livescience--2020-08-11--Book excerpt: 'The Organ Thieves' (Simon and Schuster, 2020)

Below is an excerpt of `` The Organ Thieves : The Shocking Story of the First Heart Transplant in the Segregated South '' by Chip Jones , published by Simon & Schuster on Aug. 18 , 2020 .
Read more about the landmark heart transplant surgery — one of the first in the world — that was performed in Virginia in 1968 using the heart of an African American man , obtained without his family 's knowledge or consent .
CHAPTER ONE : Case of the Missing Heart In late May 1968 , Doug Wilder was in his law office @ @ @ @ @ @ @ Virginia .
He was winding down from a long day of work when the phone rang .
“ They took my brother ’ s heart !
” the man on the other end of the line exclaimed in horror .
As one of the best-known African American trial lawyers practicing in the state capital , Wilder was accustomed to taking random phone calls day or night .
Accusations of rape , robbery , and murder were not uncommon , nor were other desperate pleas from mothers and fathers seeking help for loved ones @ @ @ @ @ @ @ legal system .
Even as halting steps toward progress had begun to bring incremental improvements in schools , housing , and jobs , his home state of Virginia was still moving at a snail ’ s pace from under the heavy burden of centuries of discrimination .
But taking a man ’ s heart from his own body ?
Wilder had never heard of such a thing .
“ I don ’ t understand what you ’ re talking about , not having a heart , ” he told the caller , William @ @ @ @ @ @ @ ?
What happened to it ?
” He started taking notes as Tucker described a deeply disturbing series of events that had just unfolded over the weekend .
It all started when his brother Bruce went missing after work on Friday .
It took a series of frantic phone calls—prompted by an insider ’ s tip—to finally locate him at the Medical College of Virginia ( MCV ) on Saturday night .
Then some bureaucrats hemmed and hawed before finally delivering the shocking bad news : his brother—who ’ d been rushed to @ @ @ @ @ @ @ than a day before—had died only a few hours earlier on an operating table .
Bruce ’ s body had been claimed and taken to a funeral home near the family farm .
William was given Bruce ’ s final possessions—among them his driver ’ s license and a business card .
His business card , William realized .
It was for his shoe repair shop only a few blocks from the hospital .
Why hadn ’ t anyone called him sooner ?
A day later , still numb from the news of @ @ @ @ @ @ @ began the hour-long drive to the farm .
He wanted to personally break the news to his eighty-year-old mother , Emma , and to Bruce ’ s teenage son , Abraham , who lived with her .
First , though , he would check with the local undertaker about the upcoming funeral .
William ’ s best-laid plans were shattered , though , when he learned more shocking details of his brother ’ s treatment in an operating room at the Medical College of Virginia .
William Tucker ’ s ordeal started with @ @ @ @ @ @ @ the hospital .
“ Something ’ s going on with Bruce , ” the friend whispered .
William put down a pair of shoes he was working on .
It was early Saturday afternoon .
He asked his friend to speak up and explain himself .
His friend whispered something about a heart operation involving Bruce .
Then the line went dead .
William stared at the phone and laid it back on its cradle .
What was that about ?
He tried calling the hospital a couple of times but couldn ’ @ @ @ @ @ @ @ took him a few hours to close up shop and drive over to MCV .
By then it was after 7:00 p.m .
When the hospital finally sent out some men to talk to him , he asked them a simple question : “ Where is my brother ?
” William , a polio victim who used crutches , braced himself for the reply .
Bruce was dead , he was told , and “ you ’ ll need to make funeral arrangements.
” Nothing was said about an operation or anything about @ @ @ @ @ @ @ morning , William Tucker swung by Jones Funeral Home in Stony Creek , Virginia .
Mack Jones , the owner and mortician , apologetically informed William that while preparing the body for burial he noticed something bizarre : Bruce was missing his heart—and his kidneys .
As William related his tale , Wilder put down his pen .
This was too much to write down .
After a silence , William asked Wilder if he ’ d represent him and the family and try to get to the bottom of what happened .
@ @ @ @ @ @ @ Wilder agreed .
Though he tried to sound confident , he also knew there was something about the sound of this case he couldn ’ t quite put his finger on .
It was something that went to the dark heart of the city and state of his birth .
It had been almost ten years since Wilder graduated from Howard University School of Law in Washington , DC , but he still practiced law in the long , lingering shadow of the Jim Crow South .
The courtrooms , jailhouses , and @ @ @ @ @ @ @ the times and observed strict segregation .
A black Virginian had no chance of having his or her trial being adjudicated by an African American judge for the simple reason that there weren ’ t any black judges .
Black jurors were also a rarity , since any defense attorney worth his salt would use the law to strike anyone of color from a jury panel .
William Tucker went on to describe more of the peculiar circumstances surrounding his brother ’ s demise .
Bruce had been working at an egg-processing plant @ @ @ @ @ @ @ office .
After work that past Friday , he was relaxing with friends and passing a bottle of wine in the shade behind an Esso station .
He was sitting on a wall but lost his balance and hit his head , rendering him unconscious .
An ambulance was called .
Bruce was quickly transported to the nearby MCV , the state ’ s largest teaching hospital .
That ’ s how it started .
But what happened after Bruce was treated in the emergency room and later by the hospital ’ s @ @ @ @ @ @ @ attract the notice of its heart surgeons ?
Wasn ’ t it his head—not his heart—that was injured ?
From what Wilder could piece together from William ’ s first account , something simply didn ’ t add up .
It reminded Wilder of some kind of science fiction movie where doctors experiment on humans in the dead of night .
As William ’ s friend had whispered from inside the hospital , “ They ’ re doing some kind of experimental heart operation.
” But who ?
Wilder wondered .
And why @ @ @ @ @ @ @ the big hospital on the hill ?
From `` THE ORGAN THIEVES : The Shocking Story of the First Heart Transplant in the Segregated South '' by Chip Jones .
Copyright © 2020 by Chip Jones .
Reprinted by permission of Jeter Publishing/Gallery Books , an imprint of Simon & Schuster , Inc .

Below is an excerpt of "The Organ Thieves: The Shocking Story of the First Heart Transplant in the Segregated South" by Chip Jones, published by Simon & Schuster on Aug. 18, 2020.
Read more about the landmark heart transplant surgery — one of the first in the world — that was performed in Virginia in 1968 using the heart of an African American man, obtained without his family's knowledge or consent.
CHAPTER ONE: Case of the Missing Heart
In late May 1968, Doug Wilder was in his law office on a tree-lined street in Richmond, Virginia. He was winding down from a long day of work when the phone rang.
“They took my brother’s heart!” the man on the other end of the line exclaimed in horror.
As one of the best-known African American trial lawyers practicing in the state capital, Wilder was accustomed to taking random phone calls day or night. Accusations of rape, robbery, and murder were not uncommon, nor were other desperate pleas from mothers and fathers seeking help for loved ones who’d run afoul of the legal system. Even as halting steps toward progress had begun to bring incremental improvements in schools, housing, and jobs, his home state of Virginia was still moving at a snail’s pace from under the heavy burden of centuries of discrimination.
But taking a man’s heart from his own body? Wilder had never heard of such a thing. “I don’t understand what you’re talking about, not having a heart,” he told the caller, William Tucker. “What do you mean? What happened to it?”
He started taking notes as Tucker described a deeply disturbing series of events that had just unfolded over the weekend. It all started when his brother Bruce went missing after work on Friday. It took a series of frantic phone calls—prompted by an insider’s tip—to finally locate him at the Medical College of Virginia (MCV) on Saturday night. Then some bureaucrats hemmed and hawed before finally delivering the shocking bad news: his brother—who’d been rushed to the hospital with a head injury less than a day before—had died only a few hours earlier on an operating table.
Bruce’s body had been claimed and taken to a funeral home near the family farm. William was given Bruce’s final possessions—among them his driver’s license and a business card. His business card, William realized. It was for his shoe repair shop only a few blocks from the hospital. Why hadn’t anyone called him sooner?
A day later, still numb from the news of his brother’s death, William began the hour-long drive to the farm. He wanted to personally break the news to his eighty-year-old mother, Emma, and to Bruce’s teenage son, Abraham, who lived with her. First, though, he would check with the local undertaker about the upcoming funeral. William’s best-laid plans were shattered, though, when he learned more shocking details of his brother’s treatment in an operating room at the Medical College of Virginia.
✭ ✭ ✭
William Tucker’s ordeal started with a hushed call from a friend inside the hospital. “Something’s going on with Bruce,” the friend whispered.
William put down a pair of shoes he was working on. It was early Saturday afternoon. He asked his friend to speak up and explain himself. His friend whispered something about a heart operation involving Bruce. Then the line went dead.
William stared at the phone and laid it back on its cradle. What was that about?
He tried calling the hospital a couple of times but couldn’t get a straight answer. It took him a few hours to close up shop and drive over to MCV. By then it was after 7:00 p.m. When the hospital finally sent out some men to talk to him, he asked them a simple question: “Where is my brother?” William, a polio victim who used crutches, braced himself for the reply.
Bruce was dead, he was told, and “you’ll need to make funeral arrangements.” Nothing was said about an operation or anything about Bruce’s heart.
✭ ✭ ✭
On Monday morning, William Tucker swung by Jones Funeral Home in Stony Creek, Virginia. Mack Jones, the owner and mortician, apologetically informed William that while preparing the body for burial he noticed something bizarre: Bruce was missing his heart—and his kidneys.
As William related his tale, Wilder put down his pen. This was too much to write down. After a silence, William asked Wilder if he’d represent him and the family and try to get to the bottom of what happened.
“Yes, I will,” Wilder agreed. Though he tried to sound confident, he also knew there was something about the sound of this case he couldn’t quite put his finger on. It was something that went to the dark heart of the city and state of his birth.
It had been almost ten years since Wilder graduated from Howard University School of Law in Washington, DC, but he still practiced law in the long, lingering shadow of the Jim Crow South. The courtrooms, jailhouses, and white-controlled bar association were all woefully behind the times and observed strict segregation. A black Virginian had no chance of having his or her trial being adjudicated by an African American judge for the simple reason that there weren’t any black judges. Black jurors were also a rarity, since any defense attorney worth his salt would use the law to strike anyone of color from a jury panel.
✭ ✭ ✭
William Tucker went on to describe more of the peculiar circumstances surrounding his brother’s demise. Bruce had been working at an egg-processing plant not far from Wilder’s law office. After work that past Friday, he was relaxing with friends and passing a bottle of wine in the shade behind an Esso station. He was sitting on a wall but lost his balance and hit his head, rendering him unconscious. An ambulance was called. Bruce was quickly transported to the nearby MCV, the state’s largest teaching hospital.
That’s how it started. But what happened after Bruce was treated in the emergency room and later by the hospital’s brain-injury specialists? And why would he attract the notice of its heart surgeons? Wasn’t it his head—not his heart—that was injured?
From what Wilder could piece together from William’s first account, something simply didn’t add up. It reminded Wilder of some kind of science fiction movie where doctors experiment on humans in the dead of night. As William’s friend had whispered from inside the hospital, “They’re doing some kind of experimental heart operation.”
But who? Wilder wondered. And why? What happened behind the walls of the big hospital on the hill?
From "THE ORGAN THIEVES: The Shocking Story of the First Heart Transplant in the Segregated South" by Chip Jones.
Copyright © 2020 by Chip Jones. Reprinted by permission of Jeter Publishing/Gallery Books, an imprint of Simon & Schuster, Inc.
Originally published on Live Science.


livescience--2020-08-11--Amazing photos of nocturnal animals

Amazing photos of nocturnal animals

According to the Royal Society for the Protection of Birds in the U.K. , the long-eared owl ( Asio otus @ @ @ @ @ nocturnal owl and is so secretive , it 's rarely seen other than during migration @ @ @ @ @ returning to , a communal roost site in winter .
Its ear tufts are actually @ @ @ @ @ raise when alarmed .
Not all owls are nocturnal , as Live Science previously reported @ @ @ @ @ , while some owls are sleeping , the northern hawk owl ( Surnia ulula ) @ @ @ @ @ ( Glaucidium gnoma ) are hunting for meals , making them diurnal — that is @ @ @ @ @ , '' said Marc Devokaitis , a public information specialist at the Cornell Lab of @ @ @ @ @ York .

Owls
According to the Royal Society for the Protection of Birds in the U.K., the long-eared owl (Asio otus, pictured) is a nocturnal owl and is so secretive, it's rarely seen other than during migration or when leaving, or returning to, a communal roost site in winter. Its ear tufts are actually just feathers, which they raise when alarmed.
Not all owls are nocturnal, as Live Science previously reported: "During the daytime, while some owls are sleeping, the northern hawk owl (Surnia ulula) and the northern pygmy owl (Glaucidium gnoma) are hunting for meals, making them diurnal — that is, active during the daytime," said Marc Devokaitis, a public information specialist at the Cornell Lab of Ornithology in Ithaca, New York.


livescience--2020-08-10--2 captive beluga whales finally freed to a seawater sanctuary in Iceland

After a 30-hour journey by land , air and sea , two young that were on show in an aquarium in Shanghai for years have now arrived at a new home — a cool seawater sanctuary off the coast of Iceland .
This is the first time the cuties have dipped their smiling snouts into the sea in more than a decade .
The belugas , named Little White and Little Grey , have spent the last three days and nights in a netted-off `` care pool '' within the sanctuary at Klettsvik Bay on the island of Heimaey , @ @ @ @ @ @ @ Because these captive whales could n't survive in the open ocean , the sanctuary is the next best thing .
The island is home to about 4,000 people in a town about a 10-minute boat ride away , and the belugas will have lots of room to spread out — the sanctuary covers around 344,445 square feet ( 32,000 square meters ) of seawater and is divided from the rest of the bay by netting that runs from the bottom to the surface .
The young whales will spend about a month in @ @ @ @ @ @ @ , said Audrey Padgett , the general manager of the Sea Life Trust 's Beluga Whale Sanctuary .
The pool is fitted with underwater gates that the belugas can use to pass into another pool ; eventually other underwater gates will be opened so they can explore the entire sanctuary .
So far , the two belugas seem content with their new surroundings , especially Little Grey , who spent some of Monday morning ( Aug. 10 ) investigating a diving seabird — a razorbill — that had flown into the area .
@ @ @ @ @ @ @ Little White , was `` taking her time , taking everything in , '' Padgett told Live Science .
`` They are both eating and interacting with the care staff , so that 's a really positive sign . ''
The two belugas are the first inhabitants of the new sanctuary at Klettsvik Bay .
They are both about 12 years old and are expected to live into their 40s , so the sanctuary could be their home for years to come .
Padgett explained that Little Grey and Little White were captured @ @ @ @ @ @ @ of Russia when they were about a year old , and then sold to Changfeng Ocean World in Shanghai in China .
There they lived in an indoor pool , until a new owner started looking for more natural conditions for them .
This is the first time in more than 10 years that Little Grey and Little White have experienced the sea , she said , but it 's taken a lot of work to get them here .
The two whales each weigh about 1,980 pounds ( 900 kilograms ) and @ @ @ @ @ @ @ journey to Iceland was a tricky one .
Each was placed inside specially-built transportation tanks that were lifted by a crane and placed on two trucks in Shanghai ; they were then transferred to a Cargolux Airlines cargo jet , which flew them to Iceland 's Keflavik Airport .
From there , they were transferred onto trucks , which then took a ferry to Heimaey Island .
That was in 2019 .
And since then , the two belugas have lived in a pool at the Beluga Whale Sanctuary 's visitor center at @ @ @ @ @ @ @ assessments and acclimating to cooler water temperatures that better suit an Arctic whale species , Padgett said .
The Klettsvik Bay sanctuary has room for about 10 belugas , but there are no firm plans right now to add more , Padgett said .
`` Our focus is still firmly on Little White and Little Grey , and getting them out into the larger sanctuary space , '' she said .
`` When [ they ] are out in that sanctuary , that opens the door for conversations about future belugas that could @ @ @ @ @ @ @ 300 belugas are kept in captivity around the world ; most of them were raised in captivity and could n't survive on their own in the open ocean , so a seawater sanctuary with 24-hour human care is their best bet , she said .

After a 30-hour journey by land, air and sea, two young beluga whales that were on show in an aquarium in Shanghai for years have now arrived at a new home — a cool seawater sanctuary off the coast of Iceland. This is the first time the cuties have dipped their smiling snouts into the sea in more than a decade.
The belugas, named Little White and Little Grey, have spent the last three days and nights in a netted-off "care pool" within the sanctuary at Klettsvik Bay on the island of Heimaey, in Iceland's southern Vestmannaeyjar archipelago. Because these captive whales couldn't survive in the open ocean, the sanctuary is the next best thing.
The island is home to about 4,000 people in a town about a 10-minute boat ride away, and the belugas will have lots of room to spread out — the sanctuary covers around 344,445 square feet (32,000 square meters) of seawater and is divided from the rest of the bay by netting that runs from the bottom to the surface.
Related: Photos: See the world's cutest sea creatures
The young whales will spend about a month in the pool acclimating to their new environment, said Audrey Padgett, the general manager of the Sea Life Trust's Beluga Whale Sanctuary.
The pool is fitted with underwater gates that the belugas can use to pass into another pool; eventually other underwater gates will be opened so they can explore the entire sanctuary.
So far, the two belugas seem content with their new surroundings, especially Little Grey, who spent some of Monday morning (Aug. 10) investigating a diving seabird — a razorbill — that had flown into the area.
The quieter of the two whales, Little White, was "taking her time, taking everything in," Padgett told Live Science. "They are both eating and interacting with the care staff, so that's a really positive sign."
Image 1 of 4 Little Grey and Little White are the first two belugas at the Sea Life Trust sanctuary at Klettsvik Bay in Iceland. The trust will consider finding more when they are used to their new environment. (Image credit: PA Media/Aaron Chown) Little White is transferred into the "care pool," a netted-off area of the seawater sanctuary in Klettsvik Bay. The two belugas will live in the pool for about a month before they are released into the sanctuary. (Image credit: PA Media/Aaron Chown) The beluga whale named Little Grey is transferred from a truck to a tugboat that will transport it to the seawater sanctuary at Klettsvik Bay. (Image credit: PA Media/Aaron Chown) Little Grey and Little White were caught near Russia when they were about 1 year old; they are now 12, and this will be the first time in more than 10 years they will experience the sea. (Image credit: PA Media/Aaron Chown)
Beluga sanctuary
The two belugas are the first inhabitants of the new sanctuary at Klettsvik Bay. They are both about 12 years old and are expected to live into their 40s, so the sanctuary could be their home for years to come.
Padgett explained that Little Grey and Little White were captured in Arctic waters on the north coast of Russia when they were about a year old, and then sold to Changfeng Ocean World in Shanghai in China. There they lived in an indoor pool, until a new owner started looking for more natural conditions for them.
Related: Marine marvels: Spectacular photos of sea creatures
This is the first time in more than 10 years that Little Grey and Little White have experienced the sea, she said, but it's taken a lot of work to get them here.
The two whales each weigh about 1,980 pounds (900 kilograms) and so the 6,000-mile (9,600 km) journey to Iceland was a tricky one.
Each was placed inside specially-built transportation tanks that were lifted by a crane and placed on two trucks in Shanghai; they were then transferred to a Cargolux Airlines cargo jet, which flew them to Iceland's Keflavik Airport. From there, they were transferred onto trucks, which then took a ferry to Heimaey Island.
That was in 2019. And since then, the two belugas have lived in a pool at the Beluga Whale Sanctuary's visitor center at Klettsvik Bay, going through quarantine, assessments and acclimating to cooler water temperatures that better suit an Arctic whale species, Padgett said.
Seawater sanctuary
The Klettsvik Bay sanctuary has room for about 10 belugas, but there are no firm plans right now to add more, Padgett said.
"Our focus is still firmly on Little White and Little Grey, and getting them out into the larger sanctuary space," she said. "When [they] are out in that sanctuary, that opens the door for conversations about future belugas that could come and join them."
Roughly 300 belugas are kept in captivity around the world; most of them were raised in captivity and couldn't survive on their own in the open ocean, so a seawater sanctuary with 24-hour human care is their best bet, she said.
Originally published on Live Science.


livescience--2020-08-10--Canada's last intact ice shelf just collapsed

Milne Ice Shelf was Canada 's last intact ice shelf — and it just collapsed .
On July 30 and July 31 , the northern part of the ice shelf began to break off .
A mass of ice measuring about 31 square miles ( 81 square kilometers ) — bigger than Manhattan — then detached from the ice shelf and began drifting north , representatives of the Water and Ice Research Laboratory ( WIRL ) at Carleton University in Ontario , Canada , .
By Aug. 3 , the escaping ice island had split : one piece measured about @ @ @ @ @ @ @ ) , while another measured about 9 square miles ( 24 square km ) , and both were about 230 to 260 feet ( 70 to 80 meters ) thick , according to WIRL .
And other preexisting fractures in the remains of the ice shelf hint that there may be more ice loss to come , WIRL representatives said .
Located on the northwestern coast of Ellesmere Island in Nunavut , the Milne Ice Shelf is about 4,000 years old .
Signs of the impending breakup were spotted by Adrienne White , @ @ @ @ @ @ @ Service , Environment and Climate Change Canada ( ECCC ) , according to WIRL .
On Aug. 2 , the Canadian Ice Service shared satellite images , reporting that `` above normal air temperatures , offshore winds and open water in front of the ice shelf are all part of the recipe for ice shelf breakup . ''
The shelf 's sudden collapse was a close call for scientists studying ice loss in that precarious location , said Arctic ice researcher Derek Mueller , an associate professor in Carleton University 's Department of @ @ @ @ @ @ @ camp area and instruments were all destroyed in this event , '' Mueller .
`` It is lucky that we were not on the ice shelf when this happened . ''
Ellesmere Island has been losing ice for more than a century .
About 100 years ago , a vast , single ice shelf extended along the island 's northern coast , spanning more than 3,300 square miles ( 8,600 square km ) .
By 2000 , the shelf was reduced to around 405 square miles ( 1,050 square km ) divided among @ @ @ @ @ @ @ Ice Shelf — as well as a few smaller ones , .
Since 2003 , there have been five major calving events on the Ellesmere Island coast , and there 's no question that is driving the drastic ice loss , according to Luke Copland , University Research Chair in Glaciology in the Department of Geography at the University of Ottawa .
And with the region warming at approximately two to three times the global rate — not to mention several summers of record-breaking warmth — `` the Milne and other ice shelves @ @ @ @ @ @ @ longer and will disappear in the coming decades , '' Copland said in the university statement .
Indeed , on July 30 , NASA imagery revealed that two of Ellesmere Island 's giant ice caps had vanished .
They had dominated the landscape for hundreds of years , but were erased by climate change in just 40 years , .
For now , the enormous ice islands are drifting close to the coastline , their movement restricted by other large chunks of floating ice ; the Canadian Ice Service will continue to track @ @ @ @ @ @ @ nearby ships or oil rigs , according to the statement .

Satellite animation shows the collapse of the last fully intact ice shelf in Canada, from July 30 to August 4.
Milne Ice Shelf was Canada's last intact ice shelf — and it just collapsed.
On July 30 and July 31, the northern part of the Arctic ice shelf began to break off. A mass of ice measuring about 31 square miles (81 square kilometers) — bigger than Manhattan — then detached from the ice shelf and began drifting north, representatives of the Water and Ice Research Laboratory (WIRL) at Carleton University in Ontario, Canada, said in a statement .
By Aug. 3, the escaping ice island had split: one piece measured about 21 square miles (55 square km), while another measured about 9 square miles (24 square km), and both were about 230 to 260 feet (70 to 80 meters) thick, according to WIRL.
And other preexisting fractures in the remains of the ice shelf hint that there may be more ice loss to come, WIRL representatives said.
Related: Images of melt: Earth's vanishing ice
Located on the northwestern coast of Ellesmere Island in Nunavut, the Milne Ice Shelf is about 4,000 years old. Signs of the impending breakup were spotted by Adrienne White, an ice analyst at the Canadian Ice Service, Environment and Climate Change Canada (ECCC), according to WIRL. On Aug. 2, the Canadian Ice Service shared satellite images in a Tweet , reporting that "above normal air temperatures, offshore winds and open water in front of the ice shelf are all part of the recipe for ice shelf breakup."
The shelf's sudden collapse was a close call for scientists studying ice loss in that precarious location, said Arctic ice researcher Derek Mueller, an associate professor in Carleton University's Department of Geography and Environmental Studies.
"Our camp area and instruments were all destroyed in this event," Mueller said in a WIRL blog post . "It is lucky that we were not on the ice shelf when this happened."
(Image credit: Image courtesy of Environment and Climate Change Canada)
Ellesmere Island has been losing ice for more than a century. About 100 years ago, a vast, single ice shelf extended along the island's northern coast, spanning more than 3,300 square miles (8,600 square km). By 2000, the shelf was reduced to around 405 square miles (1,050 square km) divided among six large ice shelves — including Milne Ice Shelf — as well as a few smaller ones, Carleton University representatives said .
Since 2003, there have been five major calving events on the Ellesmere Island coast, and there's no question that climate change is driving the drastic ice loss, according to Luke Copland, University Research Chair in Glaciology in the Department of Geography at the University of Ottawa.
And with the region warming at approximately two to three times the global rate — not to mention several summers of record-breaking warmth — "the Milne and other ice shelves in Canada are simply not viable any longer and will disappear in the coming decades," Copland said in the university statement. Indeed, on July 30, NASA imagery revealed that two of Ellesmere Island's giant ice caps had vanished. They had dominated the landscape for hundreds of years, but were erased by climate change in just 40 years, Live Science previously reported .
For now, the enormous ice islands are drifting close to the coastline, their movement restricted by other large chunks of floating ice; the Canadian Ice Service will continue to track them to determine if they could threaten nearby ships or oil rigs, according to the statement.
Originally published on Live Science.


livescience--2020-08-10--Is our solar system shaped like a deflated croissant?

Our solar system 's protective bubble may not be comet-shaped after all .
Scientists have traditionally posited that , the huge bubble of charged particles that the sun blows around itself , has a rounded leading edge , where the solar system barrels through space , with a long tail streaming behind it .
But the heliosphere 's true shape is weirder and more complex , a recent study suggests — something akin to a deflated croissant .
It 's tough to map out the heliosphere , because its closest edge is still a whopping 10 billion miles ( 16 @ @ @ @ @ @ @ two spacecraft , NASA 's , have directly sampled the boundary , and two data points are far from sufficient to outline the heliosphere 's contours .
So scientists have done so by other means .
For example , they 've studied measurements of , super-energetic charged particles that zoom into our neighborhood from very far away .
Researchers have also carefully tracked `` energetic neutral atoms '' that bounced sunward after interacting with the interstellar medium , the vast cosmic sea that lies beyond the heliosphere .
Such tracking has been done @ @ @ @ @ @ @ NASA 's Interstellar Boundary Explorer and the .
Scientists feed this information into computer models , which use it to map out the heliosphere 's shape .
The recent study takes a new look at such data and also includes measurements of `` pick-up ions '' made by NASA 's , which is currently more than 4.3 billion miles ( 6.9 billion km ) from Earth .
Pick-up ions are carried along by the solar wind , the stream of charged particles flowing continuously from .
( This flow is blocked by the @ @ @ @ @ @ @ the heliosphere . )
Pick-up ions are much hotter than the particles that make up most of the solar wind , which contributes to the heliosphere 's weird shape , study team members found .
`` There are two fluids mixed together .
You have one component that is very cold and one component that is much hotter , the pick-up ions , '' lead author Merav Opher , a professor of astronomy at Boston University , .
`` If you have some cold fluid and hot fluid , and you put them @ @ @ @ @ @ @ — they will evolve mostly separately , '' Opher said .
`` What we did was separate these two components of and model the resulting 3D shape of the heliosphere . ''
That shape , they determined , is croissant-like : a curving central bulge with two jets curling away from it .
`` Because the pick-up ions dominate the thermodynamics , everything is very spherical , '' Opher said .
`` But because they leave the system very quickly beyond the termination shock , the whole heliosphere deflates . ''
The is @ @ @ @ @ @ @ wind particles begin pressing into the interstellar medium and slow to less than the speed of sound .
Gaining a better understanding of the heliosphere 's shape has multiple applications , Opher and her colleagues said .
For example , the bubble blocks about 75 % of galactic cosmic rays , which can damage spacecraft and the DNA of voyaging astronauts .
Knowing in detail which regions of space are protected could aid mission planners .
( Life on Earth does n't have much to worry about from galactic cosmic rays ; our @ @ @ @ @ @ @ effective shielding . )
was published in March 2020 in the journal Nature Astronomy .
Mike Wall is the author of `` Out There '' ( Grand Central Publishing , 2018 ; illustrated by Karl Tate ) , a book about the search for alien life .
Follow him on Twitter @ michaeldwall .
Follow us on Twitter @ Spacedotcom or Facebook .

An updated model suggests the shape of the sun’s bubble of influence, the heliosphere (seen in yellow), may be a deflated croissant shape, rather than the long-tailed comet shape suggested by other research.
Our solar system's protective bubble may not be comet-shaped after all.
Scientists have traditionally posited that the heliosphere , the huge bubble of charged particles that the sun blows around itself, has a rounded leading edge, where the solar system barrels through space, with a long tail streaming behind it. But the heliosphere's true shape is weirder and more complex, a recent study suggests — something akin to a deflated croissant.
It's tough to map out the heliosphere, because its closest edge is still a whopping 10 billion miles (16 billion kilometers) from Earth. Just two spacecraft, NASA's Voyager 1 and Voyager 2 probes , have directly sampled the boundary, and two data points are far from sufficient to outline the heliosphere's contours.
Related: How the sun's magnetic field works (infographic)
So scientists have done so by other means. For example, they've studied measurements of galactic cosmic rays , super-energetic charged particles that zoom into our neighborhood from very far away. Researchers have also carefully tracked "energetic neutral atoms" that bounced sunward after interacting with the interstellar medium, the vast cosmic sea that lies beyond the heliosphere.
Such tracking has been done by a variety of spacecraft, including NASA's Interstellar Boundary Explorer and the Cassini Saturn probe . Scientists feed this information into computer models, which use it to map out the heliosphere's shape.
The recent study takes a new look at such data and also includes measurements of "pick-up ions" made by NASA's New Horizons Pluto probe , which is currently more than 4.3 billion miles (6.9 billion km) from Earth.
Pick-up ions are carried along by the solar wind, the stream of charged particles flowing continuously from the sun . (This flow is blocked by the interstellar medium to form the boundary of the heliosphere.) Pick-up ions are much hotter than the particles that make up most of the solar wind, which contributes to the heliosphere's weird shape, study team members found.
"There are two fluids mixed together. You have one component that is very cold and one component that is much hotter, the pick-up ions," lead author Merav Opher, a professor of astronomy at Boston University, said in a statement .
"If you have some cold fluid and hot fluid, and you put them in space, they won't mix — they will evolve mostly separately," Opher said. "What we did was separate these two components of the solar wind and model the resulting 3D shape of the heliosphere."
The heliosphere blocks many cosmic rays, shown as bright streaks in this animated image, from reaching the planets of our solar system. (Image credit: NASA’s Goddard Space Flight Center/Conceptual Image Lab)
That shape, they determined, is croissant-like: a curving central bulge with two jets curling away from it.
"Because the pick-up ions dominate the thermodynamics, everything is very spherical," Opher said. "But because they leave the system very quickly beyond the termination shock, the whole heliosphere deflates."
The termination shock is the heliosphere boundary region, where solar wind particles begin pressing into the interstellar medium and slow to less than the speed of sound.
Gaining a better understanding of the heliosphere's shape has multiple applications, Opher and her colleagues said. For example, the bubble blocks about 75% of galactic cosmic rays, which can damage spacecraft and the DNA of voyaging astronauts. Knowing in detail which regions of space are protected could aid mission planners. (Life on Earth doesn't have much to worry about from galactic cosmic rays; our planet's magnetic field and atmosphere provide effective shielding.)
The study was published in March 2020 in the journal Nature Astronomy.
Mike Wall is the author of "Out There" (Grand Central Publishing, 2018; illustrated by Karl Tate), a book about the search for alien life. Follow him on Twitter @michaeldwall. Follow us on Twitter @Spacedotcom or Facebook.


livescience--2020-08-10--What is brain death? New guidelines offer answers.

What is brain death ?
Though the term is used to unhook ventilators and guide organ donation , there has n't been a single process that determines when brain death has occurred .
That may be about to change : New guidelines may make the process for declaring someone brain dead more uniform .
Brain death is a fairly old concept , dating back to the advent of mechanical ventilation and other technologies that can keep a person 's body infused with oxygen even as their brain function irrevocably disappears .
The first clinical definition of brain death was published @ @ @ @ @ @ @ apply : death is diagnosed when the patient loses the capacity for , shows no brainstem reflexes such as the reaction of the pupils to light , and can not breathe independently .
In some high-profile cases , however , family members of a patient do not accept a diagnosis of brain death .
In some of these cases , the patient 's body can survive for a long time if kept on a ventilator and nourished via feeding tube .
In 2013 , for example , a 13-year-old California girl named Jahi @ @ @ @ @ @ @ surgery .
McMath 's family refused to accept the declaration and instituted a legal battle to keep the child on life support ; eventually , the hospital released McMath to her mother , who moved to New Jersey and kept the child on a ventilator and feeding tube .
Controversy followed , in part because some doctors claimed she regained signs of brain function such as electrical activity in subsequent years while others argued that there had been no recovery .
McMath 's and failed in 2018 , and she was removed from @ @ @ @ @ @ @ McMath ’ s case highlights some of the variability in how brain death is determined medically and legally .
McMath ’ s mother moved to New Jersey because while her daughter was legally dead in California , New Jersey has more lenient religious exemptions to the concept of death by neurologic criteria ; in New Jersey , McMath was considered alive and could continue to receive insurance-funded healthcare .
Criteria for determining brain death vary from state to state , says Dr. Gene Song Yung , a clinical neurologist at the Keck School @ @ @ @ @ @ @ California .
One 2008 study published in the journal found that different health centers had variations in the ways they determined brain death , ranging from differences in how the clinical examination to determine brain death was done to what additional testing was performed during the procedure for removing mechanical ventilation to see if the patient could breath on his or her own .
`` That is a problem , because in one respect someone could be declared dead in one location and not dead in another , but also because it leads @ @ @ @ @ @ @ population and even among doctors about how to determine brain death , '' Yung told Live Science .
Yung led an international effort , the World Brain Death Project , to clarify what brain death is and the basic requirements for determining brain death .
Published Aug. 3 in the journal .
The new recommendations define brain death , also known as `` death by neurologic criteria '' as `` the complete and permanent loss of brain function as defined by an unresponsive coma with loss of capacity for consciousness , brainstem reflexes @ @ @ @ @ @ @ . ''
( Critics of the concept of brain death sometimes point to the possibility of brain functions not covered in this definition , such as the secretion of hormones to maintain blood volume .
These functions might still occur in some people whose capacity for consciousness and brainstem function are destroyed . )
While many professional societies and individual health systems have released their own guidelines and procedures , this is the first collaborative international effort between societies to do so .
The recommendations outline the specifics of how to tell if @ @ @ @ @ @ @ , such as excluding conditions that might mimic the criteria for brain death .
For example , someone on a medication that induces paralysis would not show limb movement in response to pain or other similar reflexes .
Other steps include ensuring that a sufficient amount of time has passed to make the diagnosis — 24 hours at the very minimum for death caused by lack of to the brain — and testing a series of basic reflexes controlled by the brainstem .
The final test is apnea testing , which determines whether @ @ @ @ @ @ @ her own , another process controlled by the brainstem .
The guidelines also provide the first formal recommendations of how to determine brain death in a person who is being supported by extracorporeal membrane oxygenation ( ECMO ) , a process that circulates the person 's blood outside of the body to oxygenate it by machine rather than through the heart and lungs .
People on ECMO are not on ventilators , so the usual process of halting ventilation to see if a person can breath on his or her own doesn ’ @ @ @ @ @ @ @ call for adjusting the machine so that it doesn ’ t remove carbon dioxide from the blood on its own .
The buildup of dioxide is what triggers inhalation in a living person .
If the carbon dioxide buildup doesn ’ t cause the person to breathe , it is a sign that he or she is dead .
The new guidelines discuss ways for healthcare professionals to handle situations in which a family disagrees with the need to perform a brain-death evaluation or denies the results of such an evaluation .
Practitioners @ @ @ @ @ @ @ of the community their hospital serves , and should collaborate with a multidisciplinary team , including spiritual advisors and palliative-care specialists , when dealing with a patient who may be brain dead .
In some cases , it might be reasonable to keep the patient on a ventilator for a short period even after the declaration of death is made , such as when family members are traveling to be by the bedside , the recommendations state .
However , the guidelines likely won ’ t end debate over the fundamental nature of @ @ @ @ @ @ @ recommendation that hospital administration attempt to handle disagreements internally rather than escalating to the legal system .
More research is needed on why next-of-kin request that a person who has been declared brain-dead remain on a ventilator , and how often such requests are made , the World Brain Death Project authors concluded .
Despite the rise in new technology , such as functional magnetic resonance imaging ( fMRI ) that can measure brain activity , the diagnosis of brain death is still best made by a clinical , bedside exam , the @ @ @ @ @ @ @ That 's because the definition of brain death is centered on the patient 's function , says Dr. Claude Hemphill , the division chief of neurology at Zuckerberg San Francisco General Hospital , who was not involved in drafting the recommendations .
`` It 's based on the person , not on some physiology or anatomy of ‘ s there blood flow ?
’ , or 'is there a neuron that 's intact somewhere ? '
'' Hemphill told Live Science .
San Francisco General 's procedures for declaring death by neurologic criteria @ @ @ @ @ @ @ Hemphill said , though the hospital may integrate some of the newer guidance , such as the recommendations on ECMO patients .
The guidance will likely be important for standardizing the diagnosis of brain death across the United States , but will also be particularly useful internationally , said Dr. Jose Suarez , the director of Neurosciences Critical Care at Johns Hopkins University .
Many less-developed nations lack criteria for brain death at all , and the new recommendations can aid those countries in developing their own consistent frameworks .
`` We have @ @ @ @ @ @ @ people from all continents bringing their expertise to the matter and agreeing , which is amazing , '' Suarez , who was not involved in the project , told Live Science .

What is brain death? Though the term is used to unhook ventilators and guide organ donation, there hasn't been a single process that determines when brain death has occurred.
That may be about to change: New guidelines may make the process for declaring someone brain dead more uniform. Brain death is a fairly old concept, dating back to the advent of mechanical ventilation and other technologies that can keep a person's body infused with oxygen even as their brain function irrevocably disappears. The first clinical definition of brain death was published in 1968, and the fundamentals still apply: Brain death is diagnosed when the patient loses the capacity for consciousness , shows no brainstem reflexes such as the reaction of the pupils to light, and cannot breathe independently.
In some high-profile cases, however, family members of a patient do not accept a diagnosis of brain death. In some of these cases, the patient's body can survive for a long time if kept on a ventilator and nourished via feeding tube. In 2013, for example, a 13-year-old California girl named Jahi McMath was declared brain-dead after a routine surgery. McMath's family refused to accept the declaration and instituted a legal battle to keep the child on life support; eventually, the hospital released McMath to her mother, who moved to New Jersey and kept the child on a ventilator and feeding tube. Controversy followed, in part because some doctors claimed she regained signs of brain function such as electrical activity in subsequent years while others argued that there had been no recovery. McMath's kidneys and liver failed in 2018, and she was removed from life support.
Related: 10 things we’ve learned about the brain
The differing opinions in McMath’s case highlights some of the variability in how brain death is determined medically and legally. McMath’s mother moved to New Jersey because while her daughter was legally dead in California, New Jersey has more lenient religious exemptions to the concept of death by neurologic criteria; in New Jersey, McMath was considered alive and could continue to receive insurance-funded healthcare.
Criteria for determining brain death vary from state to state, says Dr. Gene Song Yung, a clinical neurologist at the Keck School of Medicine at the University of Southern California. One 2008 study published in the journal Neurology found that different health centers had variations in the ways they determined brain death, ranging from differences in how the clinical examination to determine brain death was done to what additional testing was performed during the procedure for removing mechanical ventilation to see if the patient could breath on his or her own.
"That is a problem, because in one respect someone could be declared dead in one location and not dead in another, but also because it leads to a little confusion among the general population and even among doctors about how to determine brain death," Yung told Live Science.
Clarifying death
Yung led an international effort, the World Brain Death Project, to clarify what brain death is and the basic requirements for determining brain death. Published Aug. 3 in the journal JAMA . The new recommendations define brain death, also known as "death by neurologic criteria" as "the complete and permanent loss of brain function as defined by an unresponsive coma with loss of capacity for consciousness, brainstem reflexes, and the ability to breathe independently." (Critics of the concept of brain death sometimes point to the possibility of brain functions not covered in this definition , such as the secretion of hormones to maintain blood volume. These functions might still occur in some people whose capacity for consciousness and brainstem function are destroyed.)
While many professional societies and individual health systems have released their own guidelines and procedures, this is the first collaborative international effort between societies to do so.
The recommendations outline the specifics of how to tell if someone meets the criteria for brain death, such as excluding conditions that might mimic the criteria for brain death. For example, someone on a medication that induces paralysis would not show limb movement in response to pain or other similar reflexes. Other steps include ensuring that a sufficient amount of time has passed to make the diagnosis — 24 hours at the very minimum for death caused by lack of oxygen to the brain — and testing a series of basic reflexes controlled by the brainstem. The final test is apnea testing, which determines whether the person can breathe on his or her own, another process controlled by the brainstem. The guidelines also provide the first formal recommendations of how to determine brain death in a person who is being supported by extracorporeal membrane oxygenation (ECMO), a process that circulates the person's blood outside of the body to oxygenate it by machine rather than through the heart and lungs. People on ECMO are not on ventilators, so the usual process of halting ventilation to see if a person can breath on his or her own doesn’t work. Instead, the recommendations call for adjusting the machine so that it doesn’t remove carbon dioxide from the blood on its own. The buildup of carbon dioxide is what triggers inhalation in a living person. If the carbon dioxide buildup doesn’t cause the person to breathe, it is a sign that he or she is dead.
The new guidelines discuss ways for healthcare professionals to handle situations in which a family disagrees with the need to perform a brain-death evaluation or denies the results of such an evaluation. Practitioners should be trained to understand the cultures of the community their hospital serves, and should collaborate with a multidisciplinary team, including spiritual advisors and palliative-care specialists, when dealing with a patient who may be brain dead. In some cases, it might be reasonable to keep the patient on a ventilator for a short period even after the declaration of death is made, such as when family members are traveling to be by the bedside, the recommendations state. However, the guidelines likely won’t end debate over the fundamental nature of brain death, as evidenced by the recommendation that hospital administration attempt to handle disagreements internally rather than escalating to the legal system. More research is needed on why next-of-kin request that a person who has been declared brain-dead remain on a ventilator, and how often such requests are made, the World Brain Death Project authors concluded.
Despite the rise in new technology, such as functional magnetic resonance imaging (fMRI) that can measure brain activity, the diagnosis of brain death is still best made by a clinical, bedside exam, the World Brain Death Project researchers found. That's because the definition of brain death is centered on the patient's function, says Dr. Claude Hemphill, the division chief of neurology at Zuckerberg San Francisco General Hospital, who was not involved in drafting the recommendations.
"It's based on the person, not on some physiology or anatomy of ‘s there blood flow?’, or 'is there a neuron that's intact somewhere?'" Hemphill told Live Science.
San Francisco General's procedures for declaring death by neurologic criteria already match the new recommendations closely, Hemphill said, though the hospital may integrate some of the newer guidance, such as the recommendations on ECMO patients.
The guidance will likely be important for standardizing the diagnosis of brain death across the United States, but will also be particularly useful internationally, said Dr. Jose Suarez, the director of Neurosciences Critical Care at Johns Hopkins University. Many less-developed nations lack criteria for brain death at all, and the new recommendations can aid those countries in developing their own consistent frameworks.
"We have had a truly international cooperation here, people from all continents bringing their expertise to the matter and agreeing, which is amazing," Suarez, who was not involved in the project, told Live Science.
Originally published on Live Science.


livescience--2020-08-10--New Zealand goes 100 days with no COVID-19 transmission

New Zealand , a country of about 4.8 million , has now gone 100 days without a single locally transmitted case of COVID-19 , according to news reports .
The last COVID-19 case acquired locally from an unknown source was reported on May 1 , , around the time that lockdown measures began to ease .
In late March , the South Pacific island implemented one of the strictest lockdowns in the world , `` a lockdown so severe that even retrieving a lost cricket ball from a neighbor 's yard was banned , '' .
To date , New @ @ @ @ @ @ @ cases and 22 related deaths , according to the Johns Hopkins virus dashboard .
Just 21 cases are considered active , and those people are isolating , .
Since the second week of June , life in New Zealand has gone nearly back to pre-pandemic ways .
Then and now officials warned that letting down their guard could lead to a second wave .
`` Achieving 100 days without community transmission is a significant milestone .
However , as we all know , we ca n't afford to be complacent , '' Dr. @ @ @ @ @ @ @ , said on Sunday ( Aug. 9 ) , BBC News reported .
`` We have seen overseas how quickly the virus can re-emerge and spread in places where it was previously under control , and we need to be prepared to quickly stamp out any future cases in New Zealand . ''
That was the case for Vietnam , which showed no community transmission of COVID-19 for 99 days , and then a 57-year-old man in the city of Da Nang in central Vietnam tested positive for the novel coronavirus that causes @ @ @ @ @ @ @ , according to news reports , Da Nang became the epicenter of a outbreak , reporting the country 's first pandemic death .
Other countries have been successful at blazing by the 100-day milestone .
For instance , Taiwan , which could have experienced a severe outbreak given its nearness to China and the fact that so many Taiwanese work in China , also has gone more than 100 days without any community transmission .
Since July 22 , when Taiwan reported 455 cases and more than 100 days of no local transmission @ @ @ @ @ @ @ new cases ; none of the new cases appeared to have been locally transmitted , according to news reports .
The success in Taiwan has been partly attributed to a culture that both takes infectious diseases seriously ( after suffering from the SARS outbreak in 2003 ) and is acclimated to wearing face masks , .
Though New Zealand has not been strict about mandating face masks in public , the country has such a low density — about 47 people per square mile compared with 93 per square mile in the U.S. @ @ @ @ @ @ @ for five weeks .

New Zealand, a country of about 4.8 million, has now gone 100 days without a single locally transmitted case of COVID-19, according to news reports.
The last COVID-19 case acquired locally from an unknown source was reported on May 1, BBC News reported , around the time that lockdown measures began to ease. In late March, the South Pacific island implemented one of the strictest lockdowns in the world, "a lockdown so severe that even retrieving a lost cricket ball from a neighbor's yard was banned," The New York Times reported .
To date, New Zealand has recorded a total of 1,569 cases and 22 related deaths, according to the Johns Hopkins virus dashboard. Just 21 cases are considered active, and those people are isolating, CNN reported .
Related: Read live updates on the COVID-19 pandemic
Since the second week of June, life in New Zealand has gone nearly back to pre-pandemic ways. Then and now officials warned that letting down their guard could lead to a second wave.
"Achieving 100 days without community transmission is a significant milestone. However, as we all know, we can't afford to be complacent," Dr. Ashley Bloomfield, the Director-General of Health, said on Sunday (Aug. 9), BBC News reported. "We have seen overseas how quickly the virus can re-emerge and spread in places where it was previously under control, and we need to be prepared to quickly stamp out any future cases in New Zealand."
That was the case for Vietnam, which showed no community transmission of COVID-19 for 99 days, and then a 57-year-old man in the city of Da Nang in central Vietnam tested positive for the novel coronavirus that causes COVID-19. By the end of July, according to news reports, Da Nang became the epicenter of a coronavirus outbreak, reporting the country's first pandemic death.
Other countries have been successful at blazing by the 100-day milestone. For instance, Taiwan, which could have experienced a severe outbreak given its nearness to China and the fact that so many Taiwanese work in China, also has gone more than 100 days without any community transmission. Since July 22, when Taiwan reported 455 cases and more than 100 days of no local transmission, the island has logged just 22 new cases; none of the new cases appeared to have been locally transmitted, according to news reports.
The success in Taiwan has been partly attributed to a culture that both takes infectious diseases seriously (after suffering from the SARS outbreak in 2003) and is acclimated to wearing face masks, STAT News reported .
Though New Zealand has not been strict about mandating face masks in public, the country has such a low density — about 47 people per square mile compared with 93 per square mile in the U.S. — and they practiced strict lockdown measures for five weeks.
Originally published on Live Science.


livescience--2020-08-10--Live Science podcast 'Life's Little Mysteries' Episode 46: Mysterious Elephants

In this episode of Life 's Little Mysteries , we 'll take a closer look at a mysterious animal from a family that 's been around for millions of years .
It 's the biggest land animal alive today : the elephant .
How big can elephants get , and how sensitive are their trunks ?
How intelligent are elephants , and do they really get plastered on fermented fruit and go on drunken rampages ?
Listen to Life 's Little Mysteries Episode 46 : Mysterious Elephants , to find out !
You 'll also hear about how elephants ' @ @ @ @ @ @ @ how understanding elephant cognition and psychology could help people protect these giants and even coexist with elephants in the wild .
Guest : Joshua Plotnik , assistant professor of psychology at Hunter College , The City University of New York Listen to Life 's Little Mysteries , Episode 46 : Mysterious Elephants below or on Audioboom , or subscribe on Apple Podcasts and Spotify , so you don ’ t miss out on new episodes .
Follow us on Facebook and Twitter for even more Life 's Little Mysteries , and catch up @ @ @ @ @ @ @ articles .
You can also join the conversation in our forums , where you can pose Life 's Little Mysteries questions of your own , or even suggest topics for upcoming podcast episodes .

In this episode of Life's Little Mysteries, we'll take a closer look at a mysterious animal from a family that's been around for millions of years. It's the biggest land animal alive today: the elephant.
How big can elephants get, and how sensitive are their trunks? How intelligent are elephants, and do they really get plastered on fermented fruit and go on drunken rampages? Listen to Life's Little Mysteries Episode 46: Mysterious Elephants, to find out!
You'll also hear about how elephants' big brains shape their behavior, and how understanding elephant cognition and psychology could help people protect these giants and even coexist with elephants in the wild.
Co-hosts: Jeanna Bryner and Mindy Weisberger
Guest: Joshua Plotnik, assistant professor of psychology at Hunter College, The City University of New York
Listen to Life's Little Mysteries, Episode 46: Mysterious Elephants below or on Audioboom, or subscribe on Apple Podcasts and Spotify, so you don’t miss out on new episodes.
Follow us on Facebook and Twitter for even more Life's Little Mysteries, and catch up on the latest Life's Little Mysteries articles. You can also join the conversation in our forums, where you can pose Life's Little Mysteries questions of your own, or even suggest topics for upcoming podcast episodes.
Originally published on Live Science.


livescience--2020-08-10--Decoys could trick COVID-19, keep humans safe from infection

The coronavirus that causes COVID-19 infects cells by plugging into a receptor on their surface .
Now , by crafting a `` decoy '' of that receptor , scientists aim to foil the virus 's attack .
In a new study , published Aug. 4 in the journal , researchers engineered such a decoy and found that the bound tightly to the imposter receptor , and once attached , the virus could n't infect primate cells in a lab dish .
The decoy binds to the virus as tightly as a neutralizing , a Y-shaped molecule generated by the to @ @ @ @ @ @ @ infecting cells .
Neutralizing antibodies are the `` best that the human body makes … so that 's our target '' — to have a decoy receptor that sticks to the coronavirus just as snuggly , study author Erik Procko , an assistant professor of biochemistry at the University of Illinois at Urbana-Champaign , told Live Science .
The team found that their newly designed decoy , known as sACE2.v2.4 , tightly binds both the novel coronavirus and SARS-CoV , a related virus that caused outbreaks of severe acute respiratory syndrome in the @ @ @ @ @ @ @ in animals as it does in cell culture , it could be developed into a COVID-19 treatment and preventative therapy for humans .
That said , the research is still in very early stages and no decoy receptor has ever been approved as a treatment for an infectious disease , Procko said .
`` This would be something new , if it is successful , '' being that it would be the first decoy approved as an antiviral , he said .
A few decoy receptors have been approved by the U.S. Food @ @ @ @ @ @ @ the treatment of inflammatory- and immune system-related diseases , such as the rare that causes recurrent fevers , joint pain and inflammation of the eyes , according to a 2013 report in the journal .
However , decoy receptors developed as antiviral treatments have historically hit roadblocks on their way to approval .
The first decoy designed to thwart a virus mimicked a natural receptor found on immune cells called CD4 , which binds to , according to a 2008 report in the journal .
While promising in studies that used lab-grown HIV @ @ @ @ @ @ @ effectively to strains isolated from HIV/AIDS patients , according to the report .
To this day , no CD4 decoys have graduated from clinical trials and been approved for use in patients .
The same is true of the decoys designed to treat rhinovirus , , hepatitis A and SARS-CoV .
Procko noted that , to be a successful antiviral , a decoy receptor must meet two major criteria : First , it must not disrupt important bodily functions , given that natural receptors often play multiple roles in the body .
For @ @ @ @ @ @ @ COVID-19 exploits as a gateway into cells , also helps control blood volume and lower blood pressure , he said .
By infecting cells with ACE2 receptors , COVID-19 actually interferes with ACE2 activity in the body — a decoy ACE2 receptor could potentially `` rescue '' some of this lost activity by leaving natural receptors open for business , rather than bound to the coronavirus , Procko said .
Related : 20 of the worst epidemics and pandemics in history However , decoy ACE2 receptors could cause unanticipated side effects , so @ @ @ @ @ @ @ in animal studies and early clinical trials , he added .
In addition to being safe to administer , a decoy receptor must show high affinity for the virus it targets , meaning it binds tightly to the virus in human cells .
`` To be a good binder , with high affinity , you need to bind on your target quickly and you need to come off your target slowly , '' Procko said .
To find a decoy that binds well to SARS-CoV-2 , Procko and his colleagues ruled out thousands @ @ @ @ @ @ @ technique known as `` deep mutagenesis . ''
So what is deep mutagenesis ?
Think of a Vegas slot machine — a mix of three different fruits equals a certain payout ( or not ) .
DNA is similar : a set of three letters code for a single amino acid , or protein building block .
In this case , the team scrambled the three-letter segments in 117 spots in human DNA that past studies suggested affected how tightly coronavirus bound to the ACE2 receptor .
This allowed the researchers to essentially @ @ @ @ @ @ @ over and over to study how swapping out each amino acid ( a single spin of the slot machine ) for another affected the ACE2 receptor 's coronavirus binding .
In this case , the scrambled DNA was expressed in different versions of human cells in a lab dish .
`` You can exhaustively test many , many thousands of mutations , to see which are relevant , '' Procko said .
After producing cells with mutant ACE2 receptors — ones based on scrambled DNA segments — the researchers exposed the cells to @ @ @ @ @ @ @ the ACE2 receptor , known as the receptor-binding domain .
They found that sACE2.v2.4 showed the highest affinity for the virus ; the researchers then developed a version of the decoy that can exist in the body without being attached to a cell , as the detached receptor is all that would be needed for a future drug .
Compared with an unmodified ACE2 receptor , `` less than 1 % of the entire protein sequence has been changed '' to craft the decoy , Proko noted .
If fully developed as a @ @ @ @ @ @ @ would likely be delivered into the body through an injection or inhaled as a mist , he said .
Drugs derived from living things , like the decoy receptor , are `` frequently long-lived , '' and can persist in the body for a week or more , he said .
A decoy receptor would serve a similar purpose to designed to treat COVID-19 , which would include multiple antibodies that bind in different ways to SARS-CoV-2 .
However , a report published June 15 in the journal suggests that the virus can @ @ @ @ @ @ @ antibodies — a decoy receptor might be more reliable in the long run , as the virus would be less likely to mutate in such a way that it no longer binds to ACE2 , Procko said .
The fact that sACE2.v2.4 tightly binds both SARS-CoV-2 and its predecessor SARS-CoV supports this notion , given that both viruses use ACE2 to break into cells .
Procko founded a start-up called Orthogonal Biologics to continue work on the ACE2 decoy earlier this year , along with study author Kui Chan who serves as Chief @ @ @ @ @ @ @ to do animal studies , and should the treatment advance to human studies , they have to show the decoy can be manufactured reliably at large scales .
Interestingly , anACE2 decoy that was developed by researchers tied to Apeiron Biologics is already being tested in clinical trials for the treatment of COVID-19 , and so far , appears safe in both healthy people and those with lung disease , from the company .
The major difference is that the existing decoy closely resembles the natural ACE2 receptor , and has not been @ @ @ @ @ @ @ to SARS-CoV-2 , while sACE2.v2.4 has .
( Procko and his colleagues were not involved in the design of the Apeiron decoy . )
Apeiron developed the existing decoy following the SARS epidemic as a treatment for the coronavirus , but has also tested the drug for the treatment of various lung conditions , including acute respiratory distress syndrome ( ARDS ) and pulmonary arterial hypertension .
Based on early data , patients appear to tolerate the treatment well , without major side effects .
Though the Apeiron product is different from the @ @ @ @ @ @ @ the early results are encouraging , Procko said .
`` We know that you can inject [ the Apeiron decoy ] into people and it does n't hurt them , '' which gives hope for their mutated ACE2 decoy , Procko said .
Procko 's team has begun testing their decoy in mice infected with COVID-19 and has `` not yet observed any toxicity , '' he noted .

The coronavirus that causes COVID-19 infects cells by plugging into a receptor on their surface. Now, by crafting a "decoy" of that receptor, scientists aim to foil the virus's attack.
In a new study, published Aug. 4 in the journal Science , researchers engineered such a decoy and found that the coronavirus bound tightly to the imposter receptor, and once attached, the virus couldn't infect primate cells in a lab dish. The decoy binds to the virus as tightly as a neutralizing antibody , a Y-shaped molecule generated by the immune system to grab the virus and prevent it from infecting cells.
Neutralizing antibodies are the "best that the human body makes … so that's our target" — to have a decoy receptor that sticks to the coronavirus just as snuggly, study author Erik Procko, an assistant professor of biochemistry at the University of Illinois at Urbana-Champaign, told Live Science. The team found that their newly designed decoy, known as sACE2.v2.4, tightly binds both the novel coronavirus and SARS-CoV, a related virus that caused outbreaks of severe acute respiratory syndrome in the early 2000s.
Related: 14 coronavirus myths busted by science
If the decoy works in animals as it does in cell culture, it could be developed into a COVID-19 treatment and preventative therapy for humans. That said, the research is still in very early stages and no decoy receptor has ever been approved as a treatment for an infectious disease, Procko said.
"This would be something new, if it is successful," being that it would be the first decoy approved as an antiviral, he said.
Designing a decoy
A few decoy receptors have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of inflammatory- and immune system-related diseases, such as the rare "familial cold autoinflammatory syndrome" that causes recurrent fevers, joint pain and inflammation of the eyes, according to a 2013 report in the journal Frontiers in Immunology . However, decoy receptors developed as antiviral treatments have historically hit roadblocks on their way to approval.
The first decoy designed to thwart a virus mimicked a natural receptor found on immune cells called CD4, which binds to HIV , according to a 2008 report in the journal Current Opinion in Biotechnology . While promising in studies that used lab-grown HIV strains, CD4 decoys did not bind effectively to strains isolated from HIV/AIDS patients, according to the report. To this day, no CD4 decoys have graduated from clinical trials and been approved for use in patients. The same is true of the decoys designed to treat rhinovirus, foot-and-mouth disease virus , hepatitis A and SARS-CoV.
Procko noted that, to be a successful antiviral, a decoy receptor must meet two major criteria:
First, it must not disrupt important bodily functions, given that natural receptors often play multiple roles in the body. For example, the ACE2 receptor, which COVID-19 exploits as a gateway into cells, also helps control blood volume and lower blood pressure, he said. By infecting cells with ACE2 receptors, COVID-19 actually interferes with ACE2 activity in the body — a decoy ACE2 receptor could potentially "rescue" some of this lost activity by leaving natural receptors open for business, rather than bound to the coronavirus, Procko said.
Related: 20 of the worst epidemics and pandemics in history
However, decoy ACE2 receptors could cause unanticipated side effects, so the researchers need to monitor for these in animal studies and early clinical trials, he added.
In addition to being safe to administer, a decoy receptor must show high affinity for the virus it targets, meaning it binds tightly to the virus in human cells.
"To be a good binder, with high affinity, you need to bind on your target quickly and you need to come off your target slowly," Procko said. To find a decoy that binds well to SARS-CoV-2, Procko and his colleagues ruled out thousands of inadequate ACE2 copycats using an experimental technique known as "deep mutagenesis."
So what is deep mutagenesis? Think of a Vegas slot machine — a mix of three different fruits equals a certain payout (or not). DNA is similar: a set of three letters code for a single amino acid, or protein building block. In this case, the team scrambled the three-letter segments in 117 spots in human DNA that past studies suggested affected how tightly coronavirus bound to the ACE2 receptor. This allowed the researchers to essentially "pull the slot machine lever" over and over to study how swapping out each amino acid (a single spin of the slot machine) for another affected the ACE2 receptor's coronavirus binding. In this case, the scrambled DNA was expressed in different versions of human cells in a lab dish.
"You can exhaustively test many, many thousands of mutations, to see which are relevant," Procko said.
After producing cells with mutant ACE2 receptors — ones based on scrambled DNA segments — the researchers exposed the cells to the portion of SARS-CoV-2 that locks into the ACE2 receptor, known as the receptor-binding domain. They found that sACE2.v2.4 showed the highest affinity for the virus; the researchers then developed a version of the decoy that can exist in the body without being attached to a cell, as the detached receptor is all that would be needed for a future drug.
The next steps
Compared with an unmodified ACE2 receptor, "less than 1% of the entire protein sequence has been changed" to craft the decoy, Proko noted. If fully developed as a treatment for humans, the decoy receptor would likely be delivered into the body through an injection or inhaled as a mist, he said. Drugs derived from living things, like the decoy receptor, are "frequently long-lived," and can persist in the body for a week or more, he said.
A decoy receptor would serve a similar purpose to antibody cocktails designed to treat COVID-19, which would include multiple antibodies that bind in different ways to SARS-CoV-2. However, a report published June 15 in the journal Science suggests that the virus can mutate to escape the grasp of specific antibodies — a decoy receptor might be more reliable in the long run, as the virus would be less likely to mutate in such a way that it no longer binds to ACE2, Procko said. The fact that sACE2.v2.4 tightly binds both SARS-CoV-2 and its predecessor SARS-CoV supports this notion, given that both viruses use ACE2 to break into cells.
Procko founded a start-up called Orthogonal Biologics to continue work on the ACE2 decoy earlier this year, along with study author Kui Chan who serves as Chief Operating Officer. The next step is to do animal studies, and should the treatment advance to human studies, they have to show the decoy can be manufactured reliably at large scales.
Interestingly, anACE2 decoy that was developed by researchers tied to Apeiron Biologics is already being tested in clinical trials for the treatment of COVID-19, and so far, appears safe in both healthy people and those with lung disease, according to a statement from the company. The major difference is that the existing decoy closely resembles the natural ACE2 receptor, and has not been mutated to bind as tightly as possible to SARS-CoV-2, while sACE2.v2.4 has. (Procko and his colleagues were not involved in the design of the Apeiron decoy.)
Apeiron developed the existing decoy following the SARS epidemic as a treatment for the coronavirus, but has also tested the drug for the treatment of various lung conditions, including acute respiratory distress syndrome (ARDS) and pulmonary arterial hypertension. Based on early data, patients appear to tolerate the treatment well, without major side effects. Though the Apeiron product is different from the decoy Procko and his colleagues developed, the early results are encouraging, Procko said. "We know that you can inject [the Apeiron decoy] into people and it doesn't hurt them," which gives hope for their mutated ACE2 decoy, Procko said.
Procko's team has begun testing their decoy in mice infected with COVID-19 and has "not yet observed any toxicity," he noted.
Originally published on Live Science.


livescience--2020-08-10--Pandemic childcare is way more stressful for moms than dads

Fathers forced to work from home by the coronavirus take on more childcare than their usual , new research finds .
But moms are more often stuck juggling kids and work at the same time .
Moms are also more stressed than men about new work-at-home arrangements .
The closure of schools and many childcare centers has put working parents in a bind , according to the new briefing , which was written by Yale sociologists Thomas Lyttelton and Emma Zang and Kelly Musick , the chair of policy analysis and management at Cornell University , for the Council on @ @ @ @ @ @ @ nonprofit research organization .
In April and May of 2020 , 55 % of employed parents were working from home , the researchers wrote .
During this time , most public schools were closed .
Lyttelton and Zang used data from the American Time Use Survey ( ATUS ) collected between 2003 and 2018 to measure how telecommuting affected the division of labor pre-pandemic .
This survey is run by the U.S. Bureau of Labor Statistics and asks participants to log their daily time spent doing activities such as paid work , house @ @ @ @ @ @ @ call center that runs the ATUS surveys shut down due to COVID-19 between March 19 and May 11 , meaning that data from those dates were missing .
To measure at least some changes during the pandemic , the researchers turned to the , run by the Data Foundation , a nonprofit think tank that seeks to use data to improve policy , which gathered data on time use in April and May .
The pre-pandemic data showed that a parent who telecommutes typically takes on more of the domestic load .
Telecommuting @ @ @ @ @ @ @ extra childcare on work-from-home days : 67 more minutes than non-work-from-home days , to be exact .
This increase actually closed the normally-seen gender gap in which women spend more time on childcare than men .
When women telecommuted pre-pandemic , they added 47 minutes of childcare to their day , compared to the days when they worked away from home .
But dads do n't do any extra housework when they telecommute , while telecommuting moms take on 49 more minutes of housework .
Pre-pandemic , telecommuting dads also seemed to maintain @ @ @ @ @ @ @ working at home .
Men reported that children were with them for an average of 21 minutes a day while they worked from home , whereas women reported that they were working with their children present for 54 minutes a day .
Many women feel pressure to keep up housework and attend to their children every time the kids interrupt , said Stephanie Coontz , a sociologist at The Evergreen State University in Washington and the director of research at CCF .
`` This is a form of work-family conflict people often ignore @ @ @ @ @ @ @ from home , and as this report shows , it 's a source of gender inequality at home and at work . ''
Given the shutdown of ATUS data collection , the researchers couldn ’ t directly compare these pre-pandemic results to the situation during the pandemic .
The COVID-19 Impact Survey did show , however , that all parents who worked from home during the pandemic were more depressed than those still reporting to a workplace .
Mothers were hit particularly hard .
Moms telecommuting during the pandemic reported more anxiety , @ @ @ @ @ @ @ Moms who did their work outside the home reported no such increase , and telecommuting dads actually felt less anxiety than dads who were reporting to a workplace .
Notably , the data showed that the worst position to be in was to be unemployed : Unemployed mothers and fathers were consistently more anxious , depressed , lonely and hopeless than parents who still had jobs .
In May , a of 1,060 parents in different-sex couples found that both men and women agreed that men were carrying more of the domestic load @ @ @ @ @ @ @ they did pre-pandemic .
Pre-pandemic , 26 % of couples reported sharing housework relatively equally , a number that rose to 41 % in April .
Forty-one percent of couples pre-pandemic reported sharing the care of young children equally , which rose to 52 % after the pandemic began .
That survey also found that stay-at-home orders had lessened some of the domestic load by eliminating tasks like hauling children to extracurricular activities or planning their daily schedules .
However , the picture gets murkier when zooming in specifically on homeschooling children .
@ @ @ @ @ @ @ York Times found that 80 % of women said they were doing most of the schooling of their children , compared to 45 % of men .
Clearly , given that these numbers add up to more than 100 % , a significant number of couples disagree about who is doing the most .
Only 3 % of women agreed that their male partners were doing the most when it came to teaching kids at home .
Editor 's note : This article was updated to correct the spelling of Emma Zang 's @ @

Fathers forced to work from home by the coronavirus pandemic take on more childcare than their usual, new research finds. But moms are more often stuck juggling kids and work at the same time. Moms are also more stressed than men about new work-at-home arrangements.
The closure of schools and many childcare centers has put working parents in a bind, according to the new briefing, which was written by Yale sociologists Thomas Lyttelton and Emma Zang and Kelly Musick, the chair of policy analysis and management at Cornell University, for the Council on Contemporary Families (CCF), a nonprofit research organization. In April and May of 2020, 55% of employed parents were working from home, the researchers wrote. During this time, most public schools were closed.
Lyttelton and Zang used data from the American Time Use Survey (ATUS) collected between 2003 and 2018 to measure how telecommuting affected the division of labor pre-pandemic. This survey is run by the U.S. Bureau of Labor Statistics and asks participants to log their daily time spent doing activities such as paid work, house work and childcare. Unfortunately, the call center that runs the ATUS surveys shut down due to COVID-19 between March 19 and May 11, meaning that data from those dates were missing. To measure at least some changes during the pandemic, the researchers turned to the COVID Impact Survey , run by the Data Foundation, a nonprofit think tank that seeks to use data to improve policy, which gathered data on time use in April and May.
Related: Coronavirus outbreak: Live updates
The effects of telecommuting
The pre-pandemic data showed that a parent who telecommutes typically takes on more of the domestic load. Telecommuting dads, in particular, take on extra childcare on work-from-home days: 67 more minutes than non-work-from-home days, to be exact. This increase actually closed the normally-seen gender gap in which women spend more time on childcare than men. When women telecommuted pre-pandemic, they added 47 minutes of childcare to their day, compared to the days when they worked away from home.
But dads don't do any extra housework when they telecommute, while telecommuting moms take on 49 more minutes of housework. Pre-pandemic, telecommuting dads also seemed to maintain better boundaries between work and childcare while working at home. Men reported that children were with them for an average of 21 minutes a day while they worked from home, whereas women reported that they were working with their children present for 54 minutes a day.
Many women feel pressure to keep up housework and attend to their children every time the kids interrupt, said Stephanie Coontz, a sociologist at The Evergreen State University in Washington and the director of research at CCF. "This is a form of work-family conflict people often ignore when they tout the advantages of working from home, and as this report shows, it's a source of gender inequality at home and at work."
Related: Doting dads: 6 of history's finest fathers
Pandemic work-from-home
Given the shutdown of ATUS data collection, the researchers couldn’t directly compare these pre-pandemic results to the situation during the pandemic. The COVID-19 Impact Survey did show, however, that all parents who worked from home during the pandemic were more depressed than those still reporting to a workplace. Mothers were hit particularly hard. Moms telecommuting during the pandemic reported more anxiety, loneliness and depression than telecommuting dads. Moms who did their work outside the home reported no such increase, and telecommuting dads actually felt less anxiety than dads who were reporting to a workplace.
Notably, the data showed that the worst position to be in was to be unemployed: Unemployed mothers and fathers were consistently more anxious, depressed, lonely and hopeless than parents who still had jobs.
In May, a previous CCF survey of 1,060 parents in different-sex couples found that both men and women agreed that men were carrying more of the domestic load during the COVID-19 pandemic compared with what they did pre-pandemic. Pre-pandemic, 26% of couples reported sharing housework relatively equally, a number that rose to 41% in April. Forty-one percent of couples pre-pandemic reported sharing the care of young children equally, which rose to 52% after the pandemic began. That survey also found that stay-at-home orders had lessened some of the domestic load by eliminating tasks like hauling children to extracurricular activities or planning their daily schedules.
However, the picture gets murkier when zooming in specifically on homeschooling children. An April survey commissioned by The New York Times found that 80% of women said they were doing most of the schooling of their children, compared to 45% of men. Clearly, given that these numbers add up to more than 100%, a significant number of couples disagree about who is doing the most. Only 3% of women agreed that their male partners were doing the most when it came to teaching kids at home.
Editor's note: This article was updated to correct the spelling of Emma Zang's name.
Originally published on Live Science.


livescience--2020-08-09--Why do we develop lifelong immunity to some diseases, but not others?

Some diseases , like the measles , infect us once and usually grant us immunity for life .
For others , like , we have to get vaccinated year after year .
So why do we develop lifelong immunity to some diseases but not others ?
And where does the novel coronavirus fit into all this ?
Whether or not we develop immunity to a disease often depends on our , which are proteins we produce in response to infection .
Antibodies are one of the body ’ s most well-known defenses : They coat invading cells and , in @ @ @ @ @ @ @ from hijacking our cells and replicating .
After we clear an infection , antibody levels often wane , but at least a few stick around , ready to ramp up production again if that same disease attacks again .
That 's why an antibody test can tell you if you were infected in the past .
It 's also what keeps us from getting sick a second time — usually .
Related : Can you get 2 colds at once ?
`` The body does n't really forget , '' said Marc Jenkins @ @ @ @ @ @ @ Minnesota Medical School .
Usually , when we get reinfected with a disease , it 's not because our body has lost immunity .
We get reinfected either because the pathogen mutated and our immune system no longer recognizes it , or because our bodies tend to mount a much lower immune response , he said .
Take the flu .
This is a virus that can change its genes easily , Jenkins said .
Just as our kill off one version of the virus , another emerges that our immune systems do @ @ @ @ @ @ @ so readily .
For example , the ca n't easily change its genome , Jenkins said .
That 's why we 've been so successful at ( almost ) eradicating it .
The common cold , and other viruses that don ’ t typically get past our upper respiratory tract , reinfect us not necessarily because they mutate rapidly , but because our body does n't usually produce many antibodies against these pathogens in the first place , said Mark Slifka , an immunologist at the Oregon National Primate Research Center .
`` @ @ @ @ @ @ @ upper respiratory tract , '' he said .
That 's what we 're seeing with mild cases of COVID-19 .
The virus sticks to the upper respiratory tract , where the body does not treat it like a threat .
In a 2020 preprint study ( meaning it has n't been peer reviewed yet ) published in the database , 10 out of 175 patients who had mild symptoms recovered from COVID-19 without developing detectable antibodies .
For diseases that do n't fall into either of these categories — meaning they don ’ @ @ @ @ @ @ @ a strong immune response — immunity tends to last much longer .
A 2007 study published in the found that it would take more than 200 years for even half of your antibodies to disappear after a or a infection .
The same study found similar results for Epstein-Barr virus , which causes .
Still , antibody responses do n't always last a lifetime .
That same study found that it takes around 50 years to lose half of our chickenpox antibodies , and 11 years to lose half of our tetanus antibodies @ @ @ @ @ @ @ shot , you could theoretically become infected with one of these diseases as an adult .
Scientists still are n't sure why we maintain our antibody responses longer for some diseases compared with others .
It 's possible that some of these more common diseases , such as chickenpox and mono , actually are reinfecting us more frequently than we realize , but that the antibodies we do have crush the infection before we notice , Jenkins said .
And in those cases , the immune system would be at full capacity again @ @ @ @ @ @ @ `` It keeps our immunity vigilant , '' he noted .
In contrast , `` with tetanus , we 're probably very rarely getting exposed , we 're not stepping on a [ dirty ] nail very often . ''
Related : Do rusty nails really give you tetanus ?
Other scientists point out that the human immune system is trained to target pathogens that `` look '' a certain way , Slifka said .
and viruses tend to be symmetrical with a repetitive pattern of proteins across their surfaces .
( Think @ @ @ @ @ @ @ with evenly spaced spikes all over it . )
One theory suggests that we mount a larger and longer-lasting immune response to more repetitive-looking pathogens .
For example , the antibodies we produce against variola , the highly repetitively-structured , last a lifetime .
Tetanus , however , is n't repetitive at all .
It 's the toxin produced by tetanus bacteria , not the bacteria itself , that makes us sick .
Based on this theory , it 's possible that our bodies are n't as well-trained to target this single , @ @ @ @ @ @ @ , will immunity to the new — whether that comes from infection or a vaccine — be as long-lived as our immunity to smallpox , or will we need a new vaccine every year ?
While it ’ s true that some people aren ’ t mounting large antibody responses , Jenkins is still hopeful for the former .
All the evidence both from natural infections and from vaccine trials suggest that most people are making neutralizing antibodies , the variety which prevents viruses from entering our cells , Jenkins said .
And @ @ @ @ @ @ @ virus that causes COVID-19 , is n't mutating quickly , Jenkins noted .
`` This virus has the features of viruses that we 've been very successful in vaccinating against , '' Jenkins said .

Some diseases, like the measles, infect us once and usually grant us immunity for life. For others, like the flu , we have to get vaccinated year after year.
So why do we develop lifelong immunity to some diseases but not others? And where does the novel coronavirus fit into all this?
Whether or not we develop immunity to a disease often depends on our antibodies , which are proteins we produce in response to infection. Antibodies are one of the body’s most well-known defenses: They coat invading cells and, in the best case, prevent those invaders from hijacking our cells and replicating. After we clear an infection, antibody levels often wane, but at least a few stick around, ready to ramp up production again if that same disease attacks again. That's why an antibody test can tell you if you were infected in the past. It's also what keeps us from getting sick a second time — usually.
Related: Can you get 2 colds at once?
"The body doesn't really forget," said Marc Jenkins, an immunologist at the University of Minnesota Medical School. Usually, when we get reinfected with a disease, it's not because our body has lost immunity. We get reinfected either because the pathogen mutated and our immune system no longer recognizes it, or because our bodies tend to mount a much lower immune response, he said.
Take the flu. This is a virus that can change its genes easily, Jenkins said. Just as our immune systems kill off one version of the virus, another emerges that our immune systems don't recognize. Not all viruses mutate so readily. For example, the polio virus can't easily change its genome, Jenkins said. That's why we've been so successful at (almost) eradicating it.
The common cold, and other viruses that don’t typically get past our upper respiratory tract, reinfect us not necessarily because they mutate rapidly, but because our body doesn't usually produce many antibodies against these pathogens in the first place, said Mark Slifka, an immunologist at the Oregon National Primate Research Center. "Our bodies are not worried about the upper respiratory tract," he said. That's what we're seeing with mild cases of COVID-19. The virus sticks to the upper respiratory tract, where the body does not treat it like a threat. In a 2020 preprint study (meaning it hasn't been peer reviewed yet) published in the database MedRxiv , 10 out of 175 patients who had mild symptoms recovered from COVID-19 without developing detectable antibodies.
For diseases that don't fall into either of these categories — meaning they don’t mutate rapidly and they generally prompt a strong immune response — immunity tends to last much longer. A 2007 study published in the New England Journal of Medicine found that it would take more than 200 years for even half of your antibodies to disappear after a measles or a mumps infection. The same study found similar results for Epstein-Barr virus, which causes mono . Still, antibody responses don't always last a lifetime. That same study found that it takes around 50 years to lose half of our chickenpox antibodies, and 11 years to lose half of our tetanus antibodies. That means that without a booster shot, you could theoretically become infected with one of these diseases as an adult.
Scientists still aren't sure why we maintain our antibody responses longer for some diseases compared with others. It's possible that some of these more common diseases, such as chickenpox and mono, actually are reinfecting us more frequently than we realize, but that the antibodies we do have crush the infection before we notice, Jenkins said. And in those cases, the immune system would be at full capacity again and again because of the reinfections. "It keeps our immunity vigilant," he noted. In contrast, "with tetanus, we're probably very rarely getting exposed, we're not stepping on a [dirty] nail very often."
Related: Do rusty nails really give you tetanus?
Other scientists point out that the human immune system is trained to target pathogens that "look" a certain way, Slifka said. Bacteria and viruses tend to be symmetrical with a repetitive pattern of proteins across their surfaces. (Think about COVID-19 — it's a ball with evenly spaced spikes all over it.) One theory suggests that we mount a larger and longer-lasting immune response to more repetitive-looking pathogens. For example, the antibodies we produce against variola, the highly repetitively-structured smallpox virus , last a lifetime. Tetanus, however, isn't repetitive at all. It's the toxin produced by tetanus bacteria, not the bacteria itself, that makes us sick. Based on this theory, it's possible that our bodies aren't as well-trained to target this single, asymmetrical protein, Slifka said.
So, will immunity to the new coronavirus — whether that comes from infection or a vaccine — be as long-lived as our immunity to smallpox, or will we need a new vaccine every year? While it’s true that some people aren’t mounting large antibody responses, Jenkins is still hopeful for the former. All the evidence both from natural infections and from vaccine trials suggest that most people are making neutralizing antibodies, the variety which prevents viruses from entering our cells, Jenkins said. And unlike the flu, SARS-CoV-2, the virus that causes COVID-19, isn't mutating quickly, Jenkins noted.
"This virus has the features of viruses that we've been very successful in vaccinating against," Jenkins said.
Originally published on Live Science.