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neurosciencestuff:

Children as young as three recognise ‘cuteness’ in faces of people and animals

Children as young as three are able to recognise the same ‘cute’ infantile facial features in humans and animals which encourage caregiving behaviour in adults, new research has shown.

A study investigating whether youngsters can identify baby-like characteristics – a set of traits known as the ‘baby schema’ – across different species has revealed for the first time that even pre-school children rate puppies, kittens and babies as cuter than their adult counterparts.

The discovery that young children are influenced by the baby schema – a round face, high forehead, big eyes and a small nose and mouth – is a significant step towards understanding why humans are more attracted to infantile features, the study authors believe.

The baby schema has been proven to engender protective, care-giving behaviour and a decreased likelihood of aggression toward infants from adults.

The research was carried out by PhD student Marta Borgi and Professor Kerstin Meints, members of the Evolution and Development Research Group in the School of Psychology at the University of Lincoln, UK.

Marta said: “This study is important for several reasons. We already knew that adults experience this baby schema effect, finding babies with more infantile features cuter.

“Our results provide the first rigorous demonstration that a visual preference for these traits emerges very early during development. Independently of the species viewed, children in our study spent more time looking at images with a higher degree of these baby-like features.

“Interestingly, while participants gave different cuteness scores to dogs, cats and humans, they all found the images of adult dog faces cuter than both adult cats and human faces.”

The researchers carried out two experiments with children aged between three and six years old: one to track eye movements to see which facial areas the children were drawn to, and a second to assess how cute the children rated animals and humans with infantile traits.

Pictures of human adults and babies, dogs, puppies, cats and kittens were digitally manipulated to appear ‘cuter’ by applying baby schema characteristics. The same source images were also made less cute by giving the subjects more adult-like features: a narrow face, low forehead, small eyes, and large nose and mouth – making this study more rigorous than previous work.

The children rated how cute they thought each image was and their eye movements were analysed using specialist eye-tracking software developed by the University of Lincoln.

The research could also lead to improved education in teaching children about safe behaviour with dogs.

Professor Kerstin Meints, Professor in Developmental Psychology at Lincoln’s School of Psychology, supervised the research.

She said: “We have also demonstrated that children are highly attracted to dogs and puppies, and we now need to find out if that attractiveness may override children’s ability to recognise stress signalling in dogs.”

“This study will also lead to further research with an impact on real life, namely whether the ‘cuteness’ of an animal in rescue centres makes them more or less likely to be adopted.”

This research was published in the scientific journal Frontiers in Psychology.

neurosciencestuff:

Study Links Autistic Behaviors to Enzyme
Fragile X syndrome (FXS) is a genetic disorder that causes obsessive-compulsive and repetitive behaviors, and other behaviors on the autistic spectrum, as well as cognitive deficits. It is the most common inherited cause of mental impairment and the most common cause of autism.
Now biomedical scientists at the University of California, Riverside have published a study that sheds light on the cause of autistic behaviors in FXS. Appearing online today (July 23) in the Journal of Neuroscience, and highlighted also on the cover in this week’s print issue of the journal, the study describes how MMP-9, an enzyme, plays a critical role in the development of autistic behaviors and synapse irregularities, with potential implications for other autistic spectrum disorders.
MMP-9 is produced by brain cells. Inactive, it is secreted into the spaces between cells of the brain, where it awaits activation. Normal brains have quite a bit of inactive MMP-9, and the activation of small amounts has significant effects on the connections between neurons, called synapses. Too much MMP-9 activity causes synapses in the brain to become unstable, leading to functional deficits.
“Our study targets MMP-9 as a potential therapeutic target in Fragile X and shows that genetic deletion of MMP-9 favorably impacts key aspects of FXS-associated anatomical alterations and behaviors in a mouse model of Fragile X,” said Iryna Ethell, a professor of biomedical sciences in the UC Riverside School of Medicine, who co-led the study. “We found that too much MMP-9 activity causes synapses to become unstable, which leads to functional deficits that depend on where in the brain that occurs.”
Ethell explained that mutations in FMR1, a gene, have been known for more than a decade to cause FXS, but until now it has been unclear how these mutations cause unstable synapses and characteristic physical features of this disorder. The new findings expand on earlier work by the research group that showed that an MMP-9 inhibitor, minocycline, can reduce behavioral aspects of FXS, which then led to its use to treat FXS.
To further establish a causative role for MMP-9 in the development of FXS-associated features, including autistic behaviors, the authors generated mice that were missing both FMR1 and MMP-9. They found that while mice with a single FMR1 mutation showed autistic behaviors and macroorchidism (abnormally large testes), mice that also lacked MMP-9 showed no autistic behaviors.
“Our work points directly to MMP-9 over-activation as a cause for synaptic irregularities in FXS, with potential implications for other autistic spectrum disorders and perhaps Alzheimer’s disease,” said Doug Ethell, the head of Molecular Neurobiology at the Western University of Health Sciences, Pomona, Calif., and a coauthor on the study.
The research paper represents many years of bench work and effort by a dedicated team led by the Ethells. The work was primarily done in mice, but human tissue samples were also analyzed, with findings found to be consistent. Specifically, the work involved assessing behaviors, biochemistry, activity and anatomy of synaptic connections in the brain of a mouse model of FXS, as well as the creation of a new mouse line that lacked both the FXS gene and MMP-9.
FXS affects both males and females, with females often having milder symptoms than males. It is estimated that about 1 in 5,000 males are born with the disorder.
The Ethells were joined in the study by UCR’s Harpreet Sidhu (first author of the research paper), Lorraine E. Dansie, and Peter Hickmott. Sidhu and Dansie are neuroscience graduate students; Hickmott is an associate professor of psychology.
Next, the researchers plan to understand how MMP-9 regulates synapse stability inside the neurons. They also plan to find drugs that specifically target MMP-9 without side effects such as new tetracycline derivatives that are potent inhibitors of MMP-9 but lack antibiotic properties.
“Although minocycline was successfully used in clinical trial in FXS, it has some side effects associated with its antibiotic properties, such gastrointestinal irritation,” Iryna Ethell said. “We, therefore, plan to test new non-antibiotic minocycline derivatives. These compounds lack antibiotic activity but still act as non-competitive inhibitors of MMP-9 similar to minocycline.”
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neurosciencestuff:

Study Links Autistic Behaviors to Enzyme

Fragile X syndrome (FXS) is a genetic disorder that causes obsessive-compulsive and repetitive behaviors, and other behaviors on the autistic spectrum, as well as cognitive deficits. It is the most common inherited cause of mental impairment and the most common cause of autism.

Now biomedical scientists at the University of California, Riverside have published a study that sheds light on the cause of autistic behaviors in FXS. Appearing online today (July 23) in the Journal of Neuroscience, and highlighted also on the cover in this week’s print issue of the journal, the study describes how MMP-9, an enzyme, plays a critical role in the development of autistic behaviors and synapse irregularities, with potential implications for other autistic spectrum disorders.

MMP-9 is produced by brain cells. Inactive, it is secreted into the spaces between cells of the brain, where it awaits activation. Normal brains have quite a bit of inactive MMP-9, and the activation of small amounts has significant effects on the connections between neurons, called synapses. Too much MMP-9 activity causes synapses in the brain to become unstable, leading to functional deficits.

“Our study targets MMP-9 as a potential therapeutic target in Fragile X and shows that genetic deletion of MMP-9 favorably impacts key aspects of FXS-associated anatomical alterations and behaviors in a mouse model of Fragile X,” said Iryna Ethell, a professor of biomedical sciences in the UC Riverside School of Medicine, who co-led the study. “We found that too much MMP-9 activity causes synapses to become unstable, which leads to functional deficits that depend on where in the brain that occurs.”

Ethell explained that mutations in FMR1, a gene, have been known for more than a decade to cause FXS, but until now it has been unclear how these mutations cause unstable synapses and characteristic physical features of this disorder. The new findings expand on earlier work by the research group that showed that an MMP-9 inhibitor, minocycline, can reduce behavioral aspects of FXS, which then led to its use to treat FXS.

To further establish a causative role for MMP-9 in the development of FXS-associated features, including autistic behaviors, the authors generated mice that were missing both FMR1 and MMP-9. They found that while mice with a single FMR1 mutation showed autistic behaviors and macroorchidism (abnormally large testes), mice that also lacked MMP-9 showed no autistic behaviors.

“Our work points directly to MMP-9 over-activation as a cause for synaptic irregularities in FXS, with potential implications for other autistic spectrum disorders and perhaps Alzheimer’s disease,” said Doug Ethell, the head of Molecular Neurobiology at the Western University of Health Sciences, Pomona, Calif., and a coauthor on the study.

The research paper represents many years of bench work and effort by a dedicated team led by the Ethells. The work was primarily done in mice, but human tissue samples were also analyzed, with findings found to be consistent. Specifically, the work involved assessing behaviors, biochemistry, activity and anatomy of synaptic connections in the brain of a mouse model of FXS, as well as the creation of a new mouse line that lacked both the FXS gene and MMP-9.

FXS affects both males and females, with females often having milder symptoms than males. It is estimated that about 1 in 5,000 males are born with the disorder.

The Ethells were joined in the study by UCR’s Harpreet Sidhu (first author of the research paper), Lorraine E. Dansie, and Peter Hickmott. Sidhu and Dansie are neuroscience graduate students; Hickmott is an associate professor of psychology.

Next, the researchers plan to understand how MMP-9 regulates synapse stability inside the neurons. They also plan to find drugs that specifically target MMP-9 without side effects such as new tetracycline derivatives that are potent inhibitors of MMP-9 but lack antibiotic properties.

“Although minocycline was successfully used in clinical trial in FXS, it has some side effects associated with its antibiotic properties, such gastrointestinal irritation,” Iryna Ethell said. “We, therefore, plan to test new non-antibiotic minocycline derivatives. These compounds lack antibiotic activity but still act as non-competitive inhibitors of MMP-9 similar to minocycline.”

currentsinbiology:

Ketamine can be a wonder drug for ER patients

For critically ill patients arriving at the emergency department, the drug ketamine can safely provide analgesia, sedation and amnesia for rapid, life-saving intubation, despite decades-old studies that suggested it raised intracranial pressure. The results of a systematic review of 10 recent studies of what many emergency physicians regard as a “wonder drug” are published online in Annals of Emergency Medicine.

"Apprehension for many years about ketamine’s effects on blood pressure or injured brains inhibited its use for intubation, especially in North America compared to Europe, but our review shows those concerns are likely overblown," said lead study author Corinne Hohl, MD, of the Department of Emergency Medicine at Vancouver General Hospital in Vancouver, Canada. "In view of recent concerns about the potential negative effects of an alternative induction agent, etomidate, ketamine should be considered routinely in patients with life-threatening infections and more regularly for patients who have been ‘found down,’ or unconscious, before being transported to the ER."

Lindsay Cohen, Valerie Athaide, Maeve E. Wickham, Mary M. Doyle-Waters, Nicholas G.W. Rose, Corinne M. Hohl. The Effect of Ketamine on Intracranial and Cerebral Perfusion Pressure and Health Outcomes: A Systematic Review. Annals of Emergency Medicine, 2014; DOI: 10.1016/j.annemergmed.2014.06.018

neurosciencestuff:

Missing sleep may hurt your memory
Lack of sleep, already considered a public health epidemic, can also lead to errors in memory, finds a new study by researchers at Michigan State University and the University of California, Irvine.
The study, published online in the journal Psychological Science, found participants deprived of a night’s sleep were more likely to flub the details of a simulated burglary they were shown in a series of images.
Distorted memory can have serious consequences in areas such as criminal justice, where eyewitness misidentifications are thought to be the leading cause of wrongful convictions in the United States.
“We found memory distortion is greater after sleep deprivation,” said Kimberly Fenn, MSU associate professor of psychology and co-investigator on the study. “And people are getting less sleep each night than they ever have.”
The Centers for Disease Control and Prevention calls insufficient sleep an epidemic and said it’s linked to vehicle crashes, industrial disasters and chronic diseases such as hypertension and diabetes.
The researchers conducted experiments at MSU and UC-Irvine to gauge the effect of insufficient sleep on memory. The results: Participants who were kept awake for 24 hours – and even those who got five or fewer hours of sleep – were more likely to mix up event details than participants who were well rested.
“People who repeatedly get low amounts of sleep every night could be more prone in the long run to develop these forms of memory distortion,” Fenn said. “It’s not just a full night of sleep deprivation that puts them at risk.”
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Nikon D4
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neurosciencestuff:

Missing sleep may hurt your memory

Lack of sleep, already considered a public health epidemic, can also lead to errors in memory, finds a new study by researchers at Michigan State University and the University of California, Irvine.

The study, published online in the journal Psychological Science, found participants deprived of a night’s sleep were more likely to flub the details of a simulated burglary they were shown in a series of images.

Distorted memory can have serious consequences in areas such as criminal justice, where eyewitness misidentifications are thought to be the leading cause of wrongful convictions in the United States.

“We found memory distortion is greater after sleep deprivation,” said Kimberly Fenn, MSU associate professor of psychology and co-investigator on the study. “And people are getting less sleep each night than they ever have.”

The Centers for Disease Control and Prevention calls insufficient sleep an epidemic and said it’s linked to vehicle crashes, industrial disasters and chronic diseases such as hypertension and diabetes.

The researchers conducted experiments at MSU and UC-Irvine to gauge the effect of insufficient sleep on memory. The results: Participants who were kept awake for 24 hours – and even those who got five or fewer hours of sleep – were more likely to mix up event details than participants who were well rested.

“People who repeatedly get low amounts of sleep every night could be more prone in the long run to develop these forms of memory distortion,” Fenn said. “It’s not just a full night of sleep deprivation that puts them at risk.”

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