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Hall & Oates’ Restraining Order Mystery Solved: Daryl Hall Wants to Block John Oates From Selling His Share of Their Joint Venture to Primary Wave – Yahoo Entertainment
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Double Moon crater riddle solved? Spent Chinese rocket booster carrying mystery payload crash landed – The Register
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Molecular Mystery Solved – Harvard Scientists Discover a Previously Unknown Way Cells Break Down Proteins – SciTechDaily
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Brightest cosmic explosion of all time: How we may have solved the mystery of its puzzling persistence – Phys.org
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Mysteries About Leading Biomarker for Alzheimer’s Solved
Summary: Researchers identify how taupT217, a toxic form of the Tau protein, spreads through the brain as Alzheimer’s disease progresses.
Source: University of Virginia
University of Virginia neuroscientists have revealed how a toxic form of tau protein, notorious for forming tangles in the brains of people with Alzheimer’s disease and several other neurodegenerative disorders, spreads through the brain as the disease progresses.
The tau protein helps cause cognitive decline associated with those diseases. The research shows what provokes its accumulation and how it harms nerve cells called neurons. Scientists may be able to leverage these findings to develop new Alzheimer’s treatments that prevent or delay symptom onset, or slow disease progression once symptoms develop.
UVA’s new research also advances efforts to develop blood tests to detect Alzheimer’s at its earliest stages, when it is, in principle, most amenable to treatment. The researchers found that antibodies used in blood tests for measuring this toxic, chemically modified form of tau, called “taupT217,” can easily be fooled into detecting other proteins, which compromises test accuracy. Fortunately, they also showed how this problem can be avoided.
The new research from UVA’s Dr. George Bloom and collaborators is the most comprehensive examination yet of where and how taupT217 accumulates in the brain. The results provide vital insights into the development of Alzheimer’s and possibly other neurological conditions called “non-Alzheimer’s tauopathies.”
Those include Parkinson’s disease and chronic traumatic encephalopathy.
“The past few years have witnessed exciting advances in early Alzheimer’s detection by measuring the amount of taupT217 in blood or cerebrospinal fluid, but until now almost nothing has been learned about what causes this type of tau to form in the brain or how it affects neuron health,” said Bloom, of UVA’s Departments of Biology, Cell Biology and Neuroscience, as well as the UVA Brain Institute, the Virginia Alzheimer’s Disease Center and UVA’s Program in Fundamental Neuroscience.
“Knowing what provokes taupT217 to build up in the brain and how it harms neurons provides new openings for therapeutic intervention,” he said.
Understanding Alzheimer’s
Tau plays important roles in the healthy brain, where, among other things, it helps build and maintain the “microtubules” that serve as highways for transporting important materials within the neurons that form the brain’s circuitry. But in people with Alzheimer’s, tau becomes chemically modified and misshapen in ways that prevent its normal functioning and make it toxic. This eventually leads to two phenomena that account for cognitive decline in Alzheimer’s: destruction of neuronal circuitry and neuron death.
Why this occurs has been only partially understood, but UVA’s new research offers more answers. For example, the researchers found that they could trigger taupT217 buildup inside cultured neurons by exposing them to clusters, or oligomers, of tau. Those are known to accumulate in the Alzheimer’s brain and have long been suspected as a harmful contributor to the disease.
They also found that the chemical modification that converts normal tau into taupT217 dramatically decreases tau’s ability to stick to microtubules, which in turn may make it easier for the tau to form toxic oligomers.
“In terms of immediate clinical value, we hope that our findings about the challenge of antibody specificity for measuring taupT217 in blood will quickly resonate with companies that are striving to develop commercially available tests to identify Alzheimer’s patients years before symptoms become evident,” Bloom said.
“Because massive irreversible brain damage has already occurred by symptom onset, accurate early diagnosis will be crucial for development of drugs that effectively combat Alzheimer’s.”
That’s just one example of the practical insights generated by UVA’s research that will benefit the efforts to better diagnose and treat Alzheimer’s.
“Alzheimer’s disease reflects a multi-dimensional breakdown of normal brain cells, so there is nothing simple about it,” Bloom said. “Focusing research on the earliest processes that convert normal brains into Alzheimer’s brains, though, provides the best hope for eventually conquering this terrible disease.”
The researchers have published their findings in the journal Alzheimer’s & Dementia. The first author of the paper is Binita Rajbanshi, a recently graduated pharmacology Ph.D. student. The other team members were Anuj Guruacharya, James Mandell and Bloom. The scientists reported that they have no financial interests in the work.
See also
About this Alzheimer’s disease research news
Author: Josh Barney
Source: University of Virginia
Contact: Josh Barney – University of Virginia
Image: The image is in the public domain
Original Research: Open access.
“Localization, induction, and cellular effects of tau phosphorylated at threonine 217 1” by Binita Rajbanshi et al. Alzheimer’s & Dementia
Abstract
Localization, induction, and cellular effects of tau phosphorylated at threonine 217 1
Introduction
Tau phosphorylation at T217 is a promising Alzheimer’s disease (AD) biomarker, but its functional consequences were unknown.
Methods
Human brain and cultured mouse neurons were analyzed by immunoblotting and immunofluorescence for total tau, taupT217, taupT181, taupT231, and taupS396/pS404. Direct stochastic optical reconstruction microscopy (dSTORM) super resolution microscopy was used to localize taupT217 in cultured neurons. Enhanced green fluorescent protein (EGFP)-tau was expressed in fibroblasts as wild type and T217E pseudo-phosphorylated tau, and fluorescence recovery after photobleaching (FRAP) reported tau turnover rates on microtubules.
Results
In the brain, taupT217 appears in neurons at Braak stages I and II, becomes more prevalent later, and co-localizes partially with other phospho-tau epitopes. In cultured neurons, taupT217 is increased by extracellular tau oligomers (xcTauOs) and is associated with developing post-synaptic sites. FRAP recovery was fastest for EGFP-tauT217E.
Conclusion
TaupT217 increases in the brain as AD progresses and is induced by xcTauOs. Post-synaptic taupT217 suggests a role for T217 phosphorylation in synapse impairment. T217 phosphorylation reduces tau’s affinity for microtubules.
Astronomers May Have Solved The Mystery of The Bubbles Towering Over The Milky Way : ScienceAlert
When the Fermi Gamma-Ray Space Telescope entered low-Earth orbit in 2008, it opened our eyes to a whole new Universe of high-energy radiation.
One of its more curious discoveries was the Fermi Bubbles: giant, symmetrical blobs extending above and below the galactic plane, 25,000 light-years on each side from the Milky Way’s center, glowing in gamma-ray light – the highest energy wavelength ranges on the electromagnetic spectrum.
Then, in 2020, an X-ray telescope named eROSITA found another surprise: even bigger bubbles extending over 45,000 light-years on each side of the galactic plane, this time emitting less energetic X-rays.
Scientists have since concluded that both sets of bubbles are probably the result of some sort of outburst or outbursts from the galactic center and the supermassive black hole therein. The mechanism producing the gamma- and X-radiation, however, has been a little harder to pin down.
Now, using simulations, physicist Yutaka Fujita from Tokyo Metropolitan University in Japan has come up with a single explanation that explains both sets of bubbles in one fell swoop.
The X-ray emission, he has found, is the product of a powerful, fast-moving wind that slams into the tenuous gas filling interstellar space, producing a shock wave that reverberates back through the plasma, causing it that energetic glow.
The supermassive black hole that powers the heart of the Milky Way – Sagittarius A* – is pretty quiet as far as black holes go. Its feeding activity is minimal; it’s classified as “quiescent”. It hasn’t always been that way, though. And an active black hole can have all sorts of effects on the space around it.
As material falls towards the black hole, it heats up and blazes with light. Some of the material gets channeled away along magnetic field lines outside the black hole, which act as a synchrotron to accelerate particles to near-light speed. These are launched as powerful jets of ionized plasma from the black hole’s poles, punching out into space for up to millions of light-years.
In addition, there are cosmic winds: streams of charged particles that are whipped up by the material orbiting the black hole that then blast out into space.
While Sagittarius A* may be quiet now, that hasn’t necessarily always been the case. Look hard enough, and relics of past activity, such as the Fermi bubbles, can be found lurking in the space around the galactic plane. By studying these relics we can understand when and how that activity took place.
Fujita’s foray into the Fermi bubbles is based on data from the now-retired Suzaku X-ray satellite, jointly operated by NASA and the Japanese Space Agency (JAXA). He took Suzaku observations of the X-ray structures associated with the bubbles and performed numerical simulations to try to reproduce them based on black hole feeding processes.
“We show that a combination of the density, temperature, and shock age profiles of the X-ray gas can be used to distinguish the energy-injection mechanisms,” he writes in his paper.
“By comparing the results of numerical simulations with observations, we indicate that the bubbles were created by a fast wind from the galactic center because it generates a strong reverse shock and reproduces the observed temperature peak there.”
The most likely scenario, he found, is a black hole wind blowing at a speed of 1,000 kilometers per second (621 miles) from a past feeding event that was metered out over the course of 10 million years and ended fairly recently. As the wind propagates outwards, the charged particles collide with the interstellar medium, producing a shock wave that bounces back into the bubble. These reverse shock waves heat the material inside the bubbles, causing it to glow.
The numerical simulations developed by Fujita accurately reproduced the temperature profile of the X-ray structure.
He also investigated the possibility of a single explosive eruption from the galactic center and was unable to reproduce the Fermi bubbles. This suggests that a slow, steady wind from the galactic center was the most likely progenitor of the mysterious structures. And the power of the wind can only be attributed to Sagittarius A*, not star formation – another phenomenon that produces cosmic winds.
“Thus,” he writes in his paper, “the wind may be the same as active galactic nuclei outflows often observed in other galaxies and thought to regulate the growth of galaxies and their central black holes.”
The paper has been published in the Monthly Notices of the Royal Astronomical Society.
Mystery of Smell Loss After Covid-19 Might Be Solved
The nose knows why some people still can’t smell long after recovering from Covid-19.
A haywire immune response in the olfactory system was found to explain why some people still can’t smell long after symptoms of the disease have abated, according to a small, peer-reviewed study published Wednesday in the journal Science Translational Medicine. In some cases, the immune or inflammatory response was detected in patients with smell loss up to 16 months after recovery from Covid-19.
Compared with people who can smell normally, patients with long-term smell loss had fewer olfactory sensory neurons, cells in the nose responsible for detecting smells and sending that information to the brain. Patients with lingering loss of smell had an average of 75% fewer of the neurons compared with healthy people, said
Brad Goldstein,
a study co-author and sinus surgeon at Duke University.
“We think the reduction of sensory neurons is almost definitely related to the inflammation,” Dr. Goldstein said.
Loss of smell is a common Covid-19 symptom, though its prevalence varies widely depending on factors including which variant caused the infection, head and neck specialists said.
Most Covid-19 patients who experience smell loss regain the sense within weeks of infection. But the symptom can stick around for a year or longer for up to 7% of patients, a February analysis said.
Dr. Goldstein said he and his colleagues sought to identify what was damaged or altered in people with long-term smell loss. “If we don’t know what’s broken, it’s hard to tell how to fix it,” he said.
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They took samples from the nose tissue of nine patients who couldn’t smell long after Covid-19 infections and compared them with cells from healthy people. Patients with persistent smell loss had more T-cells, a type of white blood cell that plays a critical part in immune response, in their noses, the study said. The T-cells were making interferon-gamma, a substance linked to inflammation, Dr. Goldstein said, and support cells appeared to be reacting to it.
The support cells protect and nourish olfactory sensory neurons. Without them, the olfactory sensory neurons can’t survive. Research has shown that the virus that causes Covid-19 doesn’t infect olfactory sensory neurons directly, but that it can attack such support cells.
Patients with smell loss also had fewer of a certain type of anti-inflammatory cell and more of a particular inflammatory cell than healthy people, said the study of 24 patients. The healthy group included two people who had recovered from Covid-19 but didn’t have long-term smell loss.
Covid-19 researchers said the study bolstered evidence that inflammation could be a culprit in long-Covid symptoms. An April study in the journal JAMA Neurology found inflammation among deceased Covid-19 patients in the olfactory bulb, the part of the brain responsible for receiving and processing information from olfactory sensory neurons in the nose.
Neuroinflammation could be a contributor to loss of smell and other neurological symptoms related to long-Covid such as brain fog, said
Cheng-Ying Ho,
a co-author of the April study and an associate professor of pathology at Johns Hopkins University School of Medicine.
Dr. Ho, who wasn’t involved in the new study, said inflammation that starts in the nasal cavity could extend to the brain. She said that the new study was compelling but that its small sample size necessitated further work in more patients. Because the vaccination status of participants wasn’t collected, she said it wasn’t clear whether getting the shots played a role in the olfactory system’s inflammatory response.
In a survey published last year of more than 400 patients with smell loss, more than 40% reported depressive symptoms and almost 90% reported enjoying food less.
“People might think smell loss is not really an important Covid symptom compared with severe symptoms such as pneumonia, but it can really bother some patients,” Dr. Ho said.
Researchers said regions of the brain linked to the sense of smell are closely associated with brain regions that control memory and emotion.
Sandeep Robert Datta,
a co-author of the new study and a professor of neurobiology at Harvard Medical School, said he and others are conducting more research into the reasons for smell loss following Covid-19 infection smell loss. The research could lead to potential targets for treatment. There are no effective treatments for long-term smell loss, Dr. Datta said.
“Smell gives you a sense of place. It can be very disorienting without it,” Dr. Datta said.
Write to Dominique Mosbergen at dominique.mosbergen@wsj.com
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Cosmological enigma of Milky Way’s satellite galaxies solved
Astronomers say they have solved an outstanding problem that challenged our understanding of how the universe evolved—the spatial distribution of faint satellite galaxies orbiting the Milky Way.
These satellite galaxies exhibit a bizarre alignment—they seem to lie on an enormous thin rotating plane—called the “plane of satellites.”
This seemingly unlikely arrangement had puzzled astronomers for over 50 years, leading many to question the validity of the standard cosmological model that seeks to explain how the universe came to look as it does today.
Now, new research jointly led by the Universities of Durham, U.K., and Helsinki, Finland, has found that the plane of satellites is a cosmological quirk which will dissolve over time in the same way that star constellations also change.
Their research removes the challenge posed by the plane of satellites to the standard model of cosmology.
This model explains the formation of the universe and how the galaxies we see now formed gradually within clumps of cold dark matter—a mysterious substance that makes up about 27% of the universe.
The findings are published in the journal Nature Astronomy.
The Milky Way’s satellites seem to be arranged in an implausibly thin plane piercing through the galaxy and, oddly, they are also circling in a coherent and long-lived disk.
There is no known physical mechanism that would make satellites planes. Instead, it was thought that satellite galaxies should be arranged in a roughly round configuration tracing the dark matter.
Since the plane of satellites was discovered in the 1970s, astronomers have tried without success to find similar structures in realistic supercomputer simulations that track the evolution of the universe from the Big Bang to the present day.
The fact that the arrangement of satellites could not be explained led researchers to think that the cold dark matter theory of galaxy formation might be wrong.
However, this latest research saw astronomers use new data from the European Space Agency’s Gaia space observatory. Gaia is charting a six-dimensional map of the Milky Way, providing precise positions and motion measurements for about one billion stars in our galaxy (about 1% of the total), and its companion systems.
These data allowed scientists to project the orbits of the satellite galaxies into the past and future and see the plane form and dissolve in a few hundred million years—a mere blink of an eye in cosmic time.
The researchers also searched new, tailor-made cosmological simulations for evidence of planes of satellites.
They realized that previous studies based on simulations had been misled by failing to consider the distances of satellites from the center of the Galaxy, which made the virtual satellite systems appear much rounder than the real one.
Taking this into account, they found several virtual Milky Ways which boast a plane of satellite galaxies very similar to the one seen through telescopes.
The researchers say this removes one of the main objections to the validity of the standard model of cosmology and means that the concept of dark matter remains the cornerstone of our understanding of the universe.
Study co-author Professor Carlos Frenk, Ogden Professor of Fundamental Physics in the Institute for Computational Cosmology, at Durham University, U.K., said, “The strange alignment of the Milky Way’s satellite galaxies in the sky had perplexed astronomers for decades, so much so that it was deemed to pose a profound challenge to cosmological orthodoxy.
“But thanks to the amazing data from the Gaia satellite and the laws of physics, we now know that the plane is just a chance alignment, a matter of being in the right place at the right time, just as the constellations of stars in the sky.
“Come back in a billion years, and the plane will have disintegrated, as will today’s constellations.
“We have been able to remove one of the main outstanding challenges to the cold dark matter theory. It continues to provide a remarkably faithful description of the evolution of our universe.”
Study lead author Dr. Till Sawala, of the University of Helsinki, said, “The plane of satellites was truly mind boggling.
“It is perhaps unsurprising that a puzzle which has endured for almost fifty years required a combination of methods to solve it—and an international team to come together.”
More information:
Till Sawala, The Milky Way’s plane of satellites is consistent with ΛCDM, Nature Astronomy (2022). DOI: 10.1038/s41550-022-01856-z. www.nature.com/articles/s41550-022-01856-z
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A Decade-Old Coyote Attack Mystery May Be Solved
In 2009, a pack of coyotes living in Canada’s Cape Breton Highlands National Park killed a 19-year-old hiker in a seemingly unprovoked attack. It was the first coyote-related killing ever documented in Canada and only the second in North America, following the 1981 death of a toddler in California. More than a decade later, scientists now believe that they have figured out exactly why the tragedy occurred. They argue that the park’s coyotes had started hunting large animals like moose due to their limited resources, which then made them more likely to go after humans. They ruled out other possible causes, such as the coyotes becoming more familiar with humans or their food over time.
The death of singer-songwriter Taylor Mitchell in late October 2009 shocked many, including coyote experts. Despite public perception, coyotes aren’t known to be aggressive toward humans. Even in urban areas shared by the two species, the animals will often avoid human contact.
A team of scientists in Canada and the U.S. have been studying the possible circumstances behind Mitchell’s death. Their investigation has included the capture of nearly two dozen coyotes in the area between 2011 and 2013, which allowed the team to outfit them with devices to track their movements. They also collected whisker samples from the coyotes (including the animals implicated in Mitchell’s death) and fur samples from potential prey in the area, as well as hair samples from a local barbershop. By studying the nitrogen and carbon contents of these samples, the team was able to estimate the recent diet of the coyotes, including whether they had eaten food meant for humans.
Coyotes generally hunt or scavenge small prey, though they’re omnivores that can eat most anything if the opportunity is there. But the team found that the Cape Breton coyotes were mostly eating moose, with the large animal accounting for half to two-thirds of their diets on average, followed by small mammals and deer. The same pattern was true for the coyotes responsible for Mitchell’s death. And unlike coyotes elsewhere, there was little seasonal variation in their diets, suggesting they were primarily hunting moose throughout the year.
The switch to large prey seen in this coyote population would likely only happen out of sheer necessity, the authors argue, and it’s this unique adaptation that predisposed them to attacking Mitchell.
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“We’re describing these animals expanding their niche to basically rely on moose. And we’re also taking a step forward and saying it’s not just scavenging that they were doing, but they were actually killing moose when they could. It’s hard for them to do that, but because they had very little if anything else to eat, that was their prey,” said lead author Stan Gehrt, a wildlife ecologist at OSU, in a statement from the university. “And that leads to conflicts with people that you wouldn’t normally see.”
Gehrt and his team also collected evidence that points away from other common theories for the attack. The coyotes in the park had an expansive range, but they still tended to avoid areas that overlapped with human activity. They also moved more often at night during periods of the year when humans were most active in the daytime. And only a handful of the coyotes had recently eaten human food (including one of the coyotes involved in attacks on humans), further reducing the possibility that these animals are spending much time near us. Lastly, hunting and trapping isn’t allowed in the park, meaning that local coyotes may not fear humans as much as they typically do elsewhere.
“It’s a big area for these coyotes to live in and never have a negative experience with a human—if they have any experience at all,” Gehrt said. “That also leads to the logical assumption that we’re making, which is that it’s not hard for these animals to test to see whether or not people are a potential prey item.”
All in all, the findings, published last month in the Journal of Applied Ecology, suggest that what happened to Taylor Mitchell was a tragic but “quite rare” occurrence, the study authors say. The conditions that led to her death are especially unlikely to happen in places where coyotes have plenty of food and natural prey to eat, including urban areas shared with humans. At the same time, people visiting the park or other areas with similar environmental conditions “should be made aware of the risks coyotes pose and encouraged to take precautions,” they wrote, such as bringing along a partner and animal deterrents like bear spray. Park managers in these areas may also need to carefully monitor coyote behavior and be willing to take action earlier than usual, which could include the culling of aggressive coyotes.
Though there have been reports of coyote attacks in the park in the years since, no other deaths appear to have occurred.