I Hate When People Get All Snobby Like “uhm, Humans Didn’t EVOLVE From Apes, Humans And Apes Share

Slime mold was grown on an agar gel plate shaped like America and food sources were placed where America’s large cities are. 

The result? A possible look at how to best build public transportation. 

I just really like the idea of slime mold on a map of the US. It’s beautiful.

Zoos prevent extinction. This is why I support zoos. This is why the world should support zoos.

Meme credit goes to the zookeepers at www.facebook.com/ZoosSavingSpecies @zoossavingspecies

Neuroscientist Discovers Potential New Source for Pain Inhibition

A UT Dallas scientist has found a new neurological mechanism that appears to contribute to a reduction in pain.

According to Dr. Ted Price, associate professor in the School of Behavioral and Brain Sciences, the discovery of neuroligin-2 as a cause exacerbating chronic pain is significant for the research community. Although the findings likely won’t immediately lead to new pain therapies, the findings offer a potential new therapeutic direction to investigate, he said.

Price’s research on the topic has recently been published online in Pain, the journal of the International Association for the Study of Pain.

The study focused on the body’s inhibitory networks — a series of biochemical reactions that decrease certain neurological activity, such as pain. Price said a great deal of previous research in this area has focused on the activity of the neurotransmitter GABA, a chemical released by nerve cells in the brain.

Normally, a GABA neurotransmitter acts to inhibit neuronal activity, such as pain. However, when pain becomes chronic there is strong evidence that a process called GABAergic plasticity can cause GABA to lose its inhibitory activity, sometimes making the pain even worse.

The source of these excitatory actions in neuronal circuits has been broadly attributed to chloride ions, but Price’s research has found another potential cause of GABAergic plasticity: synaptic adhesion molecules called neuroligin-2.

“From a basic science perspective, we’re really excited about it because it demonstrates that the types of GABAergic plasticity that can occur in the setting of chronic pain are more diverse than we’ve appreciated before,” he said.

Price, who heads the undergraduate research program in neuroscience in the school, focuses much of his research on understanding the neuroscience behind pain, particularly chronic pain. He said individuals with chronic pain typically don’t receive the pain-reduction benefits delivered by inhibitory systems. Instead, they often experience increased pain.

“When you hit your hand with a hammer, almost everybody has the same reflex reaction — that is, to rub your finger which, in turn, helps to reduce pain. The reason that works is because it increases GABAergic inhibition in the spinal cord,” Price said. “However, people who have chronic pain — if they do the same thing — find that rubbing it actually makes the pain worse. That’s because the GABAergic system loses its efficacy and, in fact, can become excitatory.”

Price said the research is another step in determining why the GABAergic system stops working correctly in some people and provides a second theory for what drives the system.

“Having two ideas and different models will allow us to determine what the therapeutic opportunities are — creating something that will change that back to normal. The lack of performance in the inhibitory system is very detrimental to those who are in chronic pain,” he said.

Price said the development of chronic pain is, in essence, one’s body “learning” something that is bad.

“It’s changing the way the body functions — it’s learning. That learning, in the case of chronic pain, is aberrant — it’s causing the situation to get worse. If we can figure out what that form of learning was, then we can potentially reverse it. Understanding that the GABAergic system changes during this form of learning potentially offers a new therapeutic avenue,” he said.

My tummy is blushing now. 

People Were Asked: ‘What’s The Coolest Thing Most People Don’t Know About Their Own Body?’

Asteroid Terms: Explained

There are interesting asteroid characters in our solar system, including an asteroid that has its own moon and even one that is shaped like a dog bone! Our OSIRIS-REx mission launches at 7:05 p.m. EDT today and will travel to asteroid Bennu.

Scientists chose Bennu as the target of the OSIRIS-REx mission because of its composition, size and proximity to Earth. Bennu is a rare B-type asteroid (primitive and carbon-rich), which is expected to have organic compounds and water-bearing minerals like clays.

Our OSIRIS-REx mission will travel to Bennu and bring a small sample back to Earth for study.

When talking about asteroids, there are some terms scientists use that might not be in your typical vocabulary…but we’ll help with that!

Here are a few terms you should know:

Orbital Eccentricity: This number describes the shape of an asteroid’s orbit by how elliptical it is. For asteroids in orbit around the sun, eccentricity is a number between 0 and 1, with 0 being a perfectly circular orbit and 0.99 being a highly elliptical orbit.

Inclination: The angle, in degrees, of how tilted an asteroid’s orbit is compared to another plane of reference, usually the plane of the Earth’s orbit around the sun.

Orbital Period: The number of days it takes for an asteroid to revolve once around the sun. For example, the Earth’s orbital period is 365 days.

Perihelion Distance: The distance between an asteroid and the sun when the asteroid is closest to the sun.

Aphelion Distance: The distance between the asteroid and the sun when the asteroid is farthest away from the sun.

Astronomical unit: A distance unit commonly used to describe orbits of objects around the sun. The distance from the Earth to the sun is one astronomical unit, or 1 AU, equivalent to about 93 million miles or 150 million kilometers.

Diameter: A measure of the size of an asteroid. It is the length of a line from a point on the surface, through the center of the asteroid, extending out to the opposite surface. Irregularly shaped asteroids may have different diameters depending on which direction they are measured.

Rotation Period: The time it takes for an asteroid to complete one revolution around its axis of rotation. For example, the rotation period of the Earth is approximately 24 hours, or 1 day.

Spectral Type: The classification of an asteroid, based on a measurement of the light reflected by the asteroid. 

Watch live launch coverage of OSIRIS-REx to asteroid Bennu starting at 5:30 p.m, on NASA TV: http://www.nasa.gov/nasatv 

Make sure to follow us on Tumblr for your regular dose of space: http://nasa.tumblr.com

(Image caption: In this illustration, a pair of eyeglasses “resolves” distinct serotonin neuron subtypes (shown as brightly colored cells) on a simple map of a region called the raphe in the mouse brain. By viewing serotonin neurons through multiple “lenses”—such as single-neuron and population-scale global gene expression, developmental lineage and anatomy—researchers have revealed diverse subtypes and principles of subtype organization in the brain. Credit: Mallory Rice)

Time for a New Definition

It used to be enough to call a serotonergic neuron a serotonergic neuron.

These brain cells make the neurotransmitter serotonin, which helps regulate mood, appetite, breathing rate, body temperature and more.

Recently, however, scientists have begun to learn that these neurons differ from one another—and that the differences likely matter in dysfunction and disease.

Last year, a team led by Harvard Medical School genetics professor Susan Dymecki defined a subgroup of serotonergic neurons in mice by showing that those cells specifically, among all serotonergic neurons, were responsible for increasing the breathing rate when too much carbon dioxide builds up in the body.

Now, Dymecki and colleagues have taken a first stab at systematically characterizing serotonergic neurons at the molecular level and defining a full set of subtypes, again in mice.

The researchers report in Neuron that serotonergic neurons come in at least six major molecular subtypes defined by distinct expression patterns of hundreds of genes. In many cases, the subtypes modulate different behaviors in the body.

By conducting a cross-disciplinary series of experiments, the researchers found that the subtypes also vary in their developmental lineage, anatomical distribution, combinations of receptors on the cell surface and electrical firing properties.

“This work reveals how diverse serotonin neurons are at the molecular level, which may help to explain how, collectively, they are able to perform so many distinct functions,” said Benjamin Okaty, a postdoctoral researcher in the Dymecki lab and co-first author of the paper.

“To have the list of molecular players that make each of these subtypes different from one another gives us an important handle on learning more about what that cell type does and how we can manipulate only that subtype,” said Dymecki. “It holds enormous therapeutic potential.”

“This is an ancient neurotransmitter system that’s implicated in many different diseases, and it’s starting to be cracked open,” said Morgan Freret, a graduate student in the Dymecki lab and co-first author of the paper. “We can now ask questions in a more systematic way about which serotonergic cells and molecules are important in, for example, pain, sleep apnea or anxiety.”

Crucially, the team also showed that a serotonergic neuron’s gene expression and function depend not only on its location in the adult brain stem, but also on its cellular ancestor in the developing brain.

“Earlier work had shown that you could explore the relationship between a mature neuronal system and the different developmental lineages that gave rise to it, but we had no idea whether it was meaningful,” said Dymecki. “We show that the molecular phenotypes of these neurons track quite tightly to their developmental origin, with anatomy making some interesting contributions as well.”

While the work was done in mice, Dymecki is optimistic that it will be replicated in humans because the serotonergic neuronal system is in a highly conserved region of the brain, meaning it tends to remain consistent across vertebrate species.

Because of this, researchers can look for the same molecular signatures in human tissue and begin to tease apart whether particular subtypes of serotonergic neurons are involved in conditions such as sudden infant death syndrome (SIDS) or autism.

Such research could ultimately reveal previously unknown contributions of the serotonergic neuronal system to disease, inform the development of biomarkers or lead to more targeted therapies.

The team’s findings could also inform stem cell research. “Which subtype of serotonergic neuron are we getting when we use current stem cell protocols?” asked Dymecki. “Can we drive the development of different subtypes? Can we watch how gene expression patterns change over time during development for each subtype?”

Finally, the study provides an example of a highly integrative approach to understanding brain function at multiple scales, “linking genes and gene networks to the properties of single neurons and populations of neuron subtypes, all the way up to the level of animal behaviors,” said Okaty. “I think it’s a useful template going forward. Imagine what we’d learn by applying this approach to all the neurotransmitter systems in the brain.”

why do we have butt cheeks i dont understand why did we evolve this way

what use do butt cheeks have 

Why do we not discuss clouds more?

I mean look at that. That’s water.

Flying water.

FLYING

FUCKING

WATER

LIKE WHAT THE FUCK, WHY DO WE EVER STOP TALKING ABOUT THIS

WHAT IS THIS

HOW IS THIS EVEN

AND NOW THE FLYING WATER IS EATING A MOUNTAIN

GOD DAMN, WHAT

Words matter when talking about Alzheimer’s

Using war metaphors in reference to Alzheimer’s disease should be replaced with messages of resilience against a complex, age-associated condition that may not be fully defeatable, according to a team of researchers.

Framing a health issue through comparisons to warfare is common in popular media and medical and research communities. While it can motivate efforts to deal with the issue, this type of language and messaging can also create fear and stigma, turn patients into victims and divert resources from critically important prevention and care, said Daniel R. George, assistant professor of medical humanities, Penn State College of Medicine.

Despite decades of failures in Alzheimer’s drug development, scientific attention continues to focus on drugs that “attack” a molecular compound called beta amyloid, with the goal of curing the disease. Amyloid is a key component of the plaques in the brain that are a hallmark of Alzheimer’s disease. Research, however, shows that the appearance of amyloid does not correlate with clinical symptoms and beta amyloid has repeatedly been found in the brains of one-third of “normal” elderly people. This suggests that amyloid may be a symptom rather than a cause of damage. A growing number of researchers believe that declaring “war” on Alzheimer’s by “attacking” amyloid may ultimately be an exercise in self-harm, particularly if amyloid is representative of the brain’s repair response, and may be channeling resources away from other drug-based approaches that do not assume amyloid toxicity.

Scholars have argued that metaphors and narratives that treat disease as something to be attacked can be socially damaging to those affected. The value of such metaphors may be clearer for infectious diseases caused by single pathogens. It becomes more problematic when discussing diverse, age-associated syndromes like Alzheimer’s that may not be fully curable. In this way, war metaphors in medicine can invite ways of thinking that may not be scientifically or socially productive.

“If applied in a careless manner, war metaphors can delude our sense of what’s possible therapeutically, and give false hope to people and caregivers who are suffering,” George said.

George and his co-authors propose moving toward different types of metaphors – those that encourage use of words like “slow” or “postpone” rather than “prevent” or “cure,” and emphasize building “resilience” to aging processes in the brain rather than aiming at “absolute victory” over a disease. While “fighting” and “defeating” Alzheimer’s through drug development is important, the authors argue it may be wiser to acknowledge that Alzheimer’s is not a disease disconnected from the aging process like polio or malaria. The authors note that Alzheimer’s has been classified as a disease for the past 40 years. They suggest it may be more beneficial to take a lifespan-oriented approach that includes education about known biological, psychosocial and environmental risk factors, investment in societal programs and infrastructure that support brain health, and ensuring proper care for those affected and their caregivers.

“While not as profitable as drug development, public health initiatives that reduce vascular risk factors, modulate oxidative stress and inflammation, guard against traumatic brain injuries, promote social engagement and lifelong learning, and reduce exposure to neurotoxins, and other commonsense actions should be an explicit component of our societal response (to Alzheimer’s),” the researchers wrote in the American Journal of Bioethics.

George drew particular attention to the residents of Flint, Michigan being exposed to lead, a neurotoxin, through the water supply.

“It is inexcusable that we could let our public infrastructure fail to the point where it becomes a contributor to Alzheimer’s disease risk for socio-economically disadvantaged citizens,” George said. “If we’re really serious about addressing the problem of Alzheimer’s, we must start by not poisoning our citizens.”

Moving beyond the notion of being at war against Alzheimer’s could also serve to humanize cognitive aging.

“There’s a widely-accepted myth that people who have Alzheimer’s are sort of non-people, akin to zombies,” George said. “There are ways to construct meaning around memory loss that show greater compassion and solidarity toward people with cognitive frailty rather than seeing them as passive victims in our biological war against the disease. We believe in a more humane message – that even if you have a diagnosis of ‘probable Alzheimer’s’ you can still have a life with deep purpose, social contribution and meaningful relationships.”