# MIT develops algorithm that removes unwanted reflections from photos

If you’ve ever taken a photo from behind a window, you know you’re just as likely to get a good shot of yourself reflected in the glass as you are of what’s on the other side. Researchers from MIT have developed a process that could one day extract your reflection from such pictures, leaving only the intended subject on the other side of the glass.

This process actually relies upon the most severe sort of reflections as those are easier to pick out. Specifically, anything taken through double pane glass or very thick glass tends to have two overlapping reflections, one from the inner surface and one from the outer one. If you only have one reflection, it’s a very computationally complex problem for an algorithm to figure out what’s a reflection and what isn’t. With two identical offset images that are reflections, suddenly the computer has a point of reference.

The system created by the MIT team relies on finding the edges of the reflection by looking for a repeating offset pattern. The image is split into 8×8 blocks of pixels and calculates the correlation between the pixels. When the parts of the image comprising the reflection have been identified, the computer can then selectively tune the levels to make the reflection less pronounced. You can see an example of the results in the image above. It’s far from perfect, but this is just the first iteration of the technology.

This process currently requires the offset of the double reflection to be rather large to ensure the algorithm can recognize them as distinct shapes, but things might improve in the future. The team sees possible applications for this technology in consumer imaging technologies. Your phone might just know how to reduce reflections when you snap a photo through the window. These algorithms could also be of use in improving computer vision. Despite all the research that has gone into it, computers are still pretty bad at making sense of an image.

# One billion smokers in the world now

## The study shows that almost 5% of the world’s adult population have an alcohol use disorder, around 20% smoke tobacco.

The study shows that almost 5 per cent of the world’s adult population (240 million people) have an alcohol use disorder and more than 20 per cent (1 billion people) smoke tobacco.

One billion people in the world smoke tobacco while 240 million have an alcohol use disorder, according to a new study that compiled the most up-to-date evidence on addictive disorders globally.

The study shows that almost 5 per cent of the world’s adult population (240 million people) have an alcohol use disorder and more than 20 per cent (1 billion people) smoke tobacco.

Getting good data on other drugs such as heroin and cannabis is much more difficult but for comparison the number of people injecting drugs is estimated at around 15 million worldwide, researchers said.

The “Global Statistics on Addictive Behaviours: 2014 Status Report” shows that the harm to society from legal drugs is many times the harm from illicit drugs.

“For example, alcohol use is estimated to result in loss of 257 disability adjusted life year per 100,000 of population compared with just 83 for illicit drugs,” researchers said.

There are huge regional differences in use of addictive drugs. The heaviest drinkers are in Eastern Europe where 13.6 litres of alcohol is consumed per head of population each year, followed by Northern Europe at 11.5 litres.

Central, Southern and Western Asia have the lowest consumption at 2.1 litres.

Eastern Europe also has the most smokers at 30.0 per cent of adults, closely followed by Oceania at 29.5 per cent and Western Europe at 28.5 per cent.

This compares with Africa at 14 per cent. North and Central America with the Caribbean have the highest rates of injecting drug use at 0.8 per cent, which is more than twice the rate in Northern Europe at 0.3 per cent.

The authors of the report note that there are important limitations to the data, more so for illicit than legal drugs, but believe that putting all this information in one place will make it easier for governments and international agencies to develop policies to combat this scourge.

“Bringing all this data together has been very challenging but having this global snapshot in one accessible resource should prove invaluable for policymakers and researchers,” said the report’s lead author, Associate Professor Linda Gowing, based at the University of Adelaide in South Australia.

“The most striking thing to emerge is how much more damage is done to society by legal drugs than illegal ones. It is a stark reminder of how the need to create shareholder value can work against global health and wellbeing,” said University College London Professor Robert West, an author of the report and Editor-in-Chief of the journal Addiction, which commissioned the report.

# Beekeepers see 42% of US honeybee colonies die off in a single year .

Summer deaths raise concern among entomologists as more than two in five colonies are lost: a ‘loud signal that there’s some bad things happening’

More than two out of five American honeybee colonies died in the past year, and surprisingly, the worst die-off was in the summer, according to a federal survey.

Since April 2014, beekeepers lost 42.1% of their colonies, the second-highest rate in nine years, according to an annual survey conducted by a bee partnership that includes the US Department of Agriculture.

“What we’re seeing with this bee problem is just a loud signal that there’s some bad things happening with our agro-ecosystems,” said study co-author Keith Delaplane at the University of Georgia. “We just happen to notice it with the honeybee because they are so easy to count.”

But it’s not quite as dire as it sounds. That’s because after a colony dies, beekeepers split their surviving colonies, start new ones, and the numbers go back up again, said Delaplane and study co-author Dennis vanEngelsdorp of the University of Maryland. But that pushes the bees to their limits, he said.

What shocked the entomologists is that this is the first time they have noticed bees dying more in the summer than the winter, vanEngelsdorp said. The survey found beekeepers lost 27.4% of their colonies this summer. That’s up from 19.8% the previous summer.

Seeing massive colony losses in summer is like seeing “a higher rate of flu deaths in the summer than winter,” vanEngelsdorp said. “You just don’t expect colonies to die at this rate in the summer.”

Oklahoma, Illinois, Iowa, Delaware, Maryland, Pennsylvania, Maine and Wisconsin all saw more than 60% of their hives die since April 2014, according to the survey.

“Most of the major commercial beekeepers get a dark panicked look in their eyes when they discuss these losses and what it means to their businesses,” said Pennsylvania State University entomology professor Diana Cox-Foster. She wasn’t part of the study, but praised it.

Delaplane and vanEngelsdorp said a combination of mites, poor nutrition and pesticides are to blame for the bee deaths.

Dick Rogers, chief beekeeper for pesticide maker Bayer, said the loss figure is “not unusual at all” and said the survey shows an end result of more colonies: 2.74 million hives in 2015, up from 2.64 million in 2014.

That does not mean bee health is improving or stable, vanEngelsdorp said.

# Epilepsy drug could help treat Alzheimer’s disease

University of British Columbia researchers say a new epilepsy drug holds promise as a treatment for Alzheimer’s disease.

The findings, published today in Alzheimer’s Research & Therapy, reinforce the theory that brain hyperexcitability plays an important role in Alzheimer’s disease, and that anticonvulsant drugs—drugs that prevent or reduce the severity of seizures—represent a promising treatment that deserve further human studies.

In previous studies, several groups have tested the effects of the widely used anticonvulsant drug levetiracetam in both rodent models as well as two clinical trials in patients with early signs of Alzheimer’s disease. The findings suggest it may slow some of the symptoms of the disease, including memory loss.

In this newest research, Dr. Haakon Nygaard, the Fipke Professor in Alzheimer’s Research in UBC’s Faculty of Medicine, tested the effects of brivaracetam, an anticonvulsant drug still in clinical development for epilepsy, and closely related to levetiracetam. Since it is 10 times more potent than levetiracetam, it can be used at lower dosages. Nygaard and his colleagues found that it completely reversed memory loss in a rodent model of Alzheimer’s disease.

While the drug appears effective, the researchers are unclear how it works to reverse memory loss. Nygaard also points out that the current study represents very preliminary data with respect to treating patients with Alzheimer’s disease.

“Now we have many different research groups using antiepileptic drugs that engage the same target, and all point to a therapeutic effect in both Alzheimer’s disease models, and patients with the disease,” said Nygaard, a researcher with the Djavad Mowafaghian Centre for Brain Health. “Both of these drugs are likely to be tested in larger clinical trials in Alzheimer’s disease over the next five to 10 years.”

“Larger clinical studies in human subjects will be needed before we can determine whether anticonvulsant therapy will be part of our future therapeutic arsenal against Alzheimer’s.”

Background

Alzheimer’s is the most common cause of dementia among older people. It slowly destroys memory and cognitive skills, and eventually the ability to carry out simple, daily tasks. In 2011, 747,000 Canadians were living with dementia, a number expected to rise to 1.4 million by 2031.

It’s been known for a few decades that patients with Alzheimer’s have an increased risk of seizures, especially in people with a family history of the disease. There is now a growing body of evidence that certain mechanisms related to how the brain is wired are shared between Alzheimer’s and epilepsy This led researchers to test anticonvulsant drugs as potential treatments for Alzheimer’s. While some drugs like levetiracetam and brivaracetam appear to work, others do not. In this study, Nygaard and his colleagues also tested the anticonvulsant ethosuximide but found that it was not effective in reversing symptoms in an Alzheimer’s model.

# Hello, Jurassic Park? Scientists create chickens with dinosaur features .

Scientists for the first time have created animals with dinosaur features using fossils as a guide. They have transformed chicken beaks into something similar to a dinosaur snout.

Many have pondered the idea of recreating dinosaurs while novelists and sci-fi film directors tempted our imagination with such as creations the Jurassic park film and novel series.

A research team led by Yale paleontologist and developmental biologist Bhart-Anjan S. Bhullar and Harvard developmental biologist Arhat Abzhanov, have conducted a successful experiment which allowed them to create chickens with dinosaur-like features. They published their discoveries in a study in the journal “Evolution” on Tuesday.

Researchers were able to transform chicken embryos in a laboratory into specimens with a snout and palate configuration similar to that of small dinosaurs such as Velociraptor and Archaeopteryx, according to a Yale press-release published on Tuesday.

“Our goal here was to understand the molecular underpinnings of an important evolutionary transition, not to create a ‘dino-chicken’ simply for the sake of it,” said Bhullar, lead author of the study.

Thought, the embryos were humanely euthanized after the experiment, Bhullar told MailOnline that in the future it may be possible to allow them to grow into animals with dinosaur features.

Why did scientists decide to transform the beak? According to them, it’s one of parts of avian anatomy that has not been changed much in the evolution process.

“The beak is a crucial part of the avian feeding apparatus, and is the component of the avian skeleton that has perhaps diversified most extensively and most radically – consider flamingos, parrots, hawks, pelicans, and hummingbirds, among others,” Bhullar said.

“Yet little work has been done on what exactly a beak is, anatomically, and how it got that way either evolutionarily or developmentally.”

The research team also found that major living lineages of birds have a unique, median gene expression zone of two different facial development genes early in embryonic development, which the non-beaked creatures lack. When they blocked this gene expression not only did the beak structure revert into a snout, but the process also caused the palatine bone on the roof of the mouth to go back to a dinosaur-like state.

“This was unexpected and demonstrates the way in which a single, simple developmental mechanism can have wide-ranging and unexpected effects,” Bhullar said.

In 2009 Jack Horner, a paleontologist at Montana State University, proposed in his book ways of“How to Build a Dinosaur” to reactivate the DNA found in chickens, dinosaur ancestors, to recreate a small predator. According to New York Times, he was very excited to know that this experiment succeeded calling it “fantastic”.

# Lily: the \$499 ‘selfie drone’ that’s your personal videographer

The device is capable of flying for 20 minutes, tracking its owner and shooting photos and video footage of them

“Camera. Reinvented.” claims the website for Lily, the latest consumer drone to capture people’s attention. Although “selfie drone” seems to be a more popular phrase among the media covering its launch.

Yes, in 2015 we have drones to take selfies for us, because maintaining the perfect duckface while tapping a touchscreen button are sorely testing humanity’s multi-tasking capabilities.

Actually, that’s a little unfair on Lily, which is an interesting spin on the drone formula. Its schtick is that owners will be able to throw it in the air then go about their business, while the device follows them shooting high-definition video and photographs.

Sadly (for potentially-amused bystanders) this doesn’t involve sprinting along the road in terror as a whirring hunk of metal zips towards your head like a modern, budget remake of North by Northwest.

Instead, Lily is pitched at skiers and snowboarders, athletes and other active types: a hovering alternative to strapping a GoPro camera to their helmets, with the benefit of shooting footage of them, rather than just a first-person viewpoint.

Lily can shoot 1080p HD video at 60 frames-per-second or 720p video at 120 frames-per-second for slow-motion action, as well as 12-megapixel still photographs.

It takes two hours to charge and can then stay in the air for 20 minutes before needing to be plugged in again. The device will fly a maximum of 15m and a minimum of 1.75m above its owner’s head, to avoid accidents, with an average speed of 15 miles per hour.

Those owners will wear a tracking device to ensure that Lily follows them, with the device hovering in place and trying to recover the signal if it loses the wearer, before landing “smoothly” – an action also taken if it runs out of battery.

The company was founded by a group of graduates from Berkeley University in California who’d been tinkering with robots. “Our passion for personal robotics led us to believe that there is a better way to capture and share the world around us,” explained chief executive Antoine Balaresque on Medium.

The company does not expect Lily to spark privacy arguments. “Lily is always pointing at you and less than 100ft from you. Also, Lily’s motors make noise,”explains its FAQ, in response to a question about spying on neighbours.

“So other people will most likely notice Lily and quickly figure out where you are. You are better off climbing up a tree and using binoculars.”

# Drug perks up old muscles and aging brains

Whether you’re brainy, brawny or both, you may someday benefit from a drug found to rejuvenate aging brain and muscle tissue.

Researchers at the University of California, Berkeley, have discovered that a small-molecule drug simultaneously perks up old in the brains and muscles of mice, a finding that could lead to drug interventions for humans that would make aging tissues throughout the body act young again.

“We established that you can use a single small molecule to rescue essential function in not only aged brain tissue but aged muscle,” said co-author David Schaffer, director of the Berkeley Stem Cell Center and a professor of chemical and biomolecular engineering. “That is good news, because if every tissue had a different molecular mechanism for aging, we wouldn’t be able to have a single intervention that rescues the function of multiple tissues.”

The drug interferes with the activity of a growth factor, transforming growth factor beta 1 (TGF-beta1), that Schaffer’s UC Berkeley colleague Irina Conboy showed over the past 10 years depresses the ability of various types of stem cells to renew tissue.

“Based on our earlier papers, the TGF-beta1 pathway seemed to be one of the main culprits in multi-tissue aging,” said Conboy, an associate professor of bioengineering. “That one protein, when upregulated, ages multiple stem cells in distinct organs, such as the brain, pancreas, heart and muscle. This is really the first demonstration that we can find a drug that makes the key TGF-beta1 pathway, which is elevated by aging, behave younger, thereby rejuvenating multiple organ systems.”

The UC Berkeley team reported its results in the current issue of the journal Oncotarget. Conboy and Schaffer are members of a consortium of faculty who study aging within the California Institute for Quantitative Biosciences (QB3).

Depressed stem cells lead to aging

Aging is ascribed, in part, to the failure of to generate replacements for damaged cells and thus repair the body’s tissues. Researchers have shown that this decreased stem cell activity is largely a result of inhibitory chemicals in the environment around the stem cell, some of them dumped there by the immune system as a result of chronic, low-level inflammation that is also a hallmark of aging.

In 2005, Conboy and her colleagues infused old mice with blood from young mice – a process called parabiosis – reinvigorating stem cells in the muscle, liver and brain/hippocampus and showing that the chemicals in young blood can actually rejuvenate the chemical environment of aging stem cells. Last year, doctors began a small trial to determine whether blood plasma from young people can help reverse brain damage in elderly Alzheimer’s patients.

Such therapies are impractical if not dangerous, however, so Conboy, Schaffer and others are trying to track down the specific chemicals that can be used safely and sustainably for maintaining the youthful environment for stem cells in many organs. One key chemical target for the multi-tissue rejuvenation is TGF-beta1, which tends to increase with age in all tissues of the body and which Conboy showed depresses stem cell activity when present at high levels.

Five years ago, Schaffer, who studies in the brain, teamed up with Conboy to look at TGF-beta1 activity in the hippocampus, an area of the brain important in memory and learning. Among the hallmarks of aging are a decline in learning, cognition and memory. In the new study, they showed that in old mice, the hippocampus has increased levels of TGF-beta1 similar to the levels in the bloodstream and other old tissue.

Using a viral vector that Schaffer developed for gene therapy, the team inserted genetic blockers into the brains of old mice to knock down TGF-beta1 activity, and found that hippocampal stem cells began to act more youthful, generating new nerve cells.

Drug makes old tissue cleverer

The team then injected into the blood a chemical known to block the TGF-beta1 receptor and thus reduce the effect of TGF-beta1. This small molecule, an Alk5 kinase inhibitor already undergoing trials as an anticancer agent, successfully renewed stem cell function in both brain and muscle tissue of the same old animal, potentially making it stronger and more clever, Conboy said.

“The key TGF-beta1 regulatory pathway became reset to its young signaling levels, which also reduced tissue inflammation, hence promoting a more favorable environment for stem cell signaling,” she said. “You can simultaneously improve tissue repair and maintenance repair in completely different organs, muscle and brain.”

The researchers noted that this is only a first step toward a therapy, since other biochemical cues also regulate adult stem cell activity. Schaffer and Conboy’s research groups are now collaborating on a multi-pronged approach in which modulation of two key biochemical regulators might lead to safe restoration of stem cell responses in multiple aged and pathological tissues.

“The challenge ahead is to carefully retune the various signaling pathways in the stem cell environment, using a small number of chemicals, so that we end up recalibrating the environment to be youth-like,” Conboy said. “Dosage is going to be the key to rejuvenating the stem cell environment.”

# Why Friendship Is Great For Your Brain: A Neuroscientist Explains

“When I am, as it were, completely myself, entirely alone, and of good cheer — say traveling in a carriage, or walking after a good meal, or during the night when I cannot sleep — it is on such  Read

Do you have 150 friends? Because that’s the average number of stable social relationships a person can maintain.

This number has been dubbed “Dunbar’s Number” after the scientist Robin Dunbar, who found an association between primate brain size and average social group size (and don’t forget, you’re a primate). Dunbar’s Number has been translated into the number of people you wouldn’t feel embarrassed inviting to join you for a coffee (or green juice) if you happened to bump into them in a cafe.

It’s a no-brainer that friendship is an essential ingredient in living a fulfilled life. But it turns out that neuroscience has some pretty compelling evidence for the power of friendship in maintaining brain health and well-being as we get older.

Neuroscience research shows that being socially connected protects the brain against the risk of developing dementia.

How does interacting with people make the brain resilient to aging?

Neuroscientists often talk about “cognitive reserve.” Cognitive reserve refers to how resilient the mind is to damage or decline of the brain. Think of it as a savings account for the functionality of our brain. It’s the ability to build up a resistance to mental decline and disease.

Having a healthy social life naturally involves thinking, feeling, sensing, reasoning and intuition. These mentally stimulating activities build up our reserve of healthy brain cells, and promote the formation of new connections, or synapses, between neurons.

Those good friends of yours are worth nurturing, because friends will help you live longer, too.

A meta-analysis of 148 studies, including 300,000 people studied over seven years, found that people with strong social relationships had an increased likelihood of survival (yep, they were less likely to die) than those with weaker social relationships.

Here’s how loneliness and lack of social connection compares to more well-known risk factors:

• Equivalent to smoking 15 cigarettes a day
• Equivalent to being an alcoholic
• More harmful than not exercising
• Twice as harmful as obesity

Brigham Young University Professor Julianne Holt-Lunstad, lead author on the study, says, “When someone is connected to a group and feels responsibility for other people, that sense of purpose and meaning translates to taking better care of themselves and taking fewer risks”

Another of the authors, Professor Timothy Smith, points out that modern conveniences and technology can lead some people to think that social networks aren’t necessary.

“We take relationships for granted as humans — we’re like fish that don’t notice the water,” Smith said. “That constant interaction is not only beneficial psychologically but directly to our physical health.”

# Psychiatric drugs do more harm than good, says expert

Peter Gøtzsche argues that most prescriptions could be stopped without causing harm, but other experts strongly disagree

Psychiatric drugs do more harm than good and the use of most antidepressants and dementia drugs could be virtually stopped without causing harm, an expert on clinical trials argues in a leading medical journal.

Given their lack of benefit, I estimate we could stop almost all psychotropic drugs without causing harm
Peter Gøtzsche
The views expressed in a British Medical Journal debate by Peter Gøtzsche, professor and director of the Nordic Cochrane Centre in Denmark, are strongly opposed by many experts in mental health. However, others say the debate around the use of psychiatric drugs is important and acknowledge that there has been overuse of antipsychotics to quieten aggressive patients with dementia.

Gøtzsche says more than half a million people over the age of 65 die as a result of the use of psychiatric drugs every year in the western world. “Their benefits would need to be colossal to justify this, but they are minimal,” he writes.

He claims that trials carried out with funding from drug companies into the efficacy of psychiatric drugs have almost all been biased, because the patients involved have usually been on other medication first. They stop their drugs and often experience a withdrawal phase prior to starting the trial drug, which then appears to have a big benefit. He also claims that deaths from suicide in clinical trials are under-reported.

In trials of the modern antidepressants fluoxetine and venlafaxine, says Gøtzsche, it takes only a few extra days for depression in the placebo group – given dummy pills – to lift as much as in the group given the drugs. He argues that there is spontaneous remission of the disease over time.

Results from trials of schizophrenia drugs are also disappointing, he argues, and those for ADHD (attention deficit hyperactive disorder) are uncertain. “The short-term relief seems to be replaced by long-term harms. Animal studies strongly suggest that these drugs can produce brain damage, which is probably the case for all psychotropic drugs,” he writes.

“Given their lack of benefit, I estimate we could stop almost all psychotropic drugs without causing harm – by dropping all antidepressants, ADHD drugs and dementia drugs … and using only a fraction of the antipsychotics and benzodiazepines we currently use.

“This would lead to healthier and more long-lived populations. Because psychotropic drugs are immensely harmful when used long-term, they should almost exclusively be used in acute situations and always with a firm plan for tapering off, which can be difficult for many patients.”

In the BMJ discussion, which is a curtain-raiser for the Maudsley debate at King’s College London on Wednesday, Gøtzsche’s views are countered by Allan Young, a professor of mood disorders at King’s College London, and John Crace, a psychiatric patient and Guardian writer.

They argue that the research evidence shows the drugs do work and that they are just as beneficial and effective as medication for other complex conditions. In fact, they are badly needed, they say, because psychiatric conditions are the fifth leading cause of disability worldwide. Many psychiatric patients suffer from other physical conditions, they add, which are a bigger cause of early death than suicide.

They point out that the effects and safety of drugs are monitored and studied in the general population after the research trials have ended. “Nevertheless, many concerns have been expressed about psychiatric drugs and for some critics the onus often seems to be on the drug needing to prove innocence from causing harm rather than a balanced approach to evaluating the available evidence,” they write.

“Whether concerns are genuine or an expression of prejudice is not clear, but over time many concerns have been found to be overinflated.”

They cite the example of lithium, now thought to have less severe side-effects than once feared, and clozapine, an atypical antipsychotic. Clozapine was thought to have increased patients’ risk of death, but recent data has been reassuring, they say.

Dementia experts said use of antipsychotics for elderly patients who become difficult to handle had been a problem. “The dangers of long-term use of antipsychotic drugs for symptoms of aggression and agitation in dementia were highlighted in an Alzheimer’s Research UK-funded study in 2009 and since then moves have been made to reduce their use,” said Dr Simon Ridley, of Alzheimer’s Research UK.

But he and Dr Doug Brown, director of research and development at the Alzheimer’s Society, both argued that drugs such as Aricept, specifically developed for people with dementia, had some effect and were needed.

Dr Michael Bloomfield, academic clinical fellow in psychiatry at the Medical Research Council and University College London, said Gøtzsche’s view that most psychotropic drugs could be stopped without harm was not supported by the evidence.

Long-term use of schizophrenia drugs appeared to reduce early deaths, but he added: “In practice, there need to be regular reviews of treatments between a patient and their psychiatrist in order to continually weigh up the pros and cons of any treatment.”