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Apparently this is old news, but it’s the first I’m hearing it, and, well, frogs are pretty cool.

But:

The scientists then infected frogs

What’s your fucking problem, scientists? Find some sick frogs to cure instead of infecting healthy ones you sick fucks.


Inside a “sauna,” heat helps frogs rid themselves of a deadly fungal infection. They look cozy as hell.

^Inside\ a\ “sauna,”\ heat\ helps\ frogs\ rid\ themselves\ of\ a\ deadly\ fungal\ infection^

Australia’s green and golden bell frog has suffered greatly from Batrachochytrium dendrobatidis (Bd), a fungus that has spread around the world over the past 3 decades. With its range reduced by 90%, the amphibian is teetering on the edge of extinction. Now, scientists have shown that small plastic-covered shelters can help the frogs warm up enough to kill the fungus, potentially rescuing the species—and maybe others—before it disappears.

“It’s a superinnovative and impressive paper,” says Brian Gratwicke, a conservation biologist at the Smithsonian Institution’s National Zoo and Conservation Biology Institute who was not involved with the work. “The implications are very hopeful.”

The approach, reported today in Nature, might improve the outlook for other frogs as well if the shelters could be distributed widely or put out in targeted efforts to help the last remaining populations of rare and endangered frogs, says Benedikt Schmidt, a conservation biologist at the University of Zurich, also not involved.

Bd wiped out the iconic harlequin frogs of Central America in the 1990s, causing the cloud forests to fall silent. Around the world, 90 species of frog have gone extinct, and even more have been pushed to the brink of vanishing, earning Bd the dubious distinction of the most harmful infectious disease of wildlife. The fungus spreads easily, often through the pet trade, infecting the skin of susceptible species and eventually causing heart attacks.

In the lab, antifungal medications can cure the disease. Keeping heat-loving frogs at 30°C also kills the fungus and can even assist some species in building immunity. But scientists have struggled to come up with practical ways to help animals survive the fungus in the wild. In a few heroic cases, scientists even temporarily removed the animals from remote ponds and disinfected the habitat.

Looking for a simpler approach, researchers have proposed putting small, heated enclosures into the field to allow frogs to warm themselves enough to kill the fungus. But no one had tested the idea.

Anthony Waddle, a conservation biologist at Macquarie University, wondered whether the approach might work with bell frogs. The animals like to climb into the holes of bricks, so Waddle designed a cheap, small greenhouse shelter that could surround these bricks and bring them up to 30°C. “I started to think, ‘What if the frogs can help themselves?’” he says. “Maybe all we have to do is give them an opportunity.”

First, Waddle and colleagues studied the bell frogs in the lab. They showed that when they infected animals with Bd, they preferred to be at 30°C. These frogs had milder disease than those kept at 19°C, which is an ideal temperature for the fungus. And frogs that could choose the temperature—by going in and out of various compartments in the housing—did even better, suggesting that being able to raise and lower body temperature is a particularly effective way for frogs to fight the fungus. The experiments also showed that, like some other species, bell frogs that had cleared an infection were better able to resist reinfection.

The green and gold bell frog of Australia is an endangered species. It’s really purdy, with mottled gold stripes on green.

^The\ green\ and\ gold\ bell\ frog\ of\ Australia\ is\ an\ endangered\ species^

Moving outside, Waddle and colleagues created habitats in a dozen 3.5-meter-wide tubs. They added gravel, water, some artificial plants, and flowerpots for the frogs to hide in. Every tub also housed a shelter for the frogs consisting of a stack of black bricks, each with 10 frog-size holes. This shelter was enclosed in a small greenhouse, about the size of a lawn chair, wrapped in translucent plastic. The greenhouses heated up in the Sun and created a sauna effect inside. In a variation on this setup, the scientists also covered some of these greenhouses with shade cloth, which kept the temperatures inside cooler.

The scientists then infected frogs and put them in the tubs, observing them for several months and recapturing them every week or so to check for the severity of infection.

The sick frogs seemed to prefer spending time in the greenhouses rather than outside of them; they were seen there four times more often than would be expected by chance. The higher temperatures in the unshaded greenhouses helped them fight the infection, whereas the frogs in the slightly cooler shaded shelters had infections twice as intense. “I’m glad that we have a proof-of-concept study that show that the method could work for some species,” Schmidt says.

Waddle says he hopes the findings will lead to ways to help wild frogs. “I am extremely anxious about the outlook for the species.” He has a small grant to install frog shelters in Sydney Olympic Park, which has one of the largest remaining populations of the green and golden bell frogs. So far, he's put up 50, and he will track how the frogs do over the next few years. He also hopes to look at five to six other frog species in Australia that may benefit from the shelters, because they can tolerate temperatures high enough to kill Bd.

The approach could work for the many other species of amphibians that like to bask in the Sun and heat themselves, notes Schmidt, who specializes in amphibians with info fauna, the national data and information center for Swiss fauna. He would like to see a study where the shelters are deployed and the populations recover.

But Schmidt says it may not be easy to manufacture and distribute a lot of shelters, get landowner permission, or reach the entire range of a species. “The challenges of the transition from ‘it works’ to ‘it is now widely used’ should not be underestimated.”

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Two of those eyes may have evolved into a part of the brain called the pineal gland

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https://www.dailycamera.com/2026/01/23/nsf-ncar-boulder-new-owner-mesa-lab/

The National Science Foundation announced Friday that it will consider proposals for new private or public ownership to take over the National Center for Atmospheric Research’s Mesa Lab in Boulder.

Friday’s announcement comes after the Trump administration made threats to dismantle NCAR in December, and on Dec. 17, the NSF announced its intent to restructure critical weather science infrastructure at NCAR.

The NSF published a Dear Colleague Letter requesting “expressions of interest in and/or concepts of operation” for the Mesa Lab, specifically seeking those interested in “ownership of the NSF NCAR Mesa Lab building” for private or public use. The Boulder lab is currently managed by the University Corporation for Atmospheric Research on behalf of the NSF.

“We’re in touch with NSF to better understand how this process will unfold, and we’re continuing to do our work,” Boulder NCAR media relations manager David Hosansky wrote in an email to the Daily Camera.

The Daily Camera requested a further explanation of the letter from the NSF, which did not immediately respond to a request for comment on Friday evening.

The NSF also put out a call for those interested in “management and operations” of NCAR space weather activities and NCAR weather modeling and atmospheric observing capabilities. In addition to operation proposals, the NSF posed four questions to which it’s seeking responses. The foundation is seeking to know:

• Whether NCAR activities duplicate those of other organizations.

• If there are any new ideas for NCAR’s management and operations the NSF should consider.

• If there are other “concepts for management and operations of NCAR activities” that differ from the current model that the NSF should consider.

• What the performance objectives and metrics should be for a restructured atmospheric research center. Related Articles

The NSF is requesting that interested parties submit a document, limited to two or three pages per topic, describing ideas for operations and/or addressing the questions posed in the letter. The deadline for submissions is March 13.

“The materials received will be used to inform NSF’s future actions with respect to the components of NCAR and to ensure the products, services, and tools provided in the future align with the needs and expectations of stakeholders to the extent practicable,” the letter read.

Plans to transfer stewardship of the NCAR-Wyoming Supercomputing Center, located in Cheyenne, and plans to divest from or transfer two research aircraft that NCAR manages are being considered separately from this letter.

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Answers

  • Left: An image of Europa taken by NASA's Galileo spacecraft

  • Right: The end of a rusted 500 gallon propane tank belonging to my friend and photographed by me

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Obviously domestication, deliberate or not, is bad. But also, I want a Raccoon companion sooooo bad.

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cross-posted from: https://lemmy.ml/post/41043473

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cross-posted from: https://lemmy.bestiver.se/post/821202

Editing the title to the original URL instead of the crosspost.

spoilerFor more than a century, people have considered Alzheimer's disease (AD) an irreversible illness. Consequently, research has focused on preventing or slowing it, rather than recovery. Despite billions of dollars spent on decades of research, there has never been a clinical trial of any drug to reverse and recover from AD.

A research team from Case Western Reserve University, University Hospitals (UH) and the Louis Stokes Cleveland VA Medical Center has now challenged this long-held dogma in the field, testing whether brains already badly afflicted with advanced AD could recover.

The study, led by Kalyani Chaubey, from the Pieper Laboratory, was published online Dec. 22 in Cell Reports Medicine. Using diverse preclinical mouse models and analysis of human AD brains, the team showed that the brain’s failure to maintain normal levels of a central cellular energy molecule, NAD+, is a major driver of AD, and that maintaining proper NAD+ balance can prevent and even reverse the disease.

NAD+ levels decline naturally across the body, including the brain, as people age. Without proper NAD+ balance, cells eventually become unable to execute many of the critical processes required for proper functioning and survival. In this study, the team showed that the decline in NAD+ is even more severe in the brains of people with AD, and that this same phenomenon also occurs in mouse models of the disease.

While AD is a uniquely human condition, it can be studied in the laboratory with mice that have been genetically engineered to express genetic mutations known to cause AD in people.

The researchers used two of these mouse models: One carried multiple human mutations in amyloid processing; the other carried a human mutation in the tau protein.

Amyloid and tau pathology are two of the major early events in AD. Both lines of mice develop brain pathology resembling AD, including blood-brain barrier deterioration, axonal degeneration, neuroinflammation, impaired hippocampal neurogenesis, reduced synaptic transmission and widespread accumulation of oxidative damage. These mice also develop the characteristics of severe cognitive impairments seen in people with AD.

After finding that NAD+ levels in the brain declined precipitously in both human and mouse AD, the research team tested whether preventing loss of brain NAD+ balance before disease onset or restoring brain NAD+ balance after significant disease progression could prevent or reverse AD, respectively.

The study was based on their previous work, published in Proceeding of the National Academy of Sciences USA, showing that restoring the brain's NAD+ balance achieved pathological and functional recovery after severe, long-lasting traumatic brain injury. They restored NAD+ balance by administering a now well-characterized pharmacologic agent known as P7C3-A20, developed in the Pieper lab.

Remarkably, not only did preserving NAD+ balance protect mice from developing AD, but delayed treatment in mice with advanced disease also enabled the brain to fix the major pathological events driven by the disease-causing genetic mutations.

Moreover, both lines of mice fully recovered cognitive function. This was accompanied by normalized blood levels of phosphorylated tau 217, a recently approved clinical biomarker of AD in people, providing confirmation of disease reversal and highlighting an objective biomarker that could be used in future clinical trials for AD recovery.

“We were very excited and encouraged by our results,” said Andrew A. Pieper, the study’s senior author, a professor at the Case Western Reserve School of Medicine and director of the Brain Health Medicines Center, Harrington Discovery Institute at UH. “Restoring the brain's energy balance achieved pathological and functional recovery in both lines of mice with advanced Alzheimer's. Seeing this effect in two very different animal models, each driven by different genetic causes, strengthens the new idea that recovery from advanced disease might be possible in people with AD when the brain's NAD+ balance is restored.”

Pieper also holds the Morley-Mather Chair in Neuropsychiatry at UH and the CWRU Rebecca E. Barchas, MD, DLFAPA, University Professorship in Translational Psychiatry. He serves as psychiatrist and investigator in the Louis Stokes VA Geriatric Research Education and Clinical Center.

The results prompt a paradigm shift in how researchers, clinicians and patients can think about treating AD in the future.

“The key takeaway is a message of hope—the effects of Alzheimer's disease may not be inevitably permanent,” Pieper said. “The damaged brain can, under some conditions, repair itself and regain function.”

“Through our study, we demonstrated one drug-based way to accomplish this in animal models, and also identified candidate proteins in the human AD brain that may relate to the ability to reverse AD,” Chaubey said.

Pieper emphasized that current over-the-counter NAD+-precursors have been shown in animal models to raise cellular NAD+ to dangerously high levels that promote cancer. The pharmacological approach in this study, however, uses a pharmacologic agent (P7C3-A20) that enables cells to maintain their proper balance of NAD+ under conditions of otherwise overwhelming stress, without elevating NAD+ to supraphysiologic levels.

“This is an important factor when considering patient care, and clinicians should consider the possibility that therapeutic strategies aimed at restoring brain energy balance might offer a path to disease recovery,” Pieper said.

This work also encourages new research into complementary approaches and eventual testing in patients, and the technology is being commercialized by Cleveland-based company Glengary Brain Health, which Pieper co-founded.

“This new therapeutic approach to recovery needs to be moved into carefully designed human clinical trials to determine whether the efficacy seen in animal models translates to human patients,” Pieper said. “Additional next steps for the laboratory research include pinpointing which aspects of brain energy balance are most important for recovery, identifying and evaluating complementary approaches to Alzheimer's reversal, and investigating whether this recovery approach is also effective in other forms of chronic, age-related neurodegenerative disease.”

https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(25)00608-1

Summary: Alzheimer’s disease (AD) is traditionally considered irreversible. Here, however, we provide proof of principle for therapeutic reversibility of advanced AD. In advanced disease amyloid-driven 5xFAD mice, treatment with P7C3-A20, which restores nicotinamide adenine dinucleotide (NAD+) homeostasis, reverses tau phosphorylation, blood-brain barrier deterioration, oxidative stress, DNA damage, and neuroinflammation and enhances hippocampal neurogenesis and synaptic plasticity, resulting in full cognitive recovery and reduction of plasma levels of the clinical AD biomarker p-tau217. P7C3-A20 also reverses advanced disease in tau-driven PS19 mice and protects human brain microvascular endothelial cells from oxidative stress. In humans and mice, pathology severity correlates with disruption of brain NAD+ homeostasis, and the brains of nondemented people with Alzheimer’s neuropathology exhibit gene expression patterns suggestive of preserved NAD+ homeostasis. Forty-six proteins aberrantly expressed in advanced 5xFAD mouse brain and normalized by P7C3-A20 show similar alterations in human AD brain, revealing targets with potential for optimizing translation to patient care.

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