Star From The Lizard Constellation Photobombs Hubble Observation

#DataMining

Poland A and Poland B might be real - Borders of Imperial Germany and the 2015 Polish Presidential Race Exit Poll Results.

Orange (Incumbent): PO (Civic Platform) Party - Liberal-Conservative

Blue: PiS (Law and Justice) Party - Interventionist & Social Conservative

More interesting correlations >>

What movie best represent each US state (according to subtonix)?

50.1% of the US population lives in these 244 counties.

More similar maps >>

The U.S. is increasing its attacks on sprawling ISIS oil fields in eastern Syria. https://t.co/PZyFcdonkd

Source: twitter / nytgraphics

soo cool

(Image caption: diagram of the research findings (Taken from article’s Table of Contents Image) bFGF is produced in the injured zone of the cerebral cortex. Ror2 expression is induced in some population of the astrocytes that receive the bFGF signal, restarting their proliferation by accelerating the progression of their cell cycle)

How brain tissue recovers after injury: the role of astrocytes

A research team led by Associate Professor Mitsuharu ENDO and Professor Yasuhiro MINAMI (both from the Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University) has pinpointed the mechanism underlying astrocyte-mediated restoration of brain tissue after an injury. This could lead to new treatments that encourage regeneration by limiting damage to neurons incurred by reduced blood supply or trauma. The findings were published on October 11 in the online version of GLIA.

When the brain is damaged by trauma or ischemia (restriction in blood supply), immune cells such as macrophages and lymphocytes dispose of the damaged neurons with an inflammatory response. However, an excessive inflammatory response can also harm healthy neurons.

Astrocytes are a type of glial cell*, and the most numerous cell within the human cerebral cortex. In addition to their supportive role in providing nutrients to neurons, studies have shown that they have various other functions, including the direct or active regulation of neuronal activities.

It has recently become clear that astrocytes also have an important function in the restoration of injured brain tissue. While astrocytes do not normally proliferate in healthy brains, they start to proliferate and increase their numbers around injured areas and minimize inflammation by surrounding the damaged neurons, other astrocytes, and inflammatory cells that have entered the damaged zone. Until now the mechanism that prompts astrocytes to proliferate in response to injury was unclear.

The research team focused on the fact that the astrocytes which proliferate around injured areas acquire characteristics similar to neural stem cells. The receptor tyrosine kinase Ror2, a cell surface protein, is highly expressed in neural stem cells in the developing brain. Normally the Ror2 gene is “switched off” within adult brains, but these findings showed that when the brain was injured, Ror2 was expressed in a certain population of the astrocytes around the injured area.

Ror2 is an important cell-surface protein that regulates the proliferation of neural stem cells, so the researchers proposed that Ror2 was regulating the proliferation of astrocytes around the injured areas. They tested this using model mice for which the Ror2 gene did not express in astrocytes. In these mice, the number of proliferating astrocytes after injury showed a remarkable decrease, and the density of astrocytes around the injury site was reduced. Using cultured astrocytes, the team analyzed the mechanism for activating the Ror2 gene, and ascertained that basic fibroblast growth factor (bFGF) can “switch on” Ror2 in some astrocytes.

This research showed that in injured brains, the astrocytes that show (high) expression of Ror2 induced by bFGF signal are primarily responsible for starting proliferation. bFGF is produced by different cell types, including neurons and astrocytes in the injury zone that have escaped damage. Among the astrocytes that received these bFGF signals around the injury zone, some express Ror2 and some do not. The fact that proliferating astrocytes after brain injury are reduced during aging raises the possibility that the population of astrocytes that can express Ror2 might decrease during aging, which could cause an increase in senile dementia. Researchers are aiming to clarify the mechanism that creates these different cell populations of astrocytes.

By artificially controlling the proliferation of astrocytes, in the future we can potentially minimize damage caused to neurons by brain injuries and establish a new treatment that encourages regeneration of damaged brain areas.

*Glial cell: a catch-all term for non-neuronal cells that belong to the nervous system. They support neurons in various roles.

Alan Turing and the Halting Problem

By now I’m sure most of you saw Saturday’s Google doodle, commemorating Alan Turing’s 100th birthday.

Turing, as you’ve probably either read or already knew, was a British mathematician regarded as the father of computer science. His work as a codebreaker during the second world war contributed substantially to the allied victory. Tragically, not even his invaluable service to his country was enough to save him from persecution for being homosexual, leading to his untimely death at the age of 41. 

Turing made many contributions to computer science, but the one that stands out is the concept the doodle illustrated: the Turing machine. A Turing machine isn’t an actual machine, or even a blueprint for one. It’s a mathematical idealization of a computer, conceived by Turing long before real computers existed. The centrality of the Turing machine concept in computer science is why every software engineer you know squealed with delight on seeing that doodle. 

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(Image caption: The prefrontal cortex connects to a very specific region of the brainstem (the PAG) through prefrontal cortical neurons: those labeled in purple directly project to the PAG and control our instinctive behaviours. Credit: EMBL/Livia Marrone)

Neural connection keeps instincts in check

From fighting the urge to hit someone to resisting the temptation to run off stage instead of giving that public speech, we are often confronted with situations where we have to curb our instincts. Scientists at EMBL have traced exactly which neuronal projections prevent social animals like us from acting out such impulses. The study, published online in Nature Neuroscience, could have implications for schizophrenia and mood disorders like depression.

“Instincts like fear and sex are important, but you don’t want to be acting on them all the time,” says Cornelius Gross, who led the work at EMBL. “We need to be able to dynamically control our instinctive behaviours, depending on the situation.”

The driver of our instincts is the brainstem – the region at the very base of your brain, just above the spinal cord. Scientists have known for some time that another brain region, the prefrontal cortex, plays a role in keeping those instincts in check (see background information down below). But exactly how the prefrontal cortex puts a break on the brainstem has remained unclear.

Now, Gross and colleagues have literally found the connection between prefrontal cortex and brainstem. The EMBL scientists teamed up with Tiago Branco’s lab at MRC LMB, and traced connections between neurons in a mouse brain. They discovered that the prefrontal cortex makes prominent connections directly to the brainstem.

Gross and colleagues went on to confirm that this physical connection was the brake that inhibits instinctive behaviour. They found that in mice that have been repeatedly defeated by another mouse – the murine equivalent to being bullied – this connection weakens, and the mice act more scared. The scientists found that they could elicit those same fearful behaviours in mice that had never been bullied, simply by using drugs to block the connection between prefrontal cortex and brainstem.

These findings provide an anatomical explanation for why it’s much easier to stop yourself from hitting someone than it is to stop yourself from feeling aggressive. The scientists found that the connection from the prefrontal cortex is to a very specific region of the brainstem, called the PAG, which is responsible for the acting out of our instincts. However, it doesn’t affect the hypothalamus, the region that controls feelings and emotions. So the prefrontal cortex keeps behaviour in check, but doesn’t affect the underlying instinctive feeling: it stops you from running off-stage, but doesn’t abate the butterflies in your stomach.

The work has implications for schizophrenia and mood disorders such as depression, which have been linked to problems with prefrontal cortex function and maturation.

“One fascinating implication we’re looking at now is that we know the pre-frontal cortex matures during adolescence. Kids are really bad at inhibiting their instincts; they don’t have this control,” says Gross, “so we’re trying to figure out how this inhibition comes about, especially as many mental illnesses like mood disorders are typically adult-onset.”