Category: 7. Science

A team of Chinese scientists may have cracked the secret behind the strange Canyon Diablo diamonds. Hexagonal in form rather than cubic, the process behind how these diamonds formed has, until now, remained elusive.

Diamonds are usually made of carbon atoms in a cubic arrangement (like stacked Lego blocks in a cube pattern). But there is a rarer form, the hexagonal diamond (atoms stacked in a honeycomb-like pattern), that seems to originate when meteorites smash into Earth, producing extreme heat and pressure.

The very first hexagonal-structured diamond was found within the ‘Diablo Canyon’ meteorite which is believed to have hit the Earth about 50,000 years ago and landed in what is present-day Arizona.

Now, a joint team of experts from the Centre for High Pressure Science and Technology Advanced Research and the Chinese Academy of Sciences’ Xian Institute of Optics and Precision Mechanics have claimed to have recreated the enigmatic ‘meteorite diamond’ in a laboratory.

Cracking the meteorite’s secrets

Most diamonds are forged nearly 90 miles (150 kilometers) below the Earth’s surface, where temperatures can reach more than 2,000 degrees Fahrenheit (1,093 degrees Celsius). The temperature and pressure at this depth causes carbon atoms to arrange themselves into cubic shapes.

In contrast, the Diablo Canyon meteorite contains a series of strange, alien diamonds formed during its violent path to Earth. The diamonds found inside the meteorite have a hexagonal crystal structure called lonsdaleite. This crystal structure makes the diamonds even harder than ‘traditional’ ones, perhaps by as much as 60%.

Since their discovery, there has been a decades-long debate about whether meteorite diamonds actually exist in pure form, or if these tiny crystals are just mixed phases of cubic diamond and graphite.

Earlier attempts at finding answers usually ended up making ordinary cubic diamonds or messy mixtures. For example, a team was partially successful in synthesizing them using gunpowder and compressed air on graphite disks. However, the Chinese team’s success appears to have now settled a 60-year scientific argument.

Synthesizing alien diamonds

According to reports, the team managed to make pure hexagonal diamond crystals which are 100 micrometres in width, or about the thickness of a strand of human hair. This was achieved by using extremely pure, single-crystal graphite with the idea that fewer impurities would mean less chance of ‘defaulting’ to the cubic structure.

Using this, the scientists applied controllable high pressure and temperature, plus quasi-hydrostatic conditions (meaning the pressure is uniform in all directions). They also used in-situ X-ray techniques during the process to observe the transformation real time and adjust conditions to favor hexagonal diamond growth.

The breakthrough is being touted as the first macroscopic proof that hexagonal diamond really exists as a distinct, stable structure. It also pushes the limits of what ‘superhard’ means, beyond the properties of a traditional cubic diamond.

Considering that the new synthetic hexagonal diamond promises superior hardness and thermal resistance, its could be used in manufacturing cutting tools, wear-resistant coatings, and possibly high-end electronics (diamonds are excellent thermal conductors and can handle extreme conditions).

“This synthesized hexagonal diamond is expected to pave new pathways for the development of superhard materials and high-end electronic devices,” stated Ho-kwang Mao from the Chinese Academy of Sciences.

The study has been published in the journal Nature.

Plants are essential when designing the perfect pool area. Whether you’re looking to create a super-luxe space, a tropical-inspired paradise, or a romantic retreat, the right choices truly help to set the scene. And opting for scented picks will only add to the sensory experience as you take a dip or lounge on a daybed nearby.

Below, gardening experts share their recommendations for fragrant pool planting ideas, so if you’re looking for inspiration, you’ve come to the right place. You’ll find quick tips on keeping them looking their best, too.

So much for heliocentrism.

An international team of astronomers using observations made with the James Webb Space Telescope have found evidence of massive planets out there that’re capable of forming their own planetary systems — without a star. 

These planets would be the center of something like a mini version of our solar system where other, smaller planets revolve around it. But without the light of a star, these systems, if they exist, would go largely overlooked by our telescopes, lost to the dark void of space.

The work, a new study accepted for publication in the The Astronomical Journal, focuses on free-floating “rogue” planets which are not gravitationally bound to a star. While some rogue planets are first formed around a stellar object before being ejected from their system, the astronomers believe these ones may have formed from the same mechanism that gives birth to stars.

“These discoveries show that the building blocks for forming planets can be found even around objects that are barely larger than Jupiter and drifting alone in space,” lead author Belinda Damian, an astronomer at the University of St Andrews in Scotland, said in a statement about the work. “This means that the formation of planetary systems is not exclusive to stars but might also work around lonely starless worlds.” 

Using James Webb observations taken between August and October 2024, the astronomers examined eight free-floating planets. With masses between five to ten times that of Jupiter, these belong to a class of objects believed to be the lowest mass objects that form from the collapse of the giant gas clouds that are sometimes referred to as stellar nurseries, as they’re typically associated with star formation. 

For one reason or another, these objects didn’t accumulate enough mass to sustain nuclear fusion reactions in their cores and become proper stars. These shouldn’t be confused with brown dwarfs, however, which are much more massive substellar objects that are dozens of times heavier than Jupiter that also fail to kickstart nuclear fusion, earning them the moniker of “failed” stars.

In this latest work, the astronomers detected excess emissions in the infrared spectra of these objects, showing that six of them have emissions associated with warm dust. This indicates the presence of a disk, or a circumstellar cloud of gas and dust that surrounds the planet. 

In itself, this isn’t unusual, and such disks have been detected around rogue planets before. Around stars, these disks, referred to as protoplanetary disks, are where dense regions of gas and dust can coalesce to form planets, and are the leftover material from the star’s formation which didn’t get sucked into its collapsing core.

But the kicker here is that the scientists have detected signs that the rogue planets’ disks are already exhibiting the crucial first steps of planetary formation in the form of harboring silicate grains, which appear to be growing and crystallizing. These dusty grains can clump together to form planetesimals, the large, solid objects that are the building blocks of a baby planet. 

This is the first detection of silicate grains around a planetary mass object, the authors said. And it pairs tantalizingly with their previous study which showed that the rogue planet disks can last for millions of years, providing more than enough time to incubate inchoate worlds.

“Taken together, these studies show that objects with masses comparable to those of giant planets have the potential to form their own miniature planetary systems,” coauthor Aleks Scholz, who is also a St Andrews astronomer, said in the statement. “Those systems could be like the solar system, just scaled down by a factor of 100 or more in mass and size. Whether or not such systems actually exist remains to be shown.”

Ironically, then, maybe our ancestors weren’t totally off the mark with their whole geocentrism fixation — they just had the wrong planetary system in mind.

More on exoplanets: James Webb Spots Planets Forming Into Solar System in Real Time, Like an Organism’s First Cells

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Starts With A Bang — August 9, 2025

In the search for life in the Universe, the ultimate goal is to find an inhabited planet beyond Earth. How will we know when we’ve made it?

Key Takeaways

• 
  Ever since we discovered that there were other planets and worlds than Earth, both in our own Solar System and around other stars, we’ve wondered about what life forms might exist on them.
• 
  While most of the worlds we’ve found so far appear to be indistinguishable from completely lifeless and uninhabited, there are signatures that life produces that can strongly hint at the presence of a living world.
• 
  But how will we know when we’ve gotten there? How can we distinguish between an inhabited world and a very different-from-ours uninhabited world with those same key signatures? Here’s where we are today.

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Travel the universe with Dr. Ethan Siegel as he answers the biggest questions of all.

Out there in the Universe, somewhere, a second example of an inhabit world or planet likely awaits us. It could be some other planet or moon within our own Solar System; it could be a spacefaring, interstellar civilization, or it could be an exoplanet around a different parent star. Although the search for life beyond Earth generally focuses on worlds that have similar conditions to Earth, like rocky planets with thin atmospheres and liquid water on their surfaces, that’s not necessarily the only possibility. The truth is that we don’t know what else is going to be out there, not until we look for ourselves and determine the answers.

And yet, if you’ve been paying attention to the news, you might think that super-Earth or mini-Neptune type worlds, such as the now-famous exoplanet K2-18b, might be excellent candidate planets for life. Some have even gone as far as to claim that this planet has surefire biosignatures on it, and that the evidence overwhelmingly favors the presence of life within this planet’s atmosphere. But the science backing up that claim has been challenged by many, including our two podcast guests for this episode: Dr. Luis Welbanks and Dr. Matthew Nixon.

Beyond the breathless and sensational claims, what does the actual science concerning K2-18b in particular, and of biosignatures on exoplanets in general, actually teach us? What does the evidence indicate, and if we are going to find inhabited exoplanets, what will it take for us to actually announce a positive detection with confidence and less ambiguity? That’s what this episode of the Starts With A Bang podcast is all about; I hope you enjoy it!

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Travel the universe with Dr. Ethan Siegel as he answers the biggest questions of all.

Somewhere, at some point in the history of our Universe, life arose. We’re evidence of that here on Earth, but many big puzzles remain.

The relic signal that first proved the Big Bang has been known and analyzed for 60 years. Join us at the frontiers of modern cosmology!

Once every 12 years, Earth, Jupiter, Uranus, and Neptune all line up, opening a window for a joint mission. Our next chance arrives in 2034.

Here in 2025, many of us claim to come to our own conclusions by doing our own research. Here’s why we’re mostly deluding ourselves.

The hunt for extraterrestrial life begins with planets like Earth. But our inhabited Earth once looked very different than Earth does today.

These short books offer insights and meditations on timeless themes, without the time commitment.

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Tex38 is an evolutionarily conserved gene predominantly expressed in the testis

To explore the evolutionary history of Tex38, we initially utilized the Ensembl comparative genomics resources (https://asia.ensembl.org/index.html) to construct the phylogenetic tree of Tex38. We observed that Tex38 first appeared in amniotes and is mainly expressed in mammals (Fig. S1A). Alignment analyses (https://www.uniprot.org/) of TEX38 orthologs from mice, rats, bovines, chimpanzees, horses, macaques, and humans revealed high homology throughout evolution (Fig. S1B). TEX38 orthologs exhibited significant sequence identity, ranging from 70.47% to 95.15% (Fig. S1C). The FANTOM5 dataset in the Human Protein Atlas (https://www.proteinatlas.org/) demonstrated that TEX38 is predominantly expressed in the testis, with a moderate expression level in the epididymis (Fig. S1D). Additionally, human single-cell RNA sequencing data revealed specific expression of TEX38 in both early and late spermatids (Fig. S1E). Furthermore, transcriptomic analysis of mouse tissues (https://www.ncbi.nlm.nih.gov/) indicated that Tex38 is predominantly expressed in the testis (Fig. S1F). Consistent with human data, single-cell sequencing data from databases (https://smart-db.cn/home) showed that Tex38 is primarily expressed in round spermatids in mouse testes (Fig. S1G). To elucidate the expression pattern of the Tex38 gene in mice, we performed reverse transcription polymerase chain reaction (RT-PCR) analysis using cDNA samples from multiple organs. Tex38 mRNA was detected only in the testis, with no evident PCR product bands observed in other tissues (Fig. 1A). TEX38 protein was detected with predominant expression in the testis (Fig. 1C). Additionally, we analyzed the expression patterns of Tex38 mRNA and protein in mouse testes at different developmental stages. Tex38 mRNA was first detected at 21 days postpartum (dpp), while TEX38 protein was first detected at 28 dpp. Both mRNA and protein remained at high levels until adulthood (Fig. 1B, D), coinciding with the appearance of elongating spermatids. These results demonstrate that Tex38 is predominantly expressed in the mouse testis, and this specific expression pattern suggests a potentially important role for TEX38 in spermatogenesis.

Due to limitations in antibody availability, direct detection of TEX38 localization within testicular tissue was not feasible. To elucidate its subcellular localization, we conducted an amino acid sequence analysis of TEX38, identifying a transmembrane region spanning amino acids 4-26. Subsequently, we constructed an EGFP-TEX38 plasmid encompassing the full-length TEX38 sequence and a mutant plasmid lacking the transmembrane domain (Fig. S2A). EGFP was fused to the N-terminus of the TEX38 protein. These plasmids were transfected into HeLa cells, and the distribution of the EGFP signal was observed following protein expression. The full-length EGFP-TEX38 protein exhibited predominant perinuclear localization with a punctate pattern, whereas both EGFP alone and the EGFP-TEX38 mutant protein were uniformly distributed throughout the cell (Fig. S2B). To further define the subcellular localization of the EGFP-TEX38 fusion protein, transfected HeLa cells were stained with fluorescent probes targeting the endoplasmic reticulum (ER), Golgi apparatus, mitochondria, and lysosomes. Significant co-localization between the EGFP-TEX38 fusion protein and probes for the ER and Golgi apparatus was observed in the perinuclear region, while minimal co-localization was detected with mitochondrial and lysosomal probes (Fig. S2C). These findings indicate that TEX38 plays a functional role in multiple cytoplasmic organelles, with emphasis on the ER and Golgi apparatus.

Deficiency of Tex38 causes male infertility

To further clarify the function of Tex38, we generated a Tex38^−/− mouse model through the CRISPR-Cas9 genome editing system. Two sgRNAs were designed targeting exons 1 and 2 of Tex38 (Fig. 1E). Genotyping was performed by PCR (Fig. 1F). Western blot analysis confirmed the deletion of TEX38 protein (Fig. 1G). Fertility testing revealed that Tex38^−/− male mice were completely infertile (Fig. 1H), whereas females exhibited normal fertility comparable to Tex38^+/+ females (Fig. 1I). No significant differences were observed in the morphology, testis size, body weight, testis weight, or testis-to-body weight ratio between Tex38^−/− and age-matched Tex38^+/+ mice (Fig. 1J, K, M–O). These findings suggest that Tex38 deficiency has no effect on mouse growth and development. Interestingly, a subset of Tex38^−/− mice displayed markedly enlarged epididymides compared to Tex38^+/+ mice (Fig. 1L). Tex38^−/− mice also exhibited a significantly increased epididymis weight/body weight ratio compared to Tex38^+/+ mice (Fig. 1P, Q). Overall, these results indicate that Tex38 is essential for male fertility in mice and contributes to the regulation of epididymal weight.

Deficiency of Tex38 causes oligoasthenozoospermia in male mice

To investigate the role of Tex38 in spermatogenesis, histological examination was conducted on the caput, corpus, and cauda regions of Tex38^+/+ and Tex38^−/− epididymis (Fig. 2A). Hematoxylin and eosin (H&E) staining revealed that sperm within the epididymis of Tex38^−/− mice exhibited abnormal morphology and reduced numbers, whereas the morphology of epithelial cells in the caput, corpus, and cauda epididymides appeared normal in Tex38^−/− mice (Fig. 2A). Sperm count analysis revealed that compared to Tex38^+/+, Tex38^−/− mice exhibited a significant reduction in sperm abundance released from the cauda epididymis (Fig. 2B). Furthermore, reductions in both the proportion of motile spermatozoa and sperm with progressive motility were noted (Fig. 2C, D). Morphological analysis of cauda epididymal sperm revealed a significant increase in bent-neck spermatozoa in Tex38^−/− mice (KO 63.3% vs WT 2.0%, P < 0.001), accompanied by other morphological abnormalities including spermatozoa with malformed heads (KO 26.8% vs WT 14.2%, P < 0.001) and multi-headed/flagellated (KO 5.5% vs WT 0.0%, P < 0.05) sperm (Fig. 2E, F). These aberrant morphological patterns were consistently observed through scanning electron microscopy (SEM) (Fig. 2G). To explore sperm defects in greater detail, sperm collected from the cauda epididymis were examined using transmission electron microscopy (TEM). In Tex38^−/− spermatozoa, both the head and the midpiece of the tail were simultaneously enveloped within a membranous structure (Fig. 2H). Compared to Tex38^+/+ mice, the cross-sections of sperm flagella from Tex38^−/− mice exhibited clear evidence of axoneme damage, as well as disorganization of the mitochondrial sheath and outer dense fibers (Fig. 2H). Meanwhile, acrosome morphology was examined in Tex38^+/+ and Tex38^−/− sperm using PNA-FITC immunofluorescence staining (IF). A significant deviation from the normal acrosomal pattern was observed in Tex38^−/− sperm, characterized by absent or abnormally located PNA-labeled acrosome signals. Notably, most sperm with neck bending displayed weak, diffuse acrosomal staining, with only 27.1% exhibiting normal PNA-positive signals (Fig. 2I, J). Given the abnormal head morphology (22.9%) observed in Tex38^−/− sperm, DNA damage was assessed in epididymal sperm. A significantly higher proportion of comet-positive sperm was detected in Tex38^−/− compared to Tex38^+/+ mice (KO 27.1% vs WT 3.7%, P < 0.01), indicating increased DNA damage in Tex38^−/− sperm (Fig. 2K, L). These findings collectively demonstrate that Tex38 deletion results in OAT in mice.

A H&E staining of the caput epididymis, corpus epididymis, and cauda epididymis from Tex38^+/+ mice and Tex38^−/− mice. B Count of the sperm from cauda epididymis (n = 3). Student’s t-test. C The percentage of motile spermatozoa in the cauda epididymis (n = 3). Student’s t-test. D The percentage of the sperm with progressive motility in the cauda epididymis (n = 3). Student’s t-test. E H&E staining of spermatozoa from the cauda epididymis. F The percentage of normal sperm, bent neck sperm, malformed head sperm, and multi-headed/flagellated sperm in Tex38^+/+ and Tex38^−/− cauda epididymis (n = 3). Student’s t-test. G Scanning electron microscopy (SEM) images of sperm from Tex38^+/+ and Tex38^−/− mice. H TEM analysis of mature sperm in the Tex38^+/+ and Tex38^−/− cauda epididymis. The red arrow indicates the absence and disorder of microtubules in the sperm flagella of Tex38^−/− mice. I Peanut agglutinin (PNA) staining of epididymal sperm from Tex38^+/+ and Tex38^−/− mice. Scale bar is 25 μm. J Quantification of the percentage of PNA positive sperm in Tex38^+/+ and Tex38^−/− mice (n = 3, more than 200 sperm per replicate). Student’s t-test. K, L Comet assay for DNA fragmentation of epididymal sperm from Tex38^+/+ and Tex38^−/− adult mice (n = 9, more 500 sperm per replicate). Scale bar is 50 μm. Student’s t-test.

Tex38 deficiency affects spermiogenesis but may not affect spermatogonial proliferation or meiosis

To investigate the role of Tex38 in mice, we further performed HE staining to analyze the tissue morphology of Tex38^+/+ and Tex38^−/− mice. No substantial differences were observed in the heart, liver, spleen, lungs, kidneys, and brain (Fig. S3A). These results demonstrate that Tex38 primarily functions within testicular tissue. To assess the cause of oligoasthenozoospermia induced by Tex38 deletion, we conducted a detailed analysis of the testicular histomorphology in Tex38^−/− mice. Periodic Acid-Schiff (PAS) staining revealed that the number and diameter of seminiferous tubules in Tex38^−/− mice were comparable to those in Tex38^+/+ mice. Histological examination of 12 spermatogenic stages revealed elongated spermatids with delayed release during stages IX-X, along with failed individualization at the basal compartment of seminiferous tubules, which were not observed in Tex38^+/+ mice. No significant abnormalities in cellular arrangement were detected in other spermatogenic stages (Fig. 3A). To clarify the impact of Tex38 on spermatogenesis, we quantified various types of germ cells at different stages. There was no significant difference in the number of germ cells in Tex38^−/− testes compared to Tex38^+/+ testes, except for an increase of unreleased elongated spermatids in stage IX-X seminiferous tubules (Fig. 3B).

A Different epithelium stages of seminiferous tubules in PAS-stained Tex38^+/+ and Tex38^−/− testes. The red dashed box indicates sperm with individualization failure, while the blue arrows indicate unreleased elongated sperm. Scale bar is 25 μm. B Spermatogenic cell count and statistical analysis of spermatogenic tubules at different stages. Leptotene (L), zygotene (Z), pachytene (P), diplotene (Di), round spermatid (Rst), elongated spermatid (Est), unreleased sperm (U). n = 4, Student’s t-test. C, D TUNEL staining of testis sections from Tex38^−/− and Tex38^+/+ mice (n = 3). Student’s t-test. Scale bar is 50 μm. E TEM images for testes from Tex38^−/− and Tex38^+/+ adult mice. Yellow arrows indicate abnormal vesicles. N nucleus, Ac acrosome, Mt manchette, MS mitochondrial sheath. Scale bar is 2 μm.

To determine the specific stage of spermatogenesis in which Tex38 functions, we further examined the expression of germ cell markers (VASA for germ cells, PCNA for spermatogonia, γ-H2AX for spermatocytes). There were no significant differences in terms of the expression and localization of these molecules in Tex38^+/+ and Tex38^−/− testes. Tex38^−/− did not affect the number of various spermatogenic cells, the differentiation of spermatogonia, or the meiosis of spermatocytes (Fig. S3B–D). SOX9 staining and quantification also indicated no significant impact of Tex38 deletion on the number and localization of Sertoli cells (Fig. S3E, F). We performed TUNEL staining to analyze cell apoptosis in Tex38^−/− testis, which revealed a significantly increased number of apoptotic cells than in Tex38^+/+ testis (Fig. 3C, D). Further observation of the ultrastructure of various cells in testis tissues using transmission electron microscopy (TEM) showed that most cells in Tex38^−/− testes exhibited no significant abnormalities. However, a few round spermatids with acrosome vacuolation and multinucleated cell clusters containing multiple sperm heads were observed. These clusters included sperm heads, dispersed acrosomes, sperm flagella, and multiple vacuoles (Fig. 3E). Collectively, Tex38 knockout primarily affects spermiogenesis, while potentially having no significant impact on spermatogonial proliferation and spermatocyte meiosis.

Progressive increase of bent-neck sperm during the transit in the epididymis of Tex38
^−/− mice

To study the etiology of abnormal sperm in Tex38^−/− males, spermatozoa were collected from the testis, caput epididymis, corpus epididymis, and cauda epididymis for analysis of morphological abnormalities. Abnormal sperm morphology was observed in Tex38^−/− males, including multi-headed/flagellated, bent-neck, malformed head (Fig. 4A, B). Compared with Tex38^+/+ mice, the percentages of abnormal spermatozoa from the testis, caput epididymis, corpus epididymis, and cauda epididymis of Tex38^−/− mice were significantly increased (Fig. 4B). H&E staining of testicular spermatozoa within seminiferous tubules revealed no significant difference in the proportions of bent-neck spermatozoa between Tex38^−/− and Tex38^+/+ mice (Fig. 4C). While multi-headed/flagellated spermatozoa were absent in Tex38^+/+ mice, they constituted 3.2% of spermatozoa in the testes of Tex38^−/− mice, a proportion consistent with that observed in the epididymis, suggesting that these abnormal spermatozoa originated in the testis (Fig. 4C). Statistical analysis demonstrated a progressive increase in the percentage of bent-neck spermatozoa from the caput epididymis (22.9%) to the corpus epididymis (46.2%) and cauda epididymis (62.0%), indicating that normal spermatozoa released into the lumen of seminiferous tubules subsequently undergo transformation into bent-neck spermatozoa during epididymal transit from the caput to the cauda epididymis (Fig. 4C).

A H&E staining of sperm collected from testis, caput epididymis, corpus epididymis, and cauda epididymis of Tex38^−/− and Tex38^+/+ mice (n = 3). B, C Percentages of abnormal morphology sperm in testicular suspensions, caput epididymis, corpus epididymis, and cauda epididymis of Tex38^−/− and Tex38^+/+ mice (n = 3, more than 200 sperm per replicate). Student’s t-test. D The representative images of epididymides from Tex38^+/+ and Tex38^−/−mice after ligation for 4 days. The one side epididymal ducts were ligated at the corpus region, and the other epididymis was removed from the abdominal cavity and then placed back as a sham ligation control. E H&E staining was used to analyze the sperm of the caput epididymis and cauda epididymis after ligation for 4 days. EP epididymis. F The percentages of normal sperm in caput and cauda epididymis of Tex38^−/− and Tex38^+/+ mice after ligation for 4 days (n = 3). Student’s t-test. G The percentages of bent neck sperm in caput and cauda epididymis of Tex38^−/− and Tex38^+/+ mice after ligation for 4 days (n = 3). Student’s t-test. H The percentages of malformed head sperm in caput and cauda epididymis of Tex38^−/− and Tex38^+/+ mice after ligation for 4 days (n = 3). I The percentages of multi-headed/flagellated sperm in caput and cauda epididymis of Tex38^−/− and Tex38^+/+ mice after ligation for 4 days (n = 3). Student’s t-test. Data are presented as mean ± SEM. Student’s t-test. All data are mean ± SEM and dots represent values for individual mice.

To elucidate whether the observed changes were induced by an aberrant epididymal environment due to Tex38 deficiency or prolonged sperm storage, epididymal duct ligation was performed. The left corpus epididymis was ligated for four days in both Tex38^−/− and Tex38^+/+ mice to simulate epididymal sperm storage, while the contralateral epididymis served as a control (Fig. 4D). Four days post-ligation, both Tex38^−/− and Tex38^+/+ mice exhibited a substantial accumulation of spermatozoa in the caput region. Subsequent H&E staining analysis of sperm collected from the caput and cauda was conducted (Fig. 4E). Compared to the non-ligated Tex38^−/− epididymis, the proportion of bent-neck sperm in the caput region of Tex38^−/− mice increased significantly post-ligation, while the proportion of normal sperm was significantly decreased post-ligation, reaching a similar proportion to that observed in the cauda epididymis (Fig. 4F, G). Conversely, no significant changes were observed in the percentages of multi-headed/flagellate sperm or malformed head sperm in the Tex38^−/− caput region four days post-ligation (Fig. 4H, I). These findings suggest a positive correlation between the formation of bent-neck sperm and sperm storage duration within the Tex38^−/− epididymis. Consequently, we hypothesize that the presence of bent-neck sperm in Tex38^−/− mice is primarily attributed to epididymal storage, regardless of storage in caput or cauda region.

Tex38 deficiency leads to sperm dysfunction and fertilization failure

To elucidate the underlying causes of male infertility in Tex38^−/− mice, we comprehensively evaluated the functionality of Tex38^−/− spermatozoa at various stages of fertilization, including acrosome reaction (AR), and zona pellucida (ZP) binding. To further induce the AR, capacitated sperm were exposed to the Ca²⁺ ionophore A23187 in vitro. Given that sperm undergoing the AR are not stained by PNA, this enabled quantification of AR occurrence. Unexpectedly, a substantial proportion of Tex38^−/− sperm retained PNA staining post-ionophore treatment, with only 3.3% exhibiting the AR, significantly lower than the 70.8% observed in Tex38^+/+ sperm (Fig. 5A, B). The fertilization capacity of Tex38^−/− spermatozoa was assessed through in vitro fertilization assays. In contrast to Tex38^+/+ sperm, which efficiently bound to the ZP, Tex38^−/− sperm displayed a complete failure to bind to the ZP (Fig. 5C). Furthermore, ATP levels were markedly decreased in Tex38^−/− sperm compared to Tex38^+/+ controls (Fig. 5D). Consequently, Tex38^−/− sperm demonstrated a notably diminished capacity to fertilize ZP-intact oocytes (Fig. 5E, F). Importantly, even after ZP removal, Tex38^−/− sperm remained incapable of fertilizing oocytes, indicating a defect in sperm-oocyte fusion (Fig. 5G, H). In summary, these findings demonstrate that Tex38 deficiency results in a cascade of sperm functional abnormalities, including impaired ZP binding, acrosome reaction, and fertilization.

A Sperm from Tex38^+/+ and Tex38^−/− mice was induced by calcium ionophore A23187 supplementation and PNA staining was performed. Nuclei were counterstained with DAPI. Representative images were shown. Scale bar is 25 μm. B Quantification of the percentages of acrosome reaction (AR) in (A) (n = 3, more than 200 sperm per replicate). Student’s t-test. C In vitro analysis of sperm–egg binding. Sperm heads were stained with Hoechst 33342. Scale bar is 50 μm. D ATP contents in Tex38^+/+ and Tex38^−/− sperm (n = 3). Student’s t-test. E Zona pellucida (ZP) intact oocytes after 24 h of in vitro fertilization (IVF) with epididymal sperm from adult Tex38^+/+ or Tex38^−/− mice. Scale bar is 100 μm. F Quantification comparison of 2-cell rate following IVF of Tex38^+/+ ZP intact oocytes with epididymal sperm from adult Tex38^+/+ or Tex38^−/− mice (n = 3). Student’s t-test. G ZP free oocytes after 24 h of IVF with epididymal sperm from adult Tex38^+/+ or Tex38^−/− mice. Scale bar is 100 μm. H Quantification comparison of 2-cell rate following IVF of Tex38^+/+ ZP free oocytes with epididymal sperm from adult Tex38^+/+ or Tex38^−/− mice (n = 4). Student’s t-test. Data are mean ± SEM and dots represent values for individual mice.

The absence of TEX38 impairs the processing and maturation of ADAM3 and its associated chaperone proteins in epididymal sperm

To elucidate the molecular mechanisms underlying TEX38 deletion-induced male infertility, we performed proteomic analyses on proteins extracted from testis, sperm, and epididymis. The histogram illustrates the distribution of DEPs (fold change ≥1.5), revealing 1290 DEPs in Tex38^−/− sperm and 445 DEPs in the epididymis, in contrast to only 37 DEPs identified in the testis (Fig. 6A and Supplementary Data 1). GO enrichment analysis revealed few enriched biological processes among testis DEPs in Tex38^−/− mice, whereas DEPs in sperm and epididymis were both enriched in flagellated sperm motility, spermatogenesis, and sperm-ZP binding (Fig. 6B). Sperm DEPs were additionally enriched in other biological processes, including cilium movement and sperm axoneme assembly, while epididymis DEPs were enriched in lipid metabolic process, actin filament organization, and cilium movement involved in cell motility (Fig. 6B). Among all DEPs, CALR3 exhibited the most dramatic elevation in sperm following Tex38 deletion. As a molecular chaperone, CALR3 works synergistically with CLGN and PDILT to facilitate ADAM3 folding for sperm-ZP binding^{12,13,14,15,16}. Consequently, we examined DEPs associated with ADAM3 folding. As depicted in Fig. 6D, F, mature ADAM3 was downregulated in Tex38^−/− sperm and epididymis. Correspondingly, CALR3, CLGN, and PDILT protein expression was significantly increased in the Tex38^−/− sperm and/or epididymis. Collectively, these findings suggest that TEX38 interacts with molecular chaperones to promote mature ADAM3 production for sperm-ZP binding.

Protein of adult mouse testis, sperm, and epididymis was extracted for proteomics analysis. A Histogram diagram shows the number of up-regulated and down-regulated differentially expressed proteins in the testis, epididymis, and sperm of Tex38^−/− mice. B Top biological process from GO enrichment analysis of DEPs in Tex38^−/− sperm, epididymis and testis. C Volcano plot of differentially expressed proteins between Tex38^+/+ and Tex38^−/− sperm. Red dots represent upregulated proteins, blue dots represent downregulated proteins, and gray dots represent proteins that were not differentially expressed (P < 0.05, |logFC | >1.5). D Protein expressions of ADAM3, CALR3, CLGN, PDILT in Tex38^+/+ and Tex38^−/− testis, epididymis, and sperm. E Protein expressions of TEX38, ARRDC5, ATPA14, DNAJB13, TEKT4, GK2, SPATA19, SUN5, and CETN1 in Tex38^+/+ and Tex38^−/− testis, epididymis, and sperm. F, G Quantitation of protein expressions in (D) and (E) (n = 3). Mann-Whitney U test.

Notably, flagellated sperm motility, sperm mitochondrial sheath assembly, and sperm-ZP binding were common to both sperm and epididymis DEPs. To validate these findings, Western blot analysis assessed protein expression in testis, epididymis, and sperm. Figure 6E showed that TEX38 protein expression was absent in the Tex38^−/− testis, while no signaling was detected in the epididymis and sperm. Additionally, Western blot analysis revealed significant decreases in TEKT4, GK2, and SUN5 expression in both Tex38^−/− epididymis and sperm, along with increased SPATA19 levels. ATP1A4 and DNAJB13 were significantly decreased in Tex38^−/− sperm, while CETN1 was downregulated in KO epididymis (Fig. 6E, G). Collectively, these findings demonstrate that TEX38 deficiency not only affects sperm HTCA formation and flagellar assembly proteins but also leads to significant alterations in the maturation of ADAM3 and its associated chaperone proteins in both sperm and epididymis.

ARRDC5, a novel interacting protein of TEX38, deficiency of which leads to similar spermatogenesis defects to those in Tex38
^−/− mouse

To investigate the mechanisms by which TEX38 functions in spermatogenesis and fertilization, we employed the STRING database (https://cn.string-db.org) to perform bioinformatic analysis on TEX38 and identify potential interacting proteins. Among these, ARRDC5 emerged as a candidate binding partner (Fig. 7A). We further validated the interaction between TEX38 and ARRDC5 using co-immunoprecipitation (Co-IP) in the HEK-293T cell line (Fig. 7B). Proteomic analysis revealed comparable ARRDC5 expression levels in the testes of Tex38^−/− and Tex38^+/+ mice; however, ARRDC5 was undetectable in Tex38^−/− sperm. This finding was further validated by Western blot analysis (Fig. 7C). The observed interaction prompted a critical inquiry into the fundamental process governing their interplay during spermatogenesis. Accordingly, we first analyzed the expression profile of ARRDC5. Similar to TEX38, ARRDC5 exhibited predominant expression in the mice testis at both the mRNA and protein levels (Fig. 7D, E). Furthermore, the developmental stage-specific expression pattern of ARRDC5 in Arrdc5^+/+ mice testis mirrored that of TEX38. Arrdc5 mRNA displayed weak expression from 7 dpp, with a significant increase observed from 28 dpp onwards. Protein expression initiated at 21 dpp, gradually increased and peaked in adulthood (Fig. 7F, G).

A Screen the interacting proteins of TEX38 in STRING database (https://cn.string-db.org). B ARRDC5 interacted with TEX38 in cultured HEK293T cells. C Protein expression of ARRDC5 in the Tex38^+/+ and Tex38^−/− testis, epididymis, and sperm. D RT-PCR analysis of Arrdc5 mRNA in mice tissue. Rps2 was used as loading control. E Western blot of ARRDC5 protein in mice tissue. β-actin was used as a control. F RT-PCR analysis of Arrdc5 mRNA in mice developing testis. G Western blot of ARRDC5 protein in mice developing testis. H Protein expressions of ADAM3, CALR3, CLGN, PDILT, TEX38 in Arrdc5^+/+ and Arrdc5^−/− testis and sperm. I Quantitation of protein expressions in (H) (n = 3). Mann-Whitney U test.

To explore the role of ARRDC5 in male reproduction, given its interaction with Tex38, we generated Arrdc5^−/− mice using CRISPR/Cas-mediated genome engineering (Fig. S4A, B). A three-month fertility test revealed complete infertility in Arrdc5 ^−/−male mice, while female fertility remained unaffected (Fig. S4C). To explore the underlying spermatogenic defects in Arrdc5^−/− mice, testes and epididymides from 8- to 10-week-old animals were collected for histological analysis. No significant differences were observed in testis size or testis-to-body weight ratio between Arrdc5^−/− and age-matched Arrdc5^+/+ mice (Fig. S4D, E). However, sperm counts and motility were significantly reduced in the cauda epididymis of Arrdc5^−/− mice compared to Arrdc5^+/+ controls (P < 0.05) (Fig. S4F, G). H&E staining of Arrdc5^−/− testis sections showed apparently normal spermatogenesis (Fig. S4H), whereas sperm isolated from the cauda epididymis exhibited reduced abundance and various morphological abnormalities, including bent necks, malformed heads, and multiple heads or flagella (Fig. S4H, I). SEM confirmed the abnormal sperm morphology observed in Arrdc5^−/− mice, which resembled that of Tex38^−/− sperm (Fig. S4J). Additionally, Comet assay analysis revealed significant DNA damage in Arrdc5^−/− sperm, indicating impaired sperm DNA integrity (Fig. S4K, L).

To further explore the underlying causes of abnormal sperm, we evaluated the 12 stages of the seminiferous cycle and observed unreleased sperm in stages IX-X of Arrdc5^−/− testis (red dashed box), a phenotype similar to the delayed sperm release caused by Tex38^−/− (Fig. S5A). To determine whether Arrdc5-deficient abnormal sperm originated in the epididymis, as in the case of Tex38, we compared sperm number and morphology in the testis, caput, corpus, and cauda epididymis of Arrdc5^−/− and Arrdc5^+/+ mice (Fig. S5B, C). Interestingly, while Arrdc5^−/− testicular tissue exhibited a higher proportion of malformed heads (KO 24.8% vs WT 3.3%, P < 0.05) and multi-headed/flagellated sperm (KO 8.9% vs WT 0%, P < 0.05), there was no significant difference in bent-neck sperm compared to Arrdc5^+/+ testis (KO 3.2% vs WT 4.3%, P > 0.05). However, the proportion of bent-neck sperm increased significantly upon entering the epididymis and remained elevated in the caput (KO 44.2% vs. WT 2.6%), corpus (KO 51.7% vs. WT 3.4%), and cauda (KO 49.6% vs. WT 2.0%) epididymis (P < 0.05). Similarly, the proportion of malformed heads and multi-headed/flagellated sperm showed significant increases and remained relatively stable compared to Arrdc5^+/+ testis, caput, corpus, and cauda epididymis (P < 0.05). The proportion of different abnormal sperm types did not change with prolonged sperm maturation time in the epididymis.

Given the phenotypic similarities between Arrdc5^−/− and Tex38^−/− mice, we hypothesized that ARRDC5, analogous to TEX38, regulates ADAM3 expression and maturation. Western blot analysis of testicular and sperm samples from Arrdc5^−/− mice revealed that while TEX38, ADAM3, CALR3, CLGN, and PDILT expression levels in the testes remained unchanged compared to wild-type controls, mature ADAM3 was significantly downregulated in Arrdc5^−/− sperm (Fig. 7H, I). Conversely, CALR3, CLGN, and PDILT expression levels were upregulated in Arrdc5^−/− sperm, mirroring the expression pattern observed in Tex38^−/− mice (Fig. 7H, I). In summary, ARRDC5, an interacting protein of TEX38, contributes to spermiogenesis and ADAM3 maturation, phenotypes resembling those of Tex38^−/− mice.

TEX38 and ARRDC5 interact with proteins involved in ADAM3 maturation, fertilization, protein transport, and spermiogenesis

Given the similar male infertility phenotypes observed in Tex38^−/− and Arrdc5^−/− mice, we hypothesized that shared molecular mechanisms underlie these reproductive defects. To identify potential protein interaction partners of TEX38 and ARRDC5 involved in male infertility regulation, we performed IP-MS in WT testes. As depicted in Fig. 8A, we identified 384 binding proteins for TEX38 and 365 for ARRDC5 within the testis. Overlap analysis revealed 172 proteins shared by both TEX38 and ARRDC5 (Fig. 8A and Supplementary Data 2). Gene Ontology (GO) enrichment analysis indicated that binding proteins for both proteins were enriched in biological processes including protein transport, apoptotic process, spermatogenesis, vesicle-mediated transport, and proteolysis (Fig. 8B). The top cellular components were cytoplasm, mitochondrion, and ER (Fig. 8C). The most significant molecular functions were protein binding and identical protein binding (Fig. 8D). Meanwhile, we discovered that the ER molecular chaperones calmegin (CLGN) and protein disulfide isomerase-like, testis expressed (PDILT), which are associated with ADAM3 maturation, are also shared interacting partners of TEX38 and ARRDC5. Co-IP analysis further confirmed that CLGN and PDILT can interact with TEX38 and ARRDC5 in vitro (Fig. 8E, F). These findings reinforce our hypothesis that TEX38 and ARRDC5 may be involved in sperm maturation by influencing the maturation of ADAM3.

Protein of adult mouse testis was extracted and IP-MS was performed to identify TEX38 and ARRDC5 binding proteins. A Venn diagram shows the overlap of the TEX38 binding proteins and ARRDC5 binding proteins. B Top biological process, C top cellular component, and D top molecular function from GO enrichment analysis of TEX38 and ARRDC5 binding proteins. E, F Co-IP was performed in HEK-293T cells to validate the interactions of CLGN and PDILT with TEX38 and ARRDC5.

Specifically, these binding proteins participate in various aspects of spermatogenesis and fertilization, including: (1) flagellum assembly (e.g., ATP1A4, DNAJB13, SPACA9, and MNS1); (2) flagellar energy metabolism (e.g., TEKT4); (3) mitochondrial sheath assembly (e.g., GK2, SPATA19, and ARMC3); (4) centriole arrangement (e.g., CETN1); (5) fertilization (e.g., LYZL4, CCIN, SPACA3, and PPP3CC); (6) multinucleated giant cell or multi-headed/flagellated sperm formation (e.g., HADH and ZDHHC19); and (7) ER-to-Golgi vesicle-mediated transport (e.g., ERGIC3). Figure S6 illustrates that TEX38 and ARRDC5 interact with common binding partners critical for spermatogenesis and fertilization. Additionally, Co-IP validated the interaction between TEX38 and several of these putative binding partners (Fig. S7).

Tex38
^−/− and Arrdc5
^−/− spermatozoa failed to pass through the uterine-tubal junction (UTJ)

Given the impaired ADAM3 maturation in Tex38^−/− and Arrdc5^−/− mice, along with significant differential expression of associated ER chaperones and the shared interaction of TEX38 and ARRDC5 with CLGN and PDILT, we hypothesized that knockout of either gene would disrupt sperm migration through the UTJ. To validate this, we dissected the uterus and oviducts 3.5 h post-coitum, quantified sperm numbers in each segment, and performed histological analysis of the uterine-tubal junction (UTJ) to assess in vivo sperm migration. Approximately 2 × 10⁶ sperm were recovered from the uteri of females mated with WT males. In contrast, sperm counts in females mated with Tex38^−/− or Arrdc5^−/− males were significantly reduced compared to WT controls (Fig. 9B), this reduction may result from decreased sperm counts in Tex38^−/− or Arrdc5^−/− males. Nevertheless, 4×10⁵–8×10⁵ sperm were detected in the uteri of females mated with Tex38^−/− or Arrdc5^−/− males. To further examine sperm migration capacity, we quantified sperm in the oviducts. While 150–200 sperm were present in each oviduct of females mated with WT males, no sperm were detected in the oviducts of females mated with Tex38 Tex38^−/− or Arrdc5^−/− males (Fig. 9C). Histological analysis confirmed that Tex38^−/− or Arrdc5^−/− sperm were predominantly retained in the uterus post-ejaculation and rarely reached the oviducts, whereas WT sperm were primarily localized in the oviducts (Fig. 9A). These findings collectively indicate that sperm from Tex38^−/− or Arrdc5^−/− males exhibit defective migration from the uterus to the oviduct in vivo.

A H&E Cross sections of the UTJ of female mice mated with mice and Tex38^−/− (or Arrdc5^−/−) mice, respectively. The middle and right panels are rectangular areas with higher magnification for the corresponding left panel. The red arrow represents sperm. B Sperm count in the uterus after coitus. Data are presented as the mean ± SEM. (n = 4), Student’s t-test. C Sperm count in the oviducts after coitus. Data are presented as the mean ± SEM. (n = 4), Student’s t-test.

Tex38
^−/− mice can be rescued by intracytoplasmic sperm injection

To probe the potential of intracytoplasmic sperm injection (ICSI) to overcome infertility in Tex38^−/− mice, we performed ICSI using spermatozoa from both Tex38^+/+ and Tex38^−/− males. In the control group, sperm with rapid, progressive motility and normal morphology were selected for injection, while in the experimental group, spermatozoa exhibiting the typical bent-neck phenotype associated with Tex38 deletion were utilized. Three control groups, each comprising 19, 20, and 22 eggs, were injected with tailless sperm. After 24 h of culture, 19, 20, and 22 cells developed into two-cell embryos, and subsequently, 17, 18, and 21 blastocysts formed after 96 h. Similarly, three experimental groups of 17, 17, and 16 eggs were injected. Following 24 h, 12, 15, and 15 two-cell embryos were obtained, with subsequent development into 7, 13, and 12 blastocysts after 96 h (Fig. 10A). Importantly, the rates of two-cell embryo and blastocyst formation from Tex38^−/− male mice were not significantly different from those derived from control mice (Fig. 10B). These findings suggest that Tex38 deletion does not overtly impact the development of early embryos produced via ICSI. To further assess the efficacy of ICSI in rescuing Tex38-associated infertility, two-cell embryos were transferred into pseudopregnant female mice, and successfully obtained the healthy developing pups (Fig. 10C). Genotyping of these offspring through PCR amplification of mouse tail DNA confirmed a heterozygous genotype in all cases (Fig. 10D). These results substantiate that ICSI can effectively overcome male infertility caused by Tex38 deficiency.

Abnormal spermatozoa from cauda epididymis of Tex38^−/− mice were selected for ICSI. A Two-cell and blastocyst embryos after ICSI. The oocytes were fertilized by the sperms from Tex38^−/− and Tex38^+/+ mice after ICSI. B The proportion of 2-cell and blastocyst embryos after ICSI in Tex38^−/− and Tex38^+/+ mice. Data are mean ± SEM and dots represent values for individual mice (n = 3). C The offspring of the Tex38^+/− and Tex38^+/+ mice were born and grew healthy after ICSI. D Genotyping for the newborn pups of Tex38^+/− and Tex38^+/+ mice by RT-PCR. E Diagram of proposed action of Tex38. This figure was originally created by the authors using PowerPoint.

Four astronauts returned to Earth on Saturday after hustling to the International Space Station five months ago to relieve the stuck test pilots of Boeing’s Starliner.

Their SpaceX capsule parachuted into the Pacific off the Southern California coast a day after departing the orbiting lab.

Splashing down were NASA’s Anne McClain and Nichole Ayers, Japan’s Takuya Onishi and Russia’s Kirill Peskov. They launched in March as replacements for the two NASA astronauts assigned to Starliner’s botched demo.

Starliner malfunctions kept Butch Wilmore and Suni Williams at the space station for more than nine months instead of a week. NASA ordered Boeing’s new crew capsule to return empty and switched the pair to SpaceX. They left soon after McClain and her crew arrived to take their places. Wilmore has since retired from NASA.

Before leaving the space station on Friday, McClain made note of “some tumultuous times on Earth” with people struggling.

“We want this mission, our mission, to be a reminder of what people can do when we work together, when we explore together,” she said.

McClain looked forward to “doing nothing for a couple of days” once back home in Houston. High on her crewmates’ wish list: hot showers and juicy burgers.

It was SpaceX’s third Pacific splashdown with people on board, but the first for a NASA crew in 50 years. Elon Musk’s company switched capsule returns from Florida to California’s coast earlier this year to reduce the risk of debris falling on populated areas. Back-to-back private crews were the first to experience Pacific homecomings.

The last time NASA astronauts returned to the Pacific from space was during the 1975 Apollo-Soyuz mission, a détente meet-up of Americans and Soviets in orbit.

A satellite launched when slide rules still ruled has jolted astronomers in 2025. NASA’s Relay 2, silent since the summer of 1967, fired off a single radio pulse so bright it briefly eclipsed every cosmic source above Earth.

Clancy James of Curtin University in Perth and colleagues stumbled on the flash during a routine search for fast radio burst signals.

Old hardware, new mystery

Relay 2 left Cape Canaveral on January 21, 1964 as an experimental communications craft, then slipped into bureaucratic oblivion once its battery failed.

NASA’s archival record shows the carcass still loops along an orbit ranging between 1,160 and 4,750 miles above the surface.

On June 13, 2024 Australian Square Kilometre Array Pathfinder (ASKAP) registered a 695.5-to-1031.5 MHz spike that saturated the array’s detectors.

The burst’s dispersion measure, essentially a fingerprint of electrons along its path, matched a single hop through the ionosphere, telling the team the culprit was local rather than interstellar.

“If it’s nearby, we can study it through optical telescopes really easily, so we got all excited, thinking maybe we’d discovered a new pulsar or some other object,” said James.

ASKAP’s software could not focus properly because the source lay close, inside a 12,400-mile shell around Earth. 

Catching a nanosecond flash

“That was an incredibly powerful radio pulse that vastly outshone everything else in the sky for a very short amount of time,” added James.

The team rebuilt the signal with sub-nanosecond precision and found it lasted under 30 ns while pumping at least 300 kilojanskys of flux, millions of times the brightness of Jupiter at radio wavelengths. 

ASKAP excels at rapid wide-field surveys and normally hunts distant galaxies. Its 36 twelve-meter dishes, spread over six square miles of Western Australia, feed a supercomputer that digests 100 trillion bits per second.

Because ASKAP triangulates sources, the group compared time delays across dishes and nailed the origin to Relay 2’s predicted track. No other satellite sat within the narrow uncertainty cone at that instant.

What could light up a corpse in orbit

Relay 2 carries no active transmitters, so the flash must have come from an external trigger. The leading suspect is an electrostatic discharge, a spark leaping between charged surfaces after the craft rubbed against plasma in low Earth orbit.

Spacecraft charging worries engineers on the International Space Station, where analyses show stray arcs can jolt metal tools and even astronauts during spacewalks.

The same physics applies to derelict aluminum shells tumbling through Earth’s shadow and sunlight several times a day.

A rival idea invokes a tiny micrometeoroid striking the satellite at about 22,000 mph, instantly vaporizing metal and creating an expanding plasma cloud that radiates radio noise.

Particles smaller than a pea pepper thousands of spacecraft annually, and shielding against them is limited on old buses like Relay 2.

“In a world where there is a lot of space debris and there are more small, low-cost satellites with limited protection from electrostatic discharges, this radio detection may ultimately offer a new technique to evaluate electrostatic discharges in space,” said Karen Aplin of the University of Bristol, who was not involved in the study.

Why short radio pulses matter

Bursts this short push detectors to their limits, highlighting a blind spot in modern transient surveys. Most instruments record millisecond snapshots, so any comparable events elsewhere in the sky would have slipped past unnoticed until now.

A single nanosecond pulse contains frequency components up to gigahertz levels, revealing fine structure in the ionosphere when it passes through.

That makes each flash an unintended probe of Earth’s upper atmosphere, much like lightning strokes map thunderstorms.

The new detection also reminds astronomers that local clutter can masquerade as cosmic treasure. Search pipelines looking for extragalactic fast radio burst events must now filter out possible shots from derelict satellites, lest they misclassify Earth-orbiting sparks as distant magnetars.

Debris, satellites, and hidden hazards

More than 29,000 tracked objects crowd low Earth orbit, and millions of fragments smaller than a marble remain invisible to radar. A metric-ton satellite built in the Apollo era was never screened for today’s debris environment.

Micrometeoroids travel so fast that even a flake of paint can punch dime-sized craters in solar panels. NASA modeling shows a one-centimeter chip at hypervelocity matches the kinetic energy of a 550-pound weight dropped at 60 mph on Earth.

If such an impact occurred on Relay 2, vaporized aluminum and solar-panel glass would briefly ionize, setting up currents that ring like a bell in radio.

The ASKAP detection suggests this clang can be loud enough to outshine the entire sky, at least for a few billionths of a second.

What happens next

James’s group is developing software triggers so ASKAP will save raw voltages when a nanosecond flash hits, preserving more detail.

Parallel efforts are under way at the Canadian CHIME and South African MeerKAT arrays to watch known dead satellites during meteor showers.

Engineers welcome the possibility of passive monitoring. Real-time radio surveillance could flag electrostatic discharge events on active spacecraft and warn operators before cumulative damage builds.

At the policy level, agencies may need to include radio-quiet zones in licensing rules, preventing future constellations from producing spurious flashes that muddy astrophysical data.

The Relay 2 episode proves even silent satellites can still speak, just not on purpose.

The study is published in The Astrophysical Journal Letters.

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Supersonic commercial travel could soon be coming to the U.S. following a new executive order lifting a 52-year ban on overland commercial supersonic flights.

While supersonic flights could cross the Atlantic, the U.S. Federal Aviation Administration (FAA) banned overland commercial supersonic flights in 1973 in response to public pressure over noise concerns. The new executive order, issued on June 6, lifts that ban and lays out a timeline for the introduction of noise-based certification rules for supersonic flights.

A crew of four wrapped up a nearly five-month stay on the International Space Station, splashing down in the Pacific Ocean off the coast of California under a canopy of parachutes Saturday in the same SpaceX capsule that launched NASA’s Crew-10 mission to the station back in March.

It took the capsule about 17 hours to make the trip home, experiencing re-entry temperatures of around 3,000 degrees Fahrenheit as it punched through the atmosphere following Friday’s undocking with the ISS.

The crew of NASA astronauts Anne McClain and Nichole Ayers, Japan Aerospace Exploration Agency (JAXA) astronaut Takuya Onishi, and Russia’s Roscosmos cosmonaut Kirill Peskov spent their time on the station conducting more than 200 science experiments that helped prepare humans for exploration beyond low-Earth orbit that included material studies and experiments to better understand physiological and psychological changes to the human body.

“We got to accomplish a lot of really amazing operational things. We got to see some amazing views, and we have had some really big belly laughs and a wonderful time together,” said NASA Nichole Ayers, the mission’s pilot.

It was the first space mission for Ayers and fellow crewmate Peskov. It was the second trip to the station for McClain and Onishi.

Their replacements, Crew-11, arrived at the station a week ago. NASA astronauts Zena Cardman and Mike Fincke, along with JAXA astronaut Kimiya Yui and Russian cosmonaut Oleg Platonov, will spend roughly six months on the orbiting lab conducting science experiments and maintenance.

That mission marked the 12th time SpaceX launched NASA astronauts to the ISS. In 2020, the private company began ferrying astronauts to the station as part of the agency’s Commercial Crew Program, ending a reliance on Russia for rides to the station after the retirement of the Space Shuttle program in 2011.

There has been a continual human presence on the space station since Oct. 31, 2000, but NASA and its international partners plan to retire the ISS around the end of the decade. NASA is hoping commercial companies will launch new space stations for the agency’s astronauts in the coming decade.

“All of us are keenly aware that we may never get to do this again,” said McClain, Crew-10 commander, before her departure. “We’ve been very pensive over the last days of understanding what we have all got to be a part of.”

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