In 1992 , a long-time heroin addict, shot up. Only this time was different: she had been clean for a month and her body couldn’t handle the opiate surge. The overdose would have killed her, she says, had she not been brought back from the dead by a drug that researchers call miraculous, but that the public largely hasn’t heard of. With overdose deaths on the rise, campaigners are calling for it to be supplied more widely as a potential lifesaver.

Naloxone, sold under various trade names including Narcan, could prove to be a game changer in stemming an alarming rise in deaths from prescription opiates and heroin in the US and the UK. Naloxone has long been stocked in ambulances and emergency rooms in both countries, but making it available to those who often are first on the scene of an overdose – the police and the drug-taker’s friends and family – is proving controversial. Some argue having such a “safety net” could make drug users more reckless, and some efforts to pass laws to distribute naloxone more widely have stalled.

One such opponent is Paul LePage, the governor of Maine. In June last year he that would have expanded access to naloxone in the state, justifying his stance on the grounds that the drug “would make it easier for those with substance abuse problems to push themselves to the edge, or beyond”.

Worst “flu” ever

Addiction researcher of Boston University says this argument does not tally with reality. Given via injection or nasal spray, naloxone binds powerfully with opiate receptors in the brain, repelling the drugs the user has taken and sending him or her into an instant and painful withdrawal. He says it’s akin to “the worst flu of one’s life”, accompanied by sweats and chills, vomiting and aches. Helton, who has not taken heroin for 16 years, agrees.

“A person who has received naloxone never wants to have that experience again,” she says. “You could go up to an addict overdosing on the street and say you’ll give them naloxone, and they’ll try to get up and walk away.”

With deaths due to prescription opiates and heroin overdoses skyrocketing – the US figure has quadrupled since 1999, to – legislators are taking heed. Seventeen US states already have laws expanding naloxone access to loved ones and first responders. And last month both Ohio and Wisconsin state legislatures passed similar bills that are now waiting to be signed into law. In the UK, naloxone has since 2005 been on a list of injection drugs that the general public can administer for lifesaving purposes.

What’s missing, says , an addiction researcher at King’s College London, is solid science to back up anecdotal findings and policy decisions. Strang is leading a massive study, called , that will be the largest ever to test if take-home naloxone can effectively prevent overdose deaths.

Prisoner trials

“One in 200 people coming out of prison with a history of heroin use are dead within a month,” Strang says. The overdose risk spikes more than sevenfold during that month-long window, he explains, because users who may once have become numbed to opiates regain their sensitivity while clean in jail. He has partnered with 16 prisons in the UK, and hopes to recruit 56,000 prisoners over five years into the trial.

Half of the prisoners, selected at random, will continue to be given standard prison pamphlets that explain the risk of post-release overdose. The other half will be given an “emergency kit” that includes a single dose naloxone-loaded syringe and a training DVD to watch with loved ones. Twelve weeks after release, researchers will cross-check reported overdose deaths with the identities of trial participants.

So far, the team has recruited 1000 prisoners into their pilot study, which will report preliminary results once the 5600 subjects have gone through the program.

If smaller studies are anything to go by, Strang has good reason to be optimistic. In 2003, the San Francisco Department of Health tried distributing naloxone to drug users and their loved ones through needle exchange programs. Heroin overdose deaths dropped from roughly 160 a year to 70 and has hovered in the single digits since 2009, says , who directs the city’s substance abuse research program. And in the Boston suburb of Quincy, where the police have carried naloxone nasal sprays for three years, Lieutenant Detective Patrick Glynn says officers have reversed the effects of every one of 226 heroin overdoses they encountered.

Our newest weapon against Lyme disease might be a vaccine – for mice.

Every year in the US, 300,000 people are diagnosed with the tick-borne illness caused by Borrelia bacteria, which can trigger arthritis and neurological problems. A vaccine was developed in 1998 that triggers immunity to Borrelia burgdorferi, but side effects in humans meant it was pulled from the market in 2002.

Rather than abandon the vaccine, of the University of Tennessee in Memphis wondered if it could still work if it was just given to mice, a major reservoir of B. burgdorferi. Her idea was that ticks sucking the blood of vaccinated mice would ingest antibodies made by the mice. This would kill any bacteria the ticks carried and prevent them from transmitting the disease.

Gomes-Solecki and her team developed an oral vaccine that could be mixed into an oatmeal pellet. They baited four football-pitch-sized plots of grassland with vaccine pellets and three with sham pellets. The number of infected ticks found in the vaccine-treated plots decreased with time; the plot treated for 5 years saw a 76 per cent drop. Plots receiving no vaccine saw no decline.

Gomes-Solecki has co-founded a company called in Memphis, Tennessee, to market the mouse vaccine and is now seeking approval from the US Department of Agriculture to market the vaccine pellets. She says they could be sold to homeowners along with “drive through” traps small enough that rodents, but not other larger animals, could enter, eat the bait, and return to the environment.

“Host target is a good concept, but it is difficult to achieve,” says at the University of Rhode Island Tick Encounter Resource Center.

Mather developed a similar “drive through” trap in 1987 called Damminix, which allows mice to disperse cotton balls treated with tick insecticide to their nests.

Gomes-Solecki’s vaccine wouldn’t address the spread of other tick-borne pathogens, nor target other animals such as deer or skunks that act as reservoirs for Lyme disease.

Gomes-Solecki concedes that a vaccine that could target several reservoirs of the parasite would be ideal. “You can’t realistically wipe out all mice or ticks, but this does reduce the parasite without harming the ecosystem balance,” she says.

And it could add another tool in a wide variety of strategies to ward off tick-borne illnesses, says Mather. “It’s just one bullet in the gun.”

Journal reference:

Our race radar isn’t fixed. People subconsciously identify others more strongly by how they work together than by their skin colour.

The mind evolved to recognise racial categories because historically they predicted social alliances, says , a psychologist at Yale University. Having a common enemy is one way to dilute social boundaries, but does the unifying factor have to be antagonistic?

To find out, David Pietraszewski and colleagues at the University of California Santa Barbara introduced 1272 people to life-like avatars that worked for one of two charities – one built homes for the poor, and one provided medical care abroad. Each charity had two white and two black avatars of the same gender.

The participants were first given 24 statements about charity work, each accompanied by the face of one of the eight avatars. Some statements contained a hint about their avatar’s affiliation, whereas others were general. Next, the participants were shown just the statements and were asked to match them to the correct avatar.

Spot the error

In studying the errors made, the team could tell if people tended to confuse the correct avatar with someone of the same race, or with someone who volunteered in the same charity.

When all eight avatars were male, the tendency to confuse an avatar with someone of the same race dropped by half when the statements contained clues to their charity affiliation, compared to when they were general. When the eight avatars were female, the tendency to confuse them by race dropped to zero. The team accounted for those cases where the participants’ confused two avatars of the same race within the same charity.

The results imply the participants categorised the avatars by the charity they worked for rather than their race, says Pietraszewski. “We found that people could abandon categorising people by race and instead categorise them based on their cooperative social relationships with others.”

“It suggests that race is not a built-in, unchangeable feature of the mind,” he says, although he admits the difference between male and female avatars isn’t well understood.

“This study confirms that at least one aspect of racism and ethnocentrism – namely treating all members of a group alike – is not driven up and down by a common enemy, but depends merely on signs that the members of each group cooperate with one another on goals that differ from those of another group,” says , a cognitive psychologist at Harvard University. He adds that so long as people are cooperating on a goal, even if it’s not defence against an enemy, they can be psychologically united into a single group.

Journal reference: PLoS One,

of University College London and colleagues have pinpointed the impacts of historical migrations and invasions on our DNA. As well as identifying the imprint of well-known mixing episodes like the Arab slave trade, they have found clues to unknown mixing events, including people who may be the descendants of Alexander the Great’s army.

If history records that groups of people once met and interbred, geneticists can use the DNA of modern peoples to work out when it most likely happened or which populations are descended from that event. But the methods used are flawed, Hellenthal says, because they rely on historical records that are often incomplete.

Now Hellenthal has developed a genetic technique that independently identifies the date of interbreeding and the groups involved. “We’ve tried to develop an objective means of reading DNA without having any sort of historical preconceptions,” Hellenthal says.

Hellenthal combed the DNA sequences of 1490 people from 95 groups living in different parts of the world. He then identified how much DNA the people of any one group had in common with members of any other group. The more chunks of DNA two populations shared, the more closely related they are – while the longer those shared chunks were, the more recently the ancestors of those populations had interbred.

Genetic signature

The genetics confirms claims by other researchers that the raping and pillaging committed by Genghis Khan and his Mongol army had a genetic impact across Asia. Bits of Mongolian DNA are shared by six populations from north-east Asia to as far west as Turkey. They acquired these genes between 1250 and 1300, when the Mongol empire had conquered most of Asia and was encroaching on Europe.

The Arab slave trade, which operated between 650 and 1900, also left a signature in the genes of 17 groups living in north Africa, the Mediterranean and the Persian Gulf. All carry genes from enslaved populations from sub-Saharan Africa. What’s more, the Mediterranean groups share more DNA with people from west Africa, while the Persian Gulf groups share more with people from the east. This matches what historians suspect were the main routes used by the slave trade.

Some genetic mixing events were more mysterious. The researchers found a genetic signal in the Tu people of modern China that seems to have begun around 1200 and to have come from a European population similar to modern Greeks. That could have been the result of Western merchants travelling the Silk Road, Hellenthal says.

The oldest mixing event the team found came from the Kalash, who live in the mountains of north-west Pakistan. Around 200 BC, they seem to have mixed with an as-yet unknown population, which was most similar to people from north-west Europe and west Asia. That gives a little credence to the Kalash’s long-cherished belief that they are . “The DNA signal and date would not refute the idea, though there are of course other possibilities,” Hellenthal says.

Journal reference:

Video: Flashes of life

Palm readers beware: biologists have found a way to accurately predict lifespan – at least in worms.

at the National Institute of Biological Sciences in Beijing, China, and her colleagues added proteins to nematode worms that fluoresce when they detect damaging free radical molecules in their mitochondria.

Mitochondria generate a cell’s energy. It’s long been thought that an accumulation of free radicals, produced when cells metabolise, drives the ageing process by damaging DNA and proteins. Mitochondria are particularly at risk because they produce free radicals in large quantities but lack the DNA repair mechanisms found in other parts of the cell.

Dong’s team found that the number of “mitoflashes”, caused by the presence of free radicals, emitted when a nematode was three days old could predict its lifespan. Worms typically live for 21 days and are at their peak of reproductive fitness at 3 days old. Those with low mitoflash activity at that time lived longer, while those with high mitoflash activity died before day 21.

The next step was to test how well their mitochondrial clock took genetic and environmental factors that alter lifespan into account.

Mitochondrial clock

Worms carrying a genetic mutation known to extend life to 39 days exhibited fewer mitoflash bursts than genetically healthy worms, and free radical production peaked later in their lifespan. Conversely, worms with a life-shortening mutation exhibited much higher than average mitoflash frequency which peaked earlier.

The same pattern was seen when the team exposed the worms to short periods of starvation and heat shock, environmental stresses that counter-intuitively increase lifespan, and to a toxic herbicide known to shorten lifespan.

“The finding that mitoflash frequency in early adulthood predicts lifespan corresponds well with our earlier observations that some early-life events and conditions could be good longevity predictors,” says of the University of Chicago, who researches ageing in humans.

Dong hopes that her team’s technique – the first non-invasive, lifespan predictor for live animals – will encourage others to explore whether the link between high free radical production in the mitochondria and accelerated ageing holds true in other animals.

It might eventually help clinical researchers investigate energy production in human cells from people with mitochondrial disorders, she says.

Journal reference: Nature, DOI:

The three blind mice should have kept on running. Physical activity can help ward off age-related blindness, suggests a study in mice.

is one of the leading causes of blindness in the elderly, and affects about 30 million people worldwide. Eyesight deteriorates due to the death of light-detecting cells in the eye, called photoreceptors.

and her colleagues at Emory University in Atlanta, Georgia, have now demonstrated for the first time that exercise protects the retina from the degeneration that causes this loss of sight.

Exercise has already been shown to help reduce the risk of dementia and Alzheimer’s disease, and has helped with the recovery of people with traumatic brain injuries or stroke. To explore whether exercise might also help with retinal diseases, Pardue and her team designed a month-long exercise regimen for mice.

One group was made to walk on tiny treadmills for an hour a day, five days a week for a month. Two weeks into this regimen, the team exposed the mice to harmfully bright light for 4 hours. This is a common way to artificially induce the degeneration of photoreceptors.

While this first group of mice exercised for a month, a second group remained inactive. These sedentary mice were kept in cages with stationary treadmills – to make sure they had the same visual stimuli in their habitats. Two weeks into the experiment, this group was also exposed to 4 hours of the bright light.

Twice as good

At the month’s end, Pardue and her team compared the retinal function and photoreceptor counts of the two groups. Neural firing in the retinas of the mice that exercised was twice the strength as the inactive group, showing that their eyes were functioning better. Dissections also showed that the exercised mice kept roughly twice the number of healthy photoreceptors as inactive mice.

Pardue thinks the benefits could be down to a protein called BDNF which is important in keeping neurons healthy. BDNF is produced during physical activity in both mice and humans.

At the end of the experiment, mice that had worked out had 20 per cent more of the protein in their retinas compared with the inactive mice.

When a subgroup of exercising mice was injected after each run with a protein that prevents BDNF from acting on neurons, the protective effect of the workouts seemed to disappear. These active mice showed the same reduced retinal function and low photoreceptor counts as the no-exercise mice.

Pardue hopes that these initial findings will lead the way to human clinical trials testing the benefits of exercise on retinal health.

at the Memorial University of Newfoundland in St John’s, Canada, who was not involved in the research, says she is hopeful that exercise might be a simple and effective way to slow macular degeneration, which is often treated with drugs or surgery.

Journal ref: Journal of Neuroscience, DOI: 10.1523/JNEUROSCI.2062-13.2014

Starfish, also known as sea stars, are under attack up and down the US Pacific coastline. The perpetrator isn’t a predator, but a mysterious and grisly disease known as sea star wasting syndrome that is ripping them apart from the inside. Here’s what you need to know – and what you can do to help.

What is sea star wasting syndrome?
It is the name for the mysterious illness that riddles starfish with ulcers and causes their arms to twist and even “crawl” away from their bodies until they tear off. It leaves their innards behind in a mush. Hundreds of thousands of stars, if not more, have already perished from the syndrome since divers and aquarium-goers on the US west coast spotted the disease last June.

What could make this happen to starfish?
Tissue decay and fragmentation are general indicators that a starfish is unhealthy. This “wasting” can be associated with all kinds of environmental stresses, such as unseasonably warm water currents – which were associated with smaller die-offs in southern California in 1983 and 1997. But major wasting events can also have a pathogenic cause such as a virus, bacteria or parasite.

So what is the cause behind the wasting?
The culprit in this die-off, the largest and most devastating in recent memory, is still unknown. Many guess that there is a pathogen that impairs starfish immune systems, making them susceptible to wasting by secondary bacterial infections.

Does that mean the disease is catching?
Evidence suggests that the disease is transmissible from star to star through water, if not also by contact – although it does not seem to affect other animals such as the closely related sea urchin. The pathogen might have existed in Pacific waters for a long time, but only turned deadly last year. Or it could be an exotic threat, carried to the region by ocean currents, ballast water from travelling ships, or material dumped in a harbour.

Which species are affected?
Twelve species including the ochre star (Pisaster ochraceus), mottled star (Evasterias troscheli), six-armed star (Leptasterias aequalis), and leather star (Dermasterias imbricata), have been hit – although the range and severity of symptoms differs among them. One of the most sensitive species is the sunflower star (Pycnopodia helianthoides), which can reach up to a metre in diameter. It can die of the disease within 24 hours of the first signs of infection.

How widespread is the disease?
Sick sea stars have been , with hardest-hit areas including the Puget Sound in Washington state, and California’s Monterey Bay. There was also a smaller and more isolated outbreak of wasting disease off the coast of Rhode Island and Maine on the US east coast, but scientists are not sure if the two incidents are linked.

What are the broader ecological impacts of a sea star die off?
Starfish are known as in marine ecosystems because of their potential to dramatically alter the intertidal communities they inhabit. They eat huge numbers of mussels and clams that would otherwise overrun the kelp forests that are home to an array of smaller marine organisms.

Is this connected to any of the other problems hitting US marine life at the moment?
It is unknown if the syndrome is related to a recent shrimp die-off in Maine and a viral outbreak in Atlantic bottlenose dolphins.

When will we know what is killing the starfish?
Marine biologists have begun to investigate the disease. and at Cornell University in Ithaca, New York, are working to identify the pathogenic cause by compiling genetic sequencing data of bacteria and viruses found on sick stars.

of Western Washington University in Bellingham is performing transmission experiments – such as placing sick and healthy starfish in shared tanks and in separate tanks with shared water. and his team at University of California, Santa Cruz, are mapping outbreaks up and down the coast to determine if there are single or multiple origins of infection.

What can I do?
If you are in the affected areas, you can submit photos of disease sightings to websites such and .

Defying years of shrinking habitat and disappearing roosts, bats are making a comeback in Europe.

Bat numbers – collected from 6000 hibernation sites in nine European countries – have increased by 43 per cent between 1993 and 2011, according to a (EEA). The study, which tracks 16 of Europe’s 45 bat species, is the most comprehensive population study of bats on the continent to date.

“This trend is a definite sign of hope,” says , director of science at the British Bat Conservation Trust, a partner in the study.

Armed with a statistical method that proved key in earlier EEA studies of and bird population trends, Haysom and her collaborators input decades of national bat data into a dataset that revealed how bat numbers changed from winter to winter according to species and region. Never before had such data – reported by scientists and also by thousands of amateur bat enthusiasts, who counted hibernating animals in local caves and other roosts – been consolidated over such a broad time span and geography, Haysom says.

“This is giving us a chance to put our numbers in a different and very valuable context, and think about why some bat species are doing well in some countries compared with others,” she says. Population trends were calculated in Latvia, Hungary, The Netherlands, Austria, Portugal, Slovenia, Slovakia, Germany and the UK.

The bat-phone

In the second half of the 20th century, European bat populations plummeted due to increased agriculture, intentional killing, destruction of roosts and exposure to roofs treated with a pest-repellent called dieldrin. The decline was further fuelled by bats’ naturally long lifespan and slow reproduction rate, Haysom says.

But recent conservation efforts including cave protection, bat-friendly farming practices, local bat-assistance hotlines – bat-phones, if you will – and educational campaigns like local “bat walks” may have helped turn the tide.

The EEA team found that nine bat species, including Daubenton’s bat () and the Mediterranean horseshoe bat () have increased, while several others held stable.

Citizen science

“Though the report is heartening, the job is certainly not done,” Haysom says. For instance, the grey long-eared bat () showed a continent-wide decline.

Bat specialist of the International Union for Conservation of Nature says the project demonstrates the power of citizen science in animal conservation efforts.

“To count butterflies or birds on a nice summer’s day is one thing, but counting bats hibernating in dark, damp, cold places – that’s a totally different ball game,” he says. “And yet, amazingly, thousands of volunteers and thousands of sites in Europe were committed to the work.”

We’ve been given the first glimpse of HIV in attack mode in the gut, shedding light on how the virus hijacks immune cells, multiplies and spreads throughout the body.

A team of biochemists have used electron tomography microscopes to capture the first high-resolution, 3D images of the HIV virus lurking in the intestines of “humanised” mice, whose immune systems are made up largely of human cells.

“This is the next step in studying how the virus interacts with immune cells in its natural environment, not in a Petri dish” says Mark Ladinsky, part of the team at the California Institute of Technology that carried out the work.

Although it was known that HIV hides out in the gut, Ladinsky says no one had expected to find such large pools of circulating virus.

In this video reconstruction, the team presents a sequence of intestinal cross-sections just 0.9 nanometres thick taken from a deep region of intestinal tissue that houses immune cells. These are called intestinal crypts, after their pocket-like shape.

The microscopic images are laid on top of one another to give the viewer a “zoom through” look at spherical particles of HIV virus (labelled in blue) within a small tissue volume.

Two immune cells called CD4 T-cells that have been infected with HIV lie side by side, taking up most of the frame. The HIV has commandeered the immune cells and new viruses bud from the cell surfaces to join a pool of more than 300 free, mature HIV particles circulating in the space between the cells.

In the second part of the clip, the gut tissue disappears to show only the pool of virus, which is rotated in 3D to demonstrate the spread of HIV within the intestinal crypt.

HIV house

Studying the large pools of virus in these crypts is crucial to understanding HIV’s rapid spread, Ladinsky says. The intestinal tissue, which houses 70 per cent of the body’s immune cells, is one of the first regions that HIV attacks. Within the first month of infection, the virus can ravage more than 50 per cent of the intestinal tissue’s CD4 T-cells.

The high concentration of virus in the crypts, Ladinsky says, may help to explain the rapid immune cell destruction they cause. The crypts are a reservoir for HIV in people with the virus, he says, allowing the virus to avoid any antiretroviral drugs circulating in the blood. This makes the tissue an important focus for researchers developing therapies to flush out the virus.

Wes Sundquist, a biochemist at the University of Utah in Salt Lake City, says the study is a technical feat. Producing an image with a fine-enough resolution to see an object as small as an HIV virus is notoriously difficult to achieve for delicate tissue samples, he says.

“The next step is to try and image what HIV virus looks like in the intestines of human patients, especially in those who are taking antiretroviral drugs and those who can control it on their own,” he says.

Journal reference: PLoS Pathogens,

The discovery was a happy accident. It turns out that an injection of microscopic tags made of a plastic-like polymer can help limit tissue damage after a heart attack in mice. The hope is that it could one day help treat this and other conditions in humans.

The hunt to find a therapy that shuts down inflammatory monocytes – a kind of immune cell that can damage the body after a heart attack and in other illnesses – has been long and elusive, says Stephen Miller at Northwestern University in Illinois.

He and his team have found a way to use microparticles made of the biodegradable polymer PLGA to tag these monocytes in mice. This triggered the monocytes to move away from inflamed sites to the spleen, where they are destroyed. It seems other immune cells are left unscathed.

One existing use for the microparticles, which are just 1/200th the width of a hair, is for laboratory imaging, to label and trace cells. ‘Daniel Getts was using them in this way to study how inflammatory monocytes travelled from the bloodstream to the brain of mice with West Nile virus, where they damage tissue.

Lucky mistake

By mistake, one batch of microparticles became negatively charged. Instead of seeing the majority of his infected mice die from brain inflammation, as expected, Getts found that monocytes had bound themselves to his charged microparticles and moved into the spleen.

“It was a total accident that we discovered this,” says Getts. He found that 60 per cent of the infected mice survived.

The negatively-charged microparticles had bound to a receptor protein on the surface of inflammatory monocytes called “MARCO.” This protein usually detects and sticks to negatively charged regions on pathogens, dying cells and other debris in the blood. Binding this particular receptor, the researchers suspect, signals the monocyte to go to the spleen, where cargo and cell are destroyed.

Getts says it was a natural move to try tagging monocytes in this way in diseases in which they damage tissue.

Innovative approach

Controlling inflammation after a heart attack was a priority. During the first couple of days after an attack, monocytes can target oxygen-deprived heart muscle, damaging it further. Mice injected with microparticles 12 hours after an attack had heart lesions half the size of those who did not receive therapy. The hearts of treated mice also pumped better.

The microparticles helped reduced spinal inflammation in mice with a disease similar to human multiple sclerosis, making their paralysis less severe. Those with irritable bowel syndrome similarly showed reduced inflammation of the intestinal lining. And those with kidney injuries had signs of better organ function, suggesting the tags might be effective after organ transplants.

Miller says the team hopes to begin human clinical trials to test the therapy for heart attack this year.

“The approach is innovative,” says Nick Giannoukakis, a pathologist at the University of Pittsburgh Medical Center in Pennsylvania. But he adds that a better understanding of events after MARCO binding would be helpful.

Journal reference: