Google X, the tech giant’s “moonshot” lab, has spent the last two years building an aerial drone that can deliver goods across the country. The company calls the effort Project Wing.
Revealed today in a story from The Atlantic, the project is reminiscent of work underway at Amazon.com. Amazon CEO and founder Jeff Bezos revealed the retailer’s drone ambitions this past holiday shopping season during an appearance on the popular TV news magazine 60 Minutes.
“Self-flying vehicles could open up entirely new approaches to moving things around—including options that are faster, cheaper, less wasteful, and more environmentally sensitive than the way we do things today,” a Google spokesperson said in an email to WIRED.
The experimental Ebola drug ZMapp cured all 18 of the lab monkeys infected with the virus, including those suffering the fever and haemorrhaging characteristic of the disease and just hours from death, scientists have said.
Even monkeys not treated until five days after infection survived, the scientists, who published their data in the journal Nature on Friday, said.
No other experimental Ebola therapy has ever shown success in primates when given that long after infection; the five days is analogous to nine to 11 days after infection in people.
Although two American aid workers who contracted Ebola in the West Afrucan nation of Liberia were cured after receiving ZMapp, their physicians do not know if the drug helped.
A Liberian doctor with the disease died this week despite being given the drug, as did a Spanish priest.
ZMapp, produced by San Diego-based Mapp Biopharmaceutical, has never been scientifically tested in people, and the current study was the first in primates.
The success is therefore a “monumental achievement,” virologist Thomas Geisbert of the University of Texas Medical Branch wrote in a commentary on the paper, published online in Nature.
There are no approved Ebola vaccines or treatments, but human safety trials will begin next week on a vaccine from GlaxoSmithKline Plc and this autumn on one from NewLink Genetics Corp.
The Ebola outbreak in West Africa has killed 1,552 people out of 3,069 confirmed cases, the World Health Organisation said.
The agency said the disease was on pace to infect 20,000 people. Neither governments nor private medical groups have been able to contain the outbreak, which WHO said will almost certainly continue into 2015.
Optimal mix
ZMapp is a mix of three antibodies that bind to proteins on Ebola viruses and trigger the immune system to destroy them.
ZMapp had previously developed two different cocktails of antibodies, but they protected only 43 percent of monkeys when given as late as five days after infection.
For the current study, scientists led by Gary Kobinger of the Public Health Agency of Canada set out to identify the optimal mix of antibodies from the earlier cocktails.
His team tested the antibodies in guinea pigs one at a time and in various combinations, identifying the two best performers last December.
The two graduated to tests in 12 rhesus monkeys. This spring the winner of that face-off, ZMapp, was given to another 18 infected monkeys – three doses at three-day intervals starting three, four or five days after infection.
All three untreated monkeys, in contrast, died of Ebola by day eight. With ZMapp, even advanced symptoms such as rashes, liver dysfunction and haemorrhaging disappeared, a result Kobinger called “beyond my own expectations”
“This is an extremely encouraging result,” said David Evans, professor of virology at England’s University of Warwick, who was not involved in the study.
The success suggests that ZMapp “offers the best option” for treating Ebola, Kobinger’s team wrote, and should be tested for safety in people to enable its compassionate use “as soon as possible”.
RosRAO, a subsidiary of Russian nuclear giant Rosatom, is among the three companies selected to build a system to filter radioactive tritium out of the contaminated water collected at the stricken power plant – a task that has so far defied engineers.
Fukushima Daiichi operator TEPCO, which has resorted to erecting thousands of water tanks to contain the toxic run-off from the plant, is already trialing a system that filters 62 radioactive materials. But the Advanced Liquid Processing System (ALPS) does not filter tritium, a mildly radioactive byproduct of nuclear generation, which nonetheless means that water cannot be safely discharged into the Pacific Ocean.
RosRAO, which was built on the foundations of Soviet-era waste disposal research institutions, won the TEPCO tender for a filtration system – alongside US firm Kurion Inc, and GE Hitachi Canada, a joint project between the Japanese and US corporations – beating 26 other companies.
Each of the three contractors will be given 1 billion yen – about $9.5 million – to present a working filter prototype by the March 2016 deadline, and the final value of the contract, which could last for decades, could run into hundreds of million dollars.
“We are offering a unique combined filtering technology, unlike our Western colleagues, which allows it to be more cost-efficient,” said project manager Sergey Florya in an interview with RIA Novosti news agency.
The official added that the level of tritium in Fukushima water is 10,000 times higher than the norm allowed by the WHO.
TEPCO faces an estimated bill of over $105 billion to clear up the consequences of the earthquake and tsunami that caused multiple meltdowns at the partially-antiquated plant in March 2011.
A worker wearing a protective suit and a mask looks up welding storage tanks for radioactive water, under construction in the J1 area at the Tokyo Electric Power Co’s (TEPCO) tsunami-crippled Fukushima Daiichi nuclear power plant in Okuma in Fukushima prefecture (AFP Photo / Toru Hanai)
While all reactors have been stabilized, cooling water disposal has been a prime issue. The multi-nuclide removal equipment, called ALPS (advanced liquid processing system) was installed in March 2013, but its functional usefulness has been hampered by problems, such as pipe corrosion, leaks, operator errors and design imperfections, which have forced constant shutdowns. At one point its filters were failing to decontaminate the water at all, despite purportedly working as designed.
To this day, ALPS remains in “trial mode”, despite the government ordering a $150 million expansion to the system, tentatively scheduled to begin operating in October.
Latest statistics show that there are currently 367,000 tons of contaminated water, stored in tanks inside the Fukushima Daiichi nuclear power plant.
“This is the first time this much radioactive water has been collected in any single place in the world – the scale of this project in unprecedented,” said Florya.
A continuous jolt of magnetic pulses to the brain can improve memory a study shows
Researchers from Northwestern University Feinberg School of Medicine have discovered that by using a procedure called Transcranial Magnetic Stimulation (TMS)—which has shown potential as a non-pharmacological way to treat stubborn depression—they can change memory functions in the brains of adults. The initial goal of the study was to determine whether a memory-related brain network could be manipulated, and whether that manipulation could lead to improved recall.
The researchers hypothesized that remembering events requires several brain regions to work together with the part of the brain called the hippocampus, which is involved in memory. If there was a way to stimulate these regions, they could sync up better, which would improve memory and cognition. “[The research] was more of a hunch than I’d like to admit,” says study author Joel Voss, a assistant professor of medical social sciences at Northwestern, who has studied memory for years. “I am interested in this network, and whether we can actually improve this system.”
To test this, Voss and his team of researchers had 16 healthy adults between the ages of 21 and 40 undergo MRIs so the researchers could learn the participants’ brain structures. Then, the participants took a memory test which consisted of random associations between words and images that they were asked to remember. Then, the participants underwent brain stimulation with TMS for 20 minutes a day for five days in a row. TMS uses magnetic pulses to stimulate areas of the brain. It doesn’t typically hurt, and has been described by some as a light knocking sensation. The researchers stimulated the regions of the brain involved in the memory network.
Throughout the five days, the participants were tested on recall after the stimulation and underwent more MRIs. The participants also underwent a faked placebo procedure. The results showed that after about three days, the stimulation resulted in improved memory, and they got about 30% more associations right with stimulation than without. Not only that, but the MRIs showed that the brain regions became more synchronized by the TMS.
Though the improvement was relatively small, Voss says they want to test the efficacy in other populations—like those who are aging or those who are starting to deal with the first stages of memory loss. The effects may be more pronounced in an “unhealthy” person because a healthy person will have a more normal baseline to start from, and there’s not as much room for improvement.
TMS is FDA approved as a treatment for depression. The procedure is used to stimulate regions of the brain in a depressed person that are inactive and involved in mood regulation. As TIME covered in May, TMS is currently used when a patient doesn’t respond to antidepressants, but some researchers think it could be used as a first-line treatment. Voss has been involved in some research in the past involving TMS for depression, and it was looking at that MRI data that helped him piece the puzzle together for his hunch that the brain memory system could be stimulated with positive results.
The new research is still very experimental and only looked at a small population. But it’s still intriguing. “This is not a treatment that someone could ask their doctor for. It’s still in very early stages,” says Voss. “But I think it has more promise than anything developed yet.”
The search for the fundamental units of space and time has officially begun. Physicists at the Fermi National Accelerator Laboratory near Chicago, Illinois, announced this week that the Holometer, a device designed to test whether we live in a giant hologram, has started taking data.
The experiment is testing the idea that the universe is actually made up of tiny “bits”, in a similar way to how a newspaper photo is actually made up of dots. These fundamental units of space and time would be unbelievably tiny: a hundred billion billion times smaller than a proton. And like the well-knownquantum behaviour of matter and energy, these bits of space-time would behave more like waves than particles.
“The theory is that space is made of waves instead of points, that everything is a little jittery, and never sits still,” says Craig Hogan at the University of Chicago, who dreamed up the experiment.
The Holometer is designed to measure this “jitter”. The surprisingly simple device is operated from a shed in a field near Chicago, and consists of two powerful laser beams that are directed through tubes 40 metres long. The lasers precisely measure the positions of mirrors along their paths at two points in time.
If space-time is smooth and shows no quantum behaviour, then the mirrors should remain perfectly still. But if both lasers measure an identical, small difference in the mirrors’ position over time, that could mean the mirrors are being jiggled about by fluctuations in the fabric of space itself.
So what of the idea that the universe is a hologram? This stems from the notion that information cannot be destroyed, so for example the 2D event horizon of a black hole “records” everything that falls into it. If this is the case, then the boundary of the universe could also form a 2D representation of everything contained within the universe, like a hologram storing a 3D image in 2D .
Hogan cautions that the idea that the universe is a hologram is somewhat misleading because it suggests that our experience is some kind of illusion, a projection like a television screen. If the Holometer finds a fundamental unit of space, it won’t mean that our 3D world doesn’t exist. Rather it will change the way we understand its basic makeup. And so far, the machine appears to be working.
In a presentation given in Chicago on Monday at the International Conference on Particle Physics and Cosmology, Hogan said that the initial results show the Holometer is capable of measuring quantum fluctuations in space-time, if they are there.
“This was kind of an amazing moment,” says Hogan. “It’s just noise right now – we don’t know whether it’s space-time noise – but the machine is operating at that specification.”
Hogan expects that the Holometer will have gathered enough data to put together an answer to the quantum question within a year. If the space-time jitter is there, Hogan says it could underpin entirely new explanations for why the expansion of our universe is accelerating, something traditionally attributed to the little understood phenomenon of dark energy.
Ann Nelson, a physicist at the University of Washington in Seattle, says the Holometer is a novel experiment for probing space on the smallest scales. But even if the experiment finds something, the wider implications for physics are still not well understood.
“It would mean that all our standard assumptions about space-time and effective local theories are wrong, at least when gravity is important,” she says.
The devastating Ebola outbreak in West Africa will likely grow much worse over the next several months, continuing into 2015. That grim news was delivered Wednesday afternoon by panelists from three San Diego organizations prominent in fighting the lethal disease.
Cases have doubled every 35 days in this year’s outbreak, already the worst since the disease was discovered in 1976. Medical workers are themselves contracting the disease, depleting health care resources that in many regions were already nearly nonexistent.
And the disease itself might be mutating to become less lethal but more contagious, increasing the risk of it spreading elsewhere.
What is Ebola?
A graphic description of what Ebola is, and what it does, from Ebola researcher Erica Ollmann Saphire.
But there’s still a chance some of the damage could be prevented, if governments and private charity give more aid, the panelists told an audience of nearly 200 at The Scripps Research Institute in La Jolla.
Cheap and well-known safeguards, such as gloves, gowns and disinfectant chlorine, can go a long way toward preventing medical worker deaths, said panelist Erica Ollmann Saphire, who studies Ebola and similar diseases at Scripps Research.
“A doctor shouldn’t die because he doesn’t have gloves to wear,” Ollmann Saphire said. “This is a solvable problem.”
Ollmann Saphire and the two other panelists epitomize San Diego’s extensive role in fighting Ebola, in complementary ways.
• The Ollmann Saphire lab focuses on the structure of Ebola and antibodies that neutralize the virus. This research, and that of her international collaborators, aims to find weak spots that can be exploited to stop it.
• Kevin Whaley, chief executive of Mapp Biopharmaceutical, which has developed an experimental Ebola drug called ZMapp, represented the medical role. ZMapp was given to two American medical missionaries who contracted the disease in Liberia. It’s unclear whether ZMapp aided their recovery.
What is Mapp Biopharmaceutical
Mapp Biopharmaceutical CEO Kevin Whaley tells the genesis of his company, which is developing an experimental Ebola drug, ZMapp.
• Mark O’Donnell, chief operating officer of the nonprofit development group PCI, discussed the humanitarian and economic development aspects. The group, also known as Project Concern International, was established more than 50 years ago by a San Diego doctor.
Change in virus?
PCI has been working in Liberia, one of the hardest-hit countries, for about four years, O’Donnell said. That work of economic development has been put aside for the Ebola emergency.
Ebola has periodically caused highly lethal but limited outbreaks. With an extremely high mortality rate, the disease typically burns itself out. People die before they can spread the disease very far.
But this outbreak is different, Ollmann Saphire said. It keeps spreading, doubling in size every 35 days. And the mortality has dropped from about 90 percent in the first outbreak to about 60 percent.
“There’s 68 mutations in the protein level between that (first) virus and this virus,” she said. “Did one of those mutations make it less immunosuppressive, or replicate less efficiently? We don’t know. Could the lower lethality have contributed to its greater scale?”
Ebola researcher Erica Ollmann Saphire holds a model of ZMapp, a three-antibody “cocktail” that neutralize Ebola in animal studies. ZMapp has been given to Ebola patients as an emergency measure, but has not yet been tested in clinical trials. Bradley J. Fikes
The answer will come from more intensive sequencing of viral genomes from patients to correlate mutations with the changes, she said.
In the meantime, development of anti-Ebola drugs, such as ZMapp, is being accelerated. Whaley said his company is getting federal help in preparing the drug for clinical trials, including increasing production. Other drugs are in development.
While ZMapp’s effectiveness remains to be proven in clinical trials, it belongs to a well-known class of antibody-based drugs and is not some “secret serum,” as media reports have called it, Whaley said. ZMapp is a combination of three Ebola-fighting antibodies, which in animals have shown effectiveness in protecting against the virus.
Whaley said the advantage of an antibody-based drug like ZMapp over a vaccine is that it can stop the virus quickly. Vaccines stimulate antibody production, but that process takes weeks, while Ebola can kill in days.
Doing more
Even better antibody combinations might be possible, Ollmann Saphire said, which is the reason for the global collaboration she leads.
“Kevin’s group found these three, and then a group in Japan had two, and a group in Canada had a couple,” Ollmann Saphire said. “Can you make an even more effective combination if you put all these antibodies on the same page? What if the absolute best cocktail is going to be one from San Diego, and one from Winnipeg, and one from Paris? We don’t know until we put them all together.”
She said that while the consortium she leads has been awarded $28 million, and while she’s grateful to have it, that money is spread over five years and 20 universities.
“A lot of that goes to the building rent, the electricity, the biosecurity, janitorial, all that stuff,” she said. “So on average it winds up being about $200,000 a year per lab. From that $200,000, I pay my salary and the 14 people who are working in my lab, and all the test tubes and chemicals. And so that was enough to get this work going, but it wasn’t enough to process all these samples.”
Laser-based method shows how cocaine disrupts flow in the brains of mice
Images reveal dramatic drop in blood flow speeds
Researchers have captured exactly what taking cocaine does to the flow of blood in the brain.
They created a laser-based method of measuring how cocaine disrupts blood flow in the brains of mice.
It shows for the first time how drug abuse affects the brain.
A side-by-side comparison of blood flow in a healthy mouse brain vs. a mouse brain exposed to cocaine. The image on the left (a) shows the mouse brain blood vessels before cocaine. The image on the right (b) shows the blood vessels after, revealing that many of the vessels are now darker, which signifies lower blood flow.
HOW COCAINE AFFECTS THE BRAIN
Drugs such as cocaine can cause aneurysm-like bleeding and strokes, but the exact details of what happens to the brain’s blood vessels have remained elusive—partly because current imaging tools are limited in what they can see, Pan says.
But using their new and improved methods, the team was able to observe exactly how cocaine affects the tiny blood vessels in a mouse’s brain.
The images reveal that after 30 days of chronic cocaine injection or even after just repeated acute injection of cocaine, there’s a dramatic drop in blood flow speed.
The researchers were, for the first time, able to identify cocaine-induced microischemia, when blood flow is shut down—a precursor to a stroke.
The breakthrough could help doctors and researchers better understand how drug abuse affects the brain, which may aid in improving brain-cancer surgery and tissue engineering, and lead to better treatment options for recovering drug addicts.
It was developed by a team of researchers from Stony Brook University in New York, USA and the U.S. National Institutes of Health, was published today in The Optical Society’s open-access journal.
The resulting images are the first of their kind that directly and clearly document such effects, according to co-author Yingtian Pan, associate professor in the Department of Biomedical Engineering at Stony Brook University.
‘We show that quantitative flow imaging can provide a lot of useful physiological and functional information that we haven’t had access to before,’ he said.
Drugs such as cocaine can cause aneurysm-like bleeding and strokes, but the exact details of what happens to the brain’s blood vessels have remained elusive—partly because current imaging tools are limited in what they can see, Pan says.
But using their new and improved methods, the team was able to observe exactly how cocaine affects the tiny blood vessels in a mouse’s brain.
The researchers were, for the first time, able to identify cocaine-induced microischemia, when blood flow is shut down—a precursor to a stroke.
The images reveal that after 30 days of chronic cocaine injection or even after just repeated acute injection of cocaine, there’s a dramatic drop in blood flow speed.
The researchers were, for the first time, able to identify cocaine-induced microischemia, when blood flow is shut down—a precursor to a stroke.
Researchers including Pan and his colleagues have developed another method called optical coherence Doppler tomography (ODT). In this technique, laser light hits the moving blood cells and bounces back.
By measuring the shift in the reflected light’s frequency—the same Doppler effect that causes the rise or fall of a siren’s pitch as it moves toward or away from you—researchers can determine how fast the blood is flowing.
It turns out that ODT offers a wide field of view at high resolution. ‘To my knowledge, this is a unique technology that can do both,’ Pan said.
ODT can only see down to 1-1.5 millimeters below the surface, so the method is limited to smaller animals if researchers want to probe into deeper parts of the brain.
But, Pan says, it would still be useful when the brain’s exposed in the operating room, to help surgeons operate on tumors, for example.
If people aren’t as concerned about climate change as they should be, one reason may be that the gradual rise of temperatures and ocean waters seems to give us plenty of time to take mitigating measures, such as seawalls to protect coastal cities and genetically-engineered crops that would be able to flourish in the altered environment. It’s harder to understand that climate change may endanger us in other ways that will be more difficult to combat. For example, it may cause a slew of deadly diseases, which are now seen mostly in poorer regions in the tropics, to spread to developed nations in temperate zones.
The latest concern: A newly-published study in BMC Public Health looked at dengue fever, avirus spread by mosquitoes that sickens 50 million people and kills about 12,000 people worldwide each year, mostly in tropical areas.
The researchers found that dengue eventually could become a significant health problem in parts of Europe, including Mediterranean and Adriatic coastal areas that are popular with tourists. Europe is becoming hotter and more humid, conditions that foster the growth of the mosquitoes.
The researchers studied data from Mexico about the occurrence of dengue fever and the effect of climate variables such as temperature, humidity and rainfall, as well as socioeconomic factors, such as population density and income, on the spread of the disease. They then used that data to model the infection rate in various regions of Europe over the next century. In some places, they predicted that rate of dengue fever cases will quintuple, to up to 10 cases per 100,000 inhabitants.
Almost all of the excess risk will fall on the coastal areas of the Mediterranean and Adriatic seas and the northeastern part of Italy, particularly the Po Valley, University of East Anglia medical school professor Paul Hunter said in a press release.
That comes after a 2013 study warned that people in the United States are also at risk from dengue due to climate change. Traditionally, America has only had a few hundred reported cases of dengue each year, usually involving international travelers. But the Natural Resources Defense Council says that the mosquito that transmits dengue now is found in 28 states.
Another 2014 study found that climate change may be increasing the spread of Lyme disease.
Do burgers, sugary snacks and other unhealthy foods exacerbate the effects of mental illness? David Robson investigates the evidence, and discovers a surprising new idea to help treat depression.
The people entering Felice Jacka’s offices over the next few months will be in the throes of depression. She wants to help them – but her approach is unorthodox. Her team at Deakin University in Australia won’t be trying out a new cocktail of drugs. Nor will they be mulling over the patient’s childhood, their jobs, or their marital difficulties to help them cope with their problems. Instead, she wants them to talk about food.
If Jacka is right, changing their eating habits could be a key part of these people’s recovery. She has good reason to believe this; over the last few years, a series of striking findings have begun to suggest that fatty, sugary diets are bad for the mind, as well as the body. The result is a cascade of reactions in the brain that can eventually lead to depression.
Although the link is by no means proven, the fear that we are eating our way to depression is already prompting governments to take action. The US Department of Defence is now funding a trial that will deliver daily nutrient-rich food parcels to a group of former soldiers, to see if it can reduce suicide rates in army veterans. And at the start of this year, the European Union launched the 9m euro MoodFood project to further explore the way different nutrients may influence our minds. Certainly, no one is suggesting that a new diet should immediately replace existing treatments; Jacka’s volunteers will still be taking their medications as well as changing their eating habits. But if healthier eating can improve their recovery rate – or prevent some people developing symptoms in the first place – it would make for a simple, complementary way to help tackle mental illness.
‘Mind and body’
To grasp why your favourite dishes could be influencing your mental health, you first need to understand a strange aspect of the mind-body connection that first came to light 20 years ago. At the time, doctors were concerned that the stresses of poor mental health would weaken the body’s immune response, leaving them open to infection. Instead, they found the exact opposite was true; in people with depression, the immune system seemed to be going into over-drive. For instance, the blood of depressed people was awash with a particular type of protein, called cytokines, which normally lead to inflammation after illness or injury.
(Thinkstock)
As the scientists pressed on, it became clear that this was a two-way process: not only could depression cause inflammation, but crucially,inflammation from other causes seems to be triggering depression. Some grounds for this link came from diseases that are known to send cytokines flushing through the body, like arthritis or cancer; patients often report depression before a diagnosis has even been made. “The people become depressed even before they know that they have cancer, and it ties in with the high levels of cytokines” says Michael Maes at Deakin University in Australia, who has pioneered work on the biological basis of depression.
More solid evidence comes from an ingenious experiment by Naomi Eisenberger at the University of California, Los Angeles. Her study involved injecting healthy volunteers with small fragments of the E. coli bacteria; it’s not enough to trigger food poisoning, but it nevertheless kicks the volunteer’s immune system into action, causing a release of cytokines. Although all the participants going into Eisenberger’s lab were reasonably happy and healthy, over the course of the day they began to develop many of the feelings you would normally associate with depression: their mood dipped and they were more sensitive to social slights, reporting feelings of disconnection and loneliness. And when Eisenberger asked them to play a computer game, for real cash prizes, the subjects appeared to take less pleasure in their wins than those who had not been injected with the fragment of bacteria – changes that were also reflected in scans of the brain’s reward circuits. An inability to feel pleasure, called anhedonia, is one of the most common symptoms of depression.
Evolutionary hangover
Lethargy during illness may have made sense during our evolution, says Eisenberger. “When dealing with infection, you would want to slow down, withdraw, and use your energy to recuperate instead of going out,” she says. But if, for whatever reason, the effects linger in the long-term, the results could be devastating; besides dampening your mood, inflammation can exacerbate oxidative stress in the brain. Oxidative stress, caused by toxic ‘free radicals’, could itself cause depression, since it can kill neurons, erode the brain’s long-range connections and disrupt the brain’s chemical signalling – sweeping changes that seem to come with long-term mental illness and may well contribute to the symptoms.
The upshot is that we may need to think about depression in an entirely new light – as a disease of the body as well as the mind. If so, many more things, besides life’s stresses, could put us at risk. Poor general fitness, smoking, and alcoholism are all known to increase an inflammatory response. And so, feasibly, could your diet: high fat and sugar levels – and the fatty tissue that results from it – are known to increase inflammation and oxidative stress. Conversely, certain nutrients such as omega-3 fish oils and minerals like zinc and selenium are anti-oxidants that can reduce inflammation and mop up some of the toxic chemicals, while boosting others that can help the brain to heal from damage.
Proving that this really can explain certain kinds of depression has been no mean feat, however. Although a few early studies had shown that people with depression often have a deficiency in nutrients like zinc, and that offering food supplements could improve their symptoms, the experiments were often poorly designed. “The whole area had been dogged by poor trials with small sample sizes,” says Jacka. As a result, it was difficult to know if the findings had just arisen by chance.
Fish oils showed a positive impact on mental health (SPL)
But around 2010, three landmark papers caused more doctors to sit up and take notice. One took place in southern Europe, where doctors were charting the transition from the traditional Mediterranean diets, full of seafood, olive oil and nuts, to the fast food served in the rest of the West. Besides studying the risks of heart disease and diabetes, the scientists also looked at the 10,000 participants’ mental health. The differences were striking; those who lived almost exclusively on the traditional Mediterranean diet were about half as likely to develop depression over the period as those eating more unhealthy food – even when you control for things like education and economic status.
Around the same time, psychologists examining UK civil servants – in the famous ‘Whitehall’ studies – found exactly the same pattern; over the course of five years, people who regularly indulged in processed, high-fat and high-sugar foods were about 60% more likely to develop depressionover the same period. Then Jacka confirmed the results with a further 1,000 Australian volunteers. Finally, the ball started rolling. “Over the following years we’ve seen an exponential growth in the number of studies,” says Jacka. Perhaps the best evidence came this year from the lab of Frank Hu at Harvard University, who directly traced the contributions of certain diet patterns with levels of cytokines, and depression; sure enough, foods rich in olive oil, leafy vegetables and wine reduced inflammation, and slashed the risk of depression by about 40%, compared to the ‘pro-inflammatory diet’, which includes sugary drinks, processed grains and red meat.
Getting well
Even your water supply might be having an impact, according to a recent study by Leigh Johnson at the University of North Texas Health Science Centre. She was recently studying the mental health of people in the western parts of the state – a rural population who still draw their drinking water directly from nearby wells. Crucially Johnson found that levels of the mineral selenium– an anti-oxidant that can combat inflammatory stress and which is also involved in brain signalling – in the well water had a direct impact on the chances of depression. People drawing water from wells with the highest levels of selenium, had about 17% lower scores on a standard measure of depression, compared to those in other areas. “That is very high,” says Maes. “It’s a really amazing result.”
As provocative as these findings are, the researchers will readily admit that there is still a long way to go before we can be sure of these conclusions. Eisenberger, for instance, acknowledges that certain foods can increase our inflammatory response, but she says it wouldn’t be as pronounced as the effects seen in her E. coli study. So it’s not clear that a poor diet would be enough to set you on the road to full-blown depression. And Johnson says that we should be careful not to over-generalise the results. “There are so many factors that can affect how depression could present itself in a patient,” she says. Your genes, lifestyle, and personal circumstances could all play a role. With so many different paths, it will be important to identify who would and wouldn’t benefit from better nutrition.
(SPL)
Some of these issues will be addressed in the next wave of studies. So far, the results have mostly come from observational studies watching people’s existing behaviour, but the researchers are now trying to actively change people’s diets in randomised trials, to see how it changes someone’s mental health. Success is by no means guaranteed; apparent correlations seen in observational studies can sometimes evaporate to thin air when you try more active measures to intervene in people’s lives – either because some other explanation lay behind the apparent effect, or because the interventions themselves are not practical. It is possible, for instance, that people at risk of depression may find it more difficult to change their eating habits, if they are already facing other stresses.
Surprise finding
Yet a chance finding by Charles Reynolds at the University of Pittsburgh offers some room for optimism. He had originally been testing a new form of psychotherapy in a group of older African Americans. “These people have a disproportionate burden of risk factors for depression,” he explains. Although they hadn’t been formally diagnosed with depression, his hope was that the therapy would offer some kind of protection against mental health problems in the future. As a comparison, half the group were given simple advice on how to eat more healthily – basic stuff on ways to eat delicious, nutritional meals on a low budget. Reynolds didn’t expect such a simple lifestyle change to heal his visitors’ minds – he just wanted to use it as a baseline, allowing him to measure the benefits of the ‘real’ therapy.
Two years later and it was clear that something very strange was going on. As expected, the people taking the psychotherapy had a reduced risk of developing depression; but so had the diet group, to an extraordinary degree; they were about half as likely to develop depression as you would expect for this kind of group, says Reynolds, and they reported a noticeable elevation in mood. “We were surprised, frankly,” says Reynolds. Importantly, these improvements came from minimal contact with the subjects – around 10 hour-long sessions across the two years. “That’s a remarkably short period of time to get the magnitude of effect that we saw.” His results were recently published in the American Journal of Psychiatry.
In line with Eisenberger’s earlier reservations, Reynolds points out that there are many reasons why the change in diet could have been so successful – and the potential anti-inflammatory effects are only one. Preparing more healthy meals is, in itself, a rewarding experience that boosts self-confidence, he says. “You might then believe that you can cope with other difficulties and respond adequately,” says Reynolds.
(Thinkstock)
Either way, the result has enthused Jacka about her own upcoming trial in Australia. Unlike Reynold’s study, she is trying to find out whether it can relieve the symptoms in those people already diagnosed with depression. Her subjects will have regular meetings with a dietician, who will advise them on the best ways to improve the nutritional value of their meals. Along the way, Jacka is taking blood tests to see if she can forge a more concrete link between components of the diet, levels of inflammation and oxidative stress, and the volunteers’ ongoing symptoms. If the visits to the dietician have a big enough effect on their recovery rate, she thinks it might then be possible to try out a dietary change as a treatment in its own right.
Reynolds points out that this kind of approach may appeal to people who feel uncomfortable with seeking other kinds of treatment. “Lifestyle changes may be more acceptable because they aren’t burdened by stigma – and they aren’t as expensive,” he says. Hu agrees that it holds a lot of promise: “Improving diet quality could not only reduce depression, but also the overall quality of life.”
For Jacka, a break in our love affair with fast food can’t come quickly enough. According to some predictions, nearly half of all Americans will be obese by 2030 – with countries across the world following similar trends. “If we add depression to the burden of illness that results from unhealthy diet,” she says, “no country can afford the cost.”
Initial human testing of an investigational vaccine to prevent Ebola virus disease will begin next week by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
The early-stage trial will begin initial human testing of a vaccine co-developed by NIAID and GlaxoSmithKline (GSK) and will evaluate the experimental vaccine’s safety and ability to generate an immune system response in healthy adults. Testing will take place at the NIH Clinical Center in Bethesda, Maryland.
The study is the first of several Phase 1 clinical trials that will examine the investigational NIAID/GSK Ebola vaccine and an experimental Ebola vaccine developed by the Public Health Agency of Canada and licensed to NewLink Genetics Corp. The others are to launch in the fall. These trials are conducted in healthy adults who are not infected with Ebola virus to determine if the vaccine is safe and induces an adequate immune response.
In parallel, NIH has partnered with a British-based international consortium that includes the Wellcome Trust and Britain’s Medical Research Council and Department for International Development to test the NIAID/GSK vaccine candidate among healthy volunteers in the United Kingdom and in the West African countries of Gambia (after approval from the relevant authorities) and Mali.
Additionally, the U.S. Centers for Disease Control and Prevention has initiated discussions with Ministry of Health officials in Nigeria about the prospects for conducting a Phase 1 safety study of the vaccine among healthy adults in that country.
The pace of human safety testing for experimental Ebola vaccines has been expedited in response to the ongoing Ebola virus outbreak in West Africa. According to the World Health Organization (WHO), more than 1,400 suspected and confirmed deaths from Ebola infection have been reported in Guinea, Liberia, Nigeria, and Sierra Leone since the outbreak was first reported in March 2014.
“There is an urgent need for a protective Ebola vaccine, and it is important to establish that a vaccine is safe and spurs the immune system to react in a way necessary to protect against infection,” said NIAID Director Anthony S. Fauci, M.D. “The NIH is playing a key role in accelerating the development and testing of investigational Ebola vaccines.”
“Today we know the best way to prevent the spread of Ebola infection is through public health measures, including good infection control practices, isolation, contact tracing, quarantine, and provision of personal protective equipment,” added Dr. Fauci. “However, a vaccine will ultimately be an important tool in the prevention effort. The launch of Phase 1 Ebola vaccine studies is the first step in a long process.”
“Tried and true public health interventions, strong supportive medical care and the rapid testing of Ebola vaccines and antiviral treatments can help to reduce suffering now and in the future,” said CDC Director Thomas R. Frieden, M.D., M.P.H.
The investigational vaccine now entering Phase 1 trials was designed by Nancy J. Sullivan, Ph.D., chief of the Biodefense Research Section in NIAID’s Vaccine Research Center (VRC). She worked in collaboration with researchers at the VRC, the U.S. Army Medical Research Institute of Infectious Diseases, and Okairos, a Swiss-Italian biotechnology company acquired by GSK in 2013.
Phase 1 clinical trials are the first step in what is typically a multi-stage clinical trials process). During Phase 1 studies, researchers test an investigational vaccine in a small group of people to evaluate its safety and the immune response it provokes. Phase 2 clinical trials of investigational vaccines are designed to further assess safety and immune response in larger numbers of volunteers. Under certain circumstances, the vaccine’s ability to prevent infection or disease (called efficacy) can be determined in a Phase 2 trial. Phase 3 clinical trials are directed predominantly at determining efficacy.
The NIAID/GSK Ebola vaccine candidate is based on a type of chimpanzee cold virus, called chimp adenovirus type 3 (ChAd3). The adenovirus is used as a carrier, or vector, to deliver segments of genetic material derived from two Ebola virus species: Zaire Ebola and Sudan Ebola. Hence, this vaccine is referred to as a bivalent vaccine. The Zaire species of the virus is responsible for the current Ebola outbreak in West Africa.
The vaccine candidate delivers one part of Ebola’s genetic material to human cells, but the adenovirus vector does not replicate. Rather, the Ebola gene that it carries allows the cells of the vaccine recipient to express a single Ebola protein, and that protein prompts an immune response in the individual. It is important to know that the Ebola genetic material contained in the investigational vaccine cannot cause a vaccinated individual to become infected with Ebola.
“The experimental NIAID/GSK vaccine performed extremely well in protecting nonhuman primates from Ebola infection,” Dr. Fauci noted.
The candidate vaccine builds upon three earlier NIAID-developed investigational Ebola vaccines that began Phase 1 clinical trial testing in 2003.
“The knowledge gained from each of those trials has contributed to the development of the candidate vaccine we are now studying, as well as our improved understanding of human immune responses to investigational Ebola vaccines,” said John R. Mascola, M.D., director of NIAID’s Vaccine Research Center.
The Phase 1 clinical trial, called VRC 207, will be led by principal investigator Julie E. Ledgerwood, D.O., chief of the VRC’s clinical trials program, and will be conducted among 20 healthy adults ages 18 to 50 years. Participants will be divided into two groups of 10 participants each. One group will receive an intramuscular injection of the NIAID/GSK experimental vaccine. The second group will receive a single injection of the same vaccine but at a higher dose.
A number of safety features are built into the study’s design, including daily and weekly reviews of patient data by clinical staff and the study protocol team. Additionally, the trial features a staged enrollment plan that requires interim safety reviews after three participants have been vaccinated and have undergone three days of follow up before enrolling additional study participants into the group. Participants in both groups will be seen and evaluated by clinical staff nine times over a 48-week period.
Additional Phase 1 Tests of the NIAID/GSK Vaccine
As part of the VRC 207 trial, NIAID will also test a version of the NIAID/GSK vaccine that contains genetic material from only the Zaire Ebola species. Hence, this vaccine is referred to as a monovalent vaccine. This portion of the Phase 1 safety study, which will also involve 20 healthy adults, is expected to begin in October at the NIH Clinical Center and potentially another U.S. location. Dr. Ledgerwood will also lead that effort. The VRC 207 clinical trial is being conducted based on expedited review and approval by the U.S. Food and Drug Administration.
In parallel, NIH has partnered with an international consortium that includes the British-based Wellcome Trust, as well as Britain’s Medical Research Council and Department for International Development to test the same NIAID/GSK monovalent vaccine candidate. The vaccine candidate will be tested among 60 healthy volunteers at the University of Oxford in England and among 40 healthy volunteers in Mali by the University of Maryland School of Medicine Center for Vaccine Development and its Center for Vaccine Development in Mali (a joint enterprise of the University of Maryland School of Medicine and the Ministry of Health of Mali). Additionally, the vaccine candidate is expected to be tested among 40 healthy volunteers in Gambia after approval from the relevant authorities.
The Oxford trial is expected to launch in mid-September pending ethical and regulatory approval.
“Today’s announcement shows how private and public partners can pull together to quickly respond to this critical public health emergency. Developing a new vaccine is complex with no guarantees of success, and we are still in the early days for our Ebola vaccine candidate. But we are encouraged by progress so far and will do the best we can, along with WHO and our partners, to speed up development and explore ways in which the vaccine could contribute to this or future Ebola outbreaks,” said Dr. Moncef Slaoui, chairman of Global R&D and Vaccines at GSK.
Initial safety and immunogenicity data from the Phase 1 trials of the NIAID/GSK investigational Ebola vaccine are expected in late 2014.
The NIH will also collaborate with the U.S. Department of Defense in support of efforts by NewLink Genetics Corp., a biopharmaceutical company in Ames, Iowa, to conduct Phase 1 safety studies of the investigational recombinant vesicular stomatitis virus Ebola vaccine (called VSV-EBOV) developed by and licensed from the Public Health Agency of Canada. Those clinical trials are expected to begin in the fall at the Clinical Trials Center of Walter Reed Army Institute of Research in Silver Spring, Maryland.
ARYAN'S BLOG 