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Today in the history of astronomy, a map of the innermost planet reveals a surprise.

Telomere shortening, DNA damage and elevated oxidative stress in blastocysts cultured in vitro

Figure 1a depicts the morphology of mouse blastocysts that developed in vivo and were cultured in vitro. We first compared the relative TL between in vivo and in vitro blastocysts via quantitative PCR (qPCR) (Fig. 1b). As shown in the Fig. 1b, TL was significantly lower in vitro (0.71 ± 0.47, n = 34) than in vivo (1.16 ± 0.53, n = 34) (In vivo vs. In vitro, p = 0.0005). To further define TL at different sites, we evaluated the ICM and Trophectoderm (TE) cell independently (Fig. 1c), and found that the ICM of in vitro blastocysts (0.70 ± 0.39, n = 30) had a considerably shorter TL than did the ICM of in vivo blastocysts (1.11 ± 0.70, n = 30) (In vivo vs. In vitro, p = 0.0067), the same was true for TE cell (In vivo vs. In vitro, p = 0.0071). We further analyzed the TL of embryos at different developmental stages and found no significant difference in TL between the in vivo and in vitro groups prior to the eight-cell stage (In vivo vs. In vitro, p < 0.05), however, post-eight-cell stage, TL differences between the two groups became increasingly apparent (Morula: In vivo vs. In vitro, p = 0.0409; Blastocyst: In vivo vs. In vitro, p = 0.0070; Hatching-blastocyst: In vivo vs. In vitro, p = 0.0010) (Supplementary Fig. 1a, b).

Telomeres are composed of repeated G-rich sequences and specific binding proteins that work together to stabilize chromosomal ends. These structures are closely associated with apoptosis^33,34. To evaluate whether the lineage-specific cell apoptosis exists, the in vivo and in vitro blastocysts were respectively subjected to differential cell staining and TUNEL staining, showing that compared with the in vivo blastocysts, the number of ICM (17.04 ± 7.33, n = 28 vs. 13.72 ± 3.66, n = 25, p = 0.0461), TE (31.50 ± 4.45, n = 28 vs. 28.24 ± 6.35, n = 25, p = 0.0336) and total cell (48.54 ± 10.14, n = 28 vs. 41.96 ± 9.38, n = 25, p = 0.0182) in the in vitro blastocysts significantly decreased, while the apoptotic rate significantly increased (In vivo vs. In vitro: 10.94 ± 7.74, n = 28 vs. 19.75 ± 10.55, n = 25 in the ICM, p = 0.0010; 4.66 ± 4.34, n = 28 vs. 8.48 ± 5.04, n = 25 in the TE, p = 0.0047; 6.62 ± 4.89, n = 28 vs. 12.00 ± 6.23, n = 25 in the total cell, p = 0.0009) (Fig. 1d–f), although the ICM:TE ratio of apoptotic rate did not differ between the two groups (1.88 ± 1.84, n = 28 vs. 2.11 ± 1.57, n = 25, p = 0.6183) (Fig. 1g). To further confirm the increase in DNA damage, on one hand, we evaluated DNA damage through γH2A.X staining and confirmed the presence of significantly increased DNA damage foci in in vitro cultured-blastocysts (Supplementary Fig. 2a, b); On the other hand, the activation of the p53 pathway also plays an important role, as evidenced by the increased mRNA expression of Trp53, Cdkn1a, Pmaip1, and Trp53bp1 in in vitro-cultured blastocysts. However, when the p53 pathway is inhibited, the expression shows no difference compared with the in vivo group (Supplementary Fig. 2c).

Considering that mitochondria are the main sites of reactive oxygen species (ROS) production, which is an up-regulation in response to cellular stress³⁵. By using MitoSOX (which reflects mitochondrial superoxide production) to track mitochondria in blastocysts, it was found that compared with the in vivo group (0.97 ± 0.08, n = 17), blastocysts in the in vitro group (1.12 ± 0.14, n = 19) exhibited significantly elevated mitochondrial ROS (mtROS) (In vivo vs. In vitro, p = 0.0008) (Fig. 1h). Furthermore, by analyzing the mtROS during preimplantation embryo development, it could be observed that a significant increase in oxidative stress mainly occurs during the blastocyst formation stage and persists until the hatching-blastocyst stage (Supplementary Fig. 1c, d). Collectively, these findings demonstrate that in vitro culture leads to telomere shortening, DNA damage accumulation, and mitochondrial oxidative stress in blastocysts.

Postnatal offspring born from in vitro blastocyst trasfer displayed shorter telomere length one week after birth

We then tracked the change in TL after birth by transferring in vivo and in vitro blastocysts into the uteri of pseudopregnant ICR females. In the in vivo and in vitro groups, 13 (21.67%, 13/60) and 6 (7.89%, 6/76) living F1 pups were respectively delivered (Supplementary Fig. 3a), which were born healthily and respired normally (Fig. 2a). The in vitro group exhibited a significantly higher proportion of male offspring (4/6, 66.67%) compared to the in vivo group (6/13, 46.15%) (Fig. 2b and Supplementary Fig. 3a). Furthermore, the pups were born one day earlier in the in vitro group than in the in vivo group (Supplementary Fig. 3a). Next, tail samples of pups were collected every two weeks after birth to measure TL, and body weight was monitored. The results showed that the TL of F1 pups born from in vitro blastocyst trasfer (0.84 ± 0.15,n = 6) was significantly shorter than that of those born in vivo (1.01 ± 0.26, n = 13) at one week after birth (In vivo vs. In vitro, p = 0.0217), although there was no statistically significant difference in TL between the in vivo and in vitro groups after three weeks (In vivo vs. In vitro, p > 0.05) (Fig. 2d). Furthermore, the body weights of the F1 pups in the two groups were all within the normal range for the mice at the early growth stage (before 5 weeks), whereas at the late growth stage (after 5 weeks), the body weights of the F1 pups in the in vitro group tended to increase compared with those in the in vivo group (Fig. 2c). Grouping analysis by sex revealed that particularly male pups in the in vitro group presented the same trend of weight gain (Supplementary Fig. 3c), with male pups showing greater telomere shortening (0.80 ± 0.15, n = 4) at 1 week after birth than did those in the in vivo group (1.05 ± 0.28, n = 6) (In vivo vs. In vitro, p = 0.0195) (Supplementary Fig. 3e).

We subsequently obtained the F2 generation through F1 inbreeding (Supplementary Fig. 4a). Unlike the F1 generation, we found a significant increase in the proportion of female offspring born in the in vitro group (13/20, 65%) compared with the in vivo group (11/24, 45.83%) (Supplementary Fig. 4b). Then, we measured the TL of F2 generation newborn mice. Similarly, F2 cubs from the in vitro group (0.73 ± 0.21, n = 20) displayed a different growth pattern and had significantly shorter TL than did F2 cubs from the in vivo group (0.98 ± 0.25, n = 24) at one week after birth (In vivo vs. In vitro, p < 0.0001) (Fig. 2e, f). We also found that the growth pattern and TL of F2 generation female pups was more significantly affected in vitro (0.66 ± 0.20, n = 13) than in vivo (0.87 ± 0.19, n = 11) (In vivo vs. In vitro, p = 0.0147) (Supplementary Fig. 4d, f). Overall, these results indicate that offspring produced following blastocyst transfer in vitro exhibit shorter TL one week after birth, which could have intergenerational effects and be gradually recovered later.

Profiles of differentially expressed mRNAs in blastocysts in vivo and in vitro

To investigate the mechanism of telomere shortening caused by in vitro culture, we collected inner cell masses from blastocyst stage embryos for sequencing. The sequencing study was divided into two groups: in vivo fertilization and development as the control (A, in vivo group), and in vivo fertilization and in vitro culture (B, in vitro group). Following high-throughput sequencing, the heatmap revealed hierarchical clustering of distinct mRNA expression profiles within the two groups (Fig. 3a). Using differentially expressed gene sets, a hierarchical clustering analysis was performed, dividing the samples into two major clustering branches. Three replicate samples from the in vivo group were self-clustered into one branch, whereas three samples from the in vitro group were clustered into another branch. During the differential analysis of mRNAs, 644 differentially expressed genes (DEGs) were identified between the in vivo and in vitro groups, among which the percentages of upregulated and downregulated genes were 56.5% (364/644) and 43.5% (280/644), respectively (Fig. 3e). Each dot on the volcano plot represents an mRNA. The blue dots on the left and red dots on the right represent downregulated and upregulated mRNAs with significant differences, respectively, whilst the gray dots represent mRNAs that are expressed with no significant differences. We subsequently conducted KEGG and GO analyses on DEGs (Fig. 3b, c). KEGG analysis revealed that 49 of the 644 genes were enriched in metabolic pathways (Fig. 3b). GO analysis revealed that these genes were mainly involved in intracellular anatomical structure (375 genes), metabolic processes (314 genes), organic substance metabolic processes (305 genes) and etc. (Fig. 3c). Together, these results highlight the critical function of metabolic regulation in in vitro embryo culture. Furthermore, we integrated the DEGs (644 genes) with the metabolism pathway-related genes (1642 genes) from KEGG database, and telomere-related genes (190 genes) identified based on GOTERM_BP_DIRECT: telomere maintenance (GO:0000723) (Fig. 3d). Sirt6 is an NAD⁺ dependent deacetylase that was previously identified as a critical gene in telomere and metabolism. Our RNA sequencing results demonstrated significant expression and fold changes in Sirt6 in the in vivo group compared with the in vitro group. Therefore, we hypothesized that Sirt6 may be associated with the telomere shortening of blastocysts induced by in vitro culture.

The effects of NAD⁺ dependent Sirt6 and epigenetic regulation on telomere maintenance in preimplantation embryos during in vitro culture

To dissect the potential relationship between Sirt6 and telomere shortening induced by in vitro culture, we first examined Sirt6 expression in the inner cell mass of mouse blastocysts in vivo and in vitro. Real-time quantitative PCR (RT-qPCR) analysis revealed that the relative mRNA level of Sirt6 in the in vitro group (0.43 ± 0.15, n = 21) was significantly lower than that in the in vivo group (0.95 ± 0.30, n = 30) (In vivo vs. In vitro, p < 0.0001) (Fig. 4a). In line with these findings, immunofluorescence analysis revealed an approximately 50% decrease in the intensity of Sirt6 fluorescent signals detected in the inner cell mass of mouse blastocysts in vitro (0.57 ± 0.04, n = 37) (In vivo vs. In vitro, p < 0.0001) (Fig. 4b, c). We further analyzed the expression of Sirt6 in embryos at different developmental stages, which showed that the significant decrease of Sirt6 expression mainly initiated at the blastocyst stage (Supplementary Fig. 5a). To clarify the subcellular localization of Sirt6, we found that Sirt6 is mainly expressed in the ICM and the nucleus (Supplementary Fig. 5b–d). Furthermore, we found that the expression of Tert and Terc in blastocysts was significantly increased (Supplementary Fig. 5e, f), which might be a reactive upregulation in response to telomere shortening. These data indicate that decreased expression of Sirt6 may result in shorter telomeres of in vitro blastocysts. Previous studies using in vitro models have shown that the activity of the SIRT6 promoter is regulated by transcription factors and methylation levels, with high methylation inhibiting its expression^36,37. Therefore, through whole-genome methylation analysis, we found that the methylation level of the Sirt6 promoter region in one-week-old F1 mice born from in vitro blastocyst transfer (68.02 ± 3.95, n = 3) was significantly higher than that in the in vivo group (56.61 ± 2.94, n = 3) (In vivo vs. In vitro, p = 0.016). However, there was no significant difference in the methylation level of the Sirt6 promoter region between the two groups at seven weeks (In vivo vs. In vitro: 74.76 ± 3.51, n = 3 vs. 63.91 ± 6.89, n = 3, p = 0.4128) (Supplementary Fig. 3b). These findings suggest that in vitro culture may cause an increase in methylation levels in the Sirt6 promoter region, which could affect Sirt6 expression and consequently affect telomere homeostasis.

Considering that Sirt6 activity and expression could be affected by the NAD⁺ level, we further evaluated the ratio of NAD⁺/NADH throughout mouse blastocyst development in vivo and in vitro, and found that the ratio of NAD⁺/NADH in in vitro mouse blastocysts (0.61 ± 0.11, n = 3) was much lower than that in in vivo mouse blastocysts (1.02 ± 0.18, n = 3) (In vivo vs. In vitro, p = 0.0265) (Fig. 4d). Therefore, we speculated that a decrease in the NAD⁺/NADH ratio during in vitro growth would lead to impaired function of Sirt6 and thus result in telomere shortening in vitro. To determine whether the telomere shortening phenotype of blastocysts in vitro is related to the functional loss of Sirt6 induced by the decrease in the NAD⁺ level, we added different concentrations of a Sirt6 inhibitor (JYQ-42) at the eight-cell stage to inhibit its function and subsequently examined its embryonic development (Supplementary Fig. 6a). We discovered that the TL of blastocysts decreased as the inhibitor concentration increased (DMSO: 0.85 ± 0.40, n = 15; 1 µM: 0.84 ± 0.34, n = 12; 5 µM: 0.67 ± 0.27, n = 11; 10 µM: 0.47 ± 0.22, n = 12; 20 µM: 0.31 ± 0.13, n = 17) (Supplementary Fig. 6b). Moreover, we treated embryos at the eight-cell stage with nicotinamide mononucleotide (NMN), the precursor of NAD⁺ biosynthesis, and discovered that the TL (1.15 ± 0.48, n = 32) was restored to the same level as that of the blastocyst in vivo (1.18 ± 0.56, n = 21) (In vivo vs. In vitro, p > 0.9999), but the TL (0.62 ± 0.28, n = 22) was significantly reduced to that of untreated blastocysts in vitro (0.84 ± 0.32, n = 30) after the addition of high concentrations of Sirt6 inhibitors (In vivo vs. In vitro, p = 0.3149) (Fig. 4e, f). Taken together, these results suggest that the reduction in NAD⁺ levels during the preimplantation stage of mouse embryo development affects telomere maintenance primarily by impairing the function of Sirt6.

Oocyte-specific Sirt6 knockout mice exhibited shorter telomere length

The upregulation of NAD⁺ could restore the TL of blastocysts in vitro, whereas Sirt6 suppression led to a shorter TL, implying that Sirt6, which is dependent on NAD⁺ regulation, plays a role in the regulation of the TL of preimplantation embryos. Considering that NAD⁺ may affect TL regulation through multiple pathways³⁸, we generated oocyte-specific Sirt6 knockout mice to further validate that Sirt6 causes telomere shortening in in vitro cultured-blastocysts (Fig. 5a). Since Sirt6^(-/-) mice die shortly after weaning²⁹, we generated oocyte-specific Sirt6 knockout mice using ZP3-Cre to overcome this early postnatal lethality. We first identified the genotype of Sirt6 conditional knockout (CKO) mice, and observed that using a primer pair of P1 and P2, homozygous mice could produce a 444 bp fragment, whereas wild-type (WT) mice obtained a 390 bp fragment. And homozygous mice were able to obtain a 429 bp fragment while WT mice were unable to obtain a band when a primer pair of P3 and P4 was used (Fig. 5b). Furthermore, we performed RT-qPCR analyses on Sirt6 CKO mice, respectively. Compared with that in WT ovaries (1.01 ± 0.21, n = 3), the level of Sirt6 mRNA in CKO ovaries (0.08 ± 0.03, n = 3) decreased to <10% (WT vs. CKO, p = 0.0015) (Fig. 5c). Our study of 4-month-old mice revealed significant differences in TL between Sirt6 CKO and WT mice. We discovered that the TL of CKO mice (0.70 ± 0.23, n = 4) was significantly shorter than that of WT mice (1.12 ± 0.26,n = 8) when the mouse tail genome was tested (WT vs. CKO, p = 0.0206) (Fig. 5d). Then, we compared the TL between different tissues of CKO mice and WT mice, and the results showed that CKO mice had considerably shorter telomeres than WT mice did. In particular, lung and whole blood tissues were significantly different (WT vs. CKO: 2.61 ± 1.62, n = 3 vs. 0.92 ± 0.35, n = 3 in the lung, p = 0.0355; 3.48 ± 3.29, n = 3 vs.1.67 ± 0.23, n = 3 in the blood, p = 0.0250) (Fig. 5e).

Early embryonic development of oocyte-specific Sirt6 knockout mice is characterized by delayed development and shorter telomeres

To study the early embryonic development of Sirt6 CKO mice and its impact on the TL of embryos, as well as whether NAD⁺ regulates the TL of preimplantation embryos through Sirt6, we performed ICSI on WT and CKO mouse MII oocytes, and then cultured fertilized oocytes with or without NMN. The embryonic development of the preimplantation embryos in both groups was assessed with and without the administration of NMN (Fig. 6a). As shown in Fig. 6a, CKO or CKO + NMN mouse oocyte-derived embryos presented delayed development (red asterisk) compared with the WT group. In terms of the blastocyst formation rate, we noted that the incidence in the CKO (52.4%, n = 21) and CKO + NMN groups (52.4%, n = 21) was significantly lower than that in the WT group (89.6%,n = 48) (WT vs. CKO, p < 0.001; WT vs. CKO + NMN, p < 0.001), although its cleavage capacity remained unaffected (WT vs. CKO: 90.6%, n = 53 vs. 84%, n = 25, p = 0.3970; WT vs. CKO + NMN: 90.6%, n = 53 vs. 84%, n = 25, p = 0.3970) (Fig. 6b, c). These observations suggest that when Sirt6 is deficient in oocytes, the developmental potential of early embryos is compromised and cannot be restored even in the presence of NAD⁺. Figure 6d shows that the TL of mature oocytes in CKO mice (0.30 ± 0.23, n = 18) was considerably shorter than that in WT mice (0.90 ± 0.68, n = 23) (WT vs. CKO, p = 0.0010) (Fig. 6d). Consistent with this concept, the TL of blastocysts derived from the oocytes of CKO mice (0.52 ± 0.19, n = 11) was significantly shorter than that of WT mice (0.91 ± 0.37, n = 26) (WT vs. CKO, p = 0.0340). When NMN was added, the TL in the WT group (1.24 ± 0.52, n = 24) dramatically increased (WT vs. WT + NMN, p = 0.0203). The TL in the CKO group (0.53 ± 0.21, n = 11) was not substantially different from that previously reported (CKO vs. CKO + NMN, p > 0.9999), but was much shorter than that in the WT group (WT vs. CKO + NMN, p = 0.0400) (Fig. 6e). Taken together, these results suggest that oocyte Sirt6 is critical for maintaining early embryonic telomere function and genome integrity in the presence of NAD⁺, which determines developmental capacity.

Bowhead whales can live more than 200 years. Tiny shrews barely make it a year. Some sea sponge species are over 15,000 years old. That gap raises a straightforward question: what’s different at the biological level?

Instead of hunting for a single “longevity gene,” researchers looked for patterns across sets of related genes that might scale up in species with long lives.

Biologists call these sets “gene families.” Over evolutionary time, genes sometimes duplicate. Extra copies can shift how strongly a function shows up in the body – a higher “dose” – or create room for small tweaks that help cells respond more flexibly.

Studying lifespan potential

Dr. Benjamin Padilla-Morales, from the Milner Center for Evolution and the University of Bath’s Department of Life Sciences, was the first author.

The study compared 46 mammalian species with high-quality, well-curated genomes.

For each species, the team used maximum lifespan potential (MLSP), defined as the longest confirmed age any individual of that species has reached, and matched it to the sizes of thousands of gene families.

They also accounted for traits that often track with lifespan, including body size, brain size relative to body size, how long pregnancy lasts, and when animals first reproduce.

This design allowed them to ask a clear question: across mammals, do certain families get larger in species that live longer, and if so, which ones?

Immune system and lifespan potential

The strongest signal centered on the immune system. The gene families that tended to be larger in long-lived mammals were involved in immune surveillance and clearance.

These functions help detect threats and clear cellular debris that accumulates with age.

The immune system does more than fight infections. It also removes damaged or “senescent” cells that stop dividing and release stress signals, and it helps identify early cancer cells before they grow out of control.

As an animal ages, those jobs matter more. Expanding the families that handle them can help tissues maintain stability over many decades.

Brain size link plays a role

Across mammals, species with bigger brains for their body size often live longer. In this study, many of the same gene families that grow with lifespan also grow with relative brain size.

A large brain uses substantial energy and oxygen and produces more metabolic byproducts. Extra immune and housekeeping capacity supports this load and helps keep neural tissue stable.

The link implies a shared genetic background: immune-related expansions may support both long life and the demands of a large, energy-hungry brain.

Padilla-Morales explained that scientists have long known relative brain size is linked to longevity. He said the two traits share an evolutionary path, with larger brains offering potential behavioral advantages.

He also noted that bigger-brained species don’t just live longer because of ecological factors. Their genomes show parallel expansions in genes tied to survival and maintenance.

“This shows that brain size and immune resilience seem to have walked hand-in-hand in the evolutionary journey toward longer lives,” Padilla-Morales explained.

Lifespan potential – what doesn’t matter

Body mass itself – big versus small – did not account for the gene-family trends once other factors were included.

Life-history timings such as gestation length and age at first reproduction didn’t drive the expansions either.

Those traits do correlate with lifespan in general, but they weren’t behind which gene families got larger in this analysis.

The team checked a basic concern: maybe long-lived species just carry more genes overall. They do not. The pattern wasn’t a blanket “more genes everywhere.” It was specific to certain families tied to maintenance and defense.

Humans and longevity genes

The researchers looked at how these longevity-linked genes behave in people. Human versions tend to be more active and produce more transcript variants – different “edits” of the same gene that yield slightly different proteins.

That diversity gives cells more ways to fine-tune responses, which fits the idea of a vigilant, flexible maintenance system.

The team compared their gene lists with earlier aging databases. The overlap wasn’t perfect, which is common, but the functions aligned.

Prior work points to DNA damage responses, inflammation control, and programmed cell death (apoptosis). The expanded families in this study cluster within the same biological pathways.

Maximum lifespan potential limitations

This is not “the cure for aging.” The results show correlations, not causes. Evolution is complicated, and a gene family can expand for one reason and later take on another role.

Maximum lifespan potential is a record-holder measure, not an average, and records can reflect limited data or unusual individuals.

Even with those limits, the same immune-related signal shows up across dozens of species, and that deserves attention. It shifts the focus from a single switch to scaled-up maintenance.

Future of species lifespan research

Overall, the findings point to systems-level resilience. Long-lived mammals don’t rely on a magic change in metabolism.

They tend to carry more copies of genes that help detect problems early, remove damaged cells, and keep tissues – especially the brain – stable for many years.

For anyone thinking about healthy aging, this suggests a practical target. Immune surveillance and cellular housekeeping may be as important as tweaking metabolism or chasing one-off genetic fixes.

It’s a reminder that evolution didn’t grant immortality. It boosted the systems that prevent small problems from turning into big ones, and it did so in ways we can measure – across 46 species, using maximum lifespan potential, and with clear links to brain size and immune function.

The study is published in the journal Scientific Reports.

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During this period, the moon reaches its new phase on Saturday August 23rd. On that date it will be located near the sun and will be invisible at night. As the week progresses, the waxing crescent moon will enter the evening sky and will only slightly hamper meteor observing during the evening hours late in the week. The estimated total hourly rates for evening observers this weekend should be near 4 as seen from mid-northern latitudes (45N) and 3 as seen from tropical southern locations (25S). For morning observers, the estimated total hourly rates should be near 18 as seen from mid-northern latitudes (45N) and 11 as seen from tropical southern locations (25S). The actual rates seen will also depend on factors such as personal light and motion perception, local weather conditions, alertness, and experience in watching meteor activity. Evening rates are slightly reduced during this period due to moonlight. Note that the hourly rates listed below are estimates as viewed from dark sky sites away from urban light sources. Observers viewing from urban areas will see less activity as only the brighter meteors will be visible from such locations.

The radiant (the area of the sky where meteors appear to shoot from) positions and rates listed below are exact for Saturday night/Sunday morning August 23/24. These positions do not change greatly day to day so the listed positions may be used during this entire period. Most star atlases (available online and at bookstores and planetariums) will provide maps with grid lines of the celestial coordinates so that you may find out exactly where these positions are located in the sky. I have also included charts of the sky that display the radiant positions for evening, midnight, and morning. The center of each chart is the sky directly overhead at the appropriate hour. These charts are oriented for facing south but can be used for any direction by rotating the charts to the desired direction. A planisphere or computer planetarium program is also useful in showing the sky at any time of night on any date of the year. Activity from each radiant is best seen when it is positioned highest in the sky (culmination), either due north or south along the meridian, depending on your latitude. Radiants that rise after midnight will not reach their highest point in the sky until daylight. For these radiants, it is best to view them during the last few hours before dawn. It must be remembered that meteor activity is rarely seen at its radiant position. Rather they shoot outwards from the radiant, so it is best to center your field of view so that the radiant lies toward the edge and not the center. Viewing there will allow you to easily trace the path of each meteor back to the radiant (if it is a shower member) or in another direction if it is sporadic. Meteor activity is not seen from radiants that are located far below the horizon. The positions below are listed in a west to east manner in order of right ascension (celestial longitude). The positions listed first are located further west therefore are accessible earlier in the night while those listed further down the list rise later in the night.

 

These sources of meteoric activity are expected to be active this week

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The kappa Cygnids (KCG) are active from August 3-28, with maximum occurring on August 16^th. The radiant is currently located at 19:24 (291) +58. This area of the sky is located in extreme southeastern Draco, 5 degrees north of the 4^th magnitude star known as kappa Cygni. To best see these meteors face northward near 2300 local summer time (LST) when it lies on the meridian and is located highest in the sky. With a high northern declination, these meteors are difficult to view from the southern hemisphere. Expected hourly rates this week are less than 1 no matter your location. With an entry velocity of 24 km/sec., the average meteor from this source would be of medium-slow velocity.

The large Anthelion (ANT) radiant is currently centered at 22:52 (343) -05. This position lies in central Aquarius, 2 degrees north of the 4^th magnitude star known as lambda Aquarius. This radiant is best placed near 02:00 LST when it lies on the meridian and is highest in the southern sky. Rates at this time should be near 3 no matter your location. With an entry velocity of 30 km/sec., the average Anthelion meteor would be of medium-slow velocity.

The last of the Perseids (PER) are expected this weekend from a radiant located at 04:08 (062) +58. This position lies in southwestern Camelopardalis, 10 degrees northeast of the 2nd magnitude star known as Mirfak alpha Persei. This area of the sky is best placed for viewing during the last dark hour before dawn when it lies highest in the northeastern sky. Current rates are expected to be less than 1 no matter your location. With an entry velocity of 59 km/sec., the average meteor from this source would be of swift velocity. Viewers in the southern hemisphere have a limited view of this shower as the radiant only rises just before dawn.

Sporadic meteors are those meteors that cannot be associated with any known meteor shower. All meteor showers are evolving and disperse over time to the point where they are no longer recognizable. Away from the peaks of the major annual showers, these sporadic meteors make up the bulk of the activity seen each night. As seen from the mid-northern hemisphere (45N) one would expect to see during this period approximately 12 sporadic meteors per hour during the last hour before dawn as seen from rural observing sites. Evening rates would be near 3 per hour. As seen from the tropical southern latitudes (25S), morning rates would be near 7 per hour as seen from rural observing sites and 2 per hour during the evening hours. Locations between these two extremes would see activity between these listed figures. Evening rates are slightly reduced due to moonlight.

The list below offers information in tabular form. Rates and positions in the table are exact for Saturday night/Sunday morning.

SHOWER	DATE OF MAXIMUM ACTIVITY	CELESTIAL POSITION	ENTRY VELOCITY	CULMINATION	HOURLY RATE	CLASS
		RA (RA in Deg.) DEC	Km/Sec	Local Summer Time	North-South
kappa Cygnids (KCG)	Aug 16	19:24 (291) +58	23	23:00	<1 – <1	II
Anthelion (ANT)	–	22:52 (343) -05	30	02:00	3  –  3	II
Perseids (PER)	Aug 12	04:08 (062) +58	59	08:00	<1 – <1	I

Class Explanation: A scale to group meteor showers by their intensity:

• Class I: the strongest annual showers with Zenith Hourly Rates normally ten or better.
• Class II: reliable minor showers with ZHR’s normally two to ten.
• Class III: showers that do not provide annual activity. These showers are rarely active yet have the potential to produce a major display on occasion.
• Class IV: weak minor showers with ZHR’s rarely exceeding two. The study of these showers is best left to experienced observers who use plotting and angular velocity estimates to determine shower association. These weak showers are also good targets for video and photographic work. Observers with less experience are urged to limit their shower associations to showers with a rating of I to III.
  

Until recently, Mars was studied only through telescopes and some data that was recorded from early spacecraft. It was thought that Mars’ polar regions were the only significant reservoirs of ice, mainly in the form of frozen carbon dioxide (dry ice). The rest of Mars seemed too dry for frozen water to form, and there were no means to detect what was under the surface of the planet. The glaciers on Mars were thought to be composed mainly of rock and dust, with a thin layer of ice covering them.

This view started to change with planetary science missions like the Mars Odyssey and the Phoenix Lander. Having a closer look at the red planet unveiled the existence of hydrogen in the soil and water ice just a few inches below the surface. Water was found on Mars, and it wasn’t as rare as previously thought. However, with the new study published in the journal Icarus, scientists Yuval Steinberg, Oded Aharonson, and Isaac Smith describe Martian glaciers as consisting of 80% ice. This new, radar-based study opens myriad new possibilities for planetary science and even future human-led missions to Mars.

Read more: What’s Happening To Earth Right Now Can’t Be Explained By Climate Models

What’s Special About These Glaciers?

Martian glaciers are of special interest to scientists because they help us understand the planet’s climate history. Understanding Mars’ past may help us better plan for the future of our own planet. This was the main sphere of interest for Weizmann Institute of Science graduate, Steinberg, who conducted this study alongside mentors and colleagues from the Planetary Science Institute in Tucson and York University.

They began their research by combing through old studies, just to realize many of those had been performed on different sites, with different methods. That means the results from different glaciers across the planet were not comparable. There was no discernible pattern, so the team decided to test five separate glacier sites and use the same techniques on all of them. That would allow them to process all the data in the same way, compare them, and draw a single conclusion.

They used the Shallow Radar instrument mounted on the Mars Reconnaissance Orbiter (MRO), a NASA spacecraft designed to study climate and water presence on the red planet. The Shallow Radar allowed Steinberg and the team to gather crucial data from five different spots on different glaciers. Once the analysis of the data was performed, it was clear that each glacier had the same electrical signature. In other words, all of the analyzed glaciers had the same composition. It was determined that by volume, Mars glaciers are four-fifths ice, and the rest is rocks and various debris that encase this ice. This uniformity of results means that either there was one glaciation event on Mars, or multiple ice periods that occurred under very similar circumstances.

What Does This Discovery Mean To Humankind?

Mars, as we know it today, is a barren wasteland. However, the new study suggests it wasn’t always like this. The presence of high-purity ice means Mars once had an abundance of snowfall and frost that, over time, led to the formation of these large glaciers at different latitudes over the planet’s surface. Knowing that the glaciers consist of 80% ice, scientists can now model how much water once circulated in the planet’s atmosphere. This also enables us to understand how the climate on Mars has changed with the planet’s tilt. Following these changes on the nearby planet might let us understand how to combat climate change on Earth.

That said, the presence and purity of ice also mean possibilities for future missions on Mars, especially if we plan to send people to the surface of the red planet. If we develop ways of using the water already on the planet, it would mean more efficient crewed missions. The pure ice can be mined for drinking water or even fuel, which means Mars could sustain human life on its own. There would be no need to haul all the necessary water from Earth.

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Exoplanets used to be fringe objects in astronomy. Now, they are popular subjects for testing ideas about the composition of the universe.

A new study proposes that some gas giants might steadily collect dark matter in their cores until the buildup tips into a collapse that forms a tiny black hole.

Mehrdad Phoroutan-Mehr, a graduate researcher at the University of California, Riverside (UCR), led the work with postdoctoral researcher Tara Fetherolf.

Planets help detect dark matter

Astronomers now have thousands of worlds to work with across many ages, sizes, and orbits. NASA’s exoplanet archive lists nearly 6,000 confirmed planets as of mid 2025.

Gas giants are especially handy for this kind of test. They have huge volumes and cold interiors compared with stars, which makes any extra energy source easier to notice.

The team modeled how heavy, non-annihilating dark matter would move through a Jupiter-like world. The particles would gradually lose speed, settle into the center, and pile up.

Once that central clump passes a critical mass, gravity wins. The clump collapses into a black hole that either begins to feed on the surrounding gas or evaporates if it is small enough.

How planets may form black holes

The researchers focused on the superheavy, non-annihilating case scenario because captured particles never remove themselves by destroying each other. That makes the buildup relentless.

Under those conditions, the core can collapse on observable timescales in some planets. The possibility extends to multiple collapses throughout a single planet’s lifetime if capture continues.

In plain language, if the parameters line up, a Jupiter-mass world could quietly become a Jupiter-mass black hole. The object would keep the planet’s mass but lose the planet’s bulk.

“As the central concentration of dark matter grows in gaseous planets, a black hole may form and then accrete the surrounding material. Discovering a black hole with the mass of a planet would be a major breakthrough,” noted Phoroutan-Mehr.

Signs of planet black holes

A planet that turns into a black hole would still tug its star in the same way, so radial-velocity and astrometric signals would persist. Transit dips, however, could vanish because the body shrinks far below a star-crossing silhouette.

That mismatch creates a check. If we see stellar wobbles that imply a giant planet but repeated photometry no longer shows transits, the system deserves a closer look.

Microlensing adds a different angle. A compact lens and a puffier planet of the same mass bend light nearly the same way in simple events, so single light curves will not easily separate them.

Population statistics can help. If many high-mass “planets” near the galactic center lack transits yet show dynamical signals, that pattern would be hard to blame on chance alone.

How telescopes can check

The Nancy Grace Roman Space Telescope’s Galactic Bulge Time-Domain survey will capture tens of thousands of micro-lensing events in fields rich in dark matter. That is exactly where this model expects stronger capture and faster collapses.

Roman’s microlensing plus precise astrometry can flag planetary-mass compact objects and map their distribution. If planet-mass black holes cluster where the dark matter density is higher, that would lift this idea above speculation.

There is also a thermal route. Independent work showed that dark matter annihilation could heat exoplanets, raising their infrared glow beyond what cooling alone predicts.

Small black holes could also evaporate by Hawking radiation, dumping high-energy particles into the planet or, if the particles escape, into space. Either outcome offers a potential signal, though today’s instruments lack the sensitivity to chase the faintest cases.

Limits of the idea

This is not a blanket prediction that all gas giants are doomed. Many parameters must align, from the particle mass to the scattering cross section and the local dark matter density.

The absence of planet-mass black holes would be informative as well. If Jupiter-like worlds remain intact in regions where the model expects collapses, that would carve away at the allowed properties of dark matter.

The researchers also noted that multiple observational methods must be combined. No single transit, lens, or velocity signal will settle the question in isolation.

There are limitations in the physics too. Capture and drift times depend on interior temperature and density profiles, which are still debated for many planets, and even modest changes can shift the thresholds.

Why this matters for dark matter

The research could turn an ordinary planetary survey into a particle-physics experiment. We already collect the data while hunting for new worlds.

A confirmed planet-mass black hole would point straight at a non-annihilating, very heavy particle candidate. That would push the conversation about dark matter beyond the ranges probed by common terrestrial detectors.

Even a null result tightens the net. If transit catalogs remain full and consistent with radial-velocity and astrometric counts, those absences pin down cross sections that would have produced collapses.

The framework invites new cross-checks as the exoplanet census grows. Roman’s catalogs, plus follow-up from ground observatories and future direct-imaging missions, set the stage for a decisive test.

The study is published in the journal Physical Review D.

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