New findings raise questions about the role of microbes living in the lungs. More than 35 trillion bacteria live throughout the human body, forming microbiomes in the gut, mouth, lungs, skin, and urogenital tract. Researchers increasingly recognize that these microbial communities are connected to both health and disease, but much about what individual microbes do [...]Lipid droplets in the kidneys may help cats maintain a consistent chemical “scent identity.” Scent marks can linger long after an animal has moved on, allowing urine and other chemical signals to carry information across both distance and time. Yet the molecules responsible for odor do not remain unchanged. They evaporate, break down, and shift [...]
Dear scientists: Follow the ants
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Thanks to having the “chunkiest squid butt” ever seen on an ancient cephalopod, paleontologists have discovered a 160-million-year-old octopus cousin. The newly identified fossils are described by an international research team in their study recently published in Papers in Palaeontology, which also includes a potential explanation for Wyoteuthis linsterorum’s hefty proportions. Just like today’s tentacled ocean dwellers, the Mesozoic squid ancestor likely had no problem devouring its relatives—or even members of its own species.
W. linsterorum is a belemnite, a group of prehistoric cephalopods who left behind some of paleontology’s most common fossils. Examples of their bullet-shaped structures known as a rostrum have regularly shown up at dig sites around the world for over 200 years. This includes the Sundance Formation in present-day Wyoming, which was covered by an inland sea millions of years ago.
Most of Wyoming’s belemnites are comparatively tiny—usually about two-to-four inches long and less than one inch wide. But about 30 years ago, Wyoming Dinosaur Center founder Burkhard Pohl found a fossil that “stuck out like a sore thumb,” according to study co-author Bill Wahl. While the preserved belemnite rostrum was about as long as other examples, it measured about 2.4 inches wide. Based on what they knew of belemnite proportions, paleontologists estimated this specimen’s entire body probably reached nearly two feet long.
Without any comparable examples, the thick squid butt remained in storage for nearly three decades. In 2019, fossil collector Cliff Linster finally discovered a similar cephalopod near Ten Sleep, Wyoming. He soon donated it to the Wyoming Dinosaur Center, and researchers began analyzing this pair of mystery fossils.
Computed tomography (CT) scanning allowed the team to inspect the remains without damaging them. The results confirmed the ancient sea creatures were never-before-seen belemnites.What’s more, they belonged to a family researchers previously believed went extinct millions of years earlier.
“After spending years fossil hunting in Wyoming and collecting countless fossils of the common Pachyteuthis belemnites here in Wyoming, this one is unlike anything I have ever seen,” Jessica Lippincott, a paleontologist and study co-author, said in a statement.
But why did W. linsterorum evolve to reach such bulky proportions? The team believes the answer lies in the diets of many present-day cephalopods.
“A possible explanation is that their relatively large size gave them an advantage when hunting co-occurring smaller belemnites of the genus Pachyteuthis,” explained paleontologist Alexey Ippolitov, a study co-author now at New Zealand’s Victoria University. “Modern squid, after all, are hardly picky when it comes to prey: they readily hunt not only other species of cephalopods, but sometimes even their own kind.”
An unexpected and surprising species, W. linsterorum is named in honor of Cliff Linster, who died in June 2026. While he didn’t live to see the dedication, Linster was well aware that the team was working to describe the animal he helped discover.
“It goes to show that we are still finding new species of fossils all the time, and people who rockhound or collect invertebrate fossils can also contribute to science,” said Lippincott.
The post ‘Squid butt’ fossil belongs to one of the ‘chunkiest’ cephalopods ever discovered appeared first on Popular Science.
The salmon? Eaten. The days? Shorter. The bears? Fatter.
After spending the summer eating the fatty pink salmon swimming through Katmai National Park and Preserve in Alaska, it’s time to celebrate the park’s iconic brown bears (Ursus arctos). Fat Bear Week begins on Tuesday, September 22, and here is everything you need to know.
Think March Madness, just without the basketball and significantly more bears. Fat Bear Week is a single-elimination tournament, where bear enthusiasts from around the world can vote online for their favorite chunky bear. After each round, the bear with the most votes advances until the winner is announced on September 29. According to the Katmai Conservancy, the event began as a one-day event in 2014 with 1,700 votes cast. Only 10 years later, 1.2 million votes were cast from over 100 countries.
The brown bears return to Brooks Falls for the salmon migration every year in late June, where viewers can watch them on explore.org’s livestream. There, they will feast to fatten up for the long winter ahead. By late summer, the nutritious fish will spawn and then begin to die. The bears will then move to the lower Brooks River in September and October to eat the dead and dying salmon near the river’s mouth.
Eating all of this salmon is important because the heftier the bear, the better chance they will survive their long winter hibernation. Despite being the poster species for winter hibernation, bears are not “deep hibernators,” they way that squirrels, bats, and bees are. Bears enter a state called torpor, which is an involuntary state primarily triggered by lack of food. During this time, the bears rely on stored fat reserves for energy. A torpid bear’s eating, drinking, and waste functions will cease, as its body metabolizes these stores it put on over the summer.
This year, Fat Bear Week begins on Tuesday, September 22, and a winner will be crowned on Tuesday, September 29.
Votes may be cast from noon to 9 p.m. EDT (9 a.m. to 6 p.m. PDT and 8 a.m. to 5 p.m. ADT)
from September 22 and 29 at fatbearweek.org.
Photographs comparing the bears from earlier in the summer and later in the summer will be shown, so voters can get an idea of just how much weight the bears put on during their salmon fest. An adult male bear can go from roughly 700 pounds in the early summer to over 1,200 pounds by fall.
Voters are also encouraged to get familiar with each bear’s life history and the unique challenges they face to survive.
The 2026 Fat Bear Week Bracket will be released on Friday, September 18.
In 2025, Bear #32 (Chunk) took the crown, despite beginning the salmon run with a freshly broken jaw. He was likely injured while fighting with another bear for a mate, but he still managed to catch plenty of fish. Chunk is known for his dominance and size, but also narrow-set eyes, dark fur, a prominent brow ridge, and a distinctive scar across his muzzle.
Donations can be made to Katmai Conservancy’s Otis Fund. The Otis Fund is named after Bear #480 (Otis), who won four Fat Bear Week titles before his death around 2024. All donations made between September 22 and October 3 will be matched by explore.org.
This year’s livestream featured an example of how wild (and upsetting to humans) nature can be. On Tuesday, July 28, the live-cams captured a young brown bear cub being killed and eaten by an unrelated mother bear (Bear #806). The deceased cub was born this spring and the child of Bear #909, a 10-year-old brown bear. Bear #909 started the season with two cubs, but now lost both.
On Sunday, August 2, one of Bear #335’s (Jolly) cubs died, after following three unrelated cubs up a tree. The mother of the cubs already in the tree attacked Bear #335’s cub, who did not survive the encounter. The identity of the mother bear who killed the spring cub was not confirmed.
Following the first cub’s death, naturalist Mike Fitz and park rangers Christine Loberg and Sarah Bruce said this likely the first documented case occurring at Brooks River. While there is no one answer as to why mother bears are killing cubs, some experts suspect bear adoption, food scarcity, and fights for dominance all play a role.
Additionally, this year also saw the cub with silver-hued fur, a cub who hopefully learned important lesson about porcupine quill safety, the unique fishing stylings of Bear #164 (Bucky Dent), and Bear #284’s (Electra) family who can “walk on water.”
The post Fat Bear Week kicks off September 22 appeared first on Popular Science.
In order to survive, the first humans to reach Mars will immediately need a safe and reliable place to set up shop. But building on Earth’s neighbor is immensely more challenging than construction projects at home. The Martian surface is a practically airless vacuum, constantly bombarded with radiation, and regularly reaches temperatures as low as -81 degrees Fahrenheit.
However, there is a very specific process on Earth that approximates similar conditions to the Red Planet: freeze-drying. According to researchers at The Hong Kong University of Science and Technology, the same method used to preserve perishable foods could also inspire sturdy and even recyclable 3D-printed houses on Mars. The secret ingredients? Everyday gelatin and yeast. The novel approach is detailed in a study published today in the journal Chem Circularity.
“My inspiration came from freeze-dried fruits that become harder. So I asked myself if we can take advantage of that and make some materials,” Jishen Qiu, a study co-author and civil engineer, said in a statement.
The combination of materials are simple: sand and an adhesive binder. Since gluing tiny rocks together requires specialized stickiness, Qiu’s team invented a new concoction from gelatin and lab engineered yeast. When mixed, the yeast microbes become coated with adhesive proteins similar to those used by mussels to anchor on stones underwater. The goop is then extruded through a 3D printer nozzle into an extremely cold, low-pressure environment, where it solidifies as the water instantly freezes and converts from ice to vapor. The final result is a light, porous, foam-like material that remains very resilient.
“This is actually strong enough to build a one- or two-story building on Earth—whose gravity is three times that of Mars,” explained Qiu. “So, you can probably easily build a multistory building on Mars with the material.”
Qiu and his collaborators know they must first start small before expanding to Martian neighborhoods. Their prototype domes are only about the size of a wine cork at this point, but their compressive strength is comparable to low-grade concrete.
Engineers have experimented with 3D-printed structures to use on the moon and Mars for years, but many of these still require steps like melting down rocks or lunar regolith. These methods usually require a lot of extra energy, which may limit their utility. Qiu’s technique requires comparatively little energy, although he admits it’s still unclear if yeasts can withstand life on Mars. That said, the team’s early results are a promising step towards simple, efficient, and sturdy buildings beyond Earth. If nothing else, yeast also lends itself to trial-and-error.
“As long as there’s one yeast that’s still alive, you can grow them again,” added Qiu.
The post Mars astronauts could live in houses 3D-printed from freeze-dried yeast appeared first on Popular Science.
In the wild, mimicry is an important tool for survival. Some baby hummingbirds disguise themselves as caterpillars with stinging hairs to avoid predators, while octopus, squid, and cuttlefish use camouflage to blend in with their surroundings and hide. Even plants get in on the mimicry fun, with some mimicking the small of rotten meat to attract flies and others using their petals to trick flies into pollinating on them.
True to its name, Iran’s spider-tailed horned viper (Pseudocerastes urarachnoides) has a rather novel strategy. It uses a tail that looks like a spider to lure birds trying to eat the decoy spider. When the time is right, the snake jumps into action and eats the bird.
The spider-tailed horned viper is a relatively new species to science, and a study published today in the journal The Anatomical Record is peeling back the layers of this master mimic. A team from the Field Museum in Chicago used X-ray computed tomography (XCT) scanners to take a look inside of the snake’s spidery tail and found that their tailbones appear rather normal.
“Scientists first collected a specimen of this snake in 1968, and when they brought it back to the Field Museum, people thought that it had some sort of deformity at the tip of its tail, like a tumor,” Sara Ruane, a study co-author and the Field’s Associate Curator of Herpetology and Director of the Core Laboratories, said in a statement. “It sat on the shelves of the museum for decades, but it wasn’t until another specimen with a similar tail was found in 2003 that people revisited it.”
Scientists described the snake as a new species in 2006, using the specimen housed in the Field Museum’s collections as the holotype. Holotype specimens serve as a main standard-bearer and reference point for the physical characteristics of a species, so that scientists can compare and contrast them to see if a specimen belongs to one species or another.
Shortly after naming the spider-tailed horned viper, researchers recorded video of the snake using the spider-like appendage at the tip of its tail as a way to lure in unsuspecting birds.
“I remember being a PhD student in about 2008 and first seeing the videos of this snake in the wild,” says Ruane. “The appendage at the end of its tail is so outrageous, I remember thinking it was so cool. It’s truly unique among snakes.”
In 2023, Ruane attended a conference with Georgios Georgalis, an associate professor at the Polish Academy of Sciences in Kraków. Georgalis mentioned that he was interested in studying the Field Museum’s spider-tailed horned viper holotype specimen.
“I am primarily a paleontologist, so I try to use modern snake species to make sense of fossil remains,” said Georgalis, who is also a co-author on the new study. “In vipers, the vertebral column unfortunately doesn’t give us very many clues about what kind of snake we’re looking at. When we find fossils, we often just find individual bones rather than the entire skeleton, and the individual vertebrae are so different from each other along the snake’s body that it’s hard to use them to identify a species.”
The spider-tailed horned viper offered a unique opportunity to study snake vertebrae. Georgalis said that viper vertebrae in particular have not been very well studied. They also wanted to know more about this species’ unusual tail.
To take a closer look, they used the Field Museum’s XCT lab. With XCT, scientists can scan objects and take thousands of X-ray images. These images are then stacked together to produce a 3D rendering of the object’s interior. It essentially allows scientists to study rare or one-of-a-kind specimens in detail without cutting them open or and risking damage.
“With the spider-tailed horned viper, we were particularly interested in seeing what the vertebrae at the tip of the tail look like, because the exterior of this snake’s tail is so unusual, and because it’s used for this unusual bird-luring behavior,” says Georgalis. “In some other snakes, like sand boas and rubber boas, the vertebrae at the tip of the tail have extreme shapes that look really alien. We wanted to investigate if the spider-tailed horn viper’s tail was similarly strange inside.”
Surprisingly, the scans revealed that the inside of the viper’s tail looked quite normal. The spider-tip tail is only visible on the outside of the snake and the vertebrae were the same as they would be in other vipers.
“There was nothing in the snake’s skeleton that would suggest how extreme its tail looks on the outside,” said Georgalis.
Findings like these show how fossil skeletons only tell one part of the story of what an animal looked like and how it behaved. Nothing in the spider-tailed horned viper’s skeleton would suggest it has such a unique tail, or that the tail twitches in a way that tricks birds.
“It’s one of the, let’s say, frustrations of the life of a paleontologist,” says Georgalis. “We work with beautiful animals, but most of the time, we’re trying to put together puzzles with some of the pieces missing, and in the end, we can’t be 100% sure of what the animal actually looked like.”
It’s also a reminder that prehistoric life may be even stranger than we can imagine by looking at bones alone. These findings also lay some groundwork for scientists studying how tissues evolve and develop and underscores the value of museum collections.
“Specimens that were collected 50, 100, 200 years ago are still being used all the time to learn new things,” said Ruane.
The post Snake that hunts with fake spider on its tail shocks scientists appeared first on Popular Science.
Recurrent pregnancy loss affects an estimated one in a hundred couples trying to build a family, yet in a striking proportion of cases no cause is ever identified, leaving patients and clinicians alike without answers. A new study from researchers at the Institute of Medical Sciences, Banaras Hindu University in Varanasi, India, published in the journal Biochemical Genetics, offers a detailed picture of the genetic abnormalities lurking in lost pregnancies and points to a two-tier testing strategy that could substantially improve diagnostic yield. Combining rapid aneuploidy screening with high-resolution chromosomal microarray analysis and a layer of computational biology, the team has mapped not only which chromosomes go wrong in recurrent miscarriage but also which biological pathways those errors may disrupt.
The research team, led by Shivani Mishra and corresponding author Royana Singh, recruited 125 fetal specimens from pregnancies that ended in loss, ultimately analyzing 118 samples after applying predefined exclusion criteria designed to guard against contamination and degraded tissue. The specimens, which included products of conception and fetal tissues such as skin, muscle, and cartilage obtained during autopsy, underwent DNA extraction and quantitative fluorescent PCR, a technique that amplifies short tandem repeat markers scattered across chromosomes 13, 18, 21, X, and Y. By measuring the relative quantity of fluorescent signals at these markers, QF-PCR can detect the most common whole-chromosome imbalances, the trisomies and monosomies that account for the majority of chromosomally abnormal miscarriages, often within a day or two of sample receipt.
The results were sobering but clinically rich. Of the 118 samples analyzed, QF-PCR identified aneuploidy in 36 cases, a detection rate of 30.5 percent. Twenty of these were monosomies, in which an entire chromosome is missing from the fetal genome, and sixteen were trisomies, in which an extra copy is present. The remaining 82 samples appeared normal by this rapid screen. That nearly one in three lost pregnancies carried a whole-chromosome imbalance confirms the central role of aneuploidy in early pregnancy failure, and it also carries a practical message for genetic counseling: when an aneuploidy is identified as the cause of a loss, the recurrence risk for future pregnancies is generally low, information that can meaningfully reduce anxiety for couples facing the aftermath of repeated loss.
Beyond the raw detection numbers, the study teased out clinical associations that matter for patient management. Maternal age showed a statistically significant relationship with the presence of chromosomal abnormalities, echoing decades of reproductive biology linking the aging oocyte to meiotic segregation errors. More intriguing was the finding of a weak but statistically significant negative correlation between gestational age and aneuploidy risk, with a correlation coefficient of −0.238 and a p-value of 0.008855. In other words, the earlier the loss, the more likely it was to be chromosomally abnormal, a pattern consistent with the idea that grossly imbalanced embryos tend to fail early in development, while losses later in gestation are more often driven by other mechanisms, including immunological, endocrine, thrombotic, and anatomical factors.
But QF-PCR has a well-known blind spot. It interrogates a limited set of chromosomes and cannot see submicroscopic copy number variations, the deletions and duplications of genomic segments too small to alter chromosome number but large enough to remove or duplicate genes. To peer beneath that resolution floor, the team selected a subset of 30 samples, stratified by their QF-PCR outcomes, and subjected them to array comparative genomic hybridization. In aCGH, differentially labeled fetal and reference DNA are co-hybridized to a microarray carrying hundreds of thousands of immobilized genomic probes, and the fluorescence ratio at each probe reveals whether the corresponding region is deleted or duplicated in the fetal genome. This technique can detect imbalances ranging from roughly 100 kilobases upward, an order of magnitude finer than conventional karyotyping.
The aCGH analysis proved its worth. Within the 30-sample cohort, the researchers identified clinically relevant copy number variations spanning the spectrum of pathogenicity, including pathogenic and likely pathogenic variants as well as variants of uncertain significance, the latter category reflecting regions whose dosage sensitivity has not yet been firmly established. Each variant was interpreted according to the joint guidelines of the American College of Medical Genetics and the Clinical Genome Resource, the standard framework that weighs factors such as gene content, inheritance pattern, and overlap with established disease loci before assigning a clinical classification.
Among the genes caught in deleted or duplicated segments were several with compelling biological narratives. CFHR3, a member of the complement factor H-related gene family, participates in the regulation of the complement cascade, the arm of innate immunity whose dysregulation has been implicated in inflammatory damage at the maternal-fetal interface. TNFRSF4 encodes a tumor necrosis factor receptor superfamily member with roles in immune cell signaling and tolerance. UGT2B17 belongs to the uridine diphosphate glucuronosyltransferase family, a set of metabolic detoxification enzymes whose variation has previously been linked to recurrent miscarriage, possibly through altered clearance of environmental and endogenous compounds. CD24 and MSR1 are involved in immune signaling and macrophage scavenger function, respectively, while the pregnancy-specific glycoprotein gene family, or PSG genes, is expressed almost exclusively in the placenta and is thought to modulate maternal immune tolerance of the fetus.
To move from gene lists to mechanism, the authors turned the implicated genes loose on a battery of bioinformatics tools. Using FunRich and WebGestalt for functional annotation, KEGG for pathway enrichment, and STRING for protein-protein interaction network construction, the team asked what biological themes united the disrupted loci. The answer converged on a coherent set of processes: immune-inflammatory signaling, endocrine regulation, lipid metabolism, extracellular matrix remodeling, and placental development. The involvement of TNF receptor signaling, MAPK cascades, and interleukin-1-related pathways emerged from the network analyses, weaving the copy number variations into the same immunological tapestry that independent studies have implicated in unexplained recurrent loss, including work on maternal B cell signaling and natural killer cell-mediated immunopathology.
The authors are careful, appropriately so, to frame the pathway findings as exploratory. The cohort of 30 microarray samples is modest, and several of the variants of uncertain significance may prove benign as genomic databases mature. The statistical associations between individual CNVs and miscarriage phenotypes will require validation in larger, well-powered cohorts with matched controls before they can inform clinical decision-making. Still, the architectural message of the study is clear: sequential testing with QF-PCR followed by aCGH captures abnormalities that neither method detects alone, and it does so at a fraction of the cost and turnaround time of broader approaches such as whole-genome sequencing.
That message lands at a moment of ferment in reproductive genetics. European Society of Human Reproduction and Embryology guidelines define recurrent pregnancy loss as two or more consecutive losses, and professional societies have been wrestling with the optimal diagnostic workup of lost pregnancy tissue for years. Previous studies comparing karyotyping with molecular methods have shown that conventional cytogenetics suffers from culture failure and maternal cell contamination, problems that DNA-based methods largely sidestep. The Banaras Hindu University team’s approach, anchored in a real clinical diagnostic laboratory serving a population with limited access to advanced genomic testing, demonstrates that a tiered molecular protocol is feasible and productive outside of well-funded Western centers.
For couples enduring the grief of repeated loss, the study’s findings translate into a concrete recommendation worth discussing with a genetic counselor: comprehensive cytogenetic analysis of lost pregnancy tissue is not merely an academic exercise. Identifying an aneuploidy or a pathogenic copy number variant can close the diagnostic loop, refine recurrence risk estimates, and in some cases guide the management of subsequent pregnancies, including targeted prenatal or preimplantation genetic testing. Conversely, a normal molecular karyotype redirects the clinical search toward the non-genetic contributors, from antiphospholipid syndrome to uterine anomalies.
The work also adds to a growing map of the genomic landscape of pregnancy failure, in which the PSG gene cluster on chromosome 19, the complement factor H-related locus, and immune receptor genes recur across independent cohorts. As genome-wide datasets accumulate and functional studies test the dosage sensitivity of these loci, variants of uncertain significance will gradually be reclassified, and the exploratory pathway signals reported here may harden into causal mechanisms. Until then, the study stands as both a practical diagnostic template and a hypothesis-generating catalog of the fragile genetic architecture underlying one of medicine’s most quietly devastating problems.
Article Title: Decoding Genetic Risk Factors in Recurrent Pregnancy Loss: An Integrative Chromosomal and Bioinformatics Approach
Article References: Mishra, S., Ashish, A., Rai, S., Yadav, A. K., & Singh, R. (2026). Decoding Genetic Risk Factors in Recurrent Pregnancy Loss: An Integrative Chromosomal and Bioinformatics Approach. Biochemical Genetics. https://doi.org/10.1007/s10528-026-11424-z
Image Credits: AI Generated
DOI: 10.1007/s10528-026-11424-z
Keywords: recurrent pregnancy loss, QF-PCR, aCGH microarray, copy number variations, aneuploidy, gene ontology, chromosomal abnormalities, placental development, immune-inflammatory pathways, bioinformatics
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