Journal List
ID6120
Title Educa - Revista Multidisciplinar Em Educação
E ISSN 2359-2087
P ISSN -
Country Brasil
Impact Factor Awaiting
Publication year 2014
Publisher NameJosé Lucas Pedreira Bueno
FrequencyTriennial
Indexed Yes
Website http://revistaeduca.unir.br


SIS Advertise









News

"I think rejuvenating the immune system could rectify a lot of problems," said Roel de Maeyer, an immunologist at the University of Oxford. "We know hospitals are full of older people suffering from infections that younger people don't need to go to [the] hospital for."

The aim of these rejuvenating therapies would be to help people live healthier for longer, he told Live Science.

How do cells turn into zombies?

The immune system constantly gets rid of old, dysfunctional and dead cells to keep tissues healthy, but that cleanup gets less effective with age.

When cells die, they display proteins on their surfaces that act as "eat me" signals for immune cells, called macrophages, to engulf and destroy them. However, some cells refuse to die and instead become senescent. These zombified cells can lurk in tissues for years, releasing chemicals that drive inflammation and damage.

Senescent cells can form due to DNA damage from oxidative stress, radiation, or even normal cell division. Cells lose bits of DNA each time they make copies of themselves, and they have intricate mechanisms to decide when it becomes a "bit too dangerous to keep dividing," de Maeyer said. If a cell can no longer divide, it usually undergoes a process called programmed cell death or becomes senescent, he said.

Senescence can be beneficial in some contexts; it helps heal wounds, for example. But an accumulation of senescent cells is linked to damaging inflammation and impaired organ function.

"If there are many senescent cells in a tissue, that's usually a bad sign," de Maeyer said. The number of senescent cells goes up with age and is linked to many age-related conditions, such as heart disease and dementia.

Slaying zombies

Studies in mice have shown that using drugs to kill senescent cells can reverse inflammation and some signs of cellular aging. These drugs, called senolytics, force senescent cells to enter programmed cell death, thus reducing their numbers, said Jure Povsin, a biochemist at the Max Planck Institute of Biochemistry in Germany. This ultimately reduces inflammation and improves tissue function, he told Live Science.

But while senolytics can help rid the body of zombie cells, it's not clear why the immune system fails to eliminate senescent cells in the first place. To find answers, scientists began looking at macrophages, the cells tasked with devouring dying cells.

Research pointed to a receptor on macrophages called EP2. One study, published in July in the journal Science, found that old macrophages have a greater number of these receptors and cannot eat senescent cells effectively.

Genetically deleting the EP2 receptor in lab mice restored the macrophages' function and reduced the number of senescent cells. Compared with normal mice of the same age, the genetically tweaked mice showed less cognitive decline, muscle loss, cardiac dysfunction and systemic inflammation.

On some of these metrics, such as the ability to remember familiar objects, the modified mice were comparable to younger mice.

Gobbling up cells requires a ton of energy.

Dr. Katrin Andreasson, a neurologist at Stanford University

A problem with energy

Why is the EP2 receptor at the root of this problem? Scientists found a clue in a huge study of older adults.

A molecule called PGE2 plugs into the EP2 receptor. It's a type of prostaglandin — a molecule that helps cells communicate during stress and injury and contributes to fever, pain and swelling. Drugs such as ibuprofen reduce inflammation by blocking prostaglandin production.

In 2001, a large study uncovered a connection between these prostaglandin-blocking drugs and Alzheimer's disease: People ages 55 and older who routinely took the drugs for at least two years had a lower risk of developing Alzheimer's than nonusers did. The study could not prove that the drugs directly prevented the disease, but it added to growing evidence that inflammation related to EP2 activity plays a role in Alzheimer's.

This caught the attention of Dr. Katrin Andreasson, a neurologist at Stanford University and co-author of the recent Science study.

"I thought, 'Wow, this is interesting,'" she told Live Science. "I wondered if there's a connection."

Andreasson and colleagues had an important breakthrough in 2021: They found that aging macrophages had higher levels of the EP2 receptor and that increased EP2 activity disrupted how the cells used their energy. Instead of burning glucose to produce energy like young macrophages do, these cells stashed it away.

As a result, the cells could not do their job properly, as "gobbling up cells requires a ton of energy," Andreasson said. Blocking the EP2 receptor restored normal energy use in the macrophages. In old mice, it also led to reduced inflammation and better scores on cognitive tests, compared with mice in which EP2 activity remained high.

Making senescent cells vulnerable

In their recent study, Andreasson's team uncovered another consequence of aging: Old mice accumulated many senescent neutrophils, a type of short-lived immune cell that acts as the body's first line of defense against germs. Neutrophils normally die within days and are then cleared away, but with age, they become more prone to senescence and accumulate.

"I think that's kind of an odd concept because they're [usually] very short-lived cells," said de Maeyer, who was not involved in the Science study. "Neutrophils are inherently quite inflammatory, so wanting to clear them from tissues is very valuable."

Old mice have too much EP2 activity in their macrophages, and that means they can't get rid of these neutrophils, Andreasson's team found. That may be why deleting EP2 seems to have anti-aging effects in multiple organs, they concluded.

But increased EP2 activity is just one side of the story; some studies suggest that zombie cells actively suppress macrophages' ability to eat them. They do this by using a tricky protein called CD47.

CD47 is a "don't eat me" signal that stops macrophages from destroying cells, Povsin said. "It signals that the cell is healthy, alive and doesn't need to be eaten."

However, that signal gets amplified in senescent cells, Max Planck researchers showed in a 2023 study. That means that, when macrophages interact with senescent cells, macrophages' function becomes impaired. Afterward, they even lose the ability to engulf dying, nonsenescent cells. This allows a ton of cellular debris to accumulate.

Microscope images show red and blue stained macrophages engulf senescent cells (fluorescent green)

Top row: Macrophages (stained blue and red) incubated with young, proliferating cells will engulf dead cells and debris (green) when they encounter it. By contrast, macrophages grown in culture with senescent cells will not engulf dead cells, allowing cellular trash to accumulate (bottom row). This is because the aging cells release a strong "don't eat me" signal. (Image credit: Adapted from Schloesser et al, J. Cell Biology, 2022.)

So, rather than just blocking EP2, it could also be beneficial to reduce that "don't eat me" signal in senescent cells, this research hints. But CD47 is found on all living cells, so scientists can't just deplete its numbers across the body.

A specific enzyme modifies CD47 on senescent cells, and in the 2023 study, blocking the enzyme helped spare macrophages from the effects of CD47. Therefore, blocking the enzyme could be a more selective approach to weaken the "don't eat me" signal on senescent cells, Povsin said.

A long road to treatments for people

Translating these ideas into anti-aging treatments for humans would be a major success in the science of aging, but experts say there are significant problems to overcome.

Although blocking EP2 had consistent results in lab mice, the rodents are genetically identical and bred in controlled environments. Humans are inherently more variable in their biology and the environmental factors they're exposed to, introducing confounding factors that would need to be addressed, de Maeyer said.

Additionally, in clinical trials, EP2-blocking drugs have so far been explored as cancer treatments, but they are "underexplored" in the context of aging, he added.

Drugs targeting CD47 are in an even earlier stage of development. In the 2023 research from Max Planck, the team used both human and mouse macrophages in their experiments, but the approach has not been tested as an anti-aging treatment in living mice or humans yet.

In 2020, de Maeyer's team used a different strategy to rejuvenate macrophages in older adults. They blocked a protein called p38, whose activity was high in the macrophages of older adults. Blocking the protein helped macrophages better recognize and eat dying cells in specific tests.

In that study, the team gave adults ages 65 and up an experimental drug called losmapimod to block p38. Although it helped restore their immune cell function, it was not suitable for long-term use because it caused liver problems in later trials, de Maeyer said.

In their mouse studies, Andreasson's team was able to block EP2 without causing any negative side effects. But she cautioned that we "really need to drill down on the research and confirm all this stuff in humans."

"The next logical step," she said, "would be to figure out how to inhibit this receptor in a safe way."

This article is for informational purposes only and is not meant to offer medical advice.

Help us improve Live Science Pro: We're always trying to make our content better. Leave us feedback about Pro here.

'> Zombified cells may drive aging, and scientists are devising new ways to get rid of them
  • Eerily humanlike AI-powered robot enters mass production in China — its makers say it could soon be helping you out at home
  • "Because the design rules depend on the rod’s shape and how its ends are moved, they work across different sizes and scales," Khalid Jawed, an associate professor at UCLA's School of Engineering and co-first author of the study, said in the statement.. "This opens a promising path toward miniaturized robots just a few millimeters in size that turn small motor movements into powerful bursts of motion," said Jawed, whose lab worked on the simulation and robot arm experiments.

    The final form of the prototype was a frog-like robot with a pair of snapping rods at the rear of its main body. Tests included hopping over a broad range of surfaces, including solid materials like wood and glass, as well as trickier soft and slippery surfaces that used materials like leather. The scientists also tested the robot outdoors on sand and grass, noting that it could even climb and descend steps and, with paddle attachments, swim.

    By using only one of the snapping rods, the team enabled the robot to turn and, with a remote control, navigate a small obstacle course.

    '> Roboticists showcase tiny, frog-like robot that can hop across wet surfaces and swim

    Comparison between the astronomical images of IRAS 18293-0941 (left) and the artist's impression (right). (Image credit: B. Marcote (JIVE/ASTRON).)

    These objects, as well as microquasars in general, are tricky to observe, Martí said. "Because of stellar evolution, you need to catch the system at the right time," he added. "The microquasar phase of evolution is very short, and so it is difficult to find one in that phase."

    Theorists predicted that microblazars would have special characteristics that should help define them. These features include powerful emissions across the electromagnetic spectrum, rapid changes in brightness (variability), and a hotspot behind them where its opposing jet heats up the interstellar medium in the opposite direction of Earth.

    To observe IRAS 18293-0941, the study authors used a variety of instruments ‪—‬ including the Calar Alto Astronomical Observatory in Spain, a network of radio astronomy telescopes called the European VLBI Network, and the MeerKAT radio telescope array in South Africa ‪—‬ as well as archival data from the Very Large Array in New Mexico.

    They found that IRAS 18293-0941 has all of the expected microblazar characteristics, except one ‪—‬ variability. Microblazars have rapid variability, which means their brightness changes a lot in a short period, because one of the jets is facing Earth and small changes in brightness are amplified by an effect called Doppler boosting.

    Martí said IRAS 18293−0941's lack of rapid variability could be explained by the dense cloud of gas surrounding it, which could smooth out quick fluctuations in brightness.

    The researchers are currently investigating whether the observed area behind the microblazar is in fact a hotspot, study co-author Pedro Luque-Escamilla, an astronomer at the University of Jaén, told Live Science.

    Even with one of the expected features missing, this object is a promising candidate for the first known microblazar. "The claims and the results of the paper are sensible and there are no questionable hidden assumptions," Kinwah Wu, a theoretical astrophysicist at University College London who was not involved in the research, told Live Science in an email. "The source in this paper had shown signatures of interactions between the jets and the ambient material, which naturally leads to [particle] interaction."

    Svetlana Jorstad, a senior research scientist at the Institute for Astrophysical Research at Boston University who was not involved in the research, told Live Science in an email that the new study was "very interesting, important and comprehensive."

    Itumeleng Monageng, an astronomer at the University of Cape Town who was also not involved in the research, added that the team's observations "presents a previously overlooked mechanism for generating some of the highest energy emissions observed."

    Microblazars "may power some of the universe's most energetic processes," Monageng told Live Science in an email.

    Martí, J., Luque-Escamilla, P. L., Marcote, B., Abaroa, L., Aguasca-Cabot, A., Combi, J. A., Romero, G. E., Paredes, J. M., García, F., Fogantini, F., Saavedra, E. A., Del Ser, D., & Van Den Eijnden, J. (2026). A Galactic microblazar as a potential accelerator of ultra-high-energy particles. Astronomy and Astrophysics. https://doi.org/10.1051/0004-6361/202661105

    See how much you know about black holes with our black hole quiz!

    '> Earth is in the firing line of a strange new type of cosmic object, astronomers say

    During the Scandinavian Iron Age and Viking Age (from roughly 500 B.C. to A.D. 1050), violent encounters between individuals and communities steadily increased, resulting in archaeological evidence of elite warrior burials and mass graves from battles.

    To better understand the context of violence in the Iron and Viking ages, researchers analyzed 192 human bones from people buried in domestic areas at settlements in what are now Denmark, Norway and Sweden.

    "The fact is that not all bodies ended up in monumental burial mounds in the Iron and Viking Ages, or even in more modest urnfields and cemeteries," the researchers wrote in a study published Sept. 28 in the Journal of Archaeological Method and Theory. Rather, some bodies — or pieces of bodies — were placed in postholes, pits, floors, wells, houses, yards and feasting halls.

    The archaeologists discovered that at least 12 of the individuals had sustained a violent injury around the time of death. Half of those cases involved head trauma, while four people suffered multiple injuries. Most of the victims of violence were adult males, but there were two females and a child as well.

    In one Iron Age house in Denmark, built sometime between 500 and 1 B.C., archaeologists discovered a frontal bone from the skull of a child who died between the ages of 2 and 4 years old.

    four views of the frontal bone of the skull of a human child showing injuries

    The skull of a child aged 2 to 4 from Aalborg, seen from different angles, and showing the damage from a sword cut. The skull was later placed on the floor of a house. (Image credit: National Museum of Denmark)

    "Our DNA analyses show that it is a small boy who has been cut with a sword," study first author Marianne Hem Eriksen, an archaeologist at the National Museum of Denmark, said in a translated statement. "The child's skull was placed on the floor of a house where people continued to live. This means that someone has walked over a child's skull day after day."

    Radiocarbon dating revealed that the child's skull is significantly older than the house itself, by as many as two centuries, suggesting the bone may have been kept for some time before being placed in the house floor, according to the study.

    At a Viking Age site dated to around 750 to 1050, archaeologists found a young woman's skull in a well near a cluster of four small houses. "The woman's skull bore traces of blows and was buried in a well," Eriksen said. She may have been cut or slashed with a sword or ax and, like the child, her bones may have been kept for a significant amount of time before being buried in the well. "These glimpses of lives lived from the past show how fascinatingly different people must have thought about life and death," Eriksen said.

    And at the Viking Age site of Gammel Lejre, a royal feasting hall that many experts consider to be the inspiration for the epic Old English poem "Beowulf," archaeologists found the burial of a man whose skeleton bore numerous blunt force injuries, several of which had healed, and which attested to a difficult and likely painful life. His skeleton was discovered directly south of the feasting hall.

    The study of bones in domestic areas "opens up a completely new understanding of Iron Age society, of the occurrence of violence and of the handling of the dead," Eriksen said. "The results show a much greater complexity in the everyday life and world of imagination of the time than we often attribute to Iron Age people."

    But it is unclear exactly why these particular people were the victims of violence and why they were buried in such unusual ways. One possible scenario, the researchers wrote in the study, is that these were victims of violent domestic encounters rather than warfare. Their deaths may also have been the result of socially acceptable corporal punishment or some form of aggression within the community.

    Given the increase in social inequality and rise in violence in the Iron and Viking ages, the researchers suspect that precarious community members may have been targeted.

    "Not all lives were equally grieved and commemorated in the Iron and Viking Ages of Scandinavia," the researchers wrote. "We may question whether some lives were already considered disposable."

    See how much you know about ancient norsemen with our Viking quiz!

    '> Archaeologists discover a child's skull built into the floor of a 2,500-year-old Scandinavian house Photograph 51, which was taken in May 1952 and later published to show the double-helix structure, was specifically taken for the purpose of publication — not, as some narratives have held, an experimental shot that Franklin believed was insignificant. The new research revealed that Photograph 51 was a new exposure of a sample Franklin had already photographed. She started Photograph 51 the same day she saw that photograph, Photograph 49.

    "She took it because she wanted to get a really refined version," said study co-author Alistair Sponsel, a historian of science at the Science History Institute in Philadelphia. Making the effort to take a better photograph of the same sample is "a sign she knew she had something really important on her hands," Sponsel told Live Science.

    Francis Crick, James Watson and Maurice Wilkins shared the Nobel Prize in Medicine for the discovery of the double-helix structure of DNA in 1962. As Watson told it in his 1968 autobiography, "The Double Helix: A Personal Account of the Discovery of the Structure of DNA," Franklin's photographs were his "aha" moment: "The black cross of reflections which dominated the picture could only arise from a helical structure," he wrote.

    Rosalind Franklin (1920-1958) first took Photograph 49 and then Photograph 51, clues that she was aware of DNA's helical structure. (Image credit: Donaldson Collection via Getty Images)

    Watson further implied that Franklin was a laboratory automaton, good at the X-ray crystallography techniques used to capture the images of the DNA molecule but bad at interpreting her own data. The new archival work, published Monday (Oct. 5) in the Journal of the History of Biology, suggests otherwise.

    Franklin's dearth of published notes about Photograph 51 has been used to suggest she missed a major discovery. But Sponsel said her journals show she noted the possible helical shape and rich structural data in her notes for her first picture of the sample, Photograph 49, which she followed up with the more refined image in Photograph 51.

    "In Franklin's mind, they were two different types of scientific image," Sponsel said. Photograph 49 was the experimental image revealing exciting new data. Photograph 51 was the showpiece to convey these findings with the most clarity and sharpness possible.

    This new understanding of the relationship between the two images, and how Franklin perceived them, is the most important feature of the new work, Sponsel said, which he conducted with molecular biophysicist Brian Sutton of King's College London. The project began when the Science History Institute acquired a new collection of archival material from Rosalind Franklin and her graduate student Raymond Gosling. The two researchers also combed through the archives at King’s College London, where Franklin was working when she took the famous photos.

    Sponsel and Sutton think that Franklin's notes and actions reveal why she didn't rush to publish Photograph 51 right away. Her scientific goals, laid out in a report she wrote in February 1952, were to understand the two separate structures of DNA, then known as A and B. Structure B, illustrated in Photographs 49 and 51, turned out to be the double helix that occurs in nature. Structure A is a form DNA takes when it's dehydrated in the lab.

    Structure A, when photographed, appeared more data-rich, so Franklin decided to characterize that structure first before studying structure B. But while she did this painstaking work, Wilkins showed Watson her photographs of structure B. The two scientists, together with Crick, then built a detailed model of DNA's double helix and scooped the discovery from under her nose.

    Those three men shared the Nobel Prize for the work less than a decade later. Franklin died of ovarian cancer in 1958, making her ineligible for the prize — and leaving her insights to come to light only much later.

    Editor's note: This article was updated at 3:23 p.m. ET to fix the caption and subhead, noting that Rosalind Franklin had likely discovered DNA's helical, but not double-helix structure. Also, the top photo is not Photograph 51, but another photo taken by Franklin.

    '> 'She knew she had something really important on her hands': Rosalind Franklin figured out DNA's helical structure before Watson and Crick, study s...
    Visits
    Online User :
    Today Visit :
    Week Visit :
    Month Visit :
    Total Visit :
    • © 2013-2026
    • |
    • Scientific Indexing Services
    3505 Brewster Drive, Plano, Texas, 75025, USA