Ebola virus is rapidly mutating.


A study of some of the earliest Ebola cases in Sierra Leone reveals more than 300 genetic changes in the virus as it has leapt from person to person.

These rapid changes could blunt the effectiveness of diagnostic tests and experimental treatments now in development, say researchers.

“We found the virus is doing what viruses do. It’s mutating,” says study lead author Pardis Sabeti of Harvard Universityand the Broad Institute.

The study is based on samples from 78 people in Sierra Leone, all of whose infections could be traced to a faith healer whose claims of a cure attracted Ebola patients from Guinea, where the virus first took hold.

The findings, published in Science , suggests the virus is mutating quickly and in ways that could affect current diagnostics and future vaccines and treatments, such as GlaxoSmithKline’s Ebola vaccine, which was just fast-tracked to begin clinical trials, or the antibody drug ZMapp, being developed by California biotech Mapp Biopharmaceutical.

Study coauthor Robert Garry of Tulane University says the virus is mutating at twice the rate in people as it was in animal hosts, such as fruit bats.

Garry says the study shows changes in the glycoprotein, the surface protein that binds the virus to human cells, allowing it to start replicating in its human host.

“It’s also what your immune system will recognise,” he says.

In an unusual step, the researchers posted the sequences online as soon as they became available, giving other researchers early access to the data.

Erica Ollmann Saphire of the Scripps Research Institute in La Jolla, California, has already checked the data to see if it impacts the three antibodies in ZMapp, a drug in short supply that has been tried on several individuals, including the two US missionaries who contracted Ebola in Sierra Leone and who have since recovered.

“It appears that they do not (affect ZMapp),” says Saphire, who directs a consortium to develop antibody treatments for Ebola and related viruses. But she says the data “will be critical to seeing if any of the other antibodies in our pool could be affected.”

Saphire says the speed with which Sabeti and colleagues mapped genetic changes in the virus gives researchers information that “will also be critical” to companies developing RNA-based therapeutics.

That could impact treatments under way from Vancouver-based Tekmira Pharmaceuticals Corp and privately held Profectus BioSciences of Tarrytown, New York.

Unfolding epidemic

Part of what makes the data useful is the precise picture it paints as the epidemic unfolded. Sabeti credits years of work by her lab, colleagues at Tulane and the Sierra Leone Ministry of Health and Sanitation in developing a response network for Lassa fever, a virus similar to Ebola that is endemic in West Africa.

Several of the study authors gave their lives to the work, including Dr Sheik Humarr Khan, the beloved “hero” doctor from the Kenema Government Hospital, who died from Ebola.

The team had been doing surveillance for two months when the first case of Ebola arrived from Guinea on 25 May. That case involved a “sowei” or tribal healer, whose claim of a cure lured sick Ebola victims from nearby Guinea.

“When she contracted Ebola and died, there were a lot of people who came to her funeral,” says Garry said. One of these was a young pregnant woman who became infected and travelled to Kenema Government Hospital, where she was diagnosed with Ebola.

With the Lassa surveillance team in place, they quickly began testing samples.

“We’ve been able to capture the initial spread from that one person and to follow all of these contacts and everything with sequencing,” Garry says.

The team used a technique called deep sequencing in which sequences are done repeatedly to generate highly specific results, allowing them to see not only how the virus is mutating from person to person, but how it is mutating in cells within the same person.

What is not clear from the study is whether the mutations are fueling the epidemic by allowing the virus to grow better in people and become easier to spread. That will require further tests in the lab, says Garry.

The findings come as the World Health Organization (WHO) says the epidemic could infect more than 20,000 people and spread to more countries.

A WHO representative could not be reached for comment.

Autism and vaccine study results questioned


The debate over a link between autism and vaccines continues.

A study published earlier this month concluded African-American boys are more at risk for autism if they’re given the measles, mumps and rubella vaccine before the age of 2. The study author says researchers at the Centers for Disease Control and Prevention knew about the link in 2004 — and covered it up.

CDC researchers are standing by their original findings: that there is no link between autism and vaccination schedules.

The new study was funded by the Focus Autism Foundation, which says it is dedicated to exposing the causes of autism, “focusing on the role of vaccinations.”

The study has since been removed from the public domain pending further investigation, according to Translational Neurodegeneration.

In an online statement, the scientific journal said the paper had been removed “because of serious concerns about the validity of its conclusions.”

CNN first became aware of the study when an iReport was posted about its publication and the controversy surrounding it. iReport is CNN’s user-generated news community.

Life with Autism: Your stories
Life with Autism: Your stories

Brian Hooker, author of the study and a biochemical engineer, found African-American boys who were given the MMR vaccine before age 24 months were more likely to be diagnosed with autism. To reach this conclusion, Hooker said he analyzed the same set of data that was the basis for a 2004 study done by researchers at the U.S. Centers for Disease Control and Prevention.

Living with autism as an adult
Living with autism as an adult

In 2004, scientists at the CDC’s National Immunization Program published their study in the journal Pediatrics. Researchers compared 624 children with autism, age 3 to 10, with 1,824 developmentally healthy children. Most of the children, according to the study, were vaccinated between 12 and 17 months of age in accordance with vaccination recommendations.

The CDC study authors found no link between the age children were given their first MMR vaccination and autism diagnoses. Nor did they find a statistically significant increased risk for a particular racial group.

Dad’s pictures connect with autistic son

The CDC’s raw data was made available for other scientists to use when its study was published in 2004. Hooker said he began his research after he was contacted by one of the original study authors, William Thompson, in November 2013. Thompson is a senior scientist with the CDC, where he has worked since 1998.

Hooker said he believes the increased risk for African-American boys he found was not identified in the CDC study because the researchers, including Thompson, deliberately limited the number of participants they included in their analysis, which he said altered the results. Hooker said that by excluding children without birth certificates, the CDC study results were skewed.

“I regret that my co-authors and I omitted statistically significant information in our 2004 article,” Thompson said in a statement sent to CNN by his lawyer. “I have had many discussions with Dr. Brian Hooker over the last 10 months regarding studies the CDC has carried out regarding vaccines and neurodevelopmental outcomes, including autism spectrum disorders. I share his belief that CDC decision-making and analyses should be transparent.”

However, Thompson went on to say that Hooker had recorded these conversations without his consent, and had posted them online without his knowledge.

In a statement to CNN on Monday, the CDC said its study presented results for two sets of children: all children initially recruited for the study, and a subset of children for whom a Georgia birth certificate was available.

“Access to the information on the birth certificates allowed researchers to assess more complete information on race, as well as other important characteristics,” the CDC statement said.

Dr. Frank DeStefano, lead author of the 2004 study, said he and his colleagues stand by their findings. DeStefano said all the study authors, including Thompson, agreed on the analysis and interpretation before the study was submitted for publication 10 years ago. However, he said he plans to review his notes and will decide whether to run another analysis on the data.

The new study by Hooker has been publicized by groups like Focus Autism, which say vaccines have contributed to the “current autism epidemic and rise of chronic illness in children.” Hooker is a scientific adviser for the Focus Autism Foundation. He also has a 16-year-old son with developmental delays who he said is “vaccine injured.”

Dr. Max Wiznitzer, a pediatric neurologist at Rainbow Babies and Children’s Hospital in Cleveland, said the design of Hooker’s study is questionable, and that his analysis is “not fine-tuned enough to give you meaningful information.”

“If you analyze data enough times and enough ways, you’re bound to find something that is statistically significant,” said Witznitzer, after looking at both studies. “This does not mean that the result is a true positive (vs. a false positive) or meaningful.”

The debate over whether autism spectrum disorders are caused by vaccines started when researcher Andrew Wakefield published a now-retracted study in The Lancet in 1998 that linked the MMR vaccine to autism.

Most of Wakefield’s co-authors withdrew their names from the study when they learned Wakefield had been compensated by a law firm intending to sue manufacturers of the vaccine in question. In 2010, Wakefield lost his medical license. And in 2011, The Lancet retracted the study after an investigation found Wakefield altered or misrepresented information on the 12 children who were the basis for the conclusion of his study.

Other researchers have not been able to replicate Wakefield’s findings. In fact, several subsequent studiestrying to reproduce the results have found no link between vaccines and autism, including several reviews by the Institute of Medicine. Most recently, a study published in Pediatrics on July 1 concluded that vaccines do not cause autism spectrum disorders.

An editorial published with the Pediatrics study added that the debate should be put to rest. This review was done by the RAND Corporation at the request of the Agency for Healthcare Research and Quality, and claims to be the most comprehensive review on the safety of vaccines.

“I want to be absolutely clear that I believe vaccines have saved and continue to save countless lives,” Thompson said in his statement. “I would never suggest that any parent avoid vaccinating children of any race.”

While the cause of autism is not known, several studies indicate it starts in utero, long before a child is given the MMR or any other vaccinations. As such, DeStefano and other experts in the field have said it is biologically implausible for vaccines to cause autism.

“We know the brain and cellular features for children begin when the child is still in the womb. The brain is already developing the wiring that will manifest in autism,” DeStefano said.

Hooker said his results raise more questions than answers and pointed to the need for additional studies.

The advocacy group Autism Speaks, which declined to comment on Hooker’s study, referred CNN to its “Vaccine and Autism” statement, which says:

“We strongly encourage parents to have their children vaccinated for protection against serious disease. We recognize that some parents still have concerns about vaccines, particularly if they have a child or relative with autism. We urge them to find a health practitioner who will consider their concerns and help them ensure the well-being of their child.”

Did physicists just solve the construction mystery of the Great Pyramid?


Physicists might have finally figured out how the Great Pyramid of Giza in Egypt was built – namely, how 2.4 million limestone blocks weighing up to 80 tonnes each were moved into place.

great-pyramid

Exactly how the colossal Great Pyramid of Giza was built has been debated furiously for centuries. While Egyptologists generally agree that the 146.5-metre-high structure was built over a period of 10 to 20 years, no one has been able to prove how 2.4 million enormous limestone blocks were transported from several nearby quarries and stacked so perfectly in a pyramid shape using nothing but whatever basic construction technologies were available at the time.

One popular theory is that the blocks were dragged across strips of sand that had been loosened with water to reduce friction. But this raises the question of how the workers would have transported all the water they needed to the location of the blocks, because just like limestone blocks, water is incredibly heavy too!

Perhaps, proposes a different theory, the workers attached quarter-circle wheels to the flat surfaces of the blocks, turning them into easy-rolling cylinder shapes. But the problem with this hypothesis is that it’s not particularly practical when you consider it in relation to the roads these cylinders would need to roll along. The pressure exerted by the blocks on the roads as they were rolled towards the construction would have effortlessly torn them up, necessitating constant maintenance by the otherwise engaged workers.

But a new study led by physicist Joseph West from Indiana State University in the US has offered up a pretty promising theory. The Physics arXiv Blog explains:

“Their approach considerably reduces the ground pressure but at the same time allows the blocks to be moved with significantly less effort than dragging. They have even tested the idea to measure the amount of force workers would have had to use to move the blocks. Their idea is remarkably simple. They strap wooden rods to a block, turning its profile from a square into a dodecagon, which can then be moved more easily by rolling.”

pyramid-logs

West and his colleagues tried their theory out on a scale model made from a concrete block weighing almost 30 kg. After they strapped the four sets of three wooden rods to each side of the block, they attached a rope to the top, which could be used to pull on the crude wheel-like structure and get it rolling. They measured how much force would be needed to set the stone rolling, and found that it was only around 0.15 times the entire weight of the stone, which is feasible, even for the largest stones used in the Great Pyramid.

“Of course, these researchers do not address the question of whether there is any evidence that the pyramids were constructed in this way, only that this would certainly seem a good option, not least because of the reduced wear and tear on the thoroughfares to and from the pyramid,” says the Physics arXiv Blog. “Indeed, they say the mechanism would work without a formal, engineered road.”

The team is in agreement with that assessment, concluding the study by asserting the need for further research into the theory: “It would seem that some variation of rolling the blocks should now be considered to be among the ‘best’ and most likely method used to move the stones for the great pyramids.”

Ebola Doctor Reveals How Infected Americans Were Cured .


Techniques used in the U.S. to treat symptoms and subdue the virus in patients could work overseas, Bruce Ribner says
Last week two American aid workers who had contracted Ebola while working in west Africa were released from a U.S. hospital and pronounced “recovered.” They had been flown to Emory University Hospital in Atlanta from Liberia earlier this month to receive care in the hospital’s specialized infectious disease unit. Kent Brantly, a physician with the humanitarian group Samaritan’s Purse, and missionary Nancy Writebol, of SIM USA, beat the strain of the disease they had contracted, which kills 52 percent of its victims. Bruce Ribner, medical director of the hospital’s Infectious Disease Unit, sat down with Scientific American to explain how the two Americans were cared for, the lessons that could be applied to help patients across Africa and why the hysteria over flying the two individuals back to the U.S. was unfounded.

Are Brantly and Writebol now immune to the Zaire strain of Ebola?
In general, patients who have recovered from Ebola virus infection do develop a very robust immunity to the virus. They develop antibodies against the virus and they also develop cell-mediated immunity—the lymphocytes important to form viral control of pathogens. In general, the finding is it’s basically like being immunized—it would be unusual to get infection with the same strain.

Will that immunity afford them protection against other strains of Ebola?
We are still evaluating that in our two patients. Cross-protection is not quite as robust. There are five strains of Ebola viruses. Even though that data is not great, the feeling is there is potential for being infected if you go to a different part of Africa and get exposed to a different strain.

You said “still evaluating.” Are you still caring for Brantly and Writebol?
We are going to be following those two patients as outpatients, and as part of our evaluation they have agreed to undergo additional testing so we can better understand immunity to Ebola virus. We are meeting with them periodically.

What sort of lessons has Emory learned from caring for these two people that would be transferrable to patients in west Africa?
We are not being critical of our colleagues in west Africa. They suffer from a terrible lack of infrastructure and the sort of testing that everyone in our society takes for granted, such as the ability to do a complete blood count—measuring your red blood cells, your white blood cells and your platelets—which is done as part of any standard checkup here. The facility in Liberia where our two patients were didn’t even have this simple thing, which everyone assumes is done as part of your annual physical.

What we found in general is that among our Ebola patients, because of the amount of fluid they lost through diarrhea and vomiting, they had a lot of electrolyte abnormalities. And so replacing that with standard fluids [used in hospital settings] without monitoring will not do a very good job of replacing things like sodium and potassium. In both of our patients we found those levels to be very low. One of the messages we will be sending back to our colleagues is even if you don’t have the equipment to measure these levels, do be aware this is occurring when patients are having a lot of body fluid loss.

Our two patients also gained an enormous amount of fluid in their tissues, what we call edema. In Ebola virus disease there is damage to the liver and the liver no longer makes sufficient amount of protein; the proteins in the blood are very low and there is an enormous amount of fluid leakage out into the tissues. So one of the takeaway messages is to pay closer attention to that and perhaps early on try to replace some of these proteins that patients’ livers lack.

Considering how limited resources are in some of these facilities, could health care workers really act on this information?
I think the world is becoming aware that issues like this are not going to go away. The developed countries of the world will have to do our part to assist our colleagues with less developed infrastructure to care for sick people. I think one of the messages that is going out from many sources is we really have to help countries such as the ones involved in this outbreak to develop their medical infrastructure. Hopefully in five years they will have this infrastructure.

You have said that you are helping to develop new Ebola care guidelines based on your experience. How will those be disseminated?
We have several articles that we have submitted to major medical journals, which are read overseas, where we will be pointing this out. We are working with several government agencies, including the U.S. State Department, to help them come up with lessons learned—guidelines which they will distribute in turn to other countries. It is our goal to help our colleagues overseas.

Alternatively, what lessons did you learn from those health care workers?
Mostly the clinical course of the patients—much like any physician sending a patient to a referral center. They admitted they knew they were kind of flying blind. They’d say, “this is what we observed but we had no way to test it.”

The World Health Organization maintains that patients can continue to be infectious via their sexual fluids for several months after recovery. What did you recommend to Brantly and Writebol?
There are data that go back several decades—over several outbreaks—that suggest when you have individuals that have recovered from Ebola virus infection they may still be shedding nuclear material [genetic material from the virus which could potentially help spread it] in semen in males and vaginal secretions in females and also, potentially in urine. People have done this by doing assays looking specifically at the nuclear material of the virus. There has been very little attempt to demonstrate if this is viable virus that these individuals are shedding. It’s important when looking at epidemiological investigations that no one has been able to show people shedding these nuclear materials as a source of infection after they are discharged.

Looking at Ebola survivors who were discharged and successfully resolved the infection, following up several months later and evaluating their family members, there has never been any evidence that family members became infected. A lot of the thinking now is this probably was not live and is not important in terms of control of infection. We did give both of our patients the standard recommendations, which are contained on the CDC [U.S. Centers for Disease Control] Web site—not having unprotected sex for three months.

How many doctors and nurses were on your team caring for these two Ebola patients?
Twenty-one nurses, five physicians and we had the support of hundreds. Just making sure all the disposables coming out of those rooms were sterilized before we put them on the federal highway system, for example—we had to certify to the contractor that takes our regulated medical waste that it didn’t have active Ebola virus inside it. We didn’t have the equipment to handle all of the waste but in two hours facilities brought in industrial autoclaves [which sterilize materials with extreme heat] to replace the system that we had. We would have been drowning in garbage without them.

It has been reported that Brantly received a blood transfusion from a recovered patient. What role might that have played and is it being tried in other contexts?
I wouldn’t be able to tell you what I read in his chart. The most accurate thing to say is we don’t have a clue [what role a blood transfusion could play]. It’s not part of our standard treatment in our country. We wouldn’t have any idea whether he benefited or it was detrimental.

Are current diagnostics to identify Ebola virus disease adequate for this outbreak?
Certainly in the United States they are adequate. The major way one would diagnose Ebola virus disease is through a process called PCR or polymerase chain reaction, where you take the patient’s blood, put it in a machine and it tells you in a few hours if the nuclear material from the Ebola virus is present. CDC is doing that for patients coming back from infected areas where virus is a potential. There are a number of labs, both local and courtesy of CDC, that are doing this testing in west Africa, and my sense is it’s not that difficult to get it done.

This past week WHO announced that one of its workers has been infected with Ebola virus disease and that person was given the option of being sent to a different country for treatment. A British nurse also contracted the virus and went home to the U.K. for care. What’s the value of getting treated elsewhere?
Given that there is no treatment for Ebola virus disease, the main intervention that will determine if someone lives or dies with this infection is supportive care: The ability to replace fluid and electrolytes if a patient is losing them. The ability to replace platelets if that count is low and a patient is starting to bleed. The ability to replace protein in the blood that may be deficient. A developed country has the capability because of our infrastructure to provide that level of support is at a much higher level than a hospital dealing with patients in west Africa.

Among the handful of patients that received the experimental drug ZMapp, some have died. Considering the mortality rate for the current Ebola strain is almost 50 percent what can we say about ZMapp?
Experimental drugs are experimental drugs because we don’t know if they will work. That is true both with the preparations patients received in Liberia and other preparations that are being considered for treating patients with this infectious disease. We are a long way from being able to say that someone that received one of these agents benefited, it had no impact or it may be that their outcome may be impeded. Until we have good studies looking at outcomes of patients who received these medications, compared to patients who didn’t receive them, we should be very cautious.

I would go further to say that there is a fair amount of almost hysteria and people feeling they must have these preparations to survive. In the past people thought they needed agents for treatment, and the agents actually turned out to impair people’s ability to survive. The focus should remain on aggressive intensive care and the ability to correct abnormalities metabolically, rather than receiving any magic vaccine or product that may or may not improve survival.

For example, there used to be a belief that patients who had bacterial sepsis did much better if you gave them high doses of steroids. Now we know that these may be detrimental instead of beneficial. We know now since we’ve done the studies. Again, it was one of those things where people felt like “yeah this should be” but when they did the study in randomized patients they found it didn’t work at all.

As you know, two upcoming clinical trials will be looking at potential Ebola vaccines, and there are also a variety of experimental therapies that are being discussed in the U.S. and elsewhere beyond ZMapp. How should such information be coordinated? Does there need to be an entity overseeing that?
Given that we have multiple countries I don’t know that you can have any one entity. It’s tricky enough having the FDA [U.S. Food and Drug Administration] monitor what is going on in the United States. Clearly if you are talking about Canadian studies or European products, I don’t know that there is any entity that can provide that sort of coordination. My guess is that most of the manufacturers are aware of what the others are doing and are comparing notes because they feel it’s to their benefit to work together.

An ethics panel from WHO recently said that it is ethical to give out experimental treatments to Ebola patients, but it has not yet specified who should have priority in such circumstances or how such drugs should be doled out. They are taking up that issue at a meeting next week. What’s your thought?
I think it’s certainly ethical to study experimental biologicals and vaccines but we have to be extremely cautious. It’s not as though we have something that we know works. To say that anyone is withholding products implies we know that there’s a benefit, which gives me pause because we are a long long way from demonstrating that these offer any benefit in humans.

Is there anything you would like to add about insights you learned from your Ebola patient care?
The major thing I hope people have appreciated is there was a lot of anxiety, a lot of negative comment about our bringing these two patients back to our facility to care for them. Most of that we attribute to poor education, and I’m hoping that since we were successful in helping them resolve their infections it helps to dispel the idea that this is a disease that by nature has to be fatal. As we have been saying all along, we feel that the high fatality rates in developing parts of the world where this infection occurs are because of the lack of resources. We had always felt that the survival of patients with proper support would be a lot better than in developing countries.

The other thing I would hope we would get across to the public is this is a disease where we don’t have to have a lot of secondary infections—if we follow standard infection-control procedures. We had 26 people giving direct patient care to these patients and we did not have any secondary infections at all, and that’s as we expected.

We were using contact precautions and droplet precautions. Fortunately, we don’t have to go to that level of protection [wearing protective full-body suits like in west Africa]. You wear whatever you need so that the blood and body secretions don’t come into contact with you, depending on the quantity of fluids. We used gowns and gloves and foot coverings of the health care workers in order to prevent contact with the body materials of these individuals. Our approach was what CDC recommends: you wear a mask and goggles or a face shield to prevent that infection. Some of the nurses spending three to four hours in patients’ rooms were more comfortable wearing hoods than masks and face shields, though those would have been adequate. We can manage care with minimal chance for secondary spread. It’s not as though we brought the plague to American shores.

Bad Memories Turned to Happy Ones in Mice Brains


Memories are often associated with emotions, and these feelings can change through new experiences and over time. Now, using light, scientists have been able to manipulate mice brain cells and turn the animals’ fearful memories into happy ones, according to a new study.
Memories are encoded in groups of neurons that are activated together or in specific patterns, but it is thought that neurons in different brain regions encode different aspects of a memory of an event. For example, the place where an event occurred and the emotion associated with it may be stored in different places.
In the new study, researchers examined whether it is possible to selectively change one part of a memory — the emotion attached to it. They made male mice form fearful memories by giving them painful electrical shocks, or form pleasant memories by letting the animals interact with female mice. [Why You Forget: 5 Strange Facts About Memory]

Later, using light to control the activity of neurons (a method called optogenetics), the researchers evoked the fearful memories every time the mice went to a certain corner of their cage, which led the mice to avoid that corner. In mice that had formed pleasant memories, the researchers used those memories to make a certain corner look attractive to the rodents.
In the last step, to reverse the associations between a place and an emotion, the researchers evoked only the “place” part of the fearful memories, while letting the mice interact with female counterparts. As a result, the mice were no longer afraid of that specific corner of the cage.
The researchers were also able to do the reverse, and turn positive memories to fearful ones, according to the study published today (Aug. 27) in the journal Nature.
Shaping memory fragments
It is well-known that memories are subject to change, and may even get slightly rewritten each time we recall them during a new experience, studies suggest.
However, scientists do not entirely understand the brain mechanisms that enable memories to change and that even allow us to feel different emotions about those memories. Elucidating these mechanisms could help scientists one day develop new therapies for conditions such as depression and post-traumatic stress disorder.
In the new study, the researchers looked at neurons in a brain structure called the hippocampus, which is thought to encode the context of memories, such as where an event happened. The researchers also looked at neurons in another brain structure, the amygdala, which is believed to encode emotions.
The mice in the study were genetically engineered to make tracking their memories easier. As the animals’ fearful or pleasant memories were formed, a light-sensitive protein was expressed in the neurons that encoded the new memories. This way, the researchers were able to tag these neurons, and later use light to reactivate the memory those brain cells held.
The new experiment worked because the scientists tackled the contextual and emotional aspects of the memory separately. When the researchers activated the neurons in the hippocampus, it evoked the contextual part of the memory, while new events the mouse was experiencing rewrote the emotional part of the memory. This led to a new memory of the same place but with a different emotional association, the researchers said.
Looking at the cells under the microscope, the researchers confirmed that the relationship between the memory-holding neurons in the hippocampus and those in the amygdala was altered after the scientists’ manipulations, suggesting that the connection between the two brain regions is indeed malleable.
The new experiments followed previous studies by the same researchers last year, in which they implanted false memories in mice. In those studies, the researchers activated neurons to make mice remember a previous experience as the animals were undergoing a new and different experience. This made mice form a memory of the mixture of the two experiences, which in real life had never happened.

Smartphone app that detects jaundice in newborns within minutes


Researchers have developed a smartphone app that checks for jaundice in newborns and can deliver results to parents and pediatricians within minutes. Jaundice is a common condition in babies less than a week old. Skin that turns yellow can be a sure sign that a newborn is jaundiced and isn’t adequately eliminating the chemical bilirubin. However, that discolouration is sometimes hard to see,and severe jaundice left untreated can harm a baby.

The smartphone app can serve as a screening tool to determine whether a baby needs a blood test

The new app, developed by the University of Washington engineers and physicians, could serve as a screening tool to determine whether a baby needs a blood test – the gold standard for detecting high levels of bilirubin. “Virtually every baby gets jaundiced, and we’re sending them home from the hospital even before bilirubin levels reach their peak,” said James Taylor, a UW professor of pediatrics and medical director of the newborn nursery at UW Medical Center.

“This smartphone test is really for babies in the first few days after they go home. A parent or health care provider can get an accurate picture of bilirubin to bridge the gap after leaving the hospital,” Taylor said. The app, called BiliCam, uses a smartphone’s camera and flash and a colour calibration card.

A parent or health care professional needs to download the app, place the card on her baby’s belly, and then take a picture with the card in view. The card calibrates and accounts for different lighting conditions and skin tones. Data from the photo are sent to the cloud and are analysed by machine-learning algorithms, and a report on the newborn’s bilirubin levels is sent almost instantly to the parent’s phone.

“This is a way to provide peace of mind for the parents of newborns,” said Shwetak Patel, a UW associate professor of computer science and engineering and of electrical engineering. A noninvasive jaundice screening tool is available in some hospitals, but the instrument costs several thousand dollars and isn’t feasible for home use, researchers said.

Currently, both doctors and parents assess jaundice by looking for the yellow colour in a newborn’s skin, but this visual assessment is only moderately accurate. The UW team developed BiliCam to be easy to use and affordable for both clinicians and parents, especially during the first several days after birth when it’s crucial to check for jaundice.

The team ran a clinical study with 100 newborns and their families at UW Medical Center. They used a blood test, the current screening tool used in hospitals, and BiliCam to test the babies when they were between two and five days old. They found that BiliCam performed as well as or better than the current screening tool. Though it wouldn’t replace a blood test, BiliCam could let parents know if they should take that next step, researchers said.

Are ‘immortal’ jellyfish key to eternal life?


For centuries, man has been on a quest to find the elixir to eternal life. Alchemists struggled fruitlessly to create the legendary philosopher’s stone — a mythical substance capable of turning base metals into precious gold, and said to hold the key to immortality.

But perhaps they were going about it the wrong way. Instead of searching for answers on land, maybe they should have been looking to the sea.

For many beach-goers, jellyfish are a nuisance that blights the sea shore. But some scientists believes they could hold the key to immorality.

In the seaside town of Shirahama, in Japan, one man thinks he knows what holds the key to everlasting life — jellyfish.

Shin Kubota is a professor at Kyoto University’s Seto Marine Biological Laboratory. He began studying the gelatinous sea creatures in 1979 but there’s one type with which he’s particularly preoccupied — the scarlet jellyfish.

“They don’t die,” Kubota says, “they rejuvenate.” He adds that they are one of three jellyfish species in japan that are considered “immortal.”

“One day in my plankton net there was a small scarlet jellyfish from [the] south, which had many sharp sticks stuck into its body,” he recalls. “I thought ‘poor thing,’ and removed all of the sticks, hoping it may become better and swim again. But it didn’t and shrunk. However, it rejuvenated!”

Read: Swimming with sharks, without a cage

It’s less immortality and more regeneration but Kubota believes these tiny marine animals could hold the secret to perpetual life.

When an adult scarlet jellyfish — or medusa — is injured it goes to the bottom of the ocean floor. From there it morphs back into its infant state, known as a polyp. Then the polyp becomes a brand new medusa, allowing the Jellyfish to move between an adult and infant state in about two months.

So far, Kubota has succeeded in making one jellyfish rejuvenate an incredible 12 times in the lab. But there remain many unanswered questions.

“There should be a key to rejuvenation in the system of scarlet jellyfish,” says Kubota. “I’d like to believe it could be applied to human beings because genetically jellyfish and humans are not so different.”

Watch the video below to see more about Kubota’s work at the Seto Marine Biological Laboratory and Japan’s “immortal” jellyfish.