The Lama Has Spoken

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taco-man-andre:

monetizeyourcat:

magicpottybaby:

sizvideos:

TL;DR : Watch this incredible story in video

holy fuck! so how did the penguins taste?????

this is the cutest video in the entire world. this seal is just so afraid for this dumb weird baby she thinks she’s found out in the ocean. have a bird. have another bird. no, see, eat the bird! the bird is food! why won’t this stupid baby eat. open your mouth you idiot baby i will feed you bird if it’s the last thing i do

fuckin cool

So beautiful :)

Jul 9
Mmmhhhmm

Mmmhhhmm

Jul 6
70sscifiart:

madddscience:

Space chimp casually screams about his latest accomplishment. No big deal.

See what you’re missing by not following my Maddd Science tumblr, guys? Space chimps. Space. Chimps.

:)

70sscifiart:

madddscience:

Space chimp casually screams about his latest accomplishment. No big deal.

See what you’re missing by not following my Maddd Science tumblr, guys? Space chimps. Space. Chimps.

:)

Jul 5

asylum-art:

Donut Doubles by Brandon Voges

Yes.

darksilenceinsuburbia:

Ramona Rosales

Balloons

Jul 4

darksilenceinsuburbia:

Zoe Byland

Jul 2

I think that one of these days you’re going to have to find out where you want to go. And then you’ve got to start going there.

- J.D. Salinger, The Catcher in the Rye (via theunquotables)

ibayodeperegrino:

Pasado un tenemos todos

Bahahaha

ibayodeperegrino:

Pasado un tenemos todos

Bahahaha

Jejeje

Jejeje

archatlas:

 Siegfried Hansen

Bravo, sir. Bravo.

red-lipstick:

Tang Yau Hoong (Kuala Lumpur, Malaysia) - Danger Ahead from The Art Of Negative Space II, 2011     Graphic Arts

Details.

red-lipstick:

Tang Yau Hoong (Kuala Lumpur, Malaysia) - Danger Ahead from The Art Of Negative Space II, 2011     Graphic Arts

Details.

tracksoot:

'Sista Girls' by Bindi Cole

The term ‘Sistagirl’ is used to describe a transgender person in Tiwi Island culture. Traditionally, the term was ‘Yimpininni’.  The very existence of the word provides some indication of the inclusive attitudes historically extended towards Aboriginal sexual minorities. Colonisation not only wiped out many indigenous people, it also had an impact on Aboriginal culture and understanding of sexual and gender expression. As Catholicism took hold and many traditions were lost, this term became a thing of the past. Yimpininni were once held in high regard as the nurturers within the family unit and tribe much like the Faafafine from Samoa. As the usage of the term vanished, tribes’ attitudes toward queer indigenous people began to resemble that of the western world and religious right. Even today many Sistergirls are excluded from their own tribes and suffer at the hands of others.

Within a population of around 2500, there are approximately 50 ‘Sistagirls’ living on the Tiwi Islands. This community contains a complex range of dynamics including a hierarchy (a queen Sistergirl), politics, and a significant history of pride and shame. The Sistagirls are isolated yet thriving, unexplored territory with a beauty, strength and diversity to inspire and challenge.

Fucking western culture…

neurosciencestuff:

Blocking brain’s ‘internal marijuana’ may trigger early Alzheimer’s deficits


A new study led by investigators at the Stanford University School of Medicine has implicated the blocking of endocannabinoids — signaling substances that are the brain’s internal versions of the psychoactive chemicals in marijuana and hashish — in the early pathology of Alzheimer’s disease.
A substance called A-beta — strongly suspected to play a key role in Alzheimer’s because it’s the chief constituent of the hallmark clumps dotting the brains of people with Alzheimer’s — may, in the disease’s earliest stages, impair learning and memory by blocking the natural, beneficial action of endocannabinoids in the brain, the study demonstrates. The Stanford group is now trying to figure out the molecular details of how and where this interference occurs. Pinning down those details could pave the path to new drugs to stave off the defects in learning ability and memory that characterize Alzheimer’s.
In the study, published June 18 in Neuron, researchers analyzed A-beta’s effects on a brain structure known as the hippocampus. In all mammals, this midbrain structure serves as a combination GPS system and memory-filing assistant, along with other duties.
“The hippocampus tells us where we are in space at any given time,” said Daniel Madison, PhD, associate professor of molecular and cellular physiology and the study’s senior author. “It also processes new experiences so that our memories of them can be stored in other parts of the brain. It’s the filing secretary, not the filing cabinet.”
Surprise finding
Applying electrophysiological techniques to brain slices from rats, Madison and his associates examined a key hippocampal circuit, one of whose chief elements is a class of nerve cells called pyramidal cells. They wanted to see how the circuit’s different elements reacted to small amounts of A-beta, which is produced throughout the body but whose normal physiological functions have until now been ill-defined.
A surprise finding by Madison’s group suggests that in small, physiologically normal concentrations, A-beta tamps down a signal-boosting process that under certain conditions increases the odds that pyramidal nerve cells will transmit information they’ve received to other nerve cells down the line.


When incoming signals to the pyramidal tract build to high intensity, pyramidal cells adapt by becoming more inclined to fire than they normally are. This phenomenon, which neuroscientists call plasticity, is thought to underpin learning and memory. It ensures that volleys of high-intensity input — such as might accompany falling into a hole, burning one’s finger with a match, suddenly remembering where you buried the treasure or learning for the first time how to spell “cat” — are firmly stored in the brain’s memory vaults and more accessible to retrieval.
These intense bursts of incoming signals are the exception, not the rule. Pyramidal nerve cells constantly receive random beeps and burps from upstream nerve cells — effectively, noise in a highly complex, electrochemical signaling system. This calls for some quality control. Pyramidal cells are encouraged to ignore mere noise by another set of “wet blanket” nerve cells called interneurons. Like the proverbial spouse reading a newspaper at the kitchen table, interneurons continuously discourage pyramidal cells’ transmission of impulses to downstream nerve cells by steadily secreting an inhibitory substance — the molecular equivalent of yawning, eye-rolling and oft-muttered suggestions that this or that chatter is really not worth repeating to the world at large, so why not just shut up.
Passing along the message
But when the news is particularly significant, pyramidal cells squirt out their own “no, this is important, you shut up!” chemical — endocannabinoids — which bind to specialized receptors on the hippocampal interneurons, temporarily suppressing them and allowing impulses to continue coursing along the pyramidal cells to their follow-on peers.
A-beta is known to impair pyramidal-cell plasticity. But Madison’s research team showed for the first time how it does so. Small clusters consisting of just a few A-beta molecules render the interneuron’s endocannabinoid receptors powerless, leaving inhibition intact even in the face of important news and thus squashing plasticity.
While small A-beta clusters have been known for a decade to be toxic to nerve cells, this toxicity requires relatively long-term exposure, said Madison. The endocannabinoid-nullifying effect the new study revealed is much more transient. A possible physiological role for A-beta in the normal, healthy brain, he said, is that of supplying that organ’s sophisticated circuits with yet another, beneficial layer of discretion in processing information. Madison thinks this normal, everyday A-beta mechanism run wild may represent an entry point to the progressive and destructive stages of Alzheimer’s disease.
Exactly how A-beta blocks endocannabinoids’ action is not yet known. But, Madison’s group demonstrated, A-beta doesn’t stop them from reaching and binding to their receptors on interneurons. Rather, it interferes with something that binding ordinarily generates. (By analogy, turning the key in your car’s ignition switch won’t do much good if your battery is dead.)
Madison said it would be wildly off the mark to assume that, just because A-beta interferes with a valuable neurophysiological process mediated by endocannabinoids, smoking pot would be a great way to counter or prevent A-beta’s nefarious effects on memory and learning ability. Smoking or ingesting marijuana results in long-acting inhibition of interneurons by the herb’s active chemical, tetrahydrocannabinol. That is vastly different from short-acting endocannabinoid bursts precisely timed to occur only when a signal is truly worthy of attention.
“Endocannabinoids in the brain are very transient and act only when important inputs come in,” said Madison, who is also a member of the interdisciplinary Stanford Bio-X institute. “Exposure to marijuana over minutes or hours is different: more like enhancing everything indiscriminately, so you lose the filtering effect. It’s like listening to five radio stations at once.”
Besides, flooding the brain with external cannabinoids induces tolerance — it may reduce the number of endocannabinoid receptors on interneurons, impeding endocannabinoids’ ability to do their crucial job of opening the gates of learning and memory.

neurosciencestuff:

Blocking brain’s ‘internal marijuana’ may trigger early Alzheimer’s deficits

A new study led by investigators at the Stanford University School of Medicine has implicated the blocking of endocannabinoids — signaling substances that are the brain’s internal versions of the psychoactive chemicals in marijuana and hashish — in the early pathology of Alzheimer’s disease.

A substance called A-beta — strongly suspected to play a key role in Alzheimer’s because it’s the chief constituent of the hallmark clumps dotting the brains of people with Alzheimer’s — may, in the disease’s earliest stages, impair learning and memory by blocking the natural, beneficial action of endocannabinoids in the brain, the study demonstrates. The Stanford group is now trying to figure out the molecular details of how and where this interference occurs. Pinning down those details could pave the path to new drugs to stave off the defects in learning ability and memory that characterize Alzheimer’s.

In the study, published June 18 in Neuron, researchers analyzed A-beta’s effects on a brain structure known as the hippocampus. In all mammals, this midbrain structure serves as a combination GPS system and memory-filing assistant, along with other duties.

“The hippocampus tells us where we are in space at any given time,” said Daniel Madison, PhD, associate professor of molecular and cellular physiology and the study’s senior author. “It also processes new experiences so that our memories of them can be stored in other parts of the brain. It’s the filing secretary, not the filing cabinet.”

Surprise finding

Applying electrophysiological techniques to brain slices from rats, Madison and his associates examined a key hippocampal circuit, one of whose chief elements is a class of nerve cells called pyramidal cells. They wanted to see how the circuit’s different elements reacted to small amounts of A-beta, which is produced throughout the body but whose normal physiological functions have until now been ill-defined.

A surprise finding by Madison’s group suggests that in small, physiologically normal concentrations, A-beta tamps down a signal-boosting process that under certain conditions increases the odds that pyramidal nerve cells will transmit information they’ve received to other nerve cells down the line.

When incoming signals to the pyramidal tract build to high intensity, pyramidal cells adapt by becoming more inclined to fire than they normally are. This phenomenon, which neuroscientists call plasticity, is thought to underpin learning and memory. It ensures that volleys of high-intensity input — such as might accompany falling into a hole, burning one’s finger with a match, suddenly remembering where you buried the treasure or learning for the first time how to spell “cat” — are firmly stored in the brain’s memory vaults and more accessible to retrieval.

These intense bursts of incoming signals are the exception, not the rule. Pyramidal nerve cells constantly receive random beeps and burps from upstream nerve cells — effectively, noise in a highly complex, electrochemical signaling system. This calls for some quality control. Pyramidal cells are encouraged to ignore mere noise by another set of “wet blanket” nerve cells called interneurons. Like the proverbial spouse reading a newspaper at the kitchen table, interneurons continuously discourage pyramidal cells’ transmission of impulses to downstream nerve cells by steadily secreting an inhibitory substance — the molecular equivalent of yawning, eye-rolling and oft-muttered suggestions that this or that chatter is really not worth repeating to the world at large, so why not just shut up.

Passing along the message

But when the news is particularly significant, pyramidal cells squirt out their own “no, this is important, you shut up!” chemical — endocannabinoids — which bind to specialized receptors on the hippocampal interneurons, temporarily suppressing them and allowing impulses to continue coursing along the pyramidal cells to their follow-on peers.

A-beta is known to impair pyramidal-cell plasticity. But Madison’s research team showed for the first time how it does so. Small clusters consisting of just a few A-beta molecules render the interneuron’s endocannabinoid receptors powerless, leaving inhibition intact even in the face of important news and thus squashing plasticity.

While small A-beta clusters have been known for a decade to be toxic to nerve cells, this toxicity requires relatively long-term exposure, said Madison. The endocannabinoid-nullifying effect the new study revealed is much more transient. A possible physiological role for A-beta in the normal, healthy brain, he said, is that of supplying that organ’s sophisticated circuits with yet another, beneficial layer of discretion in processing information. Madison thinks this normal, everyday A-beta mechanism run wild may represent an entry point to the progressive and destructive stages of Alzheimer’s disease.

Exactly how A-beta blocks endocannabinoids’ action is not yet known. But, Madison’s group demonstrated, A-beta doesn’t stop them from reaching and binding to their receptors on interneurons. Rather, it interferes with something that binding ordinarily generates. (By analogy, turning the key in your car’s ignition switch won’t do much good if your battery is dead.)

Madison said it would be wildly off the mark to assume that, just because A-beta interferes with a valuable neurophysiological process mediated by endocannabinoids, smoking pot would be a great way to counter or prevent A-beta’s nefarious effects on memory and learning ability. Smoking or ingesting marijuana results in long-acting inhibition of interneurons by the herb’s active chemical, tetrahydrocannabinol. That is vastly different from short-acting endocannabinoid bursts precisely timed to occur only when a signal is truly worthy of attention.

“Endocannabinoids in the brain are very transient and act only when important inputs come in,” said Madison, who is also a member of the interdisciplinary Stanford Bio-X institute. “Exposure to marijuana over minutes or hours is different: more like enhancing everything indiscriminately, so you lose the filtering effect. It’s like listening to five radio stations at once.”

Besides, flooding the brain with external cannabinoids induces tolerance — it may reduce the number of endocannabinoid receptors on interneurons, impeding endocannabinoids’ ability to do their crucial job of opening the gates of learning and memory.

darksilenceinsuburbia:

1968: Radical Italian Furniture by DESTE Foundation and TOILETPAPER

What happens when famed art collector and Deste Foundation founder Dakis Joannou joins forces with what is arguably the most offbeat and mind-boggling publication out there? In an attempt to document his unparalleled collection of Radical Design furniture, Joannou commissioned artist/provocateur Maurizio Cattelan and photographer Pierpaolo Ferrari - the creative masterminds behind TOILETPAPER magazine - to create a book that proudly celebrates a period that marked a revolutionary shift in stylistic direction in Italian design.

Founded in the late 1960s by a progressive group of Italian designers, the Radical Design movement was firmly opposed to the ethics – and indeed the very notion of – ‘good design’ or taste. Stemming from a loathing of the sterile state that design had come to at the time due to the uninspiring prevailing trends of previous decades, groups like Archizoom and Superstudio challenged the perception of furniture design and the gravity applied to function as opposed to form, giving birth to remarkable objects of surprising proportions, playful shapes and bold colours. (by Demetrios Gkiouzelis)