Scientists find surprising sex reversal in Australian birds
A study of five common Australian species, including kookaburras, magpies and lorikeets, found around six percent of birds had the chromosomes of one sex but the reproductive organs of another.
The findings indicated a surprisingly high number of birds had reversed their sex after birth, said researchers from the University of the Sunshine Coast.
"This indicates that sex determination in wild birds is more fluid than we thought, and can persist into adulthood," said study co-author Dominique Potvin.
The study performed DNA tests on almost 500 birds.
The overwhelming majority of sex reversals involved genetically female birds growing male gonads.
"We also discovered a genetically male kookaburra who was reproductively active with large follicles and a distended oviduct, indicating recent egg production," said Potvin.
Sex reversal is well known in certain species of reptile and fish but is thought to be rare in wild birds and mammals.
Scientists have documented how pollutants and even warm temperatures can trigger sex reversal in frogs.
The cause of sex reversal in wild birds was not clear, the University of the Sunshine Coast study said.
But it could be due to environmental factors, such as hormone-disrupting chemicals building up in wild areas.
"Understanding how and why sex reversal occurs is vital for conservation and for improving the accuracy of bird research," added Potvin.
The study was published this week in peer-reviewed journal Biology Letters.
sft/tc
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Medscape
9 minutes ago
- Medscape
AI Detects Missed Interval Breast Cancer on Mammograms
TOPLINE: An artificial intelligence (AI) system flagged high-risk areas on mammograms for potentially missed interval breast cancers (IBCs), which radiologists had also retrospectively identified as abnormal. Moreover, the AI detected a substantial number of IBCs that manual review had overlooked. METHODOLOGY: Researchers conducted a retrospective analysis of 119 IBC screening mammograms of women (mean age, 57.3 years) with a high breast density (Breast Imaging Reporting and Data System [BI-RADS] c/d, 63.0%) using data retrieved from Cancer Registries of Eastern Switzerland and Grisons-Glarus databases. A recorded tumour was classified as IBC when an invasive or in situ BC was diagnosed within 24 months after a normal screening mammogram. Three radiologists retrospectively assessed the mammograms for visible signs of BC, which were then classified as either potentially missed IBCs or IBCs without retrospective abnormalities on the basis of consensus conference recommendations of radiologists. An AI system generated two scores (a scale of 0 to 100): a case score reflecting the likelihood that the mammogram currently harbours cancer and a risk score estimating the probability of a BC diagnosis within 2 years. TAKEAWAY: Radiologists classified 68.9% of IBCs as those having no retrospective abnormalities and assigned significantly higher BI-RADS scores to the remaining 31.1% of potentially missed IBCs (P < .05). Potentially missed IBCs received significantly higher AI case scores (mean, 54.1 vs 23.1; P < .05) and were assigned to a higher risk category (48.7% vs 14.6%; P < .05) than IBCs without retrospective abnormalities. Of all IBC cases, 46.2% received an AI case score > 25, 25.2% scored > 50, and 13.4% scored > 75. Potentially missed IBCs scored widely between low and high risk and case scores, whereas IBCs without retrospective abnormalities scored low case and risk scores. Specifically, 73.0% of potentially missed IBCs vs 34.1% of IBCs without retrospective abnormalities had case scores > 25, 51.4% vs 13.4% had case scores > 50, and 29.7% vs 6.1% had case scores > 75. IN PRACTICE: "Our research highlights that an AI system can identify BC signs in relevant portions of IBC screening mammograms and thus potentially reduce the number of IBCs in an MSP [mammography screening program] that currently does not utilize an AI system," the authors of the study concluded, adding that "it can identify some IBCs that are not visible to humans (IBCs without retrospective abnormalities)." SOURCE: This study was led by Jonas Subelack, Chair of Health Economics, Policy and Management, School of Medicine, University of St. Gallen, St. Gallen, Switzerland. It was published online on August 04, 2025, in European Radiology. LIMITATIONS: The retrospective study design inherently limited causal conclusions. Without access to diagnostic mammograms or the detailed position of BC, researchers could not evaluate whether AI-marked lesions corresponded to later detected BCs. DISCLOSURES: This research was funded by the Cancer League of Eastern Switzerland. One author reported receiving consulting and speaker fees from iCAD. This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Medscape
9 minutes ago
- Medscape
Cyclosporin: A Viable Option for Severe Ulcerative Colitis
TOPLINE: Cyclosporin was effective in achieving clinical response and remission in adults with severe steroid-refractory ulcerative colitis (UC), enabling more than half of the patients to avoid colectomy. METHODOLOGY: Researchers conducted a retrospective cohort study of 92 patients (mean age, 55 years; 54.4% men) with severe steroid-refractory UC between January 2001 and February 2024 to evaluate the short- and long-term effectiveness and safety of cyclosporin therapy. All patients received intravenous (IV) methylprednisolone (1 mg/kg/d) for 3-7 days as first-line therapy, and owing to unsuccessful treatment, they received IV cyclosporin (median, 3 mg/kg/d) for 5-7 days as second- or third-line rescue treatment. Clinical and endoscopic disease activity was assessed using the Mayo endoscopic subscore and the partial Mayo score (pMayo). The primary outcome was the rate of clinical response and remission to IV cyclosporin therapy. Clinical response was defined as any reduction in the pMayo score from baseline, and clinical remission was defined as a pMayo score of ≤ 2, with a rectal bleeding subscore of zero. In case of clinical response, IV cyclosporin was followed by oral cyclosporin treatment. Other assessments included colectomy-free survival rates and adverse events associated with cyclosporin therapy, with a median follow-up duration of 14 years. TAKEAWAY: Overall, 88% of patients achieved a clinical response, with 23.9% reaching remission after the IV phase of cyclosporin therapy. Among those on oral cyclosporin, 41.9% showed relapse, whereas 40.7% achieved or maintained remission. Cyclosporin therapy was discontinued in 12% of patients owing to insufficient response to IV therapy and in 14.1% due to adverse events. Adverse events associated with cyclosporin were reported in 53.3% of patients. Moreover, 51.9% of patients who showed response to cyclosporin avoided colectomy. At 1, 3, 5, and 14 years after initiating cyclosporin therapy, the probabilities of colectomy-free survival were 74.7%, 62.6%, 57.1%, and 45.6%, respectively. Concomitant immunomodulator use was the sole predictor of clinical remission after treatment with oral cyclosporin (odds ratio [OR], 6.41; P = .002), and hypoalbuminaemia (serum albumin levels < 35 g/L) at the start of therapy was the sole predictor of adverse events (OR, 0.36; P = .03). IN PRACTICE: "[The study] findings suggest that the effectiveness of CsA [cyclosporin] may be enhanced by the concomitant use of IMT [immunomodulator therapy] in active, severe, steroid-refractory UC, without compromising safety," the authors of the study concluded. SOURCE: This study was led by Bernadett Farkas, MD, Department of Internal Medicine, SZTE SZAKK Center for Gastroenterology, University of Szeged, Szeged, Hungary. It was published online on August 08, 2025, in Therapeutic Advances in Gastroenterology. LIMITATIONS: The study's retrospective design may have introduced confounding due to inherent differences in assessments. The sample size was small, and thus, the minimum effective dosage and duration of concomitant immunomodulator therapy were not identified. DISCLOSURES: This study received funding through a grant from the EU's Horizon 2020 research and innovation program, with additional support being received through grants from the National Research, Development and Innovation Office; the János Bolyai Research Grant; and the Géza Hetényi Research Grant from Albert Szent-Györgyi Medical School, University of Szeged to the authors. Two authors reported receiving speakers' honoraria from various pharmaceutical companies. This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Yahoo
37 minutes ago
- Yahoo
Understanding tick immunity may be key to preventing killer viruses from spreading
A tiny tick crawls across your skin, potentially carrying a virus so lethal it kills up to four out of every ten people it infects. Yet that same tick shows no signs of illness whatsoever – it feeds, moves and reproduces as if nothing is wrong. Scientists studying severe fever with thrombocytopenia syndrome virus (SFTSV) have long wondered why this happens. The pathogen, first identified in China in 2009, causes high fevers, bleeding and organ failure in humans, but leaves ticks completely unharmed. Alongside colleagues, I conducted research into how ticks can carry deadly viruses without becoming ill themselves. Understanding these resistance mechanisms could help scientists develop new ways to block or weaken tick-borne diseases before they spill over into humans or animals. The findings come as climate change pushes ticks into new territories around the world. The Asian longhorned tick that carries SFTSV has been identified in Australia, New Zealand and the eastern US, raising concerns the disease could spread to regions that have never seen it before. Unlike mice, humans or even mosquitoes, ticks pose a unique scientific challenge: most of the molecular tools researchers use to study infection simply don't work in ticks. Instead, we turned to data analysis. We captured detailed molecular snapshots of infected tick cells, tracking thousands of genes and more than 17,000 proteins simultaneously. This allowed the team to study the cellular response comprehensively, at different time post-infection. We found that while human cells respond to viral invasion by mounting aggressive immune responses, mobilising multiple defence systems to fight the infection, tick cells take a fundamentally different approach. Survival strategy Ticks do have immune systems but they operate very differently from ours. Like humans, ticks have cellular signalling pathways that help detect and respond to infection. Known as Toll, IMD and JAK-STAT, these pathways coordinate defensive responses and trigger the production of antimicrobial proteins. But when infected with SFTSV, the tick's immune system showed only minimal activity. Instead of launching full-scale defensive responses, these pathways remained largely quiet. The virus appears to have evolved ways to avoid triggering the tick's immune alarm bells. Instead, the tick cells made major changes to their stress response systems, their production of RNA and proteins, and the pathways that control cell death. (RNA is a molecule that carries genetic instructions – like a working copy of DNA – used by cells to make proteins.) Rather than attacking the virus head-on, tick cells seem to tolerate the infection, reorganising their internal machinery to manage the damage while continuing to function. This approach makes evolutionary sense when you consider the constraints these tiny creatures face. Mounting a full-blown immune response is energetically expensive – it requires lots of resources and can harm the host's own tissues. For ticks, which feed only a few times in their life and live off limited energy reserves, a gentler response may be more sustainable. And because this virus has likely been infecting ticks for millions of years, the two have had time to adapt to each other. Rather than killing the host, the virus may have evolved to fly under the radar, while the tick evolved ways to tolerate it – allowing both to survive and reproduce. Unexpected antiviral guardians We identified two key proteins that act as molecular RNA quality controllers. These proteins, called UPF1 and DHX9, are ancient guardians found in all complex life forms, from plants to humans. One of their normal functions involves monitoring and controlling the quality of RNA, the molecular messenger that carries genetic instructions around cells. Think of them as cellular proofreaders, constantly checking that genetic messages are accurate and functional. My research team first identified these proteins when they appeared as cellular partners that directly interact with viral proteins inside infected cells. This discovery intrigued us because UPF1 and DHX9 were unexpected candidates – they aren't typically associated with antiviral defence – yet they seemed perfectly positioned to detect or process viral RNA, likely because these proteins normally scan RNA for errors, making them well-suited to spot the unusual structures often found in viral genetic material. To test whether these proteins fight the virus, we used genetic techniques to silence the expression of UPF1 and DHX9 in tick cells, essentially removing these molecular guardians. We found that SFTSV viral growth increased significantly when these proteins were absent, demonstrating their antiviral function. This suggests that ticks may have evolved a different kind of immune defence known as non-canonical immunity. Instead of attacking viruses head-on using traditional immune systems, ticks seem to use more subtle strategies. In this case, their RNA quality-control proteins act as internal monitors. Because viral RNA often looks different from normal cellular RNA, these proteins may recognise it as unusual. Once detected, they can trigger internal control systems that slow down or block the virus from multiplying – helping the tick stay healthy without a full-blown immune response. Our research has important implications because UPF1 and DHX9 proteins exist in human cells too. Understanding how they work in ticks could reveal new ways to strengthen human antiviral defences or develop treatments that enhance these natural quality-control mechanisms. The research also opens possibilities for using these tolerance mechanisms to stop disease – either by strengthening similar defences in humans and animals, or by targeting them in ticks to break the chain of transmission. Future strategies might involve boosting antiviral proteins in wild tick populations or developing treatments that specifically target virus-tick interactions. Traditional approaches to disease control are struggling to keep up, especially as climate change helps ticks expand into new regions. To prevent future outbreaks, we need a deeper understanding of how ticks, and the viruses they carry, interact with both humans and animals. Learning how these tiny creatures tolerate deadly pathogens could be key to developing new tools that make people and animals less vulnerable to these diseases – or prevent ticks from passing them on in the first place. This article is republished from The Conversation under a Creative Commons license. Read the original article. Marine J. Petit receives funding from European Union's Horizon 2020 Research and Innovation Program under the Marie Skłodowska-Curie grant agreement No 890970.
