Category: 7. Science

The use of assisted reproductive technologies like in vitro fertilization is becoming more common worldwide. However, while these technologies successfully create viable embryos, a little over half of all embryos are lost because they fail to implant into the uterus.

Now, in an article published recently in Nature Communications, researchers describe a technique for studying embryonic implantation in mice by using uterine tissue outside the body (or “ex vivo“), which they hope will lead to improved implantation rates in humans.

Studying implantation is inherently more difficult than the prior stages of in vitro fertilization because it requires observing deep tissues in a live uterine environment. These challenges made researchers wonder: what if they could find a way to keep part of the uterus alive outside of the body, so that implantation could be observed without any barriers?

Previous studies have used model embryos, created from stem cells, to emulate embryonic development pre- and post-implantation. However, without the uterus, they cannot genuinely replicate embryo implantation, and studies have been unable to recreate this process.”

Takehiro Hiraoka, lead author

Using a specialized culture method, in which mouse uterine tissue is positioned between liquid and gas surfaces on either side, the researchers were able to place mouse embryos onto small pieces of endometrium tissue. They could then evaluate how the embryos implanted and developed. Impressively, their technique had over 90% efficacy for implantation, which was followed by embryo development and invasion of the uterine lining by the embryo.

“We also saw some features that are characteristic of what happens in implantation inside the body,” says Masahito Ikawa, senior author. “For example, the maternal implantation regulator COX-2 was induced at the site of embryonic attachment.”

To further highlight the potential of their system, the research team looked at the downstream pathways of COX-2 induction. They found that embryonic AKT, a protein that is involved in placental formation and arrangement as well as in cell survival, migration, and invasion, was affected by maternal COX-2.

“Further experiments indicated that introducing an activated form of AKT into embryos recovered defective implantation that was triggered by maternal COX-2 inhibition,” confirms Ikawa. “We were thus able to find a potential way to overcome the issue of implantation failure, indicating the strong potential of our technique for improving assisted reproduction in the future.”

Although challenges remain, such as how to keep the embryos developing past embryonic day 5.5, the results are promising. With future methodological improvements, this technique will allow for the development of treatments for people with recurrent implantation failure. It may also improve implantation rates in assisted reproductive technologies, thereby allowing families with previously untreatable conditions to achieve their dreams.

By Dean Murray

An explosive new space image reveals a star’s inner conflict hours before it blew up.

The picture shows the inside of a star turning on itself in the short time before it spectacularly exploded, according to a new study from NASA’s Chandra X-ray Observatory.

The shattered star, known as the Cassiopeia A supernova remnant, is one of the best-known, well-studied objects in the sky.

NASA explains: “Over three hundred years ago, however, it was a giant star on the brink of self-destruction.

“The new Chandra study reveals that just hours before it exploded, the star’s interior violently rearranged itself.

“This last-minute shuffling of its stellar belly has profound implications for understanding how massive stars explode and how their remains behave afterwards.”

Cassiopeia A (Cas A for short) was one of the first objects the telescope looked at after its launch in 1999, and astronomers have repeatedly returned to observe it.

“It seems like each time we closely look at Chandra data of Cas A, we learn something new and exciting,” said Toshiki Sato of Meiji University in Japan who led the study. “Now we’ve taken that invaluable X-ray data, combined it with powerful computer models, and found something extraordinary.”

The new research with Chandra data reveals a change that happened deep within the star at the very last moments of its life. After more than a million years, Cas A underwent major changes in its final hours before exploding.

“Our research shows that just before the star in Cas A collapsed, part of an inner layer with large amounts of silicon traveled outwards and broke into a neighboring layer with lots of neon,” said co-author Kai Matsunaga of Kyoto University in Japan. “This is a violent event where the barrier between these two layers disappears.”

The strong turbulent flows created by the star’s internal changes may have promoted the development of the supernova blast wave, facilitating the star’s explosion.

“Perhaps the most important effect of this change in the star’s structure is that it may have helped trigger the explosion itself,” said co-author Hiroyuki Uchida, also of Kyoto University. “Such final internal activity of a star may change its fate—whether it will shine as a supernova or not.”

The results have been published in the latest issue of The Astrophysical Journal.

The following information was released by the University of Georgia:

By

Savannah Peat

Millennials, Gen Z may not know they’re committing fraud or they may just not care

If you’re under the age of 34, you may be more willing to commit insurance fraud, according to new University of Georgia research.

The new study suggests that the younger you are, the more likely you may be to deceive a company or adjuster to get desired funds or outcomes.

But some fraudsters might not realize they’re committing a crime when they do.

“Many people, especially younger people, have an adversarial relationship with insurance companies,” said Brenda Cude, lead author of the study and a professor emerita in the UGA College of Family and Consumer Sciences. “If you’re pushed into a position of thinking you need to fight, maybe that pushes people into actions that they wouldn’t otherwise consider, especially if they’re not aware that it’s technically illegal. There are lots of major consequences that could come from that.”

2 out of 5 in younger generations unfazed by insurance fraud

The researchers relied on data from the Coalition Against Insurance Fraud, which surveyed almost 1,500 adults about their thoughts on insurance claims.

Among other questions, the survey asked respondents if they would:

Consider or had included damages that happened before a car accident on a claim (or if they had done so in the past).

Leave out information or provide false information on an insurance application to get better coverage or a lower premium.

Help a medical provider bill for treatment they hadn’t actually received and more.

Respondents were also asked if they knew anyone who had committed one of these crimes.

Two out of five respondents between the ages of 25 to 34 said they were OK with the fraudulent actions taken in the scenarios.

They saw it as a smart way to save money or a way to help a friend out of a tough situation.

“Age was significant. Part of that may be the impersonal way that younger adults relate to insurance companies,” Cude said. “They think, ‘I’m not hurting a person if I commit fraud. This is just a website.’ They might think it’s a good idea to tell the insurer their car is parked at their parents’ house when it’s actually in downtown Atlanta. But that’s technically fraud.”

Generational divide may reflect ethical, moral differences

Younger generations’ more carefree attitudes may affect their willingness to engage in insurance fraud, the researchers said.

Only about 5% of those 55 and older signaled that they were OK with fraud. Cude suggested that there might be a connection between age and ethics, with older respondents reflecting a stronger moral compass.

Millennials and Gen Z only changed their minds on insurance fraud if they perceived serious consequences; quick, wide-scale harm from their actions or felt bad about it.

“The younger generation just might have a weaker connection to morality and have a situation-based code of ethics. It doesn’t bother them to do things, even if they know that they’re wrong, because they think they’re getting cheated and in the right,” she said.

People don’t like insurance companies or understand what constitutes fraud

Overall, the way people felt about insurance companies was unanimously bad regardless of age. That feeling is unlikely to change and won’t impact whether people commit fraud, Cude said.

But one possible explanation for younger generations’ apathy toward insurance fraud may be that they don’t know what actually qualifies as fraud or how fraudulent claims may impact others.

“We need to think more about how to approach younger folks in terms of insurance fraud. Part of that solution might be experience, but maybe part of that solution is also education,” said Cude. “I don’t think people really understand their insurance very well or the difference between a legit claim practice and something that is actually considered fraudulent.”

Education might include learning how insurance works as well as why insurers make the decisions they do.

This study was published in the Journal of Consumer Affairs and was co-authored by Hanchun Zhang.

By Stephen Beech

DNA dating back over one million years has been identified in the woolly mammoth remains.

Scientists who discovered some of the world’s oldest microbial DNA also identified for the first time bacteria that may have caused disease in the now extinct tusked mammals.

An international team, led by researchers from the Centre for Palaeogenetics in Sweden, analyzed microbial DNA from 483 mammoth specimens, of which 440 were sequenced for the first time.

Among them was a steppe mammoth that lived about 1.1 million years ago.

Using advanced genomic and bioinformatic techniques, the researchers distinguished microbes that once lived alongside the mammoths from those that invaded their remains after death.

Study lead author Dr. Benjamin Guinet, of the Centre for Palaeogenetics, said: “Imagine holding a million-year-old mammoth tooth.

“What if I told you it still carries traces of the ancient microbes that lived together with this mammoth?

“Our results push the study of microbial DNA back beyond a million years, opening up new possibilities to explore how host-associated microbes evolved in parallel with their hosts.”

The team identified six microbial groups consistently associated with mammoth hosts, including relatives of Streptococcus, Actinobacillus, Pasteurella and Erysipelothrix.

They said some of the microbes may have been pathogenic. For instance, one Pasteurella-related bacterium identified in the study is closely related to a pathogen that has caused fatal outbreaks in African elephants.

Since African and Asian elephants are the closest living relatives of mammoths, the researchers say that their findings raise questions about whether mammoths may also have been vulnerable to similar infections.

The team reconstructed partial genomes of Erysipelothrix from a 1.1-million-year-old steppe mammoth, representing the oldest known host-associated microbial DNA ever recovered.

They say that pushes the limits of what researchers can learn about the interactions between ancient hosts and their microbiomes.

Study senior author Dr. Tom van der Valk, also of the Centre for Palaeogenetics, said: “As microbes evolve fast, obtaining reliable DNA data across more than a million years was like following a trail that kept rewriting itself.

“Our findings show that ancient remains can preserve biological insights far beyond the host genome, offering us perspectives on how microbes influenced adaptation, disease, and extinction in Pleistocene ecosystems.”

Although the exact impact of the identified microbes on mammoth health is difficult to determine due to DNA degradation and limited comparative data, the researchers say the study provides an “unprecedented” glimpse into the microbiomes of extinct big beasts.

The findings, published in the journal Cell, suggest that some microbial lineages coexisted with mammoths for hundreds of thousands of years, spanning both wide geographic ranges and evolutionary timescales, from over one million years ago to the extinction of woolly mammoths on Wrangel Island about 4,000 years ago.

Ancient DNA expert Love Dalén, Professor of Evolutionary Genomics at the Centre for Palaeogenetics, added: “This work opens a new chapter in understanding the biology of extinct species.

“Not only can we study the genomes of mammoths themselves, but we can now begin to explore the microbial communities that lived inside them,”

An analysis of the bones and teeth of ancient mammoths (Mammuthus) has identified some of the microorganisms that lived in the animals’ mouths and bodies more than one million years ago.

The study, published in Cell on 2 September¹, describes the oldest microbial DNA ever sequenced, and reveals that some species of pathogenic bacteria that have been linked to the deaths of African elephants (Loxodonta africana) once infected the mouths of their ancient cousins.

The findings offer “a good opportunity to get a global picture about what kind of bacteria or viruses we could find in this extinct species”, says study co-author Benjamin Guinet, a palaeomicrobiologist at the Centre for Palaeogenetics in Stockholm, Sweden. Further research could provide insights into how microbes might have helped ancient animals to adapt to varied environments, and whether they might have been involved in the extinction of these species.

Pathogenic microbes

Previous research on ancient remains has focused mainly on the DNA of humans and human-associated microorganisms, and few studies have looked at microbe–host interactions in prehistoric animals.

To investigate the relationship between mammoths and microorganisms, the researchers analysed ancient microbial DNA from samples of teeth, skulls and skin from 483 mammoths. The specimens encompass a range of geographical locations, from North America and Britain to Siberia, and date from the Early Pleistocene — around one million years ago — to the extinction of the last mammoths on Wrangel Island (a remote island off the coast of Siberia) during the Holocene, 4,000 years ago.

The researchers identified 310 microbial species that were associated with the mammoth tissues. Many of these were environmental microorganisms that would have colonized the tissues after death, so the team first filtered out the DNA sequences of these post-mortem bacteria. This allowed them to focus on the bacteria that lived inside the mammoths when they were alive.

Using metagenomic screening — a technique for sequencing genetic material in samples that contain genomes from a mixture of organisms — the researchers analysed the DNA present in the mammoth specimens. They then used phylogenetic inference to identify the bacterial genera, by comparing the ancient microbial sequences with those of modern bacteria..

The analysis found six microbial groups associated with the hosts, some of which might have caused diseases in the mammoths. These included a strain similar to Actinobacillus, which has previously been isolated from pig (Sus domesticus) faeces and is thought to be part of the mammoth oral microbiome. They also identified Pasteurella, a bacterial genus closely related to a pathogen that has been linked to the deaths of several African elephants in Botswana and Zimbabwe in 2020. The pathogen infected the mouths of the elephants, then made its way to the bloodstream, causing fatal septicaemia.

The team also reconstructed genomes of a family of bacteria called Erysipelothrix from samples from four woolly mammoths and from a 1.1-million-year-old steppe mammoth, which is the oldest host-associated microbial DNA yet discovered. Unlike the other bacterial groups, which were associated only with teeth cells, this microorganism was, in the case of the woolly mammal specimens, found in bone tissue.

Ancient microbiomes

The exact effects that these bacterial colonies had on the health of mammoths is difficult to elucidate from this genetic analysis, but the researchers say their study provides a first look at the microbes of ancient animals.

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A new multimodal atlas constructed by researchers at the Massachusetts Institute of Technology reveals that the progression of Alzheimer’s disease involves widespread changes in the regulation of gene expression in brain cells. The findings, published in Cell, offer a high-resolution account of how disruptions in epigenomic integrity correlate with both the severity of brain pathology and the extent of cognitive decline.

The study analyzed 384 post-mortem brain samples from 111 individuals, spanning 6 brain regions. In total, more than 3.5 million cells were profiled using single-cell RNA sequencing and ATAC-seq. This allowed the team to map both the transcriptome and the epigenome – the machinery responsible for which genes are activated or repressed in different cell types.

Two central patterns of epigenomic deterioration

Comparative analysis of brains with and without Alzheimer’s pathology revealed two main trends in epigenomic disruption. First, cells in vulnerable brain regions lost the compartmental organization of their nuclear architecture, leading to inappropriate opening and closing of DNA regions involved in gene expression. Second, these same cells exhibited a loss of epigenomic information, indicating they could no longer sustain the regulatory patterns that define their identity and function.

“To understand the circuitry, the logic responsible for gene expression changes in Alzheimer’s disease, we needed to understand the regulation and upstream control of all the changes that are happening, and that’s where the epigenome comes in.”

Dr. Manolis Kellis.

The researchers created an epigenomic information score to quantify these changes at the single-cell level. Cells from the hippocampus and entorhinal cortex – regions typically affected early in Alzheimer’s – showed marked decreases in these scores as disease advanced. The most vulnerable cell types included microglia, oligodendrocytes and certain excitatory neurons.

Link between chromatin state and cognitive decline

The breakdown of epigenomic regulation appeared to coincide with the activation of disease-related gene networks and a decline in cognitive ability. Where cells preserved compartmental structure and regulatory control, cognition tended to be maintained. Conversely, cells with more disordered chromatin states were associated with increased expression of genes involved in inflammation and oxidative stress.

The researchers also identified over 1 million gene-regulatory control regions that different cell types use to sustain their specific function. Comparing patterns across the disease continuum, they observed that regions typically repressed in healthy cells became accessible in advanced disease, allowing harmful gene expression programs to emerge.

Insights into Alzheimer’s risk genes

The study also explored how genetic risk factors for Alzheimer’s intersect with epigenomic changes. For instance, in individuals carrying two copies of the APOE4 variant, microglia initially increased their regulatory complexity – suggesting an early compensatory response – but later showed steep declines as the disease progressed. This trajectory may help explain the high risk associated with this genotype.

Neurons expressing the RELN gene, previously identified as susceptible in Alzheimer’s, also showed early and severe epigenomic information loss. However, in cognitively resilient individuals, these neurons retained their regulatory patterns, highlighting a potential axis of disease resistance.

Chromatin guardians and nuclear disorder

Cells undergoing epigenomic erosion showed increased accessibility in genomic regions that are normally repressed by proteins such as Polycomb group regulators. These findings suggest that the loss of “chromatin guardians” may be a key feature of disease vulnerability. In contrast, cells from resilient individuals continued to express genes associated with synaptic function and neural connectivity.

By assembling a comprehensive gene-regulatory map of Alzheimer’s disease across multiple brain regions and stages, the study offers a reference point for future research into the molecular underpinnings of neurodegeneration. While the work does not identify direct therapeutic targets, it emphasizes the role of epigenomic control in maintaining neuronal identity and function.

“The key to developing new and more effective treatments for Alzheimer’s disease depends on deepening our understanding of the mechanisms that contribute to the breakdowns of cellular and network function in the brain.”

Dr. Li-Huei Tsai.

Reference: Liu Z, Zhang S, James BT, et al. Single-cell multiregion epigenomic rewiring in Alzheimer’s disease progression and cognitive resilience. Cell. 2025:S0092867425007330. doi: 10.1016/j.cell.2025.06.031

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A bus-size asteroid, first spotted just over a week ago, will zoom past Earth tomorrow (Sept. 3). The space rock will not get this close to us again until Sept. 4, 2125 — almost 100 years to the day.

The asteroid, dubbed 2025 QV5, was first spotted on Aug. 24. It is approximately 35 feet (11 meters) across, or around the same width as a school bus is long, and is hurtling toward us at more than 13,900 mph (22,400 km/h), according to NASA’s Jet Propulsion Laboratory (JPL) Asteroid Watch.

A groundbreaking study by researchers from Wuhan University, York University (UK), and Peking University has uncovered how Escherichia coli (E. coli) persister bacteria survive antibiotics by protecting their genetic instructions. The work, published in Nature Microbiology, offers new hope for tackling chronic, recurring infections.

Persister bacteria, which enter a dormant state to survive antibiotics that target active cells, are linked to over 20% of chronic infections and resist current treatments. Understanding their survival mechanisms could lead to new ways to combat recurring infections. This study utilized E. coli bacteria as a model and found that prolonged stress leads to the increased formation of aggresomes (membraneless droplets) and the enrichment of mRNA (molecules that carry instructions for making proteins) within them, which enhances the ability of E. coli to survive and recover from stress.

Key Findings

They used multiple approaches, including imaging, modelling, and transcriptomics, to show that prolonged stress leading to ATP(fuel for all living cells) depletion in Escherichia coli results in increased aggresome formation, their compaction, and enrichment of mRNA within aggresomes compared to the cytosol(the liquid inside of cells). Transcript length was longer in aggresomes compared to the cytosol. Mass spectrometry showed exclusion of mRNA ribonuclease(an enzyme that breaks down RNA) from aggresomes, which was due to negative charge repulsion. Experiments with fluorescent reporters and disruption of aggresome formation showed that mRNA storage within aggresomes promoted translation and was associated with reduced lag phases during growth after stress removal. These findings suggest that mRNA storage within aggresomes confers an advantage for bacterial survival and recovery from stress.

Future Implications

This breakthrough illuminates how persister cells survive and revive after antibiotic treatment. By targeting aggresomes, new drugs could disrupt this protective mechanism, preventing bacteria from storing mRNA and making them more vulnerable to elimination, thus reducing the risk of infection relapse.

*This article is featured in PKU News “Why It Matters” series. More from this series.