Until today, precise observations and analyses of the cosmic microwave background (CMB) and large-scale structure (LSS) have led to the establishment of the standard framework of the universe, the so-called ΛCDM model, where cold dark matter (CDM) and dark energy (the cosmological constant, Λ) are significant characteristics.

This model suggests that primordial fluctuations were generated at the beginning of the universe, or in the early universe, which acted as triggers, leading to the creation of all things in the universe including stars, galaxies, galaxy clusters, and their spatial distribution throughout space. Although they are very small when generated, fluctuations grow with time due to the gravitational pulling force, eventually forming a dense region of dark matter, or a halo. Then, different halos repeatedly collided and merged with one another, leading to the formation of celestial objects such as galaxies.

Since the nature of the spatial distribution of galaxies is strongly influenced by the nature of the primordial fluctuations that created them to begin with, statistical analyses of galaxy distributions have been actively conducted to observationally explore the nature of primordial fluctuations. In addition to this, the spatial pattern of galaxy shapes distributed over a wide area of the universe also reflects the nature of the underlying primordial fluctuations.

However, conventional analysis of large-scale structure has focused only on the spatial distribution of galaxies as points. More recently, researchers have started studying galaxy shapes, because it not only provides additional information, but it also provides a different perspective into the nature of the primordial fluctuations.

A team of researchers, led by at-the-time Kavli Institute for the Physics and Mathematics of the Universe (Kavli IPMU) graduate student Toshiki Kurita (currently a postdoctoral researcher at the Max Planck Institute for Astrophysics), and Kavli IPMU Professor Masahiro Takada developed a method to measure the power spectrum of galaxy shapes, which extracts key statistical information from galaxy shape patterns by combining the spectroscopic data of spatial distribution of galaxies and imaging data of individual galaxy shapes.

The researchers simultaneously analyzed the spatial distribution and shape pattern of approximately one million galaxies from the Sloan Digital Sky Survey (SDSS), the world’s largest survey of galaxies today.

As a result, they successfully constrained statistical properties of the primordial fluctuations that seeded the formation of the structure of the entire universe.

They found a statistically significant alignment of the orientations of two galaxies’ shapes more than 100 million light years apart. Their result showed correlations exist between distant galaxies whose formation processes are apparently independent and causally unrelated.

“In this research, we were able to impose constraints on the properties of the primordial fluctuations through statistical analysis of the ‘shapes’ of numerous galaxies obtained from the large-scale structure data. There are few precedents for research that uses galaxy shapes to explore the physics of the early universe, and the research process, from the construction of the idea and development of analysis methods to the actual data analysis, was a series of trial and error. Because of that, I faced many challenges. But I am glad that I was able to accomplish them during my doctoral program. I believe that this achievement will be the first step to open up a new research field of cosmology using galaxy shapes ,” said Kurita.

Furthermore, a detailed investigation of these correlations confirmed they are consistent with the correlations predicted by inflation, and do not exhibit a non-Gaussian feature of the primordial fluctuation.

“This research is the result of Toshiki’s doctoral dissertation. It’s a wonderful research achievement in which we developed a method to validate a cosmological model using galaxy shapes and galaxy distributions, applied it to data, and then tested the physics of inflation. It was a research topic that no one had ever done before, but he did all three steps: theory, measurement, and application. Congratulations! I am very proud of the fact that we were able to do all three steps. Unfortunately, I did not make the great discovery of detecting a new physics of inflation, but we have set a path for future research. We can expect to open up further areas of research using the Subaru Prime Focus Spectrograph,” said Takada.

The methods and results of this study will allow researchers in the future to further test inflation theory.

Details of this study were published on October 31 in Physical Review D as an Editors’ Suggestion.

This protein comes in two different varieties termed “isoforms,” which are known as gamma actin and beta actin. The difference between the two proteins is miniscule, only a few amino acids at just one part of the molecule vary. Yet this small change has a big impact on the cell. In nature, normally only mixtures of the two isoforms are found. In their study, the researchers separated out the two isoforms and analyzed them individually. The results were published in the journal Nature Communications.

The researchers studied the behaviour of networks of filaments, particularly focusing on the unique properties of the individual isoforms. They employed specialized techniques allowing them to assess the mechanics and dynamics of research models of cytoskeletal networks, drawing on expertise in biophysics at Göttingen and bioengineering at Warwick.

The results indicate that gamma actin prefers to form rigid networks near the cell’s apex, while beta actin preferentially forms parallel bundles with a distinct organizational pattern. This difference is likely to be due to the stronger interaction of gamma actin with specific types of positively charged ions, rendering its networks stiffer than those formed by beta actin. “Our findings are compelling because they open up new avenues for understanding the intricate dynamics of protein networks within cells,” explains Professor Andreas Janshoff, Institute for Physical Chemistry, University of Göttingen. The research advances scientists’ understanding of fundamental cellular processes by shedding light on specific biological functions of actin, and this will have particular relevance for processes involving cellular mechanics such as growth, division and maturation of cells in tissue. “The implications of these discoveries extend to the broader field of cellular biology, offering insights that could impact many areas of research and applications, for instance in developmental biology,” adds Janshoff.

Vision is a complex process. The visual perception of the environment is created by a combination of different wavelengths of light, which are decoded as colours and brightness in the brain. Photoreceptors in the retina first convert the light into electrical impulses: with sufficient light, the cones enable sharp, detailed, and coloured vision. Rods only contribute to vision in low light conditions allowing for different shades of grey to be distinguished but leaving vision much less precise. The electrical nerve impulses are finally transmitted to ganglion cells in the retina and then via the optic nerve to the visual cortex in the brain. This region of the brain processes the neural activity into a coloured image.

What influences the internal clock?

Ambient light however does not only allow us to see, it also influences our sleep-wake rhythm. Specialised ganglion cells are significantly involved in this process, which — like the cones and rods — are sensitive to light and react particularly strongly to short-wavelength light at a wavelength of around 490 nanometres. If light consists solely of short wavelengths of 440 to 490 nanometres, we perceive it as blue. If short-wavelength light activates the ganglion cells, they signal to the internal clock that it is daytime. The decisive factor here is how intense the light is per wavelength; the perceived colour is not relevant.

“However, the light-sensitive ganglion cells also receive information from the cones. This raises the question of whether the cones, and thereby the light colour, also influence the internal clock. After all, the most striking changes in brightness and light colour occur at sunrise and sunset, marking the beginning and end of a day,” says Dr. Christine Blume. At the Centre for Chronobiology of the University of Basel, she investigates the effects of light on humans and is the first author of a study investigating the effects of different light colours on the internal clock and sleep. The team of researchers from the University of Basel and the TUM has now published its findings in the scientific journal “Nature Human Behaviour.”

Light colours in comparison

“A study in mice in 2019 suggested that yellowish light has a stronger influence on the internal clock than blueish light,” says Christine Blume. In humans, the main effect of light on the internal clock and sleep is probably mediated via the light-sensitive ganglion cells. “However, there is reason to believe that the colour of light, which is encoded by the cones, could also be relevant for the internal clock.”

To get to the bottom of this, the researchers exposed 16 healthy volunteers to a blueish or yellowish light stimulus for one hour in the late evening, as well as a white light stimulus as a control condition. The light stimuli were designed in such a way that they differentially activated the colour-sensitive cones in the retina in a very controlled manner. However, the stimulation of the light-sensitive ganglion cells was the same in all three conditions. Differences in the effect of the light were therefore directly attributable to the respective stimulation of the cones and ultimately the colour of the light.

“This method of light stimulation allows us to separate the light properties that may play a role in how light effects humans in a clean experimental way,” says Manuel Spitschan, Professor of Chronobiology and Health at the Technical University of Munich, who was also involved in the study.

In order to understand the effects of the different light stimuli on the body, in the sleep laboratory the researchers determined whether the internal clock of the participants had changed depending on the colour of the light. Additionally, they assessed how long it took the volunteers to fall asleep and how deep their sleep was at the beginning of the night. The researchers also enquired about their tiredness and tested their ability to react, which decreases with increasing sleepiness.

Ganglion cells are crucial

The conclusion: “We found no evidence that the variation of light colour along a blue-yellow dimension plays a relevant role for the human internal clock or sleep,” says Christine Blume. This contradicts the results of the mouse study mentioned above. “Rather, our results support the findings of many other studies that the light-sensitive ganglion cells are most important for the human internal clock,” says the scientist.

Manuel Spitschan sees the study as an important step towards putting basic research into practice: “Our findings show that it is probably most important to take into account the effect of light on the light-sensitive ganglion cells when planning and designing lighting. The cones and therefore the colour play a very subordinate role.”

It remains to be seen whether the colour of the light also has no effect on sleep if the parameters change and, for example, the duration of the light exposure is extended or takes place at a different time. Follow-up studies should answer questions like these.

Night mode on screens — useful or not?

We often hear that the short-wavelength component of light from smartphone and tablet screens affects biological rhythms and sleep. The recommendation is therefore to put your mobile phone away early in the evening or at least use the night shift mode, which reduces the short-wavelength light proportions and looks slightly yellowish. Christine Blume confirms this. However, the yellowish colour adjustment is a by-product that could be avoided. “Technologically, it is possible to reduce the short-wavelength proportions even without colour adjustment of the display, however this has not yet been implemented in commercial mobile phone displays,” says the sleep researcher.

Scientists are now one step closer to eliminating that threat, thanks to a Texas A&M University-led collaboration that has developed a new family of polymers capable of killing bacteria without inducing antibiotic resistance by disrupting the membrane of these microorganisms.

“The new polymers we synthesized could help fight antibiotic resistance in the future by providing antibacterial molecules that operate through a mechanism against which bacteria do not seem to develop resistance,” said Dr. Quentin Michaudel, an assistant professor in the Department of Chemistry and lead investigator in the research, published Dec. 11 in the Proceedings of the National Academy of Sciences (PNAS).

Working at the interface of organic chemistry and polymer science, the Michaudel Laboratory was able to synthesize the new polymer by carefully designing a positively charged molecule that can be stitched many times to form a large molecule made of the same repeating charged motif using a carefully selected catalyst called AquaMet. According to Michaudel, that catalyst proves key, given that it has to tolerate a high concentration of charges and also be water-soluble — a feature he describes as uncommon for this type of process.

After achieving success, the Michaudel Lab put its polymers to the test against two main types of antibiotic-resistant bacteria — E. coli and Staphylococcus aureus (MRSA) — in collaboration with Dr. Jessica Schiffman’s group at the University of Massachusetts Amherst. While awaiting those results, the researchers also tested their polymers’ toxicity against human red blood cells.

“A common issue with antibacterial polymers is a lack of selectivity between bacteria and human cells when targeting the cellular membrane,” Michaudel explained. “The key is to strike a right balance between effectively inhibiting bacteria growth and killing several types of cells indiscriminately.”

Michaudel credits the multidisciplinary nature of scientific innovation and the generosity of dedicated researchers across the Texas A&M campus and country as factors in his team’s success in determining the perfect catalyst for their molecule assembly.

“This project was several years in the making and would not have been possible without the help of several groups, in addition to our UMass collaborators,” Michaudel said. “For instance, we had to ship some samples to the Letteri Lab at the University of Virginia to determine the length of our polymers, which required the use of an instrument that few labs in the country have. We are also tremendously grateful to [biochemistry Ph.D. candidate] Nathan Williams and Dr. Jean-Philippe Pellois here at Texas A&M, who provided their expertise in our assessment of toxicity against red blood cells.”

Michaudel says the team will now focus on improving the activity of its polymers against bacteria — specifically, their selectivity for bacterial cells versus human cells — before moving on to in vivo assays.

“We are in the process of synthesizing a variety of analogs with that exciting goal in mind,” he said.

The team’s paper, which features Michaudel Lab member and Texas A&M chemistry Ph.D. graduate Dr. Sarah Hancock ’23 as first author, can be viewed online along with related figures and captions. Other key contributors from the Michaudel Lab are chemistry graduate student An Tran ’23, postdoctoral scholar Dr. Arunava Maity and former postdoctoral scholar Dr. Nattawut Yuntawattana, who is now an assistant professor of materials science at Kasetsart University in Thailand.

This research was funded primarily by Michaudel’s National Institutes of Health Maximizing Investigators’ Research Award (MIRA) through the National Institute of General Medical Sciences.

A native of La Rochelle, France, Michaudel joined the Texas A&M Chemistry faculty in 2018 and holds a joint appointment in the Department of Materials Science and Engineering. In addition to an NIH MIRA in 2020, his career honors to date include a 2022 National Science Foundation Faculty Early Career Development (CAREER) Award, a 2022 American Chemical Society Polymeric Materials: Science and Engineering (PMSE) Young Investigator Award and a 2021 Thieme Chemistry Journals Award.

A research team based in Japan has revealed that stem-like proliferative cells — which are actively growing and dividing but not yet differentiating into specific cell types — appear at the site of injury and help form the blastema.

The findings were published in the scientific journal PLOS Biology.

“Importantly, these stem-like proliferative cells in blastema are different from the resident stem cells localized in the tentacle,” said corresponding author Yuichiro Nakajima, lecturer in the Graduate School of Pharmaceutical Sciences at the University of Tokyo. “Repair-specific proliferative cells mainly contribute to the epithelium — the thin outer layer — of the newly formed tentacle.”

The resident stem cells that exist in and near the tentacle are responsible for generating all cellular lineages during homeostasis and regeneration, meaning they maintain and repair whatever cells are needed during the jellyfish’s lifetime, according to Nakajima. Repair-specific proliferative cells only appear at the time of injury.

“Together, resident stem cells and repair-specific proliferative cells allow rapid regeneration of the functional tentacle within a few days,” Nakajima said, noting that jellyfish use their tentacles to hunt and feed.

This finding informs how researchers understand how blastema formation differs among different animal groups, according to first author Sosuke Fujita, a postdoctoral researcher in the same lab as Nakajima in the Graduate School of Pharmaceutical Sciences.

“In this study, our aim was to address the mechanism of blastema formation, using the tentacle of cnidarian jellyfish Cladonema as a regenerative model in non-bilaterians, or animals that do not form bilaterally — or left-right — during embryonic development,” Fujita said, explaining that the work may provide insight from an evolutionary perspective.

Salamanders, for example, are bilaterian animals capable of regenerating limbs. Their limbs contain stem cells restricted to specific cell-type needs, a process that appears to operate similarly to the repair-specific proliferative cells observed in the jellyfish.

“Given that repair-specific proliferative cells are analogues to the restricted stem cells in bilaterian salamander limbs, we can surmise that blastema formation by repair-specific proliferative cells is a common feature independently acquired for complex organ and appendage regeneration during animal evolution,” Fujita said.

The cellular origins of the repair-specific proliferative cells observed in the blastema remain unclear, though, and the researchers say the currently available tools to investigate the origins are too limited to elucidate the source of those cells or to identify other, different stem-like cells.

“It would be essential to introduce genetic tools that allow the tracing of specific cell lineages and the manipulation in Cladonema,” Nakajima said. “Ultimately, understanding blastema formation mechanisms in regenerative animals, including jellyfish, may help us identify cellular and molecular components that improve our own regenerative abilities.”

About 200,000 people in Sweden currently live with fibromyalgia, a long-term pain syndrome that causes great suffering for patients through widespread pain, fatigue, and stiffness in the body. There is no cure for fibromyalgia. Existing drugs often have insufficient effect, raising the need for more effective treatment methods. Cognitive behavioral therapy (CBT) has shown some effect, but there is a lack of trained CBT practitioners. There is also a lack of knowledge about which form of CBT is most effective. The study compared two different forms of internet-delivered cognitive behavioral therapy in terms of how well they reduce the symptoms and functional impact of fibromyalgia.

In brief, exposure-based CBT involves the participant systematically and repeatedly approaching situations, activities, and stimuli that the patient has previously avoided because the experiences are associated with pain, psychological discomfort, or symptoms such as fatigue and cognitive problems.

In traditional CBT, the participant is presented with several different strategies to work on during treatment, such as relaxation, activity planning, physical exercise, or strategies for managing negative thoughts and improving sleep.

The study showed that traditional CBT was by and large equivalent to the newer treatment form of exposure-based CBT.

“This result was surprising because our hypothesis, based on previous research, was that the new exposure-based form would be more effective. Our study shows that the traditional form can provide an equally good result and thus contributes to the discussion in the field,” says Maria Hedman-Lagerlöf, licensed psychologist and researcher at the Center for Psychiatry Research at the Department of Clinical Neuroscience, Karolinska Institutet.

The randomized study involved 274 people with fibromyalgia, who were randomly assigned to be treated with traditional or exposure-based CBT. The treatments were delivered entirely online and all participants had regular contact with their therapist.

Participants answered questions about their mood and symptoms before, during, and after treatment. After the 10-week treatment, 60 percent of those who received exposure-based CBT and 59 percent of those who received traditional CBT reported that their treatment had helped them.

“The fact that both treatments were associated with a significant reduction in the participants’ symptoms and functional impairment and that the effects were sustained for 12 months after completion of the treatment, indicates that the internet as a treatment format can be of great clinical benefit for people with fibromyalgia,” says Maria Hedman-Lagerlöf. “This is good news because it enables more people to access treatment.”

The study is the second largest to compare different psychological treatment options for fibromyalgia, according to the researchers.

“Our study is also one of the first to compare with another active, established psychological treatment,” says Maria Hedman-Lagerlöf.

Male aggression in rodents is known to be blocked when they smell female tears. This is an example of social chemosignaling, a process that is common in animals but less common — or less understood — in humans. To determine whether tears have the same affect in people, the researchers exposed a group of men to either women’s emotional tears or saline while they played a two-person game. The game was designed to elicit aggressive behavior against the other player, whom the men were led to believe was cheating. When given the opportunity, the men could get revenge on the other player by causing them lose money. The men did not know what they were sniffing and could not distinguish between the tears or the saline, which were both odorless.

Revenge-seeking aggressive behavior during the game dropped more than 40% after the men sniffed women’s emotional tears. When repeated in an MRI scanner, functional imaging showed two aggression-related brain regions — the prefrontal cortex and anterior insula — that became more active when the men were provoked during the game, but did not become as active in the same situations when the men were sniffing the tears. Individually, the greater the difference in this brain activity, the less often the player took revenge during the game. Finding this link between tears, brain activity, and aggressive behavior implies that social chemosignaling is a factor in human aggression, not simply an animal curiosity.

The authors add, “We found that just like in mice, human tears contain a chemical signal that blocks conspecific male aggression. This goes against the notion that emotional tears are uniquely human.”

Two researchers at The Ohio State University were among a group of experts invited by the journal Science to discuss how the ESA has evolved and what its future might hold.

Tanya Berger-Wolf, faculty director of Ohio State’s Translational Data Analytics Institute, led a group that wrote on “Sustainable, trustworthy, human-technology partnership.” Amy Ando, professor and chair of the university’s Department of Agricultural, Environmental, and Development Economics, wrote on “Harnessing economics for effective implementation.”

Berger-Wolf and her colleagues wrote, “We are in the middle of a mass extinction without even knowing all that we are losing and how fast.” But technology can help address that.

For example, they note the value of tools like camera traps that survey animal species and smartphone apps that allow citizen scientists to count insects, identify bird songs and report plant observations.

New tech has allowed scientists to monitor animal and plant populations at scale for the first time, said Berger-Wolf, who is also a professor of computer science and engineering, evolution, ecology and organismal biology, and electrical and computer engineering. One challenge is to find new ways to extract all the information from these new sources of data.

“But even with all this data, we are still monitoring only a tiny fraction of the biodiversity out in the world,” she said. “Without that information, we don’t know what we have, how different species are doing and whether our policies to protect endangered species are working.”

Most important, Berger-Wolf said, is the need to make sure to keep humans in the process. Technology needs to connect data, connect different regions of the world, connect people to nature and connect people to people.

“We don’t want to sever the connection between people and nature, we want to strengthen it,” she said.

“We cannot rely on technology to save the world’s biodiversity. It has to be an intentional partnership between humans and technology and AI.”

Economics should be another partner in the fight to save endangered species, Ando said.

“There’s this tendency to think that protecting endangered species is all about biology and ecology,” Ando said. “But various tools in economics are very helpful in making sure the work we do to implement the Endangered Species Act is successful. That is not always obvious to people.”

For example, bioeconomic research is a multidisciplinary effort between economists and biologists to work together to see how human behavior interacts with ecological processes and systems.

“We have to take into account feedback effects. People take an action, and that changes the ecosystem and that changes what people do,” she said. “We need to capture those feedback effects.”

The result can be novel ways to protect endangered species, such as “pop-up” habitat modification. For example, ranchers can take down fences temporarily while elk are migrating to allow them to move freely. Rice fields can be temporarily flooded during shorebird migration to give them a place to rest and feed on their travels.

We can “draw upon economics to optimize the timing, location and extent of temporary actions to maximize their net benefits to society,” Ando wrote in Science.

Another way economics can help is to develop policies that protect species before they become so threatened that they need ESA protection.

A common issue is that multiple landowners will all need to work together to protect the habitat of threatened species. But often, if some landowners take actions to protect a species, other landowners will think they don’t have to.

“Economists have been working to understand how we can coordinate landowners where we don’t have to implement draconian land use regulations, but still protect habitat,” Ando said.

“That is a very promising tactic that can protect species and also reduce the cost to people of doing so.”

Using the latest tools in genetic sequencing, researchers at Mayo Clinic reconstructed how a collective of viral genomes colonized a human brain. The virus acquired distinct mutations that drove the spread of the virus from the frontal cortex outward.

“Our study provides compelling data that shows how viral RNA mutated and spread throughout a human organ — the brain, in this case,” says Roberto Cattaneo, Ph.D., a Mayo Clinic virologist who is a co-lead author on a new PLOS Pathogens study. “Our discoveries will help studying and understanding how other viruses persist and adapt to the human brain, causing disease. This knowledge may facilitate the generation of effective antiviral drugs.”

What is measles?

Measles is one of the most contagious diseases. The measles virus infects the upper respiratory tract where it uses the trachea, or windpipe, as a trampoline to launch and spread through droplets dispersed when an infected person coughs or sneezes.

Dr. Cattaneo pioneered studies on how the measles virus spreads throughout the body.

He first began to study the measles virus about 40 years ago and was fascinated by the rare, lethal brain disease called subacute sclerosing panencephalitis (SSPE), which occurs in about 1 in every 10,000 measles cases. It can take about five to 10 years after the initial infection for the measles virus to mutate and spread throughout the brain. Symptoms of this progressive neurological disease include memory loss, seizures and immobility. Dr. Cattaneo studied SSPE for several years until the lethal disease nearly disappeared as more people were vaccinated against measles.

However, measles is resurging due to vaccine hesitancy and missed vaccinations. During the COVID-19 pandemic, millions of children missed receiving their measles vaccinations, which has resulted in an estimated 18% increase in measles cases and 43% increase in death from measles in 2021 compared to 2022 worldwide, according to a recent Centers for Disease Control and Prevention (CDC) report.

“We suspect SSPE cases will rise again as well. This is sad because this horrible disease can be prevented by vaccination. But now we are in the position to study SSPE with modern, genetic sequencing technology and learn more about it,” says Iris Yousaf, co-lead author of the study and a fifth-year Ph.D. candidate at Mayo Clinic Graduate School of Biomedical Sciences.

Dr. Cattaneo and Yousaf had a unique research opportunity through a collaboration with the CDC. They studied the brain of a person who had contracted measles as a child and had succumbed to SSPE years later as an adult. They investigated 15 specimens from different regions of the brain and conducted genetic sequencing on each region to piece together the puzzle of how the measles virus mutated and spread.

The researchers discovered that, after the measles virus entered the brain, its genome — the complete set of genetic material for the virus — began to change in harmful ways. The genome replicated, creating other genomes that were slightly different. Then, these genomes replicated again — resulting in more genomes that were each a little different as well. The virus did this multiple times, creating a population of varied genomes.

“In this population, two specific genomes had a combination of characteristics that worked together to promote virus spread from the initial location of the infection — the frontal cortex of the brain — out to colonize the entire organ,” says Dr. Cattaneo.

The next steps in this research are to understand how specific mutations favor virus spread in the brain. These studies will be done in cultivated brain cells and in clusters of cells resembling the brain called organoids. This knowledge may help in creating effective antiviral drugs to combat virus spread in the brain. However, pharmacological intervention in advanced disease stages is challenging. Preventing SSPE through measles vaccination remains the best method.