Daryle Lockhart

ajacquelineofalltrades:

I’m not an artist, but I have more than a few friends who are, so I thought this might be a good thing to post. 

Preach it, Skottie.

designboom:

patrick dougherty weaves ‘fit for a queen’ at castle moat in nantes
all images © martin argyroglo / LVAN

set within the fortress walls, the installation invites viewers to enter and explore the tangled passageways and windows built into its tree-like expanse. see how its built, here.

neurosciencestuff:

Scientists Link Alcohol-Dependence Gene to Neurotransmitter
Scientists at The Scripps Research Institute (TSRI) have solved the mystery of why a specific signaling pathway can be associated with alcohol dependence. 
This signaling pathway is regulated by a gene, called neurofibromatosis type 1 (Nf1), which TSRI scientists found is linked with excessive drinking in mice. The new research shows Nf1 regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases feelings of relaxation.
“This novel and seminal study provides insights into the cellular mechanisms of alcohol dependence,” said TSRI Associate Professor Marisa Roberto, a co-author of the paper. “Importantly, the study also offers a correlation between rodent and human data.”
In addition to showing that Nf1 is key to the regulation of the GABA, the research, which was published recently in the journal Biological Psychiatry, shows that variations in the human version of the Nf1 gene are linked to alcohol-dependence risk and severity in patients.
Pietro Paolo Sanna, associate professor at TSRI and the study’s corresponding author, was optimistic about the long-term clinical implications of the work. “A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy,” he said.
A Genetic Culprit
Researchers have long sought a gene or genes that might be responsible for risk and severity of alcohol dependence. “Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood,” said TSRI Staff Scientist Vez Repunte-Canonigo, co-first author of the paper with TSRI Research Associate Melissa Herman.
This research showed that Nf1 is one of those rare risk genes, but the TSRI researchers weren’t sure exactly how Nf1 affected the brain. The TSRI research team suspected that Nf1 might be relevant to alcohol-related GABA activity in an area of the brain called the central amygdala, which is important in decision-making and stress- and addiction-related processes.
“As GABA release in the central amygdala has been shown to be critical in the transition from recreational drinking to alcohol dependence, we thought that Nf1 regulation of GABA release might be relevant to alcohol consumption,” said Herman.
The team tested several behavioral models, including a model in which mice escalate alcohol drinking after repeated withdrawal periods, to study the effects of partially deleting Nf1. In this experiment, which simulated the transition to excessive drinking that is associated with alcohol dependence in humans, they found that mice with functional Nf1 genes steadily increased their ethanol intake starting after just one episode of withdrawal. Conversely, mice with a partially deleted Nf1 gene showed no increase in alcohol consumption.
Investigating further, the researchers found that in mice with partially deleted Nf1 genes, alcohol consumption did not further increase GABA release in the central amygdala. In contrast, in mice with functional Nf1 genes, alcohol consumption resulted in an increase in central amygdala GABA.
In the second part of the study, a collaboration with a distinguished group of geneticists at various U.S. institutions, the team analyzed data on human variations of the Nf1 gene from about 9,000 people. The results showed an association between the gene and alcohol-dependence risk and severity.
The team sees the new findings as “pieces to the puzzle.” Sanna believes future research should focus on exactly how Nf1 regulates the GABA system and how gene expression may be altered during early development.

neurosciencestuff:

Scientists Link Alcohol-Dependence Gene to Neurotransmitter

Scientists at The Scripps Research Institute (TSRI) have solved the mystery of why a specific signaling pathway can be associated with alcohol dependence.

This signaling pathway is regulated by a gene, called neurofibromatosis type 1 (Nf1), which TSRI scientists found is linked with excessive drinking in mice. The new research shows Nf1 regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases feelings of relaxation.

“This novel and seminal study provides insights into the cellular mechanisms of alcohol dependence,” said TSRI Associate Professor Marisa Roberto, a co-author of the paper. “Importantly, the study also offers a correlation between rodent and human data.”

In addition to showing that Nf1 is key to the regulation of the GABA, the research, which was published recently in the journal Biological Psychiatry, shows that variations in the human version of the Nf1 gene are linked to alcohol-dependence risk and severity in patients.

Pietro Paolo Sanna, associate professor at TSRI and the study’s corresponding author, was optimistic about the long-term clinical implications of the work. “A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy,” he said.

A Genetic Culprit

Researchers have long sought a gene or genes that might be responsible for risk and severity of alcohol dependence. “Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood,” said TSRI Staff Scientist Vez Repunte-Canonigo, co-first author of the paper with TSRI Research Associate Melissa Herman.

This research showed that Nf1 is one of those rare risk genes, but the TSRI researchers weren’t sure exactly how Nf1 affected the brain. The TSRI research team suspected that Nf1 might be relevant to alcohol-related GABA activity in an area of the brain called the central amygdala, which is important in decision-making and stress- and addiction-related processes.

“As GABA release in the central amygdala has been shown to be critical in the transition from recreational drinking to alcohol dependence, we thought that Nf1 regulation of GABA release might be relevant to alcohol consumption,” said Herman.

The team tested several behavioral models, including a model in which mice escalate alcohol drinking after repeated withdrawal periods, to study the effects of partially deleting Nf1. In this experiment, which simulated the transition to excessive drinking that is associated with alcohol dependence in humans, they found that mice with functional Nf1 genes steadily increased their ethanol intake starting after just one episode of withdrawal. Conversely, mice with a partially deleted Nf1 gene showed no increase in alcohol consumption.

Investigating further, the researchers found that in mice with partially deleted Nf1 genes, alcohol consumption did not further increase GABA release in the central amygdala. In contrast, in mice with functional Nf1 genes, alcohol consumption resulted in an increase in central amygdala GABA.

In the second part of the study, a collaboration with a distinguished group of geneticists at various U.S. institutions, the team analyzed data on human variations of the Nf1 gene from about 9,000 people. The results showed an association between the gene and alcohol-dependence risk and severity.

The team sees the new findings as “pieces to the puzzle.” Sanna believes future research should focus on exactly how Nf1 regulates the GABA system and how gene expression may be altered during early development.

asylum-art:

New York city camouflage series by Trina Merry

Watch the video after text:

Her models meld into the grey Manhattan skyline as if they’re made of mirrors and glass.

Now body artist Trina Merry has spoken about her head-turning technique, painstakingly painting women so they blend in with New York’s landmarks, after her incredible creations made headlines around the world.

The 33-year-old shuns studios and canvases, instead letting her nude models camouflage seamlessly into the world around them.

Art imitates life: New York body painter Trina Merry’s models blend into the Manhattan Bridge (left) and Guggenheim museum (right) wearing coloured shoes and bikini bottoms. The 33-year-old began her inspiring project after moving to New York from San Francisco because she wanted to provide a ‘reflective view within the landscape’

ri-science:

In which direction is the cube spinning? Now blink, or look away and look back. Is it still spinning in the same direction?
A Necker Cube is an ambiguous line drawing. Our brain can create different interpretations of it.
This clip was part of the Christmas Lectures 2011 presented by Professor Bruce Hood - Lecture One: What’s in your head? Watch it in full on the Ri Channel.

ri-science:

In which direction is the cube spinning? Now blink, or look away and look back. Is it still spinning in the same direction?

A Necker Cube is an ambiguous line drawing. Our brain can create different interpretations of it.

This clip was part of the Christmas Lectures 2011 presented by Professor Bruce Hood - Lecture One: What’s in your head? Watch it in full on the Ri Channel.

neurosciencestuff:

Researchers discover fever’s origin
Fever is a response to inflammation, and is triggered by an onset of the signaling substance prostaglandin. Researchers at Linköping University can now see precisely where these substances are produced – a discovery that paves the way for smarter drugs.
When you take an aspirin, all production of prostaglandins in the body is suppressed. All symptoms of inflammation are eased simultaneously, including fever, pain and loss of appetite. But it might not always be desirable to get rid of all symptoms – there is a reason why they appear.
”Perhaps you want to inhibit loss of appetite but retain fever. In the case of serious infections, fever can be a good thing,” says David Engblom, senior lecturer in neurobiology at Linköping University.
Eleven years ago he had his first breakthrough as a researcher when he uncovered the mechanism behind the formation of prostaglandin E2 during fever. These signaling molecules cannot pass the blood-brain barrier, the purpose of which is to protect the brain from hazardous substances. Engblom showed that instead, they could be synthesised from two enzymes in the blood vessels on the inside of the brain, before moving to the hypothalamus, where the body’s thermostat is located.
Previous work from the research team described a very simple mechanism, but there was not yet proof that it was important in real life. The study to be published in The Journal of Neuroscience with David Engblom and his doctoral student Daniel Wilhelms as lead authors is based on tests with mice that lack the enzymes COX-2 and mPGES-1 in the brain’s blood vessels. When they were infected with bacterial toxins the fever did not appear, while other signs of inflammation were not affected.
”This shows that those prostaglandins which cause fever are formed in the blood-brain barrier – nowhere else. Now it will be interesting to investigate the other inflammation symptoms. Knowledge of this type can be useful when developing drugs that ease certain symptoms, but not all of them,” explains David Engblom.
For many years there has been debate as to where the fever signaling originates. Three alternative ideas have been proposed. Firstly, that it comes from prostaglandins circulating in the blood, secondly that it comes from immune cells in the brain, and thirdly Engblom’s theory, which stresses the importance of the brain’s blood vessels. The third proposal can now be considered confirmed.

neurosciencestuff:

Researchers discover fever’s origin

Fever is a response to inflammation, and is triggered by an onset of the signaling substance prostaglandin. Researchers at Linköping University can now see precisely where these substances are produced – a discovery that paves the way for smarter drugs.

When you take an aspirin, all production of prostaglandins in the body is suppressed. All symptoms of inflammation are eased simultaneously, including fever, pain and loss of appetite. But it might not always be desirable to get rid of all symptoms – there is a reason why they appear.

”Perhaps you want to inhibit loss of appetite but retain fever. In the case of serious infections, fever can be a good thing,” says David Engblom, senior lecturer in neurobiology at Linköping University.

Eleven years ago he had his first breakthrough as a researcher when he uncovered the mechanism behind the formation of prostaglandin Eduring fever. These signaling molecules cannot pass the blood-brain barrier, the purpose of which is to protect the brain from hazardous substances. Engblom showed that instead, they could be synthesised from two enzymes in the blood vessels on the inside of the brain, before moving to the hypothalamus, where the body’s thermostat is located.

Previous work from the research team described a very simple mechanism, but there was not yet proof that it was important in real life. The study to be published in The Journal of Neuroscience with David Engblom and his doctoral student Daniel Wilhelms as lead authors is based on tests with mice that lack the enzymes COX-2 and mPGES-1 in the brain’s blood vessels. When they were infected with bacterial toxins the fever did not appear, while other signs of inflammation were not affected.

”This shows that those prostaglandins which cause fever are formed in the blood-brain barrier – nowhere else. Now it will be interesting to investigate the other inflammation symptoms. Knowledge of this type can be useful when developing drugs that ease certain symptoms, but not all of them,” explains David Engblom.

For many years there has been debate as to where the fever signaling originates. Three alternative ideas have been proposed. Firstly, that it comes from prostaglandins circulating in the blood, secondly that it comes from immune cells in the brain, and thirdly Engblom’s theory, which stresses the importance of the brain’s blood vessels. The third proposal can now be considered confirmed.