Temper Tantrums

For more information on parenting skills and tantrums, visit ParentMagic.com

Secondhand Smoke + Bed Sharing RaiseSudden Infant Death (SID) Risk

US Health officials claimed to have helped halve cases of Sudden Infant Death Syndrome (SIDS) with a campaign that warned parents to keep their babies from sleeping face down.

The SIDS rate didn't decline further, however, indicating that other causes exist, and a new study points to secondhand smoke and bed sharing as significant risk factors.

SIDS causes more than 2,000 deaths each year in the U.S. and is the leading cause of death in children between one month and one year, according to the Centers for Disease Control and Prevention.

Remembering that the cause of SIDS is still unknown, a strong correlation has been found between putting a baby to sleep on its stomach and SIDS.

The US National Institute of Child Health and Human Development started the "Back to Sleep" campaign in 1994 to warn parents of the dangers of putting babies to sleep on their stomachs, which helped reduce the rate of SIDS by more than 50 percent since 1988, according to the US federal agency.

The campaign also led to identification of other SIDS risk factors, according to the study. Researchers found that babies who slept in a bed with other people are twice as likely to die from SIDS. The younger the child is, the higher the risk.

"Bed-sharing leads to a 17 or 18 times increase in risk if the baby is less than two or three months old," Rachel Moon, a pediatrician and SIDS researcher at Children's National Medical Center who was not involved with the study, reported.

If the baby is exposed to smoke as well, the risk increases even further.

Other risk factors for SIDS include soft bedding or toys in the crib, sleeping on an adult mattress or couch, sleeping with a blanket or with the head covered. Three out of four SIDS cases had at least one risk factor and 57 percent had at least two, according to the study.

"Most babies had two or more risk factors," Henry Krous, lead author and paediatric pathologist at the San Diego SIDS Research Project, reported. "What that says to us is that 'Back to Sleep' should emphasize multiple risk factors."

Secondhand Smoke, Bed Sharing Raises Sudden Infant Death Risk

ADHD Challenges Those Seeking a Driver’s License

The first time Jillian Serpa tried to learn to drive, the family car wound up straddling a creek next to her home in Ringwood, N.J.

Ms. Serpa, then 16, had gotten flustered trying to sort out a rapid string of directions from her father while preparing to back out of their driveway. “There was a lack of communication,” she said. “I stepped on the gas instead of the brake.”

On her second attempt to learn, Ms. Serpa recalled, she “totally freaked out” at a busy intersection.

It was four years before she tried driving again. She has made great progress, but so far has still fallen short of her goal: Two weeks ago she knocked over a cone while parallel parking and failed the road test for the fourth time.

Learning to drive is hard and scary for many teenagers, and driving is far and away the most dangerous thing teenagers do. But the challenges are significantly greater for young people who, like Ms. Serpa, have attention problems.

A number of cognitive conditions can affect driving, and instructors report a recent increase in the number of teenagers with Asperger syndrome seeking licenses.

But the largest group of challenged teenage drivers and the mostly closely studied, appears to be those with attention deficit hyperactivity disorder (ADHD, ADD).

A 2007 study, by Russell A. Barkley of the Medical University of South Carolina and Daniel J. Cox of the University of Virginia Health System, concluded that young drivers with ADHD are two to four times as likely as those without the condition to have an accident, meaning that they are at a higher risk of wrecking the car than an adult who is legally drunk.

Researchers say that many teenagers with attention or other learning problems can become good drivers, but not easily or quickly, and that some will be better off not driving till they are older or not at all.

The most obvious difficulty they face is inattention, the single leading cause of crashes among all drivers, said Bruce Simons-Morton, senior investigator at the National Institute for Child Health and Human Development in Bethesda, Md.

“When a driver takes his eyes off the road for two seconds or more, he’s doubled the risk of a crash,” he said.

Inexperienced drivers usually are distractible drivers. Dr. Simons-Morton cited a study on a closed course in which teenagers proved much more adept than adults at using cellphones while driving and missed more stop signs.

The situation isn’t helped by how “noisy” cars have become, with cellphones, iPods and Bluetooth devices, said Lissa Robins Kapust, a social worker and coordinator of a driving program at Beth Israel Deaconess Medical Center in Boston. “Driving is so busy on the inside and the outside of the car it’s the most complex thing we do.”

But ADHD involves more than distractibility (?). Its other major trait is impulsiveness, which is often linked to high levels of risk-taking, said Dr. Barkley.

“It’s a bad combination” for young drivers, he said. “They’re more prone to crashes because of inattention, but the reason their crashes are so much worse is because they’re so often speeding.” Many drivers with ADHD overestimate their skills behind the wheel, Dr. Barkley noted.

Read more in the NY Times

Dyslexia: Octavia Butler Author Extraordinaire

Despite her Dyslexia, Octavia Butler was an award-winning author of thirteen books. She was a pioneer in the science fiction genre, winning both the Nebula and the Hugo Awards.

In 1995, Butler was honoured with a MacArthur fellowship, and in 2005, she was the recipient of the City College of New York's Langston Hughes Medal.

The Pen Center West awarded her with a lifetime achievement award. Tragically, she died in 2006, after a fall outside of her home.

Throughout her life Octavia never considered herself to be very bright, much less a genius. In fact, she struggled in school, where teachers interpreted her slow reading and inability to finish assignments in the allotted time, as laziness and an unwillingness to do the work.

But when given the time to write in school, Butler would weave tales that were so out-of-the-box her teacher assumed she had copied them from a published story.

When she was thirteen, one teacher did recognize her talents as a writer and encouraged her to submit a short story to a science fiction magazine, he even typed it out for her.

That story would be the first of many she submitted for publication, and would signify the moment Butler knew that she wanted to, and could, write for a living; however, Butler was writing stories for herself long before then.

A shy loner, Butler found solace and company in words. At as young as four years old, she was making up stories for herself; and as she recalls in an interview with the literary journal Callaloo, “By the time I was ten I was writing, and I carried a big notebook around so that whenever I had some time I could write in it.

That way, I didn’t have to be lonely. I usually had very few friends, and I was lonely. But when I wrote I wasn’t, which was probably a good reason for my continuing to write as a young kid. I read a lot also, for the same reasons.”

Despite her dyslexia, she was a bookworm, reading everything that she could find. Butler described how she got her first library card: “When I was six and was finally given books to read in school, I found them incredibly dull; they were Dick and Jane books. I asked my mother for a library card. I remember the surprised look on her face. She looked surprised and happy. She immediately took me to the library and got me a card. From then on the library was my second home.”

Butler’s mother only had three years of education, but she learned to read, and worked hard as a housekeeper to make sure that her daughter learned to read and went to school.

After high school, Butler went on to graduate from Pasadena City College with an Associates of Arts degree in 1968.

Read more of Octavia Butler's story here: Octavia Butler: Author

Autism: Defective Genes May Explain Uncontrolled Brain Growth

As a baby grows inside the womb, its brain does not simply expand like a dehydrated sponge dropped in water.

Early brain development is an elaborate procession. Every minute some 250,000 neurons bloom, squirming past one another like so many schoolchildren rushing to their seats at the sound of the bell.

Each neuron grows a long root at one end and a crown of branches at the other, linking itself to fellow cells near and far.

By the end of the second trimester, neurons in the baby's brain have formed trillions of connections, many of which will not survive into adulthood—the least traveled paths will eventually wither.

Sometimes, the developing brain blunders, resulting in "neuro-developmental disorders," such as autism.

But exactly why or how early cellular mistakes cause autism has eluded medical science. Now, Eric Courchesne of the University of California, San Diego, thinks he has linked atypical gene activity to excessive growth in the autistic brain.

With the new data, he has started to trace a cascade of genetic and cellular changes that he thinks define autism.

Although intrigued by Courchesne's work, other researchers caution that explosive neural growth is not necessarily a defining feature of all autistic brains.

Since 1998 Courchesne has been searching autistic brains for unusual structural features.

His studies suggest that while in the womb, the autistic brain sprouts an excess of neurons and continues to balloon during the first five years of life, as all those extra neurons grow larger and form connections.

Sometime after age four or five, Courchesne has also found, autistic brains actually start to lose neural connections, faster than typical brains.

In a study published November 2011 in JAMA, The Journal of the American Medical Association, Courchesne reported that children with autism have 67 percent more neurons in their prefrontal cortex (PFC) than typical children.

Located in the area of the brain just behind the eyes, the PFC is responsible for what psychologists call "executive functions"—high-level thinking, such as planning ahead, inhibiting impulses and directing attention. In his 2011 study Courchesne sliced up brain tissue from six autistic children and seven typical children who had passed away and counted the number of cell bodies in the sections to estimate the total number of neurons in their PFCs.

Now, Courchesne and his colleagues have analyzed DNA and RNA in 33 cubes of brain tissue from people who passed away, 15 of whom were autistic (nine children and six adults) and 18 who had typical brains (seven children and 11 adults).

Looking at the order of DNA's building blocks reveals whether individual genes have mutations; measuring levels of RNA indicates how often those genes were translated into proteins.

Such gene expression, Courchesne and his colleagues found, varied between autistic and typical brains.

In brain tissue from both autistic children and autistic adults, genes coding for proteins that identify and repair mistakes in DNA were expressed at unusually low levels.

Additionally, all autistic brains demonstrated unusual activity levels for genes that determine when neurons grow and die and how newborn neurons migrate during early development.

Some genes involved in immune responses, cell-to-cell communication and tissue repair, however, were expressed at unusual levels in adult autistic brains, but not in autistic children's brains.

The results appear in the March 22 issue of PLoS Genetics.

You can also Read More of this article here at Scientific American: The Ballooning Brain

Mike BaBoon Design: Dr Seuss Alphabet

Depicted are: Aunt Annie (Dr Seuss’s ABC), Bartholomew Cubbins (The 500 Hats of Bartholomew Cubbins), the Cat in the Hat, Dave (Too Many Daves), Elephant-Cat (If I Ran the Zoo), Fox in Socks, the Grinch (How the Grinch Stole Christmas), Horton (Horton Hatches the Egg), Iota (If I Ran the Zoo), Jake the Pillow Snake (I Can Read with My Eyes Shut), King Bertram (The King’s Stilts), The Lorax, Daisy-Head Mayzie, North-Going Zax (The Zax), One Fish (One Fish Two Fish Red Fish Blue Fish), Pop (Hop on Pop), Quilligan Quail (I Had Trouble Getting to Solla Sollew), Rosy’s Red Rhinoceros (Dr. Seuss’s ABC), Sam-I-Am (Green Eggs and Ham), Thing One (The Cat in the Hat), Uncle Ubb (Dr. Seuss' ABC), Vipper of Vipp (Oh, the Thinks You Can Think), Wickersham Brothers (Horton Hears a Who), Little Cat X (The Cat in the Hat Comes Back), Yertle the Turtle, Zook (Butter Battle Book) 

Prints are available at http://society6.com/mbaboon/Dr-Seuss-Alphabet_Print

Mike BaBoon Design: Dr. Seuss Alphabet

Parents of sick kids distrust online medical help - ‘Dr. Google’

Parents of children with cancer not only don’t trust online medical sites, but fear them as well, preferring instead to receive information from a trusted source, like a doctor.

“Respondents were telling us they were uncertain of the information online and that they were afraid of the unknown,” says study co-author Elizabeth Gage, professor of community health and health behavior at the University at Buffalo. “They didn’t want to run into stories about ‘the worst case scenario’.”

Gage, along with Christina Panagakis, a UB graduate student in sociology and colleagues at Roswell Park Cancer Institute, interviewed 41 parents of pediatric cancer patients in the U.S. to learn how caregivers use the Internet as an information source about their child’s illness, its prognosis, and potential treatment options.

Published in the journal Sociology of Health and Illness, the study suggests that beyond a distrust and fear of health-related Internet sites, online searching for information about an illness might vary between patients dealing with routine conditions and those faced with life-threatening problems.

“The likelihood of a patient going online might depend very much on context,” Gage explains.

Previous studies looked at what Gage described as routine, contested, or stigmatized illnesses, while her research contributes a piece of knowledge relative to severe pediatric illnesses.

“One of the reasons we were interested in exploring this issue is that so much research and media coverage had examined how the Internet was breaking down barriers between patients and caregivers and their physicians,” Gage says.

“But that wasn’t the case in our study. Perhaps because of the severity of the diagnosis, parents and caregivers preferred to receive their information from sources other than the Internet.”

The information-seeking behaviour of parents and other caregivers appears to be influenced by the volume of available information, Gage says.

Patients with routine illnesses might find minor details online that better inform their conversations with health care providers, but respondents in this study who were confronting a more serious diagnosis were overwhelmed by the often conflicting sources of online material.

“Families in our study did not know where to begin or how to sift through such a huge mound of information,” Gage says.

Those who did look for information through the Internet tended to limit their searches to what they considered more credible sources, such as medical journals and hospital libraries, the study says.

“A lot of families used the Internet to establish connections with other families in a similar situation, as much for emotional support as for reasons to share medical information,” Gage says.

“However, many families ascribed a certain expert status upon these individuals, almost elevating the experience of what they call “the veterans” to the same level as that of a trusted hospital-based site.”

More news from University at Buffalo: www.buffalo.edu/news

Serotonin Levels: Protein in overdrive links to Autism (ASD)

Early disruptions in serotonin signaling in the brain may contribute to Autism Spectrum Disorder (ASD) and other “enduring effects on behavior,” researchers report.

Serotonin is a brain chemical that carries signals across the synapse, or gap between nerve cells. The supply of serotonin is regulated by the serotonin transporter (SERT).

In 2005, a team of researchers from Vanderbilt University led by Randy Blakely and James Sutcliffe identified rare genetic variations in children with ASD that disrupt SERT function.

In a new study published this week in the Proceedings of the National Academy of Sciences (PNAS), the researchers report the creation of a mouse model that expressed the most common of these variations.

The change is a very small one in biochemical terms, yet it appears to cause SERT in the brain to go into “overdrive” and restrict the availability of serotonin at synapses.

“The SERT protein in the brain of our mice appears to exhibit the exaggerated function and lack of regulation we saw using cell models,” says Blakely, director of the Vanderbilt Silvio O. Conte Center for Neuroscience Research.

“Remarkably, these mice show changes in social behavior and communication from early life that may parallel aspects of ASD,” notes first author Jeremy Veenstra-VanderWeele, assistant professor of psychiatry, pediatrics and pharmacology.

The researchers conclude that a lack of serotonin during development may lead to long-standing changes in the way the brain is “wired.”

In 1961, investigators at Yale University discovered that as many as 30 percent of children with autism have elevated blood levels of serotonin, a finding described as “hyperserotonemia.”

Since then, these findings have been replicated many times. Indeed, hyperserotonemia is the most consistently reported biochemical finding in autism, and is a highly inherited trait. Yet, the cause or significance of this biomarker has remained shrouded in mystery.

Until now. In the current study, Veenstra-VanderWeele, Blakely and their colleagues showed that they could produce hyperserotonemia in mice that express a variant of a human SERT gene associated with autism.

Because the genetic change makes the transporter more active, higher levels of serotonin accumulate in platelets and therefore in the bloodstream.

In the brain, overactive transporters should have the opposite effect—lowering serotonin levels at the synapse and producing behavioural changes relevant to autism. That’s exactly what the researchers observed.

Of course, no mouse model can completely explain or reproduce the human condition. Neither does a single genetic variation cause autism. Experts believe the wide spectrum of autistic behaviours represents a complex web of interactions between many genes and environmental factors.

But animal models are critical to exploring more deeply the basis for the developmental changes that are observed in ASD.

The scientists are using these mice to explore how altered brain serotonin levels during development may produce long-lasting changes in behaviour and impact the risk for autism.

Scientists from the National Institute of Mental Health, the Medical University of South Carolina and the University of Texas Health Science Center in San Antonio contributed to the study.

The research was supported by the National Institutes of Health, the advocacy organisation Autism Speaks (UK), and the American Academy of Child and Adolescent Psychiatry.

More news from Vanderbilt University: news.vanderbilt.edu/research

Toxoplasma Gondii: How your cat could be making you ‘crazy’

It’s long been known that a microbe found in cat's can harm people with weakened immune systems, such as people with AIDS.

It’s also been known that pregnant women should avoid cat litter so they don’t catch the microbe, lest they pass it on to their babies, causing brain damage in the infants or even death.

The microbe in question is Toxoplasma gondii (T. gondii or Toxo for short).

New research from an unconventional scientist is showing that in certain circumstances, the microbe can alter our basic personalities, making us more or less outgoing, trusting and fearful, and even making us more prone to schizophrenia, car crashes and suicides.

The circumstances that create this possibility are as follows;

• We have to be infected by the microbe
• Our bodies will eventually overcome it, 
• But the parasite can lay dormant,
• and the danger lies in whether it lodges or travels to our brain cells

The researcher, the Czech evolutionary biologist Jaroslav Flegr, claims that when you consider all its impacts, “Toxoplasma might even kill as many people as malaria, or at least a million people a year.”

Read more of this article here: How your cat could be making you ‘crazy’

The Smiley Book of Colours

When Freud came to believe he was going to die between the ages of 61 and 62, and subsequently began seeing the two numbers everywhere he looked, which only intensifying the urgency of his superstition, he came to observe the value of selective attention in focusing the unconscious.

But what if we engineered this selective attention purposefully and aligned it with our emotional and mental well-being?

That’s exactly what photographer, children’s author, and educator Ruth Kaiser did in 2008, when she began seeing smiley faces everywhere she turned.

For the past four years, she has been collecting and sharing photographs “found” everyday smileys in the Spontaneous Smiley Project — an exercise in self-induced feel-goodness, inviting others to upload their own photos and donating $1 for each uploaded photo to Operation Smile, which provides free surgeries to children born with cleft lip and cleft palate.

Four years later, The Smiley Book of Colors was born, at once teaching (eternal) kids basic color theory and instilling in them the habits of optimism — a charming, light-hearted complement to the recent grown-up exploration of the science of smiles.

The images are paired with simple, poetic meditations on the optimistic life — truths we may be tempted, through years of conditioned cynicism, to roll our eyes at, but ones that remain, at their heart, beautiful and true.

Let a neuroscientist elaborate on the optimism bias and its benefits.

Noam Chomsky: The Purpose of an Education - Video

Noam Chomsky discusses the purpose of education, impact of technology, whether education should be perceived as a cost or an investment and the value of standardised assessment.

Presented at the Learning Without Frontiers Conference - Jan 25th 2012- London (LWF 12)

www.learningwithoutfrontiers.com

A Hand-Painted Typographic Experiment by Tien-Min Liao

A Hand-Painted Typographic Experiment by Tien-Min Liao

Handmade Type is a typographic experiment by designer Tien-Min Liao wherein shapes painted on her hands are transformed by gestures to create letterforms.

However she gave herself a unique constraint: the painted figures on her hands for each individual letter had to be utilized for all variations of the letter, both upper and lowercase and sometimes even italic and handwritten. See more examples and the full alphabet over on Behance.

Prosopagnosia - Face Blidness

Prosopagnosia is a disorder of face perception where the ability to recognize faces is impaired, while the ability to recognize other objects may be relatively intact.

The term originally referred to a condition following acute brain damage, but a congenital form of the disorder has been proposed, which may be inherited by about 2.5% of the population.

The specific brain area usually associated with prosopagnosia is the fusiform gyrus.

Few successful therapies have so far been developed for affected people, although individuals often learn to use 'piecemeal' or 'feature by feature' recognition strategies.

This may involve secondary clues such as clothing, gait, hair colour, body shape, and voice. Because the face seems to function as an important identifying feature in memory, it can also be difficult for people with this condition to keep track of information about people, and socialize normally with others.

Some also use the term prosophenosia, which refers to the inability to recognize faces following extensive damage of both occipital and temporal lobes.

Children with Prosopagnosia
Developmental prosopagnosia can be a difficult thing for a child to both understand and cope with. Many adults with developmental prosopagnosia report for a long time they had no idea that they had a deficit in face processing, unaware that others could distinguish people solely on facial differences.

Children with prosopagnosia can be hard to find. They may just appear to be very shy or slightly odd due to their inabilities to recognise faces.

Children with prosopagnosia may have a hard time making friends, as they may not recognize their classmates. They often make friends with children with other distinguishing features.

Children with prosopagnosia may also have difficulties following the plots of television shows and movies, as they have trouble recognizing the different characters.

They tend to gravitate towards cartoons, where the characters always wear the same thing and have other distinguishing features.

Prosopagnosiac children may also have a hard time telling family members apart or recognizing people out of context (i.e. the teacher in a grocery store).

Additionally, those children with prosopagnosia can have a difficult time with the public school system, as many school professionals are not well versed in prosopagnosia, if they are aware of the disorder at all.

Resources
Resources to help parents and professionals cope with prosopagnosia in children are also being developed, such as Understanding Facial Recognition Disorders in Children by Nancy L. Mindick

Oliver Sacks, famous neuroscientist, author of many books including The Man Who Mistook His Wife for a Hat; although he knew what prosopagnosia was and had studied it, he did not realise he had it until people became shocked that he confused one of his brothers with the other and then, discussing it with family members, learned that a number of them had similar difficulties with face.

Dame Jane Goodall, British primatologist, ethologist, and anthropologist, best known for her 45-year study of social and family interactions of wild chimpanzees.

Listen to Jane describe her condition and how it's affected her life:

Can Playing Maternal Voice and Heartbeat Sounds Benefit Premies?

Nearly five years ago, Amir Lahav became a parent of twins born prematurely at 25 weeks. They weighed just over 1 pound each.

Welcoming two newborns into the family certainly changed his life, but as a neuroscientist, it also ended up changing the course of his research.

Lahav studies how the brain processes sounds, and worked primarily with neurologically impaired adults, but with the birth of his twins, his paternal instinct kicked in.

He approached the chief of newborn medicine at Brigham and Women’s Hospital in Boston, where the babies lay in incubators.

“Could I put a recording of my wife's voice in there?” Lahav asked, convinced that hearing their mother’s soothing tones would improve the babies’ development. The answer: It's certainly worthwhile.

Using his computer, Lahav recorded his wife’s voice telling the babies they’re fighters and urging them to be strong.

He also included some soothing piano music, figuring it could prove relaxing for preemies. Then he tinkered with the sound to make it resemble what a baby would hear in utero.

While we hear through air, babies in the womb process sound through fluid so what passes as hearing consists of more low-frequency vibrations. (Think about slipping beneath the surface of the bath as someone talks to you, or try speaking while putting a finger in each ear.) “It’s as if babies are living in a micro-subwoofer,” explains Lahav.

The twins seemed to like the recordings, and doctors and nurses in the neonatal intensive care unit (NICU) were intrigued.

Moreover, it proved therapeutic for Lahav and his wife. “It was not a controlled trial,” says Lahav, “but just a crazy father trying to do something because especially in the case of premature babies, you feel very helpless.”

Once his twins left the hospital, Lahav returned to thank the chief for letting him experiment.

One thing led to another, and they found themselves in a serious conversation about prematurity and how the focus of neonatal medicine has changed from saving the lives of these babies, doctors have grown expert at keeping preemies alive, to helping them grow into healthy children.

Studies have shown that premature infants are at greater risk of having low IQ and developing metabolic or chronic conditions in young adulthood that can shorten their lives.

Could keeping them bathed in mom’s comforting sounds lower the incidence of some of these adverse effects on their health? Lahav wound up with a job offer to find out.

Read more: Can Playing Maternal Voice and Heartbeat Sounds Benefit Premies?

Williams Syndrome: PET Brain Scans Provide insight

A peek inside the minds of hypersocial people with Williams syndrome has revealed how the genetic disorder affects the brain.

People with Williams syndrome are known for their friendliness, although this tends to be coupled with heightened anxieties.

You can contact the UK Williams Syndrome association, here

Mbemba Jabbi at the National Institutes of Health in Bethesda, Maryland, and colleagues studied MRI scans of 14 people with the syndrome. They found that the insula, a brain region involved in emotion, was smaller than in 23 people without the syndrome.

When Jabbi's team used PET scans to examine the insula in more detail, though, they found that one area of the right insula was larger in people with Williams syndrome. Those with more extreme personality differences had more grey matter here.

The findings could help predict how social symptoms of the syndrome might develop, says Debbie Riby at Newcastle University, UK.

However, the people who participated in the study have a normal IQ, which is typical of only a small percentage of those with Williams syndrome, she says.

Journal reference: Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.1114774109

Selfish, self-centred kids? Blame their immature brains

Dr. Nikolaus Steinbeis

A new study suggests that age-associated improvements in the ability to consider the preferences of others are linked with maturation of a brain region involved in self control.

The findings, published in the March 8 issue of the journal Neuron, may help to explain why young children often struggle to control selfish impulses, even when they know better, and could impact educational strategies designed to promote successful social behaviour.

Human social interactions often involve two parties who want to maximize their own outcomes while reaching a mutually satisfactory result.

It is generally accepted that over the course of childhood behaviour shifts from a more selfish focus to an increased tendency to consider the benefits to others.

However, little is known about age-related changes in this type of "strategic social behaviour" or the underlying neuronal mechanisms.

Researchers from the Max-Planck Institute for Cognitive and Brain Sciences in Leipzig conducted behavioural and brain-imaging studies comparing children of different ages as they engaged in two carefully constructed games called "The Dictator Game" and "The Ultimatum Game."

In the Dictator Game, children were asked to share a reward with another child who could only passively accept what was offered.

In the Ultimatum Game, the recipient had to accept the offer or neither child received a reward. Therefore, the games differed in the demand for strategic behavior for the child making the offer.

"We were interested in whether children would share more fairly if their counterparts could reject their offers, and to what extent strategic behaviour was dependent on age and brain development," explains lead study author, Dr. Nikolaus Steinbeis.

"We observed an age-related increase in strategic decision making between ages 6 to 13 years and showed that changes in bargaining behaviour were best accounted for by age-related differences in impulse-control abilities and underlying functional activity of the left dorsolateral prefrontal cortex, a late-maturing brain region linked with self control," explains Dr. Steinbeis.

The results suggest that egocentric behavior in children may not be a function of an inability to know "fair" from "unfair," but is instead due to an immature prefrontal cortex that does not support altruistic behaviour when faced with a situation that has a strong self-serving incentive.

"Our findings represent a critical advance in our understanding of the development of social behaviour with far-reaching implications for educational policy and highlight the importance of helping children act on what they already know," concludes Dr. Steinbeis. "Such interventions could set the foundation for increased altruism in the future."

SEN Magazine - The emotional consequences of Dyslexia

The most current research into dyslexia tends to focus upon where it exists within the human brain or what form of intervention is most likely to prevent or overcome its effects.

Essentially, such approaches are reifying the concept, giving the impression that Dyslexia is a thing that can be identified or a condition that can be diagnosed and then dealt with.

If we consider Dyslexia from a more humanistic perspective, however, we find ourselves asking a totally different set of questions of the following nature:

• how does it feel to be faced each day with the apparently simple task (in that everyone else can do it) of learning to read without being able to cope?
• do any of the significant adults in one’s life (parents, teachers, partners) seem to understand (a) how it must feel, and (b) how to help?
• if learning to read and spell is considered to be so important in our society, what effect is the inability to do so likely to have on a person’s developing sense of identity?
• is there really an effective “one solution fits all” approach to literacy?
• what are likely to be the long term effects of slipping through the net and not being recognised as suffering from specific learning difficulties of a dyslexic nature?

The comparatively limited research that has been devoted to such questions has tended to produce somewhat equivocal results.

A review of the research results relating to the self-concept of Dyslexic school children (Burden, 2008), for example, reveals that a person’s general self-esteem will not necessarily suffer irrevocably as a result of struggling at school from difficulties of a dyslexic nature, but that early recognition, intervention and emotional support are all significant factors in building resilience.

A closer investigation of this data, alongside more intensive interviews with young people who had been diagnosed as dyslexic, showed that their feelings of being understood played a vitally important role in coming to terms with early literacy difficulties (Burden, 2005).

This did not necessarily require the significant adult to understand the nature, cause or “cure” for the disability, only in the first instance that they demonstrated empathy with the dyslexic child’s feelings.

However, this was only the first stage in a long term process that would be necessary for the development of their ontological security.

As the American psychologist Martin Covington has identified, a growing child's sense of self-worth is highly likely to be closely associated with how well they are coping with school-based academic tasks.

If one is aware of not doing well, this in turn may well lead to what Covington terms “self-worth concern” and efforts to protect one’s sense of wellbeing. “… the student's sense of esteem often becomes equated with ability – to be able is to be valued as a human being but to do poorly in school is evidence of inability, and reason to despair of one’s worth” (Covington, 1992).

Read more of this article here:

Nintendo Wii™ game controllers help diagnose eye disorder (ocular torticollis)

Nintendo Wii remotes are not all about fun and games.

Scientists can use them to assess and diagnose children with an abnormal head position caused by (ocular torticollis) eye diseases.

As described in a recent Investigative Ophthalmology & Visual Science article, researchers developed a low-cost digital head posture measuring device with Nintendo Wiimotes to help diagnose this condition, medically called ocular torticollis.

"Torticollis occurs in about 1.3% of children," said author, Jeong-Min Hwang, MD, of Seoul National University College of Medicine.

"Accurate measurement of the angle of the abnormal head position is crucial for evaluating disease progression and determining treatment or surgical plans in parties with ocular torticollis."

Hwang and his colleagues point out that in clinical practice where it can be difficult to get reliable data from children whose heads move constantly, a digital head posture measuring systems using electronic devices such as the motion tracking capability offered by Wiimotes would be an ideal alternative.

Below is an old (2008) YouTube video which helps to demonstrate the Wii head tracking technique.

The researchers used two Wii controllers to develop an infrared optical head tracker (IOHT) that automatically measures and records the angle of the head in real-time.

The remotes were connected to a monitoring computer with an infrared camera and Bluetooth connectivity.

The IOHT was evaluated for accuracy, validity and reliability by comparing it with the 'Cervical Range of Motion Instrument' or CROM device, one of the most widely used head posture measuring devices in hospitals.

Results demonstrated that in measuring the head posture of normal adult subjects, the measurement of the one-dimensional and three-dimensional (3-D) positions of a human head with IOHT were very close to those of CROM.

There were slightly more deviations of measurements between IOHT and CROM than the researchers expected in 3-D movement of the head, which the researchers contribute to the structural nature of CROM rather than inaccurate measurement of IOHT.

In looking at the future, the research team hopes this new tool will play a key role in diagnosing ophthalmic patients. "Considering its high performance, ease of use and low cost, we believe IOHT has the potential to be widely used as a head posture measuring device in clinical practice."

Newly approved drug Surfaxin® for infant Respiratory Distress Syndrome (RDS)

Scientific advances at The Scripps Research Institute have led to a new drug Surfaxin® (lucinactant), approved March 7 by the U.S. Food and Drug Administration (FDA) to treat infant respiratory distress syndrome.

The FDA statement announcing the approval. 

"I am excited that our scientific findings will help save lives," said Charles Cochrane, MD, professor emeritus at Scripps Research.

"Many years of work in our basic research laboratory at The Scripps Research Institute made this landmark development possible."

The Study
In the study, the infants were treated with lucinactant (Surfaxin), colfosceril palmitate (Exosurf), or beractant (Survanta) within 30 minutes of birth. Those treated with lucinactant had significant improvement in respiratory distress syndrome at 24 hours after birth

RDS
Respiratory distress syndrome (also known as neonatal respiratory distress syndrome) is a life-threatening condition affecting pre-term infants.

The more premature an infant is, the more likely he or she is to suffer from it and die.

The condition occurs when infants are born prior to the time when natural surfactant is made in their lungs.

Surfactant is a liquid that coats the inside of the lungs, helping to keep the air sacs open and making normal breathing possible. Without enough surfactant, the lungs collapse and the body can be starved of oxygen.

In addition to mechanical ventilation, current treatments for pre-term infants involve using surfactants derived from chopped cow or pig lungs.

Current Disadvantages
However, animal-derived surfactants are expensive, contain material that can be injurious to the lungs, and cannot be produced in quantities sufficient to treat pre-term infants worldwide.

In addition, animal-derived surfactants can only be used once since they cause an immune reaction; in contrast, the new synthetic surfactant is not immunogenic.

The Cochrane lab first created a synthetic version of surfactant in the 1990s, mimicking a natural peptide known as Surfactant Protein B; the inventors of the technology are Cochrane and Susan Revak.

After this formative work at Scripps Research, the therapy was developed by Discovery Labs of Warrington, PA, which oversaw the three phases of clinical trials required by the FDA.

These clinic trials provided data on the drug's success.

Daylight saving time can throw you off your normal sleep cycle

Sunday 19th March is the start of daylight saving time and although it will throw off the clock only by an hour, it's enough to leave people feeling groggy for a day or two, sleep experts say.

By setting clocks ahead an hour, daylight saving time allows us more light through the spring, summer and fall. But when the time changes at 2 a.m. Sunday (except in Arizona and Hawaii), it will cost one hour of sleep. We'll regain that when the clocks fall back on Nov. 4.

"Losing an hour is harder than gaining an hour," says Steven Feinsilver, director of the Center for Sleep Medicine at Mount Sinai Medical Center in New York. "It's sort of like a mini jet lag."

It takes no more than 48 hours to adjust to a one-hour loss, says New York pulmonologist and sleep specialist Nicholas Rummo of Northern Westchester Hospital's Center for Sleep Medicine. "The day or two after people aren't quite alert," he says. "Most people might feel it Monday into Tuesday."

Some people will be more sluggish than others Monday morning — particularly those without regular sleep habits, such as waking up at a consistent time or snoozing seven to eight hours each night.

"Millions of people can ill afford to lose one more hour of sleep given that so many of them are so sleep-deprived," says Russell Rosenberg, board chairman for the US National Sleep Foundation.

Sleep directly affects health and safety, Rosenberg says, and the sleep loss associated with daylight saving time has been linked to increases in traffic and on-the-job accidents the Monday following the time change.

Specialists encourage people to use this, the US National Sleep Foundation's National Sleep Awareness week, to adopt good habits so that next year, it won't be quite so tiring to make the leap forward. Sleep doctors offer a few tips for making up for lost z's:

•Start early. Move your schedule up a few minutes each day, eat dinner and go to bed 10 to 15 minutes earlier every night.

•Take a nap Sunday to "build up a little sleep in your sleep bank," says Russell Rosenberg, board chairman for the National Sleep Foundation, noting that siestas should be less than an hour.


•Every minute counts Set the alarm clock for the last possible minute Monday morning.

•Soak up the sun. Sunlight jump-starts our bodies and sets our internal clocks forward, so sip your coffee in front of a window for an extra jolt. "Light in the morning makes us want to go to bed earlier," says New York pulmonologist and sleep specialist Nicholas Rummo.


•Avoid alcohol and caffeine. These interfere with the hormones and chemistry that regulate our bodies and make it more difficult to fall asleep and wake up.

Synesthesia: Laughter on the Canvas

Laughter is an uncontrollable emotion that brings joy. It's not, however, something you'd normally see depicted graphically in a painting.

Sonja Landis, 35, is a Carlsbad artist who brings laughter to life with the stroke of a paintbrush and some help from sound engineers.

Sonja Landis started The Painted Laugh about three years ago, when she heard her son laugh and saw colourful sound waves swirling around him.

She has a documented but not widely understood condition called Synesthesia. It's a neurological condition where two senses involuntarily cross. Her type allows her to see sound in the air.

When Landis first painted the sound waves of laughter, she did it for herself and hung a piece above her mantel.

Once people saw the painting, everyone wanted one. It eventually evolved into a business and she has been distributing them all over the country ever since, and plans on selling internationally.

After the paintings became popular, she decided to add actual sound. This way, parents and grandparents could hear their children's laughter whenever they wanted.

A button is placed behind the canvas of her paintings. Push it and it plays a recording of your child's laugh.

"There is a universal truth to laughter that doesn't need an explanation between cultures and between languages," Landis says. "And that's what I love about this the most."

Landis has partnered with Crayola, and has experimented with laughter therapy for children's hospitals.

Click here to watch a YouTube video made by The Painted laugh 

Sonja Landis also has a project running that is trying to create or develop a Painted Laugh APP for Smartphones and iPad devices.

The video below outlines her thinking on this.

The Black Book of Colours - The Partly Sighted Companion

Today must be the day for tickling the outer limits of our senses. From the synesthetic explorations of sound through colour earlier today, we take the creative mind-bending a step further: Experiencing colour through the lack of colour.  

The Black Book of Colours, from author Menena Cottin and illustrator Rosana Faria, is a remarkable book of simple, elegant illustrations of natural objects, from strawberries to rain to bird feathers, depicted not through colour and shading but through embossed lines, inviting the viewer to experience them tactilely rather than visually.







The book is designed as an empathy tool that allows a sighted person to step inside the world of the blind, who experience the world through their fingers rather than their eyes.



Though intended for children, The Black Book of Colours is an absolute treat for adults, not merely as a feat of aesthetic elegance, but also as a beautiful philosophical metaphor for all those things in our lives that both are and aren’t, like the nature of reality or solitude or some great love we can touch with the tender tips of our fingers but never fully grasp.

International Dyslexia Assoc: The Impact on Mathematics

While teachers and parents are well aware of the effect of dyslexia on reading, they often overlook its impact on mathematics.

The mastery of the symbolic language of mathematics involves many verbal cognitive processes that can be affected by dyslexia.

Ignoring the impact of dyslexia on the mastery of mathematics can hamper a child’s progress in school and in life.

Dyslexia is the inability to decode and obtain meaning from the printed word. It is a learning disability, not a condition due to inadequate instruction or intelligence.

Estimates of the incidence of dyslexia in school age children range from 5 to 10% (Shaywitz, Shaywitz, Fletcher, & Esteban, 1990).

Dyslexia most clearly impacts reading, spelling, and written expression. However, dyslexia may also affect mathematics achievement.

Approximately 5.9 % of students are identified with a math disability, a number similar to those with a reading disability (Fuchs, Fuchs, Powell, Seethaler, Cirino, & Fletcher, 2008).

Mathematics has a symbolic language whose practical function is to express spatial and quantitative relationships.

Number sense is acquired in developmental stages similar to those in the acquisition of language.

The process begins as soon as children begin to move and explore their environments, placing one box into another, stringing beads, learning “all gone”, etc.

 Spatial relations concepts are based on identification of objects in space, distinguishing right from left, reasoning with abstract designs, and visualizing objects in other positions.

 Children first assimilate and integrate non-verbal experiences; then they associate numerical symbols, numbers, and mathematical words such as “less” to these experiences.

 Children need to have both experiences with mathematical relationships and the words to express them.

Reading numbers and recalling number names are prerequisites for using them to represent abstract quantities.

However, associating the names with the numerals, and recalling them when needed, may be difficult for children with dyslexia.

Mastery of numerical operations also involves retrieval of basic facts. Some children work diligently to learn the multiplication tables but cannot recall them, much to the frustration of teachers and parents.

Such retrieval problems were evident when Rosie , a bright ten year old with dyslexia, and her grandmother worked on learning the names of coins in a homework assignment.

“Grandma,” she said wearily, “ I can tell you that it’s worth ten cents but I don’t know its name.” The task of recalling, sequencing, and manipulating figures, shapes, letters, designs, patterns and numerals and associating them with quantities is analogous to associating letter names with the corresponding sounds, a task many children with dyslexia find challenging.

Instruction in mathematics is most frequently verbal instruction. This may be problematic for children with poor verbal comprehension and poor short term auditory memories.

They hear the teacher but do not fully comprehend or recall the concepts and operations she is describing because of language issues.

With faulty understanding, they are unable to apply the information correctly. Since mathematical concepts build on one another, this shaky foundation can adversely affect mastery of future concepts.

Moreover, the vocabulary of mathematics is unique and can be confusing. Subtraction problems can be phrased as “less than” “ take away”, “minus”, “subtract”, all of which refer to the same process.

Such multiple meanings should be directly taught but frequently it is simply assumed that children have learned them.

Word problems embed the math calculations in language. Performance here is impacted by problems with syntax and vocabulary, as well as calculation problems.

To obtain the correct answer, children must first comprehend the syntax and vocabulary, understand what the problem is asking, ignore extraneous information, devise a strategy to solve it, and retrieve and apply the requisite facts and operations.(Bryant & Bryant, 2008)

Solving algorithms also involves performing operations in correct sequence and reading operational signs correctly.

The symbolic language of math notations, such as decimal points, using x to signify the unknown, exponents, and parentheses, can be confusing.

Some children learn this language incidentally but for others this language must be frequently reinforced.

One eleven year old requested of his teacher, “Tell me which sign it is—the add one or the times one” before starting his calculations.

Dyslexia may make mastering mathematics difficult. Teachers and parents must be aware of potential issues and provide the supports necessary to ensure success in mathematics as well as in reading.

Sunbird Educational Products Fruit & Veg Maths - YouTube

Fruit and Veg Maths is a truely interactive maths resource. Not because it can be used on an electronic whiteboard but because it can be manipulated by the teacher and/or the students.

It’s colourful and bright and guaranteed to keep your students engaged in maths lessons. Our resources are created to show students that maths lessons can be fun and interesting.

Fruit and Veg Maths allows children to practise real world situations when they are given a shopping list and have to calculate the cost.

Sunbird Educational Products

ADHD: The Youngest Students in a Class

The youngest children in a class are more likely to be diagnosed with ADHD than older children in the same class, a new study finds, and in some cases may not deserve the diagnosis.

Researchers led by Richard Morrow, a health research analyst at the Therapeutics Initiative at University of British Columbia, looked at ADHD diagnosis rates depending on whether children were born right before or after the school enrollment cutoff date.


In British Columbia, the cutoff date for kindergarten or first grade is Dec. 31, which means that kids born in December are the youngest in their class, while those born in January are the oldest.

The researchers found that children born in December were 39% more likely to be diagnosed with ADHD and 48% more likely to be receiving medication to treat it than children in the same class born in January.


In the study, which included data on 937, 943 children aged 6 to 12 over an 11-year period, Morrow and his colleagues also found that the rate of ADHD diagnoses increased steadily with each successive month from January to December.

The fact that there was such a difference in the rate of ADHD diagnoses simply based on children’s birthdates, all other things being equal, strongly suggests that less mature students may have been inappropriately being labeled with an attention deficit disorder.


“What is clear from our study is that younger children in a classroom are more likely to receive a diagnosis of ADHD and drugs to treat that ADHD,” says Morrow. “But their relative maturity should come into play.”

”Something to keep in mind when we look at behavioural problems is whether the behaviour relates to differences in age and maturity.”
Read More of this article here: ADHD: Why the Youngest Students in a Class Are Most Likely to Be Diagnosed

Autism: Researchers find another piece of the puzzle

Autism spectrum disorders (ASDs) have a complex inheritance pattern. Despite researchers having identified rare variants in synaptic proteins in patients with ASD, little work has been carried out to determine the effect at the synapse and their interactions with other genetic variations, until now.

A European team of researchers has confirmed that synaptic mutations heightens the risk of ASD.

The study, presented in the journal PLoS Genetics, was funded in part by the EUHFAUTISM ('European high-functioning autism network: translational research in a phenotypically well characterised sample') project, a Neuron-ERA-NET funded under the EU's Seventh Framework Programme (FP7) to the tune of almost EUR 370,000.

Researchers led by the Institut Pasteur in France combined genetic and neurobiological approaches to determine how ASD risk increases. They also found how modifier genes influence these disorders.

ASDs are a heterogeneous group of neurodevelopmental disorders with a complex inheritance pattern characterised by impairments in social interaction and communication. Repetitive behaviour also restricts them.

According to the researchers, ASDs emerge before the age of three years and affect 1% of children. More boys than girls have a higher risk of being affected by ASD.

The researchers say a number of genes that play a role in ASD have been identified in patients with ASD. However, researchers have only recently begun learning about their effects on neuronal functions and their interaction with other genetic variations.

'The genetic causes of ASD are diverse, but the main category of genes associated with the disorder is related to the development and function of neuronal circuits,' the authors write.

 'Mutations of genes coding for synaptic cell adhesion molecules and scaffolding proteins, such as neuroligins (NLGNs), neurexins (NRXNs) and SHANK, have been recurrently reported in patients with ASD. These proteins play a crucial role in the formation and stabilisation of synapses, as well as in synaptic homeostasis.

'SHANK2 and SHANK3 code for scaffolding proteins located in the postsynaptic density (PSD) of glutamatergic synapses. Deletions of ProSAP2/SHANK3 at chromosome 22q13 are one of the major genetic abnormalities in neurodevelopmental disorders, and mutations of ProSAP2/SHANK3 have been identified in patients with ASD, intellectual disability (ID) and schizophrenia. Mutations of ProSAP1/SHANK2 have also recently been reported in both ASD and ID. The difference in clinical outcome of mutation carriers has been attributed to the presence of still uncharacterised additional genetic, epigenetic and/or environmental factors.'

Commenting on the significance of the findings, the Institut Pasteur's Thomas Bourgeron says they emphasise the importance of a synaptic gene dysfunction in ASD, and they underline a role for modifier genes confirming 'a multiple hit model for ASD. A better knowledge of these genetic interactions will be necessary to understand the complex inheritance pattern of ASD'.

For more information, please visit:

Institut Pasteur: http://www.pasteur.fr/ip/easysite/pasteur/fr

PLoS Genetics: http://www.plosgenetics.org/home.action

Motor Neurone Disease: New Insight about how it works

When we imagine how research results can change society or help us make new bounds in medical science we think of proving a hypothesis or cracking a code, but sometimes research that refutes a theory can be just as beneficial, as scientists can eliminate a hypothesis from the mix and save years of wasted-time investigating dead ends and a team of German researchers has just done exactly that.

Writing in the journal Proceedings of the National Academy of Sciences (PNAS), the team refute a widely accepted hypothesis about a causative step in neuro-degenerative conditions.

These results deal specifically with animal models of human amyotrophic lateral sclerosis (ALS), more commonly known as Motor Neurone Disease, but the findings also have implications for other neuro-degenerative diseases such as Alzheimer's or Huntington's disease.

One of the ways neuro-degenerative diseases manifest themselves is in the loss of axons - essentially, the transmission lines for electrical signals in individual nerve cells - and synapses, the key sites for communication between them.

In the past, such damage has been attributed to deficits in the bi-directional transport of organelles, such as the intracellular power plants called mitochondria, along the axons of nerve cells.

The team, from the Technische Universitaet Muenchen (TUM) and Ludwig-Maximilians-Universitaet Muenchen (LMU), put these previously-held assumptions to the test in one of the most thorough tests carried out to date.

They used novel imaging techniques, with high resolution in both space and time, to observe changes in both axon morphology and organelle transport in several different animal models of ALS.

Their results show that transport deficits and axon degeneration can develop independently of each other, throwing into question the theory that one is a direct cause of the other.

They observed axonal organelle transport in living tissue in real time, and in a way that enabled them to track the movement of individual mitochondria, using a novel imaging approach that involves transgenic labelling.

They were also able to observe transport of another kind of organelle, endosome-derived vesicles. Several different animal models of ALS were investigated, all of which are based on human mutations associated with the disease.

One of the study authors, Professor Thomas Misgeld from the Institute of Neuroscience at the Technische Universitaet Muenchen, comments on their findings: 'We do think these insights have implications for other studies of ALS, or even studies of other neuro-degenerative diseases.

What our experiments really say is that it is not easy to develop faithful models of neuro-degenerative diseases.

So it might be worth spending more effort to get better animal models, as this is the only way forward for mechanistic studies, while always checking them against human pathology or human-derived cellular models.

In the meantime, it is probably prudent to work with several of the available models in parallel. Moreover, in more general biological terms, our results also speak to the relationship between axonal transport disruptions and degeneration - which might not be as tight as we assumed. Here we have a lot more to understand.'

The iPSoALS project brings together researchers from France, Germany, Israel and Sweden with the aim of better understanding ALS disease mechanisms.

For more information, please visit: Technische Universitaet Muenchen (TUM)