Smithsonian (CfA) have performed the first calculations that fully explain this phenomenon, with compelling evidence pointing to the Milky Way’s envelopment in an off-kilter halo of dark matter. The work also bolsters current thinking about how the galaxy evolved and may offer clues into some of the mysteries of dark matter.

The new calculations were led by Jiwon Jesse Han, a Griffin Graduate School of Arts and Sciences student affiliated with the CfA. Published in Nature Astronomy, the work includes co-authors Charlie Conroy and Lars Hernquist, both faculty members at the CfA and in the Department of Astronomy.

Our galaxy is located inside a diffuse cloud called the stellar halo, which extends much farther out into the universe. In groundbreaking work published last year, the Harvard team deduced that the stellar halo is tilted and elliptical in shape, like a zeppelin or football.

Building on that, the team assumed the same shape for the dark matter halo, the larger entity that encompasses everything in and around the Milky Way. Dark matter makes up 80 percent of the galaxy’s mass but is invisible because it doesn’t interact with light, so the shape of that halo must be inferred. Using models to calculate the orbits of stars within a tilted, oblong dark matter halo, the team found a near-perfect match to existing observations of a warped, flared galaxy.

“A tilted dark halo is actually fairly common in simulations, but no one had explored its effect on the Milky Way,” Conroy said. “It turns out that the tilt is an elegant way to explain both the magnitude and direction of our galaxy’s wobbly disk.”

Scientists had long surmised that the Milky Way formed due to a galactic collision; the astronomers’ work further underscores that hypothesis.

“If the galaxy was just evolving on its own, it would have had this nice, spherical halo, this nice, flat disk,” Han said. “So the fact that the halo is tilted and has a football-like shape suggests that our galaxy experienced a merger event, where two galaxies collide.”

Their calculation of the dark matter halo’s probable shape may also provide clues as to the properties and particle nature of dark matter itself, which remain unsolved mysteries in physics. “The fact that the galaxy is not spherical in our data implies that there is some limit to which dark matter can interact with itself,” Han explained.

Confidence in these findings might lead to better ways to cleverly study the unobservable dark matter that makes up most of the universe. This includes new ways to pick up on kinematic signatures of dark sub-halos, which are miniature dark matter halos zipping around the galaxy.