dimarts, 26 de juny de 2012

Seeking Emotional Clues Without Facial Cues // NYT

NYT // April 5, 2010 // By BENEDICT CAREY

STUDYING EXPRESSIONS Kathleen Bogart, with her husband, Beau, at Tufts University, where she is a graduate student. Ms. Bogart has Moebius syndrome, which causes facial paralysis.

Like many of the Hurricane Katrinarefugees who straggled into Baton Rouge, La., in the summer of 2005, she needed more than food and shelter. She needed company, sympathy — someone, anyone, to see and feel her loss — and searched the face of her assigned social worker in vain.

But the social worker, barely out of college, seemed somehow emotionally removed. Something was missing.

“I could see the breakdown in the emotional connection between us, could see it happening and there was nothing I could do,” said Kathleen Bogart, 28, the social worker who is now a psychology researcher at Tufts University here. Ms. Bogart has Moebius syndrome, a rare congenital condition named for a 19th-century neurologist that causes facial paralysis.

When the people she helped made a sad expression, she continued, “I wasn’t able to return it. I tried to do so with words and tone of voice, but it was no use. Stripped of the facial expression, the emotion just dies there, unshared. It just dies.”

Researchers have long known that facial expressions are crucial to social interaction and have categorized them in great detail. They know which expressions are universal; they can distinguish slight differences in expression, for example between a polite smile and a genuine one.

Still, a central question remains: How does the brain interpret others’ expressions so quickly and accurately? The answer is likely to be enormously important, experts say, both for understanding how social interactions can go smoothly and how they can go off track.

Studies so far point to what psychologists call facial mimicry. During a social exchange, people subconsciously mirror each other’s surprise, disgust or delight — and, in effect, interpret the emotion by sensing what’s embodied on their own face. Interfere with the ability to mimic, these studies suggest, and people are less adept at reading others’ expressions.

But what if a person cannot mimic any expressions, at all?

In a new study, the largest to date of Moebius syndrome, Ms. Bogart and David Matsumoto, a psychologist at San Francisco State, found that people with the disorder, whatever their social struggles, had no trouble at all recognizing others’ expressions. They do just as well as anyone else in identifying emotions in photographed faces, despite having no way to mimic.

The findings strongly suggest that the brain has other systems to recognize facial expressions, and that people with facial paralysis learn to take advantage of those. “It seems likely they would develop compensatory strategies in response to the long-term impairment,” said Tanya Chartrand, a psychologist at Duke University who is not involved in the Moebius Syndrome study, in an e-mail message. “Ones that don’t rely on the mimicry process and allow them to understand emotion through a different route.”

If such strategies are teachable, experts say, they could help others with social awkwardness, whether because of anxiety, developmental problems like autism, or common causes of partial paralysis, like Bell’s palsy.

“I had no special interest in studying facial paralysis, even though I had it; there were many other things I could have done,” Ms. Bogart said, in her office at Tufts. “But in college I looked to see what psychologists had to say about it, and there was nothing. Very, very little on facial paralysis at all. And I was just — well, I was angry.”

The emotion tightened her fist, straightened her frame and ran up into her eyes, bypassing her face: “Angry. I thought, I might as well do it because certainly no one else is.”

Moebius syndrome has no known cause; it strikes less than one in 100,000 children at birth, resulting in total, or nearly total, facial paralysis. In most cases the eyes don’t blink, and the irises move only up and down, robbing people of sideways glances and an entire vocabulary of gazes, squints and eye-rolls. The taunts tend to start early in childhood and pile up, and no one can see the embarrassment or pain in the target. “Like having a deformity and not being able to communicate, all in one,” Ms. Bogart said.

Most people with the condition adapt. “Just like for blind people, whose senses of touch, smell, hearing become sharper,” Dr. Matsumoto said. “Same thing here, I think, only it’s in the domain of nonverbal communication.” 

In the first of two studies, Ms. Bogart and Dr. Matsumoto had 36 people with Moebius syndrome look at 42 standardized photographs online of expressions, like anger, happiness and sadness. The participants correctly identified the emotions about three-quarters of the time — the same rate as adults without the condition. Their level of impairment was not related to their score. 

The results do not imply that socializing is easy or natural for people with such paralysis; most do struggle, Ms. Bogart and Dr. Matusmoto found in a follow-up study. The main reason for this (beyond the immobile features, which distract some people) has little to do with a deficit in recognizing emotions in others, the studies suggest.

It most likely comes back to mimicry, or the lack thereof. In a series of studies, psychologists have found that social bonding between conversation partners is highly dependent on a rhythmic and usually subconscious give and take of gestures and expressions that creates a kind of shared good will. “Part of that could be the buying in on the interaction itself,” Dr. Chartrand said. If the timing is not just right — the Moebius study did not account for timing — then the buy-in can feel uncertain, and interaction fizzles. The way that many people with complete, or near complete, paralysis overcome this problem is by relying on channels other than the face: eye contact, hand gestures, posture and voice tone. Many people with paralysis can make that expressive instrument as subtle and potent as a string section.
“I found my voice, figuratively and literally, in speech therapy,” said Matthew S. Joffe, the director of student services at LaGuardia Community College and a therapist in private practice, who has Moebius syndrome. Dr. Joffe described his paralysis as pronounced, “with a mouth that hangs open, and a lower lip that protrudes downward.”

“I use humor a lot,” he said. “It’s a way of showing my humanity, for one thing, and over the years people have said I have a great laugh. And I’m old enough now — I can agree. I laugh from the innards of my belly, I have many different laughs for different occasions, each one looks distinct in my body. I learned pretty early on that, given the fairly harsh standards society imposes, that if I didn’t laugh at stuff I would probably just collapse.”

Ms. Bogart, too, has a distinctive laugh. Her jaw drops,, her lips stretch and lift slightly, and her entire torso shakes. The need to rely on these peripheral channels makes people with paralysis especially sensitive to such cues in others. “At a party, I feel like I can tell whether someone will be worth talking to within seconds,” she said. “I can read people’s comfort level, or whether they can work through discomfort, very quickly.”

Taken together, some psychologists say, the evidence from people with paralysis and those without it suggests that the brain is tuning into several channels at once when it reads others’ emotional vibes. Mimicry is surely one — but it needs help. In an experiment published last year, Dutch researchers had 46 students at Leiden University pair off for a three-minute interaction with a fellow student who was either lying or telling the truth about a donation to charity. Those students told not to mimic the expressions of their conversation partner were significantly better at determining who was telling the truth than students told to mimic, or given no instructions. “Mimicry, whether spontaneous or the product of instruction, hinders observers in objectively assessing” people’s true feelings.
The gestures and tones that people with paralysis are so adept at using add more information. “And we think there may be other systems as well, in pre-motor areas of the brain, that are compiling all of this information” so that the cortex can make a judgment on the emotion, Dr. Matsumoto said.
In her current research project, Ms. Bogart is videotaping dozens of social interactions with people with all variety of paralysis, not just Moebius, but Bell’s palsy, which often stills half the face, and nerve injuries.

“The plan is to show the interviews to people to see what their impressions are, to tease apart all the elements of face, voice, gestures to see what is perceived by people as positive or negative,” she said. “The idea is that if we could learn what the best nonverbal communication techniques are, we could teach those to people who are socially awkward for any reason.”


dilluns, 18 de juny de 2012

El epigenoma cambia a lo largo de la vida

Este hallazgo sugiere que cambios dietéticos o el uso de fármacos podrían prolongar la existenciaUna investigación de colaboración internacional ha revelado que el epigenoma de los recién nacidos y el de los centenarios es distinto, incluso para un mismo tejido u órgano. Estos resultados demuestran que el centenario presenta un epigenoma distorsionado que ha perdido muchos interruptores encargados de apagar la expresión de genes inapropiados y, en cambio, ha apagado el interruptor de algunos genes protectores. La modificación de estos procesos, mediante cambios dietéticos o por el uso de fármacos, podría inducir un aumento del tiempo de vida, afirman los autores del estudio. IDIBELL/T21.

¿Qué ocurre en nuestras células tras cien años de vida? ¿En qué se diferencian a nivel molecular un recién nacido y un centenario? ¿Se trata de cambios graduales o súbitos? ¿Es posible revertir el proceso de envejecimiento? ¿Cuáles son las claves moleculares de la longevidad?Estas cuestiones centrales en biología, fisiología y medicina humana han sido foco de estudio de investigadores durante décadas.La revista internacional Proceedings of the National Academy of Sciences (PNAS) publica una investigación de colaboración internacional dirigida por Manel Esteller, director del programa de Epigenética y Biología del Cáncer del Instituto de Investigación Biomédica de Bellvitge (IDIBELL), profesor de genética de la Universidad de Barcelona e investigador ICREA, que proporciona una pista esencial en este campo: el epigenoma de los recién nacidos y de los centenarios es distinto.Mientras que el genoma de todas las células del cuerpo humano, con independencia de su aspecto y función, es idéntico, las señales químicas que lo regulan, conocidas como marcas epigenéticas, son específicas de cada tejido humano y de cada órgano.Es decir, que todos nuestros componentes tienen el mismo abecedario (genoma), pero la ortografía (epigenoma) es distinta en cada parte de nuestra anatomía.El resultado sorprendente del trabajo del grupo del Dr. Esteller es que incluso para un mismo tejido u órgano, el epigenoma varía en función de la edad de la persona.

Posibilidad de aumentar el tiempo de vida

En el estudio publicado en PNAS se han secuenciado totalmente los epigenomas de las células blancas de la sangre de un recién nacido, un individuo de edad intermedia y una persona de 103 años.Los resultados demuestran que el centenario presenta un epigenoma distorsionado que ha perdido muchos interruptores (grupo químico metilo), encargados de apagar la expresión de genes inapropiados y, en cambio, se apaga el interruptor de algunos genes protectores.“Extendiendo los resultados a un grupo numeroso de neonatos, individuos situados en el punto medio y nonagenarios o centenarios nos damos cuenta de que se trata de un proceso progresivo en el que cada día que pasa el epigenoma se va torciendo”, afirma el investigador.Sin embargo, el doctor Esteller destaca que “las lesiones epigenéticas, a diferencia de las genéticas, son reversibles y, por tanto, la modificación de los patrones de la metilación del ADN por cambios dietéticos o por el uso de fármacos podría inducir un aumento del tiempo de vida”.

Fuente: http://www.tendencias21.net/El-epigenoma-cambia-a-lo-largo-de-la-vida_a12100.html
Heyn H, Li N, Ferreira HJ, Moran S, Pisano DG, Gomez A, Diez J, Sanchez-Mut JV, Setien F, Carmona FJ, Pucaf AA Sayols S, Pujana MA, Serra-Musach J, Iglesias-Plata I, Formiga F, Fernandez AF, Fraga MF, Heath S, Valencia A, Gut IG, Wang J, Esteller M. The Distinct DNA Methylomes of Newborns and Centenarians. Proc Natl Acad Sci USA, DOI10.1073, 2012.

dimecres, 13 de juny de 2012

"When being scared twice is enough to remember"

One of the brain's jobs is to help us figure out what's important enough to be remembered. Scientists at Yerkes National Primate Research Center, Emory University have achieved some insight into how fleeting experiences become memories in the brain. 

MachinesLike Us //  Wednesday, 13 June 2012

Their experimental system could be a way to test or refine treatments aimed at enhancing learning and memory, or interfering with troubling memories. The results were published recently in the Journal of Neuroscience.

The researchers set up a system where rats were exposed to a light followed by a mild shock. A single light-shock event isn't enough to make the rat afraid of the light, but a repeat of the pairing of the light and shock is, even a few days later.

"I describe this effect as 'priming'," says the first author of the paper, postdoctoral fellow Ryan Parsons. "The animal experiences all sorts of things, and has to sort out what's important. If something happens just once, it doesn't register. But twice, and the animal remembers."

Parsons was working with Michael Davis, PhD, Robert W. Woodruff professor of psychiatry and behavioral sciences at Emory University School of Medicine, who has been studying the molecular basis for fear memory for several years.

Even though a robust fear memory was not formed after the first priming event, at that point Parsons could already detect chemical changes in the amygdala, part of the brain critical for fear responses. Long term memory formation could be blocked by infusing a drug into the amygdala. The drug inhibits protein kinase A, which is involved in the chemical changes Parsons observed.

It is possible to train rats to become afraid of something like a sound or a smell after one event, Parsons says. However, rats are less sensitive to light compared with sounds or smells, and a relatively mild shock was used.

Fear memories only formed when shocks were paired with light, instead of noise or nothing at all, for both the priming and the confirmation event. Parsons measured how afraid the rats were by gauging their "acoustic startle response" (how jittery they were in response to a loud noise) in the presence of the light, compared to before training began.

Scientists have been able to study the chemical changes connected with the priming process extensively in neurons in culture dishes, but not as much in live animals. The process is referred to as "metaplasticity," or how the history of the brain's experiences affects its readiness to change and learn. 

"This could be a good model for dissecting the mechanisms involved in learning and memory," Parsons says. "We're going to be able to look at what's going on in that first priming event, as well as when the long-term memory is triggered."

"We believe our findings might help explain how events are selected out for long-term storage from what is essentially a torrent of information encountered during conscious experience," Parsons and Davis write in their paper.