This study, published in The Astrophysical Journal, was performed by a multi-year cohort of undergraduate researchers in the Penn State branch of the Pulsar Search Collaboratory student club. Maura McLaughlin, Chair, Eberly Distinguished Professor of Physics and Astronomy, West Virginia University, created the Pulsar Search Collaboratory to engage high schoolers and undergraduates in pulsar science, and she helped facilitate access to the data used in this study. Using archival data from the Arecibo Observatory, the student team found patterns that show how pulsar signals change as they move through the interstellar medium (ISM), the gas and dust that fills the space between stars. The team measured scintillation bandwidths for 23 pulsars, including new data for six pulsars not previously studied. The results showed that in almost all cases, measured bandwidths were higher than predictions by widely used models of the galaxy, highlighting a need for updates to current ISM density models.

“This work demonstrates the value of large, archived datasets,” said Dr. Sofia Sheikh, SETI Institute researcher and lead author. “Even years after the Arecibo Observatory’s collapse, its data continues to unlock critical information that can advance our understanding of the galaxy and enhance our ability to study phenomena like gravitational waves.”

When radio light from a pulsar travels through the ISM, it gets distorted in a process known as “diffractive interstellar scintillation” (DISS). The same physics that makes light refract into patterns on the bottom of a swimming pool or causes stars to twinkle in the night sky also causes DISS. Instead of water in a pool or air in the atmosphere, DISS occurs when clouds of charged particles in space cause a pulsar’s light to “twinkle” across time and frequency.

Collaborations such as the NANOGrav Physics Frontiers Center use pulsars to study the gravitational wave background, which can help researchers understand the early Universe and the prevalence of gravitational-wave sources such as supermassive black-hole binaries. The pulsar timing measurements must be extremely precise to measure the gravitational wave background correctly. The results from this study will help better model the distortions caused by DISS, which will increase the precision of the pulsar timing measurements of projects like NANOGrav.

The study found that models incorporating galactic structures, such as spiral arms, tend to better fit the DISS data despite the challenge of accurately modeling the Milky Way’s structure. Moreover, the study showed that the models most accurately predicted the bandwidths of pulsars that were used in their development while predictions of newly discovered pulsars were worse. This suggests limitations that reinforce the need for continual updates to galactic structure models.”

This pilot study, part of the AO327 survey from Arecibo, serves as a foundation for future research on pulsar scintillation and gravitational waves. By expanding the pilot study to more recently discovered pulsars in the AO327 dataset in the future, the team hopes to further improve ISM density models for collaborations that observe pulsar timing arrays like NANOGrav.

This research involves the collaboration between authors at the SETI Institute, Penn State, and the NANOGrav Group at West Virginia University. The team includes SETI Institute researcher Michael Lam and former SETI Institute researcher Grayce Brown.

There is evidence that alcohol consumption is influenced by prenatal sex steroids so experts from Swansea University and colleagues from the Medical University of Lodz decided to use a sample of students for their research into the subject.

Their findings have just been published by the online journal American Journal of Human Biology. They found relationships between high alcohol consumption and long 4^th digits relative to 2^nd digits. This showed that high prenatal testosterone relative to oestrogen is linked to high student alcohol consumption.

Professor John Manning, of Swansea’s Applied Sports, Technology, Exercise and Medicine (A-STEM) research team, said: “Alcohol consumption is a major social and economic problem. Therefore, it is important to understand why alcohol use shows considerable differences across individuals.”

The study used a sample of 258 participants — 169 of them female — and it revealed consumption rates varied between the sexes. In comparison to women, men show higher alcohol consumption and higher mortality from alcohol abuse.

He said: “A pattern like this suggests an involvement of sex hormones, such as testosterone and oestrogen. Digit ratio (2D:4D: the relative lengths of the 2^nd [index] and 4^th [ring] fingers) is thought to be an index of early testosterone (long 4^th digit) and oestrogen (long 2^nd digit).

“It is known that alcohol-dependent patients have very long 4^th digits relative to their 2^nd digits, suggesting high testosterone relative to estrogen exposure before birth. As expected, the associations were stronger for men than women.”

Now the researchers hope their conclusions will bring a better understanding of the factors underlying the pattern of alcohol consumption, from abstinence to occasional use to harmful dependence.

This is the latest paper which has highlighted Professor Manning’s work in the field of digit ratios. Previous research has examined how digit ratio may provide vital information concerning outcomes after contracting Covid-19, as well as oxygen consumption in footballers.

All this may not be breaking news to everyone, but amid this upward march in average temperatures, a striking new phenomenon is emerging: distinct regions are seeing repeated heat waves that are so extreme, they fall far beyond what any model of global warming can predict or explain. A new study provides the first worldwide map of such regions, which show up on every continent except Antarctica like giant, angry skin blotches. In recent years these heat waves have killed tens of thousands of people, withered crops and forests, and sparked devastating wildfires.

“The large and unexpected margins by which recent regional-scale extremes have broken earlier records have raised questions about the degree to which climate models can provide adequate estimates of relations between global mean temperature changes and regional climate risks,” says the study.

“This is about extreme trends that are the outcome of physical interactions we might not completely understand,” said lead author Kai Kornhuber, an adjunct scientist at the Columbia Climate School’s Lamont-Doherty Earth Observatory. “These regions become temporary hothouses.” Kornhuber is also a senior research scholar at the International Institute for Applied Systems Analysis in Austria.

The study was just published in the journal Proceedings of the National Academy of Sciences.

The study looks at heat waves over the past 65 years, identifying areas where extreme heat is accelerating considerably faster than more moderate temperatures. This often results in maximum temperatures that have been repeatedly broken by outsize, sometimes astonishing, amounts. For instance, a nine-day wave that hammered the U.S. Pacific Northwest and southwestern Canada in June 2021 broke daily records in some locales by 30 degrees C, or 54 F. This included the highest ever temperature recorded in Canada, 121.3 F, in Lytton, British Columbia. The town burned to the ground the next day in a wildfire driven in large part by the drying of vegetation in the extraordinary heat. In Oregon and Washington state, hundreds of people died from heat stroke and other health conditions.

These extreme heat waves have been hitting predominantly in the last five years or so, though some occurred in the early 2000s or before. The most hard-hit regions include populous central China, Japan, Korea, the Arabian peninsula, eastern Australia and scattered parts of Africa. Others include Canada’s Northwest Territories and its High Arctic islands, northern Greenland, the southern end of South America and scattered patches of Siberia. Areas of Texas and New Mexico appear on the map, though they are not at the most extreme end.

According to the report, the most intense and consistent signal comes from northwestern Europe, where sequences of heat waves contributed to some 60,000 deaths in 2022 and 47,000 deaths in 2023. These occurred across Germany, France, the United Kingdom, the Netherlands and other countries. Here, in recent years, the hottest days of the year are warming twice as fast the summer mean temperatures. The region is especially vulnerable in part because, unlike places like the United States, few people have air conditioning, because traditionally it was almost never needed. The outbreaks have continued; as recently as this September, new maximum temperature records were set in Austria, France, Hungary, Slovenia, Norway and Sweden.

The researchers call the statistical trends “tail-widening” that is, the anomalous occurrence of temperatures at the far upper end, or beyond, anything that would be expected with simple upward shifts in mean summer temperatures. But the phenomenon is not happening everywhere; the study shows that maximum temperatures across many other regions are actually lower than what models would predict. These include wide areas of the north-central United States and south-central Canada, interior parts of South America, much of Siberia, northern Africa and northern Australia. Heat is increasing in these regions as well, but the extremes are increasing at similar or lower speed than what changes in average would suggest.

Climbing overall temperatures make heat waves more likely in many cases, but the causes of the extreme heat outbreaks are not entirely clear. In Europe and Russia, an earlier study led by Kornhuber blamed heat waves and droughts on wobbles in the jet stream, a fast-moving river of air that continuously circles the northern hemisphere. Hemmed in by historically frigid temperatures in the far north and much warmer ones further south, the jet stream generally confines itself to a narrow band. But the Arctic is warming on average far more quickly than most other parts of the Earth, and this appears to be destabilizing the jet stream, causing it to develop so-called Rossby waves, which suck hot air from the south and park it in temperate regions that normally do not see extreme heat for days or weeks at a time.

This is only one hypothesis, and it does not seem to explain all the extremes. A study of the fatal 2021 Pacific Northwest/southwestern Canada heat wave led by Lamont-Doherty graduate student Samuel Bartusek (also a coauthor on the latest paper) identified a confluence of factors. Some seemed connected to long-term climate change, others to chance. The study identified a disruption in the jet stream similar to the Rossby waves thought to affect Europe and Russia. It also found that decades of slowly rising temperatures had been drying out regional vegetation, so that when a spell of hot weather came along, plants had fewer reserves of water to evaporate into the air, a process that helps moderate heat. A third factor: a series of smaller-scale atmospheric waves that gathered heat from the Pacific Ocean surface and transported it eastward onto land. Like Europe, few people in this region have air conditioning, because it is generally not needed, and this probably upped the death toll.

The heat wave “was so extreme, it’s tempting to apply the label of a ‘black swan’ event, one that can’t be predicted,” said Bartusek. “But there’s a boundary between the totally unpredictable, the plausible and the totally expected that’s hard to categorize. I would call this more of a grey swan.”

While the wealthy United States is better prepared than many other places, excessive heat nevertheless kills more people than all other weather-related causes combined, including hurricanes, tornadoes and floods. According to a study out this past August, the yearly death rate has more than doubled since 1999, with 2,325 heat-related deaths in 2023. This has recently led to calls for heat waves to be named, similar to hurricanes, in order to heighten public awareness and motivate governments to prepare.

“Due to their unprecedented nature, these heat waves are usually linked to very severe health impacts, and can be disastrous for agriculture,vegetation and infrastructure,” said Kornhuber. “We’re not built for them, and we might not be able to adapt fast enough.”

The study was also coauthored by Richard Seager and Mingfang Ting of Lamont-Doherty Earth Observatory, and H.J. Schellnhuber of the International Institute for Applied Systems Analysis.

This revolutionary field still faces many challenges, including the nontrivial task of convincing stem cells to differentiate into desired cell types for treatment. And even if the correct cells or tissues are created and can function successfully in the body, immune rejection presents a formidable barrier to their use. To overcome this obstacle, regenerative medicine treatments in use today require systemic immunosuppression, leaving patients vulnerable to environmental hazards like viruses, bacteria and cancer cells.

In a novel approach to tackle these obstacles, researchers at the Medical University of South Carolina and the University of Florida recently collaborated on a novel, highly specific strategy to treat type 1 diabetes (T1D) using a tagged beta cell transplant in tandem with localized immune protection provided by specialized immune cells also tagged with a complementary but inert targeting molecule.

According to Leonardo Ferreira, Ph.D., a researcher at MUSC Hollings Cancer Center and one of the principal investigators on the study, marrying stem cell engineering and regulatory T cell (Treg) engineering allowed the first step toward a readily available, off-the-shelf solution to treating T1D.

In their recent study published in the journal Cell Reports, the researchers described a unique collaboration that leveraged the beta cell engineering expertise of the lab of Holger Russ, an associate professor of pharmacology and therapeutics at the University of Florida, combined with the delicate surgical expertise and chimeric antigen receptor (CAR) T cell expertise available at Hollings.

For T1D patients, the trouble begins with an immune system self-attack on pancreatic beta cells, the cells that produce the hormone insulin to regulate blood sugar levels. Without a reliable way to self-regulate blood glucose levels, patients are forced to live with a high-maintenance regimen of glucose monitoring and insulin management to maintain health and avoid dangerous complications like neuropathy, amputation and blindness.

For now, some patients with poorly controlled T1D may consider islet cell transplantation using beta cells from a donor. Beta cells are isolated from a donor pancreas, purified and delivered to the patient’s liver, where they can take up residence and begin secreting insulin. However, this option requires patients to undergo immunosuppression for the rest of their lives to keep the body from rejecting the foreign beta cells. It also requires the availability of donor cells, which might require long waits or may not happen at all.

To focus on an alternative solution, the researchers used an engineering strategy with tagged beta cells generated from stem cells. And to induce localized immune protection, the researchers chose to use Tregs, a type of immune cell that monitors and controls the immune response.

“Most of the cells of the immune system are focused on killing invasive elements,” Ferreira said. “But Tregs are the generals of the immune system. They make sure that nothing goes overboard, and they train the immune system on how to respond in the future.”

The researchers used a mouse model to test their strategy. By transplanting beta cells that were engineered from stem cells and included a nonreactive tag — an inactivated version of epidermal growth factor receptor — into the kidney capsules of immunodeficient mice, they showed that the cells were incorporated and began to manufacture functional insulin. In the next phase of testing, the mice were exposed to an aggressive type of immune cell to check on the viability of the transplanted beta cells in the face of a simulated immune response. As expected, all of the beta cells were killed by the immune response, the same thing that happens in people with T1D.

To avoid the killing response in the next phase, the researchers added specialized Tregs along with the immune challenge. These cells were tagged with CAR technology using a receptor that specifically recognized the inert EGFR tag present on the transplanted beta cells. With this added step, the researchers observed the immune protection they hoped for, as they observed the transplanted beta cells remaining safe, sound and functional in their new home.

Ferreira was delighted with the results and energized to take the next steps. “With this approach,” he said, “we made both the lock and the key for creating immune tolerance.”

Now that Ferreira and colleagues have shown the feasibility of their approach to T1D treatment, they plan to continue their research efforts, including building a whole library of locks and keys — differentiated stem cells and tagged protective Tregs — for multiple purposes, such as targeting certain cancers, lupus and other autoimmune diseases.

A few questions remain, such as the specific ligand that should be used for human transplantation and the longevity of Treg-mediated immune protection. The ligand or tag must be inert and have no negative impact on the function of the cells or create any reaction that could cause side effects. And it is still unknown if one Treg treatment will be effective or might need to be repeated at intervals that have yet to be established. Because Tregs can educate immune cells to maintain immune tolerance, it is possible that one treatment will be adequate, but further research is needed to understand the long-term effects.

Answering these questions and confirming the validity of the approach in humans may soon transform T1D from a chronic, high-maintenance disease with many complications to one that can be managed much more easily.

“Establishing such biomarkers could provide a key step in changing how we care for, treat, and offer interventions to people with psychosis,” said Brian Keane, PhD, assistant professor of Psychiatry, Center for Visual Science, and Neuroscience at the University of Rochester Medical Center. Keane recently co-authored an article in Molecular Psychiatry that identifies how MRI scans could reveal brain differences in people with psychosis. “Aside from potentially predicting future psychosis onset, biomarkers could also help stratify patients into clinically meaningful subgroups and suggest new options for treatment or intervention.”

Using data collected by the Human Connectome Early Psychosis Project, researchers looked at MRI scans from 159 participants. These included 105 who developed a psychotic disorder up to five years prior to testing. In the brains of participants with psychosis, researchers found that sensory regions in the cortex were more weakly connected to each other and more strongly connected to the thalamus, the brain’s information relay station. These differences were confined to the somatomotor network, which processes bodily movement and sensations, and a visual network, which generates representations of objects, faces, and complex features. Combining the dysconnectivity patterns across these two networks allowed the researchers to create a “somato-visual” biomarker.

Previous research has suggested that abnormal brain connectivity exists prominently in the sensory networks of people with schizophrenia, but it remained unclear which networks were most responsible or whether dysconnectivity could be explained by other illness factors, such as antipsychotic use, anxiety, or stress.

“What makes this biomarker unique is its large effect size, its robustness to over a dozen common confounds, and its high reliability across multiple scans. A single five-minute scan could potentially improve our ability to predict which at-risk individuals will transition to a psychotic disorder, which in turn could allow for more timely treatments or interventions,” Keane said. “It also gives us a place to keep looking. An important next step will be to determine if the somato-visual biomarker emerges before or as psychosis begins.”

Additional authors include Yonatan Abrham, Boyang Hu, and Brent Johnson of the University of Rochester, Carrisa Cocuzza of Yale University, and Michael Cole of Rutgers University. This work was supported by a K01 grant and a Psychiatry Department pilot grant at the University of Rochester.

The study, published Nov. 25 in Nature Aging, may lead to new longevity treatments that could extend human lifespan. It also establishes a mortality timer that reveals how long a cell has left before it dies.

As people get older, they are more likely to develop health conditions, such as cancer, cardiovascular disease and neurodegenerative diseases.

“Aging is the highest risk factor for these diseases,” said Dr. Jessica Tyler, professor of pathology and laboratory medicine at Weill Cornell Medicine. “Rather than treating each disease separately, a better approach would be to develop a therapeutic or supplement that will delay the onset of diseases by preventing the underlying molecular defects that cause them.” The nucleolus may hold the key.

Small Packages

The nucleus holds the cell’s chromosomes and the nucleolus where the ribosomal DNA (rDNA) is housed. The nucleolus isolates the rDNA which encodes the RNA portions of the ribosomes, the protein-building machinery. The rDNA is one of the most fragile parts of the genome, due to its repetitive nature making it more difficult to maintain and fix if damaged. If damage in the rDNA is not accurately repaired, it can lead to chromosomal rearrangements and cell death.

In organisms from yeast to worms to humans, nucleoli expand during aging. On the flip side, anti-aging strategies like calorie restriction, or eating less, result in smaller nucleoli. “Calorie restriction does so many different things, and no one knows the precise way that it is extending lifespan,” Dr. Tyler said.

Dr. Tyler and postdoctoral fellow Dr. J. Ignacio Gutierrez, the first author of the paper, suspected that keeping nucleoli small could delay aging. To test this idea, they engineered an artificial way to secure rDNA to the membrane surrounding the nucleus of yeast cells so they could control when it was anchored and when it was not. “The advantage of our system is that we could isolate the nucleolus size from all of the other effects of anti-aging strategies,” Dr. Gutierrez said.

The researchers discovered that tethering the nucleolus was enough to keep it compact, and small nucleoli delayed aging to about the same extent as calorie restriction.

Final Moments

Interestingly, nucleoli did not expand at the same rate during the entire lifespan as cells aged. They remained small for most of the yeast’s life, but at a nucleolar size threshold, the nucleoli suddenly began to grow quickly and expand to a much larger size. Cells only survived for an average of about five more cell divisions after hitting this threshold.

“When we saw it wasn’t a linear size increase, we knew something really important was happening,” said Dr. Gutierrez. Passing the threshold appears to serve as a mortality timer, ticking down the final moments of a cell’s life.

During aging, DNA accumulates damage, some of which can be devastating to the cell. In tests, the team found that large nucleoli had less stable rDNA than smaller ones. Also, when the structure is large, proteins and other factors that are usually excluded from the nucleolus are no longer kept out. It’s as if the nucleolus becomes leaky, letting in molecules that can wreak havoc on the fragile rDNA.

“The whole point of condensates is to separate biological reactions to help them work efficiently, but now when you have other proteins coming into the nucleolus, it leads to genome instability, which triggers the end of the lifespan,” Dr. Tyler said. These proteins can cause catastrophic problems, such as chromosomal rearrangements, to build up.

Next, the researchers plan to study nucleolar effects on aging in human stem cells. Stem cells are special because they have the potential to replace other cell types as they die. But eventually, the stem cells stop dividing, so the researchers hope to use the knowledge gained from this project to make them last longer.

“I was excited that we could connect the structure of the nucleolus with the repair process in a way that could be conserved from yeast to humans,” said Dr. Gutierrez.