By ALLISON HERSH LONDON I’M in line at the supermarket holding three items close to my chest. But I might as well be juggling my Kleenex box, toothpaste tube and an orange. Because — as you’d surely notice if you were behind me in line — I‘m bent forward at a sharp angle, which makes holding things difficult. I know you don’t want to stare, but you do. Maybe you think you’re being considerate when you say, apropos of nothing, “You look like you’re in pain.” Well, thanks, I am — but I’ll resist replying the way I want (“You look like you’re having a bad hair day”). I’m sorry. I know you mean well. Anyway it’s my turn at the register which means I’m closer to being at home where I can lie down and wait for the spasms to subside. Besides, if I told you what my issue was, you would probably shrug and reply that you’d never heard of it. There aren’t any public service announcements about it or telethons. No Angelina Jolies to bravely inform the world. Just people like me, in supermarket checkout lines. And this, I realize, is at the core of a problem that extends beyond me and my condition and that affects the way all of us respond to illnesses, some of which are the subject of public attention — and resources — and some of which are not. I have dystonia, a neurological disorder. Some years ago, for reasons no one knows, the muscles in my back and neck began to spasm involuntarily; the spasms multiply quickly, fatigue the muscles and force the body into repetitive movements and awkward postures like mine. There is no cure, only treatment options like deep brain stimulation, which requires a surgery I underwent last year as a last resort. © 2013 The New York Times Company

Keyword: Movement Disorders; Aggression
Link ID: 18171 - Posted: 05.20.2013

By David Brown, A team of researchers said Wednesday that it had produced embryonic stem cells — a possible source of disease-fighting spare parts — from a cloned human embryo. Scientists at the Oregon Health and Science University accomplished in humans what has been done over the past 15 years in sheep, mice, cattle and several other species. The achievement is likely to, at least temporarily, reawaken worries about “reproductive cloning” — the production of one-parent duplicate humans. But few experts think that production of stem cells through cloning is likely to be medically useful soon, or possibly ever. “An outstanding issue of whether it would work in humans has been resolved,” said Rudolf Jaenisch, a biologist at MIT’s Whitehead Institute in Cambridge, Mass., who added that he thinks the feat “has no clinical relevance.” “I think part of the significance is technical and part of the significance is historical,” said John Gearhart, head of the Institute for Regenerative Medicine at the University of Pennsylvania. “Many labs attempted it, and no one had ever been able to achieve it.” A far less controversial way to get stem cells is now available. It involves reprogramming mature cells (often ones taken from the skin) so that they return to what amounts to a second childhood from which they can grow into a new and different adulthood. Learning how to make and manipulate those “induced pluripotent stem” (IPS) cells is one of biology’s hottest fields. © 1996-2013 The Washington Post

Keyword: Stem Cells; Aggression
Link ID: 18162 - Posted: 05.16.2013

By ABIGAIL ZUGER, M.D. I hadn’t seen Larry in a dozen years when he reappeared in my office a few months ago, grinning. We were both grinning. I always liked Larry, even though he was a bit of a hustler, a little erratic in his appointments, a persistent dabbler in a variety of illegal substances. But he was always careful to avoid the hard stuff; he said he had a bad problem as a teenager and was going to stay out of trouble. It was to stay out of trouble that he left town all those years ago, and now he was back, grayer and thinner but still smiling. Then he pulled out a list of the medications he needed, and we both stopped smiling. According to Larry’s list, he was now taking giant quantities of one of the most addictive painkillers around, an immensely popular black-market drug most doctors automatically avoid prescribing except under the most exceptional circumstances. “I got a bad back now, Doc,” Larry said. Doctors hate pain. Let me count the ways. We hate it because we are (mostly) kindhearted and hate to see people suffer. We hate it because it is invisible, cannot be measured or monitored, and varies wildly and unpredictably from person to person. We hate it because it can drag us closer to the perilous zones of illegal practice than any other complaint. And we hate it most of all because unless we specifically seek out training in how to manage pain, we get virtually none at all, and wind up flying over all kinds of scary territory absolutely solo, without a map or a net. Copyright 2013 The New York Times Company

Keyword: Pain & Touch; Aggression
Link ID: 18153 - Posted: 05.14.2013

Roberta Kwok Sitting motionless in her wheelchair, paralysed from the neck down by a stroke, Cathy Hutchinson seems to take no notice of the cable rising from the top of her head through her curly dark hair. Instead, she stares intently at a bottle sitting on the table in front of her, a straw protruding from the top. Her gaze never wavers as she mentally guides a robot arm beside her to reach across the table, close its grippers around the bottle, then slowly lift the vessel towards her mouth. Only when she finally manages to take a sip does her face relax into a luminous smile. This video of 58-year-old Hutchinson illustrates the strides being taken in brain-controlled prosthetics1. Over the past 15 years, researchers have shown that a rat can make a robotic arm push a lever2, a monkey can play a video game3 and a person with quadriplegia — Hutchinson — can sip from a bottle of coffee1, all by simply thinking about the action. Improvements in prosthetic limbs have been equally dramatic, with devices now able to move individual fingers and bend at more than two dozen joints. But Hutchinson's focused stare in that video also illustrates the one crucial feature still missing from prosthetics. Her eyes could tell her where the arm was, but she could not feel what it was doing. Nor could she sense when the grippers touched the bottle, or whether it was slipping out of their grasp. Without this type of sensory feedback, even the simplest actions can be slow and clumsy, as Igor Spetic of Madison, Ohio, knows well. Fitted with a prosthetic after his right hand was crushed in an industrial accident in 2010, Spetic describes breaking dishes, grabbing fruit too hard and bruising it and dropping a can when trying to pick it up at the local shop. Having a sense of touch would be “tremendous”, he says. “It'd be one step closer to having the hand back.” © 2013 Nature Publishing Group,

Keyword: Pain & Touch; Aggression
Link ID: 18138 - Posted: 05.09.2013

National Institutes of Health researchers used the popular anti-wrinkle agent Botox to discover a new and important role for a group of molecules that nerve cells use to quickly send messages. This novel role for the molecules, called SNARES, may be a missing piece that scientists have been searching for to fully understand how brain cells communicate under normal and disease conditions. "The results were very surprising,” said Ling-Gang Wu, Ph.D., a scientist at NIH’s National Institute of Neurological Disorders and Stroke. “Like many scientists we thought SNAREs were only involved in fusion." Every day almost 100 billion nerve cells throughout the body send thousands of messages through nearly 100 trillion communication points called synapses. Cell-to-cell communication at synapses controls thoughts, movements, and senses and could provide therapeutic targets for a number of neurological disorders, including epilepsy. Nerve cells use chemicals, called neurotransmitters, to rapidly send messages at synapses. Like pellets inside shotgun shells, neurotransmitters are stored inside spherical membranes, called synaptic vesicles. Messages are sent when a carrier shell fuses with the nerve cell’s own shell, called the plasma membrane, and releases the neurotransmitter “pellets” into the synapse. SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) are three proteins known to be critical for fusion between carrier shells and nerve cell membranes during neurotransmitter release.

Keyword: Muscles; Aggression
Link ID: 18115 - Posted: 05.04.2013

By Stephani Sutherland Itching is not the only sensation to arise from unique neurons. A team at the California Institute of Technology has identified neurons that transmit the pleasurable sensations of massage, at least in mice. The cells responded to gentle rubbing but not to pinching or poking. Activation of the cells requires “a pressure component,” says lead investigator David Anderson, a neuroscientist at Caltech, “much like you would apply if you were stroking your cat.” The team first identified the mysterious cells several years ago by an unusual protein on their surface called MrgprB4—closely related to the receptor expressed by the newly identified itch cells. The rare sensory cells make up only about 2 percent of the body's peripheral neurons that respond to external stimuli, but they seem to cover about half the skin's surface with large, branching nerve endings. Whereas sensory neurons that transmit pain have been intensely studied, this is the first demonstration in live animals of a sensory cell that gives pleasure. After the scientists activated those neurons with a designer drug, the mice came to favor the place where they received the drug, according to the paper published January 31 in Nature. © 2013 Scientific American

Keyword: Pain & Touch
Link ID: 18092 - Posted: 04.30.2013

By R. Douglas Fields Scientists have speculated that it is a mild manifestation of pain or perhaps a malfunction of overly sensitive nerve endings stuck in a feedback loop. They have even wondered whether itching is mostly psychological (just think about bed bugs for a minute). Now a study rules out these possibilities by succeeding where past attempts have failed: a group of neuroscientists have finally isolated a unique type of nerve cell that makes us itch and only itch. In previous research, neuroscientists Liang Han and Xinzhong Dong of Johns Hopkins University and their colleagues determined that some sensory neurons with nerve endings in the skin have a unique protein receptor on them called MrgprA3. They observed under a microscope that chemicals known to create itching caused these neurons to generate electrical signals but that painful stimuli such as hot water or capsaicin, the potent substance in hot peppers, did not. In the new study published in Nature Neuroscience, the researchers used genetic engineering to selectively kill the entire population of MrgprA3 neurons in mice while leaving all the other sensory neurons intact. These mice no longer scratched themselves when exposed to itchy substances or allergens, but they showed no changes at all in responding to touch or pain-producing stimulation. The mice's behavior confirms that MrgprA3-containing neurons are essential for itch, but it does not rule out the possibility that these cells might respond to other sensations as well. To find out, the neuroscientists engineered a receptor that responds to capsaicin injected into the MrgprA3 neurons, in a type of mouse that lacks the capsaicin receptor in all its other cells. Now the only neurons that would be stimulated by capsaicin were the MrgprA3 neurons. If these cells are indeed itch-specific, injecting capsaicin into a tiny spot on the mouse's skin should make the rodent scratch instead of wincing in pain—which is exactly what happened. © 2013 Scientific American,

Keyword: Pain & Touch
Link ID: 18066 - Posted: 04.24.2013

By PAULA SPAN It was supposed to be a short stay. In 2006, Roger Anderson was to undergo surgery to relieve a painfully compressed spinal disk. His wife, Karen, figured the staff at the hospital, in Portland, Ore., would understand how to care for someone with Parkinson’s disease. It can be difficult. Parkinson’s patients like Mr. Anderson, for example, must take medications at precise intervals to replace the brain chemical dopamine, which is diminished by the disease. “You don’t have much of a window,” Mrs. Anderson said. “If you have to wait an hour, you have tremendous problems.” Without these medications, people may “freeze” and be unable to move, or develop uncontrolled movements called dyskinesia, and are prone to falls. But the nurses at the Portland hospital didn’t seem to grasp those imperatives. “You’d have to wait half an hour or an hour, and that’s not how it works for Parkinson’s patients,” Mrs. Anderson said. Nor did hospital rules, at the time, permit her to simply give her husband the Sinemet pills on her own. Surgery and anesthesia, the disrupted medications, an incision that subsequently became infected — all contributed to a tailspin that lasted nearly three months. Mr. Anderson developed delirium, rotated between rehab centers and hospitals, took a fall, lost 60 pounds. “People were telling me, ‘He’s never going to come home,’” Mrs. Anderson said. He did recover, and at 69 is doing well, his wife said, though his disease has progressed. But his wasn’t an unusual story, neurologists say. © 2013 The New York Times Company

Keyword: Parkinsons
Link ID: 18054 - Posted: 04.22.2013

By GRETCHEN REYNOLDS If you give a rat a running wheel and it decides not to use it, are genes to blame? And if so, what does that tell us about why many people skip exercise? To examine those questions, scientists at the University of Missouri in Columbia recently interbred rats to create two very distinct groups of animals, one of which loves to run. Those in the other group turn up their collective little noses at exercise, slouching idly in their cages instead. Then the scientists closely scrutinized and compared the animals’ bodies, brains and DNA. For some time, exercise scientists have suspected that the motivation to exercise — or not — must have a genetic component. When researchers have compared physical activity patterns among family members, and particularly among twins, they have found that close relations tend to work out similarly, exercising about as much or as little as their parents or siblings do, even if they grew up in different environments. These findings suggest that the desire to be active or indolent is, to some extent, inherited. But to what extent someone’s motivation to exercise is affected by genes — and what specific genes may be involved — has been hard to determine. There are only so many human twins around for study purposes, after all. And even more daunting, it’s difficult to separate the role of upbringing from that of genetics in determining whether and why some people want to exercise and others don’t. So the University of Missouri researchers decided to create their own innately avid runners or couch potatoes, provide them with similar upbringings, and see what happened next. Copyright 2013 The New York Times Company

Keyword: Emotions; Aggression
Link ID: 18044 - Posted: 04.18.2013

By Sandra G. Boodman, For someone who had been such a healthy child, Nancy Kennedy couldn’t figure out how she had become the kind of sickly adult whose life revolved around visits to a seemingly endless series of doctors. Beginning in 2005, shortly after a job transfer took her from Northern Virginia to St. Louis, Kennedy, then 47, developed a string of vexing medical problems. Her white blood cell count was inexplicably elevated. Her sinuses were chronically infected, although her respiratory tract seemed unusually dry. She often felt fatigued, and her joints hurt. “It felt as though an alien had invaded my body,” said Kennedy, formerly a manager at the National Geospatial-Intelligence Agency. “I felt like I was in doctors’ offices all the time.” Tests for possible ailments — including blood disorders, cancer, multiple sclerosis and rheumatoid arthritis — were negative. For seven years. Kennedy and her primary-care physician, who said she felt as though she sent Kennedy to “every specialist that walked,” had no clear idea what might be wrong. But during a physical in January 2012, her doctor, Melissa Johnson, struck by Kennedy’s trouble walking and her accelerating deterioration, decided to check for a condition not previously considered. © 1996-2013 The Washington Post

Keyword: Neuroimmunology; Aggression
Link ID: 18040 - Posted: 04.16.2013

By Gary Stix People who lose a limb often experience the sensation of still having the missing arm or leg. Phantom limbs, in fact, have spurred a whole line of independent research among neuroscientists. But it appears that all of us may be capable of these sensations, even if arms and legs remain intact. If we can conjure a phantom limb just like that, it raises all kinds of enticing questions for philosophers as well as scientists about what exactly constitutes our perception of the physical self. Karolinska Institute researchers report online in the Journal of Cognitive Neuroscience that they can induce a sensation of a phantom hand in just a short time. Watch this simple experiment here: © 2013 Scientific American

Keyword: Pain & Touch
Link ID: 18036 - Posted: 04.15.2013

Nearly half of those with Parkinson's face regular discrimination, such as having their symptoms mistaken for drunkenness, a survey suggests. The survey of more than 2,000 people was commissioned by charity Parkinson's UK. One person in 500 people is affected by the condition in Britain. Parkinson's sufferer Mark Worsfold was arrested during last year's Olympics because police thought he looked suspicious. He was detained during the cycling road race in Leatherhead, Surrey, reportedly because he was not smiling - the condition means his face can appear expressionless. Parkinson's is a progressive neurological condition that attacks the part of the brain that controls movement. The main symptoms of Parkinson's are tremors or shaking that cannot be controlled, and rigidity of the muscles, which can make movement difficult and painful. Speech, language and facial expressions can also be affected. Most people who get it are aged 50 or over but younger people can have it too. The survey found that one in five people living with Parkinson's had been mistaken for being drunk, while one in 10 had been verbally abused or experienced hostility in public because of their condition. Around 62% said they thought the public had a poor understanding of how the condition affects people. BBC © 2013

Keyword: Parkinsons
Link ID: 18035 - Posted: 04.15.2013

by Patrick Russell Many people who have had a limb amputated report feeling sensations that appear to come from their missing arm or leg. Now researchers have found that anyone can experience having such a phantom limb. "Previous research shows that you can convince a person that a rubber hand is their own by putting it on a table in front of them and stroking it in synchrony with their real hand," explains Arvid Guterstam at the Karolinska Institute in Stockholm, Sweden, who led the study. The illusion does not work with a block of wood, he says. "But our study shows that if you take away this rubber hand, people will attribute sensations to an invisible entity." Guterstam and his colleagues made volunteers sit at a table with their right arm hidden from view behind a screenMovie Camera. An experimenter then applied brush strokes to the concealed hand and, simultaneously, to a portion of empty space in full view of each volunteer. "We discovered that most participants, within less than a minute, transfer the sensation of touch to the region of empty space where they see the paintbrush move, and experience an invisible hand in that position," says Guterstam. Mock stabbing Experimenters also mimicked stabbing the phantom hand with a kitchen knife, while monitoring volunteers' stress level. To minimise any effect related to seeing the knife for the first time, the volunteers were warned that it would be used at some point. The researchers found that during the mock stabbing, stress levels, measured using a type of sweat test, went up in about 75 per cent of the 234 participants. © Copyright Reed Business Information Ltd.

Keyword: Pain & Touch; Aggression
Link ID: 18029 - Posted: 04.13.2013

by Helen Shen A thermometer is great for measuring a fever, but when it comes to pain, doctors must rely on the age-old question, "How bad is it?" Scientists have long struggled to find physiological signs that can reliably tell "ouch" from "@#%!" and everything in between. Now, a brain scanning study suggests that painful heat excites a specific pattern of neural activity that could hold the key to better diagnosis and treatment of all kinds of pain in the future. Functional magnetic resonance imaging (fMRI) studies have shown that certain areas of the brain—including the anterior cingulate cortex, somatosensory cortex, and thalamus—activate when people experience pain. But those same regions also light up in response to other experiences, such as painful thoughts or social rejection. In recent years, scientists have looked for a particular pattern of activity across these areas that single out the experience of physical pain. "What we're evolving towards is trying to predict quantitatively from patterns of brain activity how much an individual is feeling," says Tor Wager, a neuroscientist at the University of Colorado, Boulder. In the new study, Wager's group performed fMRI brain scans on a total of 114 healthy participants while delivering different amounts of heat to the volunteers' arms with a computer-controlled hot plate. In an initial experiment, the scientists used data from 20 people to find a brain-wide pattern of excitation and inhibition—a neural "signature"—that changed reliably as people experienced varying degrees of heat, ranging from painless to scalding. In the remainder of the study, Wager and his colleagues were able use the signature derived from the first group to predict pain responses in a completely different set of subjects—a promising sign for one day using such a model on patients suffering from unknown conditions, he says. © 2010 American Association for the Advancement of Science.

Keyword: Pain & Touch; Aggression
Link ID: 18024 - Posted: 04.11.2013

By GRETCHEN REYNOLDS Two new experiments, one involving people and the other animals, suggest that regular exercise can substantially improve memory, although different types of exercise seem to affect the brain quite differently. The news may offer consolation for the growing numbers of us who are entering age groups most at risk for cognitive decline. It was back in the 1990s that scientists at the Salk Institute for Biological Studies in La Jolla, Calif., first discovered that exercise bulks up the brain. In groundbreaking experiments, they showed that mice given access to running wheels produced far more cells in an area of the brain controlling memory creation than animals that didn’t run. The exercised animals then performed better on memory tests than their sedentary labmates. Since then, scientists have been working to understand precisely how, at a molecular level, exercise improves memory, as well as whether all types of exercise, including weight training, are beneficial. The new studies provide some additional and inspiring clarity on those issues, as well as, incidentally, on how you can get lab rats to weight train. For the human study, published in The Journal of Aging Research, scientists at the University of British Columbia recruited dozens of women ages 70 to 80 who had been found to have mild cognitive impairment, a condition that makes a person’s memory and thinking more muddled than would be expected at a given age. Mild cognitive impairment is also a recognized risk factor for increasing dementia. Seniors with the condition develop Alzheimer’s disease at much higher rates than those of the same age with sharper memories. Copyright 2013 The New York Times Company

Keyword: Learning & Memory
Link ID: 18015 - Posted: 04.10.2013

Ed Yong Every autumn, millions of monarch butterflies (Danaus plexippus) converge on a small cluster of Mexican mountains to spend the winter. They have journeyed for up to 4,000 kilometres from breeding grounds across eastern North America. And according to a study, they accomplish this prodigious migration without ever knowing where they are relative to their destination. The monarchs can use the position of the Sun as a compass, but when Henrik Mouritsen, a biologist at the University of Oldenburg in Germany, displaced them by 2,500 kilometres, he found that they did not correct their heading. “People seemed to assume that they had some kind of a map that allowed them to narrow in on a site a few kilometres across after travelling several thousands of kilometres,” he says. Now, “it is clear that they don’t”. His results are published in the Proceedings of the National Academy of Sciences1. For more than five decades, scientists have teamed up with amateurs to tag and monitor free-flying monarchs, creating a database of their migrations. When Mouritsen analysed these records, he realized that the monarchs tend to spread out over the course of their migration. Their distribution was a good fit with the predictions of a mathematical model that assumed that the monarchs were flying with just a compass, rather than a compass and a map. Mouritsen also captured 76 southwesterly flying monarchs from fields near Guelph in Ontario, Canada, and transported them 2,500 kilometres to the west, to Calgary in the Canadian province of Alberta. He placed the butterflies in a “flight simulator” — a plastic cylinder that kept them from seeing any landmarks except the sky — and tethered them to a rod that let them point in any direction without actually flying away. © 2013 Nature Publishing Group

Keyword: Animal Migration
Link ID: 18013 - Posted: 04.10.2013

By KATIE HAFNER While undressing for bed one night in 2009, Susan Spencer-Wendel noticed that the muscles in her left palm had disappeared, leaving a scrawny pile of tendons and bones. Her right hand was fine. She let out a yelp and showed the hand to her husband, who told her to go to the doctor. She was 42. Ms. Spencer-Wendel then entered a protracted period of denial. Adopted as an infant in Florida, she traveled from her home in West Palm Beach to find blood relatives living in Cyprus, who confirmed that there was no family history of her worst fear: amyotrophic lateral sclerosis, or A.L.S., the relentless disease that lays waste to muscles while leaving the mind intact. In June 2011, a doctor in Miami gave her a definitive diagnosis of A.L.S., smiling “like he was inviting me to a birthday party,” she writes in “Until I Say Goodbye: My Year of Living With Joy.” Patients with A.L.S., which is also known as Lou Gehrig’s disease, typically live no more than four years after the onset of symptoms. There is no cure. Ms. Spencer-Wendel thought she had prepared herself fully — that she would burst off the starting block like a sprinter to greet her fate. Instead, when she heard the news, “I dropped my head for the start ... and began to cry.” Her heart-ripping book chronicles what she did immediately after her diagnosis: she decided to embrace life while death chased her down. Instead of letting the world close in on her, she resolved to travel as far and as wide for as long as she could. She went to the Yukon with her best friend, Budapest with her husband, and the Bahamas with her sister. © 2013 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 18007 - Posted: 04.09.2013

By John McCarthy Maybe this discovery is interesting because it sheds therapeutic light on the dreaded neurodegenerative diseases that killed Woody Guthrie and Lou Gehrig. Or maybe it’s fascination with healthy cells, and yet another unsuspected complexity in how they work. What’s discovered: a previously unknown energy source in nerve cells. It propels the molecular “motors” that drag neurotransmitters from the nucleus where they’re made. The “motors” are assemblies of molecules. They walk like clumsy robots, with a staggering gait, dragging a capsule of neurotransmitter “bullets” along microtubule “highways” between nucleus and synapses. They move by flinging their boot-like feet (lavender blobs, in the image) forward, a billionth of a meter at each step. (A superb animation of “motors” in action is XVIVO’s “Life of a Cell” (at ~1:15 of playing time)). When the cargo finally arrives at the synapses, neurotransmitters are loaded into compartments at the synapse’s interior face, like bullets into a magazine. They are ready to be “fired” across a synapse to signal an adjoining neuron. It’s this transport of neurotransmitter “bullets” that failed in Guthrie’s and Gehrig’s nerve cells. Their synapses had nothing to fire. What powers the flinging that moves those boots? Previously, the answer has been specialized molecules (acronym: ATP) spewed into the cell’s fluid interior by mitochondria. The boots, it was thought, powered each step by grabbing a floating ATP and blowing it up like a firecracker. © 2013 Scientific American

Keyword: Huntingtons
Link ID: 17978 - Posted: 04.02.2013

By Emily Burns Lots of people set themselves goals – like things to do by the time you’re 30. Maybe it’s to find your dream job, meet the love of your life, or travel the world! For sufferers of Cystic Fibrosis, it’s living to see your 30th birthday. Even with all of the advances in medicine and technology, the average life expectancy of someone with Cystic Fibrosis is 33 years. Cystic Fibrosis is an inherited disease that mostly affects the lungs, but also the pancreas, liver and intestines. The body fluids we need – like the mucus in our lungs and intestines – are much thicker than normal, making it extremely difficult to breathe and digest food. Constant physiotherapy, breathing exercises, diet supplements and antibiotics are needed just to get on with daily life. And all of this suffering is caused by one tiny change in our DNA, which then messes up how one single protein folds into the right shape. It’s otherwise known as a protein misfolding disease. There are over 2 million proteins in the human body, carrying out their individual tasks to keep us breathing, thinking – enabling us to live. But their production isn’t easy. It’s an incredibly intricate and specialised process that is constantly going on inside us. If it goes wrong, there are serious consequences to our health, with Cystic Fibrosis being a prime example.... While the primary causes Alzheimer’s and Parkinson’s is still not known, one of the theories suggests that cellular and ER stress results in the cell death that we see. They are known as amyloid diseases, as they’re caused by the accumulation of amyloids in cells. We usually think of amyloids as being associated with Alzheimer’s, so you might think that they were a particular type of protein, but that’s not quite it. Instead, amyloids are protein delinquents: any protein that can form a beta sheet can become an amyloid. When a mutated protein misfolds, the side chains of amino acids (that dictate the specific fold) are no longer so important: the main chain of the polypeptide now causes these amyloid fibres to stick together. These amyloid fibres are formed regardless of the original folded protein structure (meaning that they form the same fibrous shape for every protein) and can penetrate the cells, causing cell stress and death. © 2013 Scientific American

Keyword: Alzheimers; Aggression
Link ID: 17964 - Posted: 03.28.2013

by Sid Perkins The electric fields that build up on honey bees as they fly, flutter their wings, or rub body parts together may allow the insects to talk to each other, a new study suggests. Tests show that the electric fields, which can be quite strong, deflect the bees' antennae, which, in turn, provide signals to the brain through specialized organs at their bases. Scientists have long known that flying insects gain an electrical charge when they buzz around. That charge, typically positive, accumulates as the wings zip through the air—much as electrical charge accumulates on a person shuffling across a carpet. And because an insect's exoskeleton has a waxy surface that acts as an electrical insulator, that charge isn't easily dissipated, even when the insect lands on objects, says Randolf Menzel, a neurobiologist at the Free University of Berlin in Germany. Although researchers have suspected for decades that such electrical fields aid pollination by helping the tiny grains stick to insects visiting a flower, only more recently have they investigated how insects sense and respond to such fields. Just last month, for example, a team reported that bumblebees may use electrical fields to identify flowers recently visited by other insects from those that may still hold lucrative stores of nectar and pollen. A flower that a bee had recently landed on might have an altered electrical field, the researchers speculated. Now, in a series of lab tests, Menzel and colleagues have studied how honey bees respond to electrical fields. In experiments conducted in small chambers with conductive walls that isolated the bees from external electrical fields, the researchers showed that a small, electrically charged wand brought close to a honey bee can cause its antennae to bend. Other tests, using antennae removed from honey bees, indicated that electrically induced deflections triggered reactions in a group of sensory cells, called the Johnston's organ, located near the base of the antennae. In yet other experiments, honey bees learned that a sugary reward was available when they detected a particular pattern of electrical field. © 2010 American Association for the Advancement of Science

Keyword: Pain & Touch; Aggression
Link ID: 17963 - Posted: 03.28.2013