Published today (July 1) in Astronomy & Astrophysics, the project has announced its first published major discovery – a bright exploding star.

The object underwent an extreme brightening (increasing by 2500 times) that was not seen when compared to the image taken 2 days earlier. The quick response and diligent work of the public allowed the object to be studied and classified early in its evolution, identifying it as a cataclysmic variable star, and given the name GOTO0650.

Co-lead of Kilonova Seekers, Dr. Tom Killestein, Warwick Prize Fellow in the Astronomy and Astrophysics group, University of Warwick said: “Kilonova Seekers is a unique opportunity for members of the public to take part in true real-time astrophysics. Remarkably, public volunteers identified this star as an object of interest within 3 1/2 hours of the image being taken by the GOTO telescopes – this discovery could have been missed among many other objects without their efforts.

“The involvement of the volunteers didn’t stop there, as there was a huge follow-up response from the public. It was flagged for further observations from the Swift and Einstein Probe space observatories, and GOTO0650 was bright enough for amateur astronomers to take impressively high-quality observations of with their own equipment, which formed a key part of the paper and really helping us understand the object.”

Cataclysmic variable stars sporadically increase in brightness by large amounts before dropping back to normal levels. They are compact binary star systems, consisting of a white dwarf star stealing matter from its companion donor star. Periodically, material from the donor star hits a critical density and temperature within the disc of gas that surrounds the white dwarf, which causes an explosive outburst and bright flashes of light.

The fast response of the public enabled the team to get an unusually highly complete dataset on the star, including spectroscopy, X-ray, and UV measurements, supplemented by the impressively high-quality observations of the amateur astronomers. These observations suggest it is a period bouncer, the final state of a cataclysmic variable star, and a rare object to find even in the age of widespread wide-field imaging surveys.

Co-lead of Kilonova Seekers, Dr Lisa Kelsey, Leverhulme Early Career Fellow, Institute of Astronomy and Kavli Institute for Cosmology, Cambridge said: “Citizen science is a powerful way to make novel serendipitous discoveries in vast datasets that would normally need to be analysed in depth by scientists.

“With over 2.8 million classifications so far, the discovery of GOTO0650 is really the pinnacle of 2 years of consistent hard work from our volunteers. Without the Kilonova Seekers volunteers flagging this object, rapid follow-up would not have been possible, and this object may have been missed entirely.”

The Kilonova Seekers Project is approaching its two-year anniversary of inviting members of the public to analyse near real-time data collected from the Warwick-led Gravitational-wave Optical Transient Observer (GOTO) project. This project takes all-sky survey images of space from two arrays of telescopes located on opposite sides of the planet — in Spain and Australia.

The vast numbers of observations taken in these imaging surveys will soon be beyond the capacity of individual and small teams of scientists to label and validate. Citizen Science is a viable, mutually beneficial solution to avoid objects like GOTO0650 being missed.

As a shining example of such efforts, Kilonova Seekers has provided over 3,500 members of the public with the opportunity to discover supernovae and variable stars using real data. With volunteers from around the world, there is almost always someone online looking at the data in real-time.

Svetoslav Alexandrov, Kilonova Seekers Volunteer based in Bulgaria said: “Traffic in Sofia, Bulgaria, is always awful during the mornings so I have to pass time on the bus somehow, and contributing to citizen science is an excellent way to do that! Kilonova Seekers is on the top of my list, because it’s mobile-friendly and most importantly, it offers us fresh imagery almost every single day.

“I literally screamed with joy when I saw that I was going to be a co-author of the research paper. I’m certain that people on the street raised their eyebrows when they saw me screaming and dancing, but I didn’t care. I knew I am a co-discoverer of something significant, and this was all that mattered”

Cledison Marcos da Silva, Kilonova Seekers Volunteer based in Brazil said: “This discovery was very important to me, as I was going through a serious health problem and the citizen science we do at Kilonova Seekers was distracting me from my situation. I never imagined that we would discover such a bright transient, so it was a huge surprise, and we were very happy when we found out. This discovery shows the importance of citizen science, both scientifically and personally. Even from your bed, or on the street with your cell phone, there is the possibility of making a very important discovery.”

Mayahuel Torres-Guerrero, Kilonova Seekers Volunteer based in Mexico said: “The journey from the discovery of GOTO0650 to the publication of the paper in Astronomy & Astrophysics has been personally rewarding. I had the opportunity to learn how to download data from LCO telescopes and to produce light curves that allowed us to monitor echo outbursts. It was very exciting when GOTO0650 produced an echo outburst on Christmas Day and New Year’s Day! It was a great journey for someone who has studied social sciences like me!”

GOTO is a network of telescopes that is principally funded by the Science and Technology Facilities Council (STFC) and operated by the University of Warwick at the Roque de los Muchachos Observatory on La Palma, Spain, and Siding Spring Observatory in NSW, Australia, on behalf of a consortium including the University of Warwick, Monash University, Armagh Observatory & Planetarium, the University of Leicester, the University of Sheffield, the National Astronomical Research Institute of Thailand (NARIT), the University of Turku, the University of Portsmouth, the University of Manchester and the Instituto de Astrofisica de Canarias (IAC).

The findings, presented today at the ESOT Congress 2025, mark a significant step forward in overcoming the biggest challenge in xenotransplantation: rejection by the human immune system.

Using cutting-edge spatial molecular imaging, researchers mapped how human immune cells interact with pig kidney tissue in transplanted organs, revealing critical early markers of rejection and potential intervention strategies. The study, led by Dr. Valentin Goutaudier and a collaborative international research team (Paris Institute for Transplantation and Organ Regeneration & NYU Langone Transplant Institute), highlights key molecular mechanisms that could shape the future of xenotransplantation.

One of the most striking discoveries was that human immune cells were found in every part of the pig kidney’s filtering system after the transplant. Researchers observed early molecular signs of antibody-mediated rejection as soon as Day 10 and peaking at Day 33, reinforcing previous findings that rejection begins rapidly but progresses over time.² By tracking these immune responses for up to 61 days, the team identified a crucial window for targeted therapeutic intervention.

“Our study provides the most detailed molecular map to date of how the human immune system engages with a transplanted pig kidney,” explained Dr. Goutaudier. “By pinpointing specific immune cell behaviours and gene expressions, we can refine anti-rejection treatments and improve transplant viability.”

The study’s innovative approach used a bioinformatic pipeline to distinguish human immune cells from pig structural cells, allowing for precise mapping of immune infiltration patterns. Notably, macrophages and myeloid cells were the most prevalent immune cell types across all time points, further confirming their role as key mediators in xenograft rejection.

When targeted therapeutic interventions were introduced, immune-mediated signs of rejection were successfully weakened. Combined with novel spatial insights into how immune cells interact with pig kidney tissue, this marks a major breakthrough — paving the way for more refined anti-rejection strategies. These advances come at a pivotal time as the first US-based clinical trials of pig kidney transplantation into living human recipients begin in 2025.

With xenotransplantation poised to address the global organ shortage crisis, these findings bring researchers one step closer to making genetically modified pig kidneys a viable long-term solution. The next phase will focus on optimising anti-rejection treatments, refining genetic modifications in donor pigs, and developing early detection protocols to monitor and manage rejection responses.

“Understanding the specific immune interactions at a molecular level allows us to develop targeted interventions that can prevent rejection before it escalates,” explained Dr. Goutaudier. “This research lays the groundwork for safer and more effective pig-to-human transplants in the near future.”

As scientific progress accelerates, researchers remain cautiously optimistic that genetically modified pig kidneys could become a routine transplant option within the next decade. However, regulatory approvals will require consistent demonstration of safety and efficacy in diverse patient populations.

References:

1. Goutaudier V., Williams, C., Morgand, E., et al. Application of a Novel Spatial Transcriptomic 6000-Plex Panel in Pig-to-Human Xenotransplantation. Presented at ESOT Congress 2025; 30^th June 2025; London, United Kingdom.
2. Loupy, A., Goutaudier, V., Giarraputo, A. et al. (2023). Immune response after pig-to-human kidney xenotransplantation: A multimodal phenotyping study.The Lancet, 402(10408), 1158-1169. https://doi.org/10.1016/S0140-6736(23)01855-3
3. Montgomery RA, Stern JM, Lonze BE, Tatapudi VS, Mangiola M, Wu M, Weldon E, Lawson N, Deterville C, Dieter RA, Sullivan B, Boulton G, Parent B, Piper G, Sommer P, Cawthon S, Duggan E, Ayares D, Dandro A, Fazio-Kroll A, Kokkinaki M, Burdorf L, Lorber M, Boeke JD, Pass H, Keating B, Griesemer A, Ali NM, Mehta SA, Stewart ZA. Results of Two Cases of Pig-to-Human Kidney Xenotransplantation. N Engl J Med. 2022 May 19;386(20):1889-1898. doi: 10.1056/NEJMoa2120238. PMID: 35584156.

Researchers discovered a previously unappreciated mechanism by which CMV, a herpes virus that infects the majority of the world’s adult population, enters cells that line the blood vessels and contributes to vascular disease. In addition to using molecular machinery that is shared by all herpes viruses, CMV employs another molecular “key” that allows the virus to sneak through a side door and evade the body’s natural immune defenses.

The finding might explain why efforts to develop prophylactic treatments against CMV have, so far, been unsuccessful. This research also highlights a new potential avenue for the development of future antiviral drugs and suggests that other viruses of the herpes family, such as Epstein-Barr and chickenpox, could use similar molecular structures to spread from one infected cell to the next while avoiding immune detection.

“If we don’t know what weapons the enemy is using, it is hard to protect against it,” said senior author Jeremy Kamil, Ph.D., associate professor of microbiology and molecular genetics at Pitt. “We found a missing puzzle piece that represents one possible reason why immunization efforts against CMV have been unsuccessful.”

In the United States, approximately one in every 200 babies is born with congenital CMV infection. Of the babies infected, one in five will have birth defects, such as hearing loss, or go on to have long-term health challenges. For most adults, CMV infections are asymptomatic. But a CMV infection during pregnancy presents significant health risks to the unborn child and could be deadly for people who are immunosuppressed, including organ transplant recipients.

Because of the large size of its genome and its complicated molecular machinery, CMV long evaded attempts to develop prophylactic treatments. Similar to other herpes viruses, CMV relies on a protein called gH to enter cells of the vessel lining. But unlike other herpes viruses, which use a protein partner called gL to facilitate infection, the new study found that CMV replaces gL with another partner called UL116 and recruits a protein called UL141. The resulting complex of gH-UL116-UL141, called GATE by the authors, then becomes an alternative tool for breaking into cells lining the blood vessels and causing internal damage while simultaneously preventing the body’s own immune system from recognizing the signs of infection.

The newly discovered GATE could become a potential vaccine target for CMV and other herpes viruses.

“Previous attempts to generate a CMV vaccine have failed, but that was before we identified the GATE complex. We hope that new strategies targeting GATE will improve our chances to combat CMV infection, and also perhaps cleanse our bodies of this lifelong infection,” said Chris Benedict, Ph.D., associate professor at La Jolla Institute for Immunology and co-senior author of the study with Kamil and LJI professor, president & CEO Erica Ollmann Saphire, Ph.D., MBA. “If we can develop antiviral drugs or vaccines that inhibit CMV entry, this will allow us to combat the many diseases this virus causes in developing babies and immune-compromised people.”

Other authors of this research are Michael Norris, Ph.D., of the University of Toronto; Lauren Henderson, Mohammed Siddiquey, Ph.D., both of Louisiana State University Health Shreveport; and Jieyun Yin, Ph.D., Kwangsun Yoo, Ph.D., Simon Brunel, Ph.D., Michael Mor, Ph.D., and Erica Ollmann Saphire, Ph.D., all of La Jolla Institute for Immunology.

This research was supported by the National Institutes of Health (grants AI11685, AI139749, AI101423 and T32HL155022) and by ARPA-H APECx contract 1AY1AX000055.

Glycogen is typically thought of as a reserve energy source stored in the liver and muscles. While small amounts also exist in the brain, particularly in support cells called astrocytes, its role in neurons has long been dismissed as negligible. “This new study challenges that view, and it does so with striking implications,” says Professor Pankaj Kapahi, PhD, senior scientist on the study. “Stored glycogen doesn’t just sit there in the brain; it is involved in pathology.”

The research team, led by postdoc Sudipta Bar, PhD, discovered that in both fly and human models of tauopathy (a group of neurodegenerative diseases including Alzheimer’s), neurons accumulate excessive glycogen. More importantly, this buildup appears to contribute to disease progression. Bar says tau, the infamous protein that clumps into tangles in Alzheimer’s patients, appears to physically bind to glycogen, trapping it and preventing its breakdown.

When glycogen can’t be broken down, the neurons lose an essential mechanism for managing oxidative stress, a key feature in aging and neurodegeneration. By restoring the activity of an enzyme called glycogen phosphorylase (GlyP) — which kicks off the process of glycogen breakdown — the researchers found they could reduce tau-related damage in fruit flies and human stem cell-derived neurons.

Rather than using glycogen as a fuel for energy production, these enzyme-supported neurons rerouted the sugar molecules into the pentose phosphate pathway (PPP) — a critical route for generating NADPH (nicotinamide adenine dinucleotide phosphate) and Glutathione, molecules that protect against oxidative stress. “By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies,” said Bar.

Even more promising, the team demonstrated that dietary restriction (DR) — a well-known intervention to extend lifespan — naturally enhanced GlyP activity and improved tau-related outcomes in flies. They further mimicked these effects pharmacologically using a molecule called 8-Br-cAMP, showing that the benefits of DR might be reproduced through drug-based activation of this sugar-clearing system. “This work could explain why GLP-1 drugs, now widely used for weight loss, show promise against dementia, potentially by mimicking dietary restriction,” said Kapahi.

Researchers also confirmed similar glycogen accumulation and protective effects of GlyP in human neurons derived from patients with frontotemporal dementia (FTD), strengthening the potential for translational therapies. Kapahi says the study emphasizes the power of the fly as a model system in uncovering how metabolic dysregulation impacts neurodegeneration. “Work in this simple animal allowed us to move into human neurons in a much more targeted way,” he said.

Kapahi also acknowledges the Buck’s highly collaborative atmosphere as a major factor in the work. His lab, with expertise in fly aging and neurodegeneration, took advantage of proteomics expertise in the Schilling lab and the Seyfried lab (at Emory University) as well as the Ellerby lab which has expertise in human iPSCs and neurodegeneration.

Kapahi says this study not only highlights glycogen metabolism as an unexpected hero in the brain but also opens up a new direction in the search for treatments against Alzheimer’s and related diseases. “By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell’s inner chemistry to fight age-related decline,” he says. “As we continue to age as a society, findings like these offer hope that better understanding — and perhaps rebalancing — our brain’s hidden sugar code could unlock powerful tools for combating dementia.”

Coauthors: Additional Buck collaborators include Kenneth A. Wilson, Tyler A.U. Hilsabeck, Sydney Alderfer, Jordan B Burton, Samah Shah, Anja Holtz, Enrique M. Carrera, Jennifer N. Beck, Jackson H Chen, Grant Kauwe, Tara E. Tracy, Birgit Schilling, and Lisa M. Ellerby. Other collaborators include Eric B. Dammer, Fatemeh Seifar and Nicholas T. Seyfried, Emory Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA as well as Ananth Shantaraman, Department of Biochemistry, Emory University School of Medicine, Atlanta, GA

Acknowledgments: The work was supported by NIH grants R01AG038688, R21AG054121, AG045835, R01AG071995, R01AG070193, T32AG000266-23, R01AG061879, P01AG066591 and 1S10 OD016281. Other support came from the Hevolution Foundation, American Federation of Aging Research, the Larry L. Hillblom Foundation and the Catalyst^X award from Alex and Bob Griswold

Now, a team of Northwestern Medicine scientists has developed an AI tool called iSeg that not only matches doctors in accurately outlining lung tumors on CT scans but can also identify areas that some doctors may miss, reports a large new study.

Unlike earlier AI tools that focused on static images, iSeg is the first 3D deep learning tool shown to segment tumors as they move with each breath — a critical factor in planning radiation treatment, which half of all cancer patients in the U.S. receive during their illness.

“We’re one step closer to cancer treatments that are even more precise than any of us imagined just a decade ago,” said senior author Dr. Mohamed Abazeed, chair and professor of radiation oncology at Northwestern University Feinberg School of Medicine.

“The goal of this technology is to give our doctors better tools,” added Abazeed, who leads a research team developing data-driven tools to personalize and improve cancer treatment and is a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

The study was published today (June 30) in the journal npj Precision Oncology.

How iSeg was built and tested

The Northwestern scientists trained iSeg using CT scans and doctor-drawn tumor outlines from hundreds of lung cancer patients treated at nine clinics within the Northwestern Medicine and Cleveland Clinic health systems. That’s far beyond the small, single-hospital datasets used in many past studies.

After training, the AI was tested on patient scans it hadn’t seen before. Its tumor outlines were then compared to those drawn by physicians. The study found that iSeg consistently matched expert outlines across hospitals and scan types. It also flagged additional areas that some doctors missed — and those missed areas were linked to worse outcomes if left untreated. This suggests iSeg may help catch high-risk regions that often go unnoticed.

“Accurate tumor targeting is the foundation of safe and effective radiation therapy, where even small errors in targeting can impact tumor control or cause unnecessary toxicity,” Abazeed said.

“By automating and standardizing tumor contouring, our AI tool can help reduce delays, ensure fairness across hospitals and potentially identify areas that doctors might miss — ultimately improving patient care and clinical outcomes,” added first author Sagnik Sarkar, a senior research technologist at Feinberg who holds a Master of Science in artificial intelligence from Northwestern.

Clinical deployment possible ‘within a couple years’

The research team is now testing iSeg in clinical settings, comparing its performance to physicians in real time. They are also integrating features like user feedback and working to expand the technology to other tumor types, such as liver, brain and prostate cancers. The team also plans to adapt iSeg to other imaging methods, including MRI and PET scans.

“We envision this as a foundational tool that could standardize and enhance how tumors are targeted in radiation oncology, especially in settings where access to subspecialty expertise is limited,” said co- author Troy Teo, instructor of radiation oncology at Feinberg.

“This technology can help support more consistent care across institutions, and we believe clinical deployment could be possible within a couple of years,” Teo added.

This study is titled “Deep learning for automated, motion- resolved tumor segmentation in radiotherapy.”