Archive for the ‘Boston’ Category

Police in Boston are investigating a number of overnight break-ins in the Brighton neighborhood of Boston early Tuesday morning.

Two homes on Foster Road and one on Kirkwood Road were targeted during the early morning hours.

People living in the neighborhood close to Boston College fear a serial tickler is breaking into homes and targeting men.

In one of the break-ins, David Master said he heard screaming from one of his roommates. “He felt something on his foot and thought it was the cat,” Master said. “He woke up to see a man crouched by his bed.”

Master told the Boston Globe he and his roommates did not pursue the man. The man apparently walked in through their unlocked door.

The first break-in was reported around 3:50 a.m., the Globe reported. Residents in a home on Foster Street said they found a masked man in their home. When they spotted him, he ran in an unknown direction, the Globe reported.

Gino Caligore says his apartment was another target for the tickler. “Apparently the tickler had come in, tickled my roommate, and before my friend could catch him or anything, the guy ran out of the house,” Caligore said.

Boston police asked anyone with information about the crime to contact them.

Read more: http://www.wcvb.com/news/string-of-home-invasions-could-be-tied-to-serial-tickler/26424224#ixzz34cvVuDVp

redskin

A leader of the Navajo Code Talkers who appeared at a Washington Redskins home football game said Wednesday the team name is a symbol of loyalty and courage — not a slur as asserted by critics who want it changed.

Roy Hawthorne, 87, of Lupton, Ariz., was one of four Code Talkers honored for their service in World War II during the Monday night game against the San Francisco 49ers.

Hawthorne, vice president of the Navajo Code Talkers Association, said the group’s trip was paid for by the Redskins. The four men met briefly with team owner Dan Snyder but did not discuss the name, Hawthorne said.

Still, he said he would endorse the name if asked, and the televised appearance in which three of the Indians wore Redskins jackets spoke for itself.

“We didn’t have that in mind but that is undoubtedly what we did do,” Hawthorne said when asked if he was intending to send a statement with the appearance. “My opinion is that’s a name that not only the team should keep, but that’s a name that’s American.”

Monday night’s brief, on-field ceremony came as some Indians and civil rights leaders wage a “Change the Mascot” campaign that targets the term redskins as a racial epithet.

The Navajos’ appearance drew heated comments from both sides on social media, including assertions that the Code Talkers were being used as props in a public relations stunt meant to deflect criticism over the name.

Jacqueline Pata, head of the National Congress of American Indians, called the appearance “a political play rather than a heartfelt recognition of the Code Talkers.”

Pata, a member of the Tlingit Tribe of Alaska, said she reveres the Code Talkers for the work they have done but added that people often fail to recognize that the origins of the term redskin date to a period when Indians faced efforts to annihilate their culture.

“We were outlawed during that same period the mascot was created from practicing our own religion and our own cultures,” she said. “That term is associated with getting rid of the Indians.”

Snyder has called the team name and mascot a “badge of honor.” The name dates to the team’s first years in Boston in the 1930s and has survived numerous outside efforts to change it. The team has been in the Washington, D.C., area since 1937.

Redskins Senior Vice President Tony Wyllie said there was no truth to suggestions that the Code Talkers were used to bolster the team’s resistance to a new name.

“They’re American heroes, and they deserved recognition,” he said.

Also attending Monday’s game were Code Talkers President Peter MacDonald Sr., George Willie Sr. and George James Sr.

The Navajo Code Talkers used codes derived from their native language to shield military communications from interception by Japanese troops. Hawthorne said there are now about 30 surviving Code Talkers.

The trip to Washington was the second this month for Hawthorne, who last week joined Code Talkers from other tribes who received Congressional Gold Medals for the role they played in World War I and World War II. Members of the Navajo were recognized in 2000.

The Navajo are perhaps the best known of the Code Talkers, but the Defense Department says the program began in 1918 and at its peak included more than 400 Indians who used 33 dialects to make their codes indecipherable.

http://news.yahoo.com/code-talker-says-redskins-name-not-derogatory-172147791–spt.html

Thanks to Pete Cuomo for bringing this to the attention of the It’s Interesting community.

exercise

New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules.

While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain.

Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.)

While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (and the irisin created from it) was responsible for exercise-induced benefits to the brain—in particular, increased levels of a crucial protein called brain-derived neurotrophic factor (BDNF), which is essential for maintaining healthy neurons and creating new ones. These functions are crucial to staving off neurological diseases, including Alzheimer’s and Parkinson’s. And the link between exercise and BDNF is widely accepted. “The phenomenon has been established over the course of, easily, the last decade,” says neuroscientist Barbara Hempstead of Weill Cornell Medical College in New York City, who was not involved in the new work. “It’s just, we didn’t understand the mechanism.”

To sort out that mechanism, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. First, they put mice on a 30-day endurance training regimen. They didn’t have to coerce their subjects, because running is part of a mouse’s natural foraging behavior. “It’s harder to get them to lift weights,” Spiegelman notes. The mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from physical differences between wheel-trained mice and sedentary ones—“they just look a little bit more like a couch potato,” says co-author Christiane Wrann, also of Harvard Medical School, of the latter’s plumper figures—the groups also showed neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory.

Using mouse brain cells developing in a dish, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results online today in Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. “What was weird is the same pathway is induced in the brain,” he says, “and as you know, with exercise, the brain does not move.”

So how is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it’s also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse’s bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain, Spiegelman says.

Hempstead calls the findings “very exciting,” and believes this research finally begins to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. “I think it answers the question that most of us have posed in our own heads for many years.”

The effect of liver-produced irisin on the brain is a “pretty cool and somewhat surprising finding,” says Pontus Boström, a diabetes researcher at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work doesn’t answer a fundamental question: How much of exercise’s BDNF-promoting effects come from irisin reaching the brain from muscle cells via the bloodstream, and how much are from irisin created in the brain?

Though the authors point out that other important regulator proteins likely play a role in driving BDNF and other brain-nourishing factors, they are focusing on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and to improve brain health with aging.

http://news.sciencemag.org/biology/2013/10/how-exercise-beefs-brain

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

Ernest Hartmann
Ernest Hartmann, a professor of psychiatry at Tufts University School of Medicine and the director of the Sleep Disorders Center at Newton Wellesley Hospital in Boston, Mass., explains.

The questions, “Why do we dream?” or “What is the function of dreaming?” are easy to ask but very difficult to answer. The most honest answer is that we do not yet know the function or functions of dreaming. This ignorance should not be surprising because despite many theories we still do not fully understand the purpose of sleep, nor do we know the functions of REM (rapid eye movement) sleep, which is when most dreaming occurs. And these two biological states are much easier to study scientifically than the somewhat elusive phenomenon of dreaming.

Some scientists take the position that dreaming probably has no function. They feel that sleep, and within it REM sleep, have biological functions (though these are not totally established) and that dreaming is simply an epiphenomenon that is the mental activity that occurs during REM sleep. I do not believe this is the most fruitful approach to the study of dreaming. Would we be satisfied with the view that thinking has no function and is simply an epiphenomenon–the kind of mental activity that occurs when the brain is in the waking state?

Therefore I will try to explain a current view of dreaming and its possible functions, developed by myself and many collaborators, which we call the Contemporary Theory of Dreaming. The basic idea is as follows: activation patterns are shifting and connections are being made and unmade constantly in our brains, forming the physical basis for our minds. There is a whole continuum in the making of connections that we subsequently experience as mental functioning. At one end of the continuum is focused waking activity, such as when we are doing an arithmetic problem or chasing down a fly ball in the outfield. Here our mental functioning is focused, linear and well-bounded. When we move from focused waking to looser waking thought–reverie, daydreaming and finally dreaming–mental activity becomes less focused, looser, more global and more imagistic. Dreaming is the far end of this continuum: the state in which we make connections most loosely.

Some consider this loose making of connections to be a random process, in which case dreams would be basically meaningless. The Contemporary Theory of Dreaming holds that the process is not random, however, and that it is instead guided by the emotions of the dreamer. When one clear-cut emotion is present, dreams are often very simple. Thus people who experience trauma–such as an escape from a burning building, an attack or a rape–often have a dream something like, “I was on the beach and was swept away by a tidal wave.” This case is paradigmatic. It is obvious that the dreamer is not dreaming about the actual traumatic event, but is instead picturing the emotion, “I am terrified. I am overwhelmed.” When the emotional state is less clear, or when there are several emotions or concerns at once, the dream becomes more complicated. We have statistics showing that such intense dreams are indeed more frequent and more intense after trauma. In fact, the intensity of the central dream imagery, which can be rated reliably, appears to be a measure of the emotional arousal of the dreamer.

Therefore, overall the contemporary theory considers dreaming to be a broad making of connections guided by emotion. But is this simply something that occurs in the brain or does it have a purpose as well? Function is always very hard to prove, but the contemporary theory suggests a function based on studies of a great many people after traumatic or stressful new events. Someone who has just escaped from a fire may dream about the actual fire a few times, then may dream about being swept away by a tidal wave. Then over the next weeks the dreams gradually connect the fire and tidal wave image with other traumatic or difficult experiences the person may have had in the past. The dreams then gradually return to their more ordinary state. The dream appears to be somehow “connecting up” or “weaving in” the new material in the mind, which suggests a possible function. In the immediate sense, making these connections and tying things down diminishes the emotional disturbance or arousal. In the longer term, the traumatic material is connected with other parts of the memory systems so that it is no longer so unique or extreme–the idea being that the next time something similar or vaguely similar occurs, the connections will already be present and the event will not be quite so traumatic. This sort of function may have been more important to our ancestors, who probably experienced trauma more frequently and constantly than we (at least those of us living in the industrialized world) do at present.

Thus we consider a possible (though certainly not proven) function of a dream to be weaving new material into the memory system in a way that both reduces emotional arousal and is adaptive in helping us cope with further trauma or stressful events.

http://ernesthartmann.org/ERNEST_HARTMANN_MD/HOME.html

2-bionic-handsBionic-handv1

The first bionic hand that allows an amputee to feel what they are touching will be transplanted later this year in a pioneering operation that could introduce a new generation of artificial limbs with sensory perception.

The patient is an unnamed man in his 20s living in Rome who lost the lower part of his arm following an accident, said Silvestro Micera of the Ecole Polytechnique Federale de Lausanne in Switzerland.

The wiring of his new bionic hand will be connected to the patient’s nervous system with the hope that the man will be able to control the movements of the hand as well as receiving touch signals from the hand’s skin sensors.

Dr Micera said that the hand will be attached directly to the patient’s nervous system via electrodes clipped onto two of the arm’s main nerves, the median and the ulnar nerves.

This should allow the man to control the hand by his thoughts, as well as receiving sensory signals to his brain from the hand’s sensors. It will effectively provide a fast, bidirectional flow of information between the man’s nervous system and the prosthetic hand.

“This is real progress, real hope for amputees. It will be the first prosthetic that will provide real-time sensory feedback for grasping,” Dr Micera said.

“It is clear that the more sensory feeling an amputee has, the more likely you will get full acceptance of that limb,” he told the American Association for the Advancement of Science meeting in Boston.

“We could be on the cusp of providing new and more effective clinical solutions to amputees in the next year,” he said.

An earlier, portable model of the hand was temporarily attached to Pierpaolo Petruzziello in 2009, who lost half his arm in a car accident. He was able to move the bionic hand’s fingers, clench them into a fist and hold objects. He said that he could feel the sensation of needles pricked into the hand’s palm.

However, this earlier version of the hand had only two sensory zones whereas the latest prototype will send sensory signals back from all the fingertips, as well as the palm and the wrists to give a near life-like feeling in the limb, Dr Micera said.

“The idea would be that it could deliver two or more sensations. You could have a pinch and receive information from three fingers, or feel movement in the hand and wrist,” Dr Micera said.

“We have refined the interface [connecting the hand to the patient], so we hope to see much more detailed movement and control of the hand,” he told the meeting.

The plan is for the patient to wear the bionic hand for a month to see how he adapts to the artificial limb. If all goes well, a full working model will be ready for testing within two years, Dr Micera said.

One of the unresolved issues is whether patients will be able to tolerate having such a limb attached to them all the time, or whether they would need to remove it periodically to give them a rest.

Another problem is how to conceal the wiring under the patient’s skin to make them less obtrusive. The electrodes of the prototype hand to be fitted later this year will be inserted through the skin rather than underneath it but there are plans under development to place the wiring subcutaneously, Dr Micera said.

http://www.independent.co.uk/life-style/gadgets-and-tech/news/a-sensational-breakthrough-the-first-bionic-hand-that-can-feel-8498622.html

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

sn-termites

When trekking through a forest in French Guiana to study termites, a group of biologists noticed unique spots of blue on the backs of the insects in one nest. Curious, one scientist reached down to pick up one of these termites with a pair of forceps. It exploded. The blue spots, the team discovered, contain explosive crystals, and they’re found only on the backs of the oldest termites in the colony. The aged termites carry out suicide missions on behalf of their nest mates.

After their initial observation, the team carried out field studies of Neocapritermes taracua termites and discovered that those with the blue spots also exploded during encounters with other species of termites or larger predators. The researchers report online today in Science that the secretions released during the explosion killed or paralyzed opponents from a competing termite species. However, if the scientists removed the blue crystal from the termites, their secretions were no longer toxic.

Back in their labs, scientists led by biochemist Robert Hanus of the Academy of Sciences of the Czech Republic in Prague went on to show that the blue termites always had shorter, worn-down mandibles than others from the same species, indicating that they were older. Then, the researchers removed the contents of the blue pouches and analyzed them. They contained a novel protein that is unusually rich with copper, suggesting that it’s an oxygen binding-protein. Rather than being toxic itself, it likely is an enzyme that converts a nontoxic protein into something toxic.

“What happens is when the termites explode, the contents of the back pouch actually interact with secretions from the salivary gland and the mixture is what is toxic,” explains Hanus. It’s the first time two interacting chemicals have been shown responsible for a defense mechanism in termites, he says.

Researchers already knew that many social insects change roles in their colony as they age. Moreover, it’s well known that a number of species of termites explode, often oozing sticky or smelly fluid onto their opponent. But in previously observed cases, the explosive or noxious material is found in the termites’ heads, and the suicide missions are the responsibility of a distinct caste of soldier termites, not aging workers. Since N. taracua have soldiers, it’s especially surprising to see workers exploding, says Hanus.

“This is a quirky, funny natural history,” says behavioral ecologist Rebeca Rosengaus of Northeastern University in Boston, who was not involved in the study. “What’s new and interesting here is that this is found to be an aspect of colony-related age organization,” says biologist James Traniello of Boston University. And the placement and chemistry of the blue crystals is unique, he says. The findings illustrate the vast diversity of social structures and defense mechanisms that the more than 3000 species of termites have evolved over time, Traniello says.

One question that remains is exactly how aging triggers the accumulation of the blue crystals. “We’re still not 100% sure what the role of the blue protein is,” says Hanus. “That’s definitely something which we want to perform further research on.”

http://news.sciencemag.org/sciencenow/2012/07/old-termites-blow-themselves-up-.html

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

sn-sleep

Hitting the wall in the middle of a busy work day is nothing unusual, and a caffeine jolt is all it takes to snap most of us back into action. But people with certain sleep disorders battle a powerful urge to doze throughout the day, even after sleeping 10 hours or more at night. For them, caffeine doesn’t touch the problem, and more potent prescription stimulants aren’t much better. Now, a study with a small group of patients suggests that their condition may have a surprising source: a naturally occurring compound that works on the brain much like the key ingredients in chill pills such as Valium and Xanax.

The condition is known as primary hypersomnia, and it differs from the better known sleep disorder narcolepsy in that patients tend to have more persistent daytime sleepiness instead of sudden “sleep attacks.” The unknown cause and lack of treatment for primary hypersomnia has long frustrated David Rye, a neurologist at Emory University in Atlanta. “A third of our patients are on disability,” he says, “and these are 20- and 30-year-old people.”

Rye and colleagues began the new study with a hunch about what was going on. Several drugs used to treat insomnia promote sleep by targeting receptors for GABA, a neurotransmitter that dampens neural activity. Rye hypothesized that his hypersomnia patients might have some unknown compound in their brains that does something similar, enhancing the activity of so-called GABAA receptors. To try to find this mystery compound, he and his colleagues performed spinal taps on 32 hypersomnia patients and collected cerebrospinal fluid (CSF), the liquid that bathes and insulates the brain and spinal cord. Then they added the patients’ CSF to cells genetically engineered to produce GABAA receptors, and looked for tiny electric currents that would indicate that the receptors had been activated.

In that first pass, nothing happened. However, when the researchers added the CSF and a bit of GABA to the cells, they saw an electrical response that was nearly twice as big as that caused by GABA alone. All of this suggests that the patients’ CSF doesn’t activate GABAA receptors directly, but it does make the receptors almost twice as sensitive to GABA, the researchers report today in Science Translational Medicine. This effect is similar to that of drugs called benzodiazepines, the active ingredients in antianxiety drugs such as Valium. It did not occur when the researchers treated the cells with CSF from people with normal sleep patterns.

Follow-up experiments suggested that the soporific compound in the patients’ CSF is a peptide or small protein, presumably made by the brain, but otherwise its identity remains a mystery.

The idea that endogenous benzodiazepinelike compounds could cause hypersomnia was proposed in the early 1990s by Elio Lugaresi, a pioneering Italian sleep clinician, says Clifford Saper, a neuroscientist at Harvard Medical School in Boston. But several of Lugaresi’s patients later turned out to be taking benzodiazepines, which undermined his argument, and the idea fell out of favor. Saper says the new work makes a “pretty strong case.”

Based on these results, Rye and his colleagues designed a pilot study with seven patients using a drug called flumazenil, which counteracts benzodiazepines and is often used to treat people who overdose on those drugs. After an injection of flumazenil, the patients improved to near-normal levels on several measures of alertness and vigilance, the researchers report. Rye says these effects lasted up to a couple hours.

In hopes of longer-lasting benefits, the researchers persuaded the pharmaceutical company Hoffmann-La Roche, which makes the drug, to donate a powdered form that can be incorporated into dissolvable tablets taken under the tongue and a cream applied to the skin. One 30-something patient has been taking these formulations for 4 years and has improved dramatically, the researchers report in the paper. She has resumed her career as an attorney, from which her hypersomnia had forced her to take a leave of absence.

The findings are “certainly provocative,” Saper says, although they’ll have to be replicated in a larger, double-blind trial to be truly convincing.

Even so, says Phyllis Zee, a neurologist at Northwestern University in Evanston, Illinois: “This gives us a new window into thinking about treatments” for primary hypersomnia. “These patients don’t respond well to stimulants,” Zee says, so a better strategy may be to inhibit the sleep-promoting effects of GABA—or as Rye puts it, releasing the parking brake instead of pressing the accelerator.

The next steps are clear, Rye says: Identify the mystery compound, figure out a faster way to detect it, and conduct a larger clinical trial to test the benefits of flumazenil. However, the researchers first need someone to fund such a study. So far, Rye says, they’ve gotten no takers.

http://news.sciencemag.org/sciencenow/2012/11/putting-themselves-to-sleep.html