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neuromorphogenesis:

UNDERSTANDING THE PHENOMENON OF SYNESTHESIA

The number 3 is color orange and January is moody, according to synesthetes. They are blessed with the natural ability, thought to be passed on by genes, of a blending of senses, in which the brain’s sensory centers remain connected on two levels.

by MEZZMER

science-junkie:
Inside a Changing Autumn Leaf
One of the great wonders of life is watching the leaves change colors in the fall. When temperatures get cool, chlorophyll begins to break down revealing the underlying pigments in the plants’ sap. This depiction of the inner-workings of a maple leaf shows the process in action.
Source: SciAm Blog Network

science-junkie:

Inside a Changing Autumn Leaf

One of the great wonders of life is watching the leaves change colors in the fall. When temperatures get cool, chlorophyll begins to break down revealing the underlying pigments in the plants’ sap. This depiction of the inner-workings of a maple leaf shows the process in action.

Source: SciAm Blog Network

accordingtodevin:

Scientifically accurate love story.

*95
s-c-i-guy:
Did Cancer Evolve to Protect Us? 
Could cancer be our cells’ way of running in “safe mode,” like a damaged computer operating system trying to preserve itself, when faced with an external threat? That’s the conclusion reached by cosmologist Paul Davies at Arizona State University in Tempe (A.S.U.) and his colleagues, who have devised a controversial new theory for cancer’s origins, based on its evolutionary roots. If correct, their model suggests that a number of alternative therapies, including treatment with oxygen and infection with viral or bacterial agents, could be particularly effective.
At first glance, Davies, who is trained in physics rather than biomedical science, seems an unlikely soldier in the “war on cancer.” But about seven years ago he was invited to set up a new institute at A.S.U.—one of 12 funded by the National Cancer Institute—to bring together physical scientists and oncologists to find a new perspective on the disease. “We were asked to rethink cancer from the bottom up,” Davies says.
Davies teamed up with Charley Lineweaver, an astrobiologist at The Australian National University in Canberra, and Mark Vincent, an oncologist at the London Health Sciences Center in Ontario. Together they have come up with an “atavistic” model positing cancer is the reexpression of an ancient “preprogrammed” trait that has been lying dormant. In a new paper, which appeared in BioEssays in September, they argue that because cancer appears in many animals and plants, as well as humans, then it must have evolved hundreds of millions of years ago when we shared a common single-celled ancestor. At that time, cells benefited from immortality, or the ability to proliferate unchecked, as cancer does. When complex multicellular organisms developed, however, “immortality was outsourced to the eggs and sperm,” Davies says, and somatic cells (those not involved in reproduction) no longer needed this function.
The team’s hypothesis is that when faced with an environmental threat to the health of a cell—radiation, say, or a lifestyle factor—cells can revert to a “preprogrammed safe mode.” In so doing, the cells jettison higher functionality and switch their dormant ability to proliferate back on in a misguided attempt to survive. “Cancer is a fail-safe,” Davies remarks. “Once the subroutine is triggered, it implements its program ruthlessly.”
read more

s-c-i-guy:

Did Cancer Evolve to Protect Us?

Could cancer be our cells’ way of running in “safe mode,” like a damaged computer operating system trying to preserve itself, when faced with an external threat? That’s the conclusion reached by cosmologist Paul Davies at Arizona State University in Tempe (A.S.U.) and his colleagues, who have devised a controversial new theory for cancer’s origins, based on its evolutionary roots. If correct, their model suggests that a number of alternative therapies, including treatment with oxygen and infection with viral or bacterial agents, could be particularly effective.

At first glance, Davies, who is trained in physics rather than biomedical science, seems an unlikely soldier in the “war on cancer.” But about seven years ago he was invited to set up a new institute at A.S.U.—one of 12 funded by the National Cancer Institute—to bring together physical scientists and oncologists to find a new perspective on the disease. “We were asked to rethink cancer from the bottom up,” Davies says.

Davies teamed up with Charley Lineweaver, an astrobiologist at The Australian National University in Canberra, and Mark Vincent, an oncologist at the London Health Sciences Center in Ontario. Together they have come up with an “atavistic” model positing cancer is the reexpression of an ancient “preprogrammed” trait that has been lying dormant. In a new paper, which appeared in BioEssays in September, they argue that because cancer appears in many animals and plants, as well as humans, then it must have evolved hundreds of millions of years ago when we shared a common single-celled ancestor. At that time, cells benefited from immortality, or the ability to proliferate unchecked, as cancer does. When complex multicellular organisms developed, however, “immortality was outsourced to the eggs and sperm,” Davies says, and somatic cells (those not involved in reproduction) no longer needed this function.

The team’s hypothesis is that when faced with an environmental threat to the health of a cell—radiation, say, or a lifestyle factor—cells can revert to a “preprogrammed safe mode.” In so doing, the cells jettison higher functionality and switch their dormant ability to proliferate back on in a misguided attempt to survive. “Cancer is a fail-safe,” Davies remarks. “Once the subroutine is triggered, it implements its program ruthlessly.”

read more

science-illustrated:

The Magnetosphere, as a results of the electromagnetic force, one of the four fundamental forces of the universe, is produced by convection currents in the outer liquid of Earth’s core. Basically, the Earth is like a giant magnet, with its two poles (the magnetic dipole) which differ slightly from the geographic poles.

This magnetic field is preventing the Earth from being blasted by solar winds, a stream of charged particles emanating from the Sun. Mars, as Venus, doesn’t have a magnetosphere. Therefore the planet isn’t protected against the harmful cosmic radiation and suffer a strong atmosphere erosion. The radiation on Mars ranges around 200 mSv/year, which is is 100 time more than Earth’s average!

You can see others illustrations i made for in this project here (in french sorry!)

sprigofacacia:

Gabriel’s Horn has an infinite surface area and a finite volume, which is appropriately representative of its symbolic connection between the two.

skunkbear:
At 10:02 AM on August 27th, 1883, a volcanic island in modern day Indonesia called Krakatoa erupted. The blast sent shockwaves across the ocean, triggering tsunamis that destroyed the coast of Java and Sumatra. The sound was so loud it was heard 3000 miles away.
As Aatish Bhatia notes in this recent article: “What we’re talking about here is like being in Boston and clearly hearing a noise coming from Dublin, Ireland." 
Barometric readings at the time clocked the sound pressure at 172 decibels ONE HUNDRED MILES AWAY from the island.
Here’s a handy reference:
Using a jackhammer — 100 decibels
Human threshold for pain — 130 dB
Standing next to a jet engine — 150 dB
And the scale is logarithmic - so a 10 dB increase doubles the loudness.

skunkbear:

At 10:02 AM on August 27th, 1883, a volcanic island in modern day Indonesia called Krakatoa erupted. The blast sent shockwaves across the ocean, triggering tsunamis that destroyed the coast of Java and Sumatra. The sound was so loud it was heard 3000 miles away.

As Aatish Bhatia notes in this recent article:What we’re talking about here is like being in Boston and clearly hearing a noise coming from Dublin, Ireland."

Barometric readings at the time clocked the sound pressure at 172 decibels ONE HUNDRED MILES AWAY from the island.

Here’s a handy reference:

  • Using a jackhammer — 100 decibels
  • Human threshold for pain — 130 dB
  • Standing next to a jet engine — 150 dB

And the scale is logarithmic - so a 10 dB increase doubles the loudness.

neurosciencestuff:
Why Wet Feels Wet: Understanding the Illusion of Wetness
Human sensitivity to wetness plays a role in many aspects of daily life. Whether feeling humidity, sweat or a damp towel, we often encounter stimuli that feel wet. Though it seems simple, feeling that something is wet is quite a feat because our skin does not have receptors that sense wetness. The concept of wetness, in fact, may be more of a “perceptual illusion” that our brain evokes based on our prior experiences with stimuli that we have learned are wet.
So how would a person know if he has sat on a wet seat or walked through a puddle? Researchers at Loughborough University and Oxylane Research proposed that wetness perception is intertwined with our ability to sense cold temperature and tactile sensations such as pressure and texture. They also observed the role of A-nerve fibers—sensory nerves that carry temperature and tactile information from the skin to the brain—and the effect of reduced nerve activity on wetness perception. Lastly, they hypothesized that because hairy skin is more sensitive to thermal stimuli, it would be more perceptive to wetness than glabrous skin (e.g., palms of the hands, soles of the feet), which is more sensitive to tactile stimuli.
Davide Filingeri et al. exposed 13 healthy male college students to warm, neutral and cold wet stimuli. They tested sites on the subjects’ forearms (hairy skin) and fingertips (glabrous skin). The researchers also performed the wet stimulus test with and without a nerve block. The nerve block was achieved by using an inflatable compression (blood pressure) cuff to attain enough pressure to dampen A-nerve sensitivity.
They found that wet perception increased as temperature decreased, meaning subjects were much more likely to sense cold wet stimuli than warm or neutral wet stimuli. The research team also found that the subjects were less sensitive to wetness when the A-nerve activity was blocked and that hairy skin is more sensitive to wetness than glabrous skin. These results contribute to the understanding of how humans interpret wetness and present a new model for how the brain processes this sensation.
“Based on a concept of perceptual learning and Bayesian perceptual inference, we developed the first neurophysiological model of cutaneous wetness sensitivity centered on the multisensory integration of cold-sensitive and mechanosensitive skin afferents,” the research team wrote. “Our results provide evidence for the existence of a specific information processing model that underpins the neural representation of a typical wet stimulus.”
The article “Why wet feels wet? A neurophysiological model of human cutaneous wetness sensitivity” is published in the Journal of Neurophysiology.
(Image credit)

neurosciencestuff:

Why Wet Feels Wet: Understanding the Illusion of Wetness

Human sensitivity to wetness plays a role in many aspects of daily life. Whether feeling humidity, sweat or a damp towel, we often encounter stimuli that feel wet. Though it seems simple, feeling that something is wet is quite a feat because our skin does not have receptors that sense wetness. The concept of wetness, in fact, may be more of a “perceptual illusion” that our brain evokes based on our prior experiences with stimuli that we have learned are wet.

So how would a person know if he has sat on a wet seat or walked through a puddle? Researchers at Loughborough University and Oxylane Research proposed that wetness perception is intertwined with our ability to sense cold temperature and tactile sensations such as pressure and texture. They also observed the role of A-nerve fibers—sensory nerves that carry temperature and tactile information from the skin to the brain—and the effect of reduced nerve activity on wetness perception. Lastly, they hypothesized that because hairy skin is more sensitive to thermal stimuli, it would be more perceptive to wetness than glabrous skin (e.g., palms of the hands, soles of the feet), which is more sensitive to tactile stimuli.

Davide Filingeri et al. exposed 13 healthy male college students to warm, neutral and cold wet stimuli. They tested sites on the subjects’ forearms (hairy skin) and fingertips (glabrous skin). The researchers also performed the wet stimulus test with and without a nerve block. The nerve block was achieved by using an inflatable compression (blood pressure) cuff to attain enough pressure to dampen A-nerve sensitivity.

They found that wet perception increased as temperature decreased, meaning subjects were much more likely to sense cold wet stimuli than warm or neutral wet stimuli. The research team also found that the subjects were less sensitive to wetness when the A-nerve activity was blocked and that hairy skin is more sensitive to wetness than glabrous skin. These results contribute to the understanding of how humans interpret wetness and present a new model for how the brain processes this sensation.

“Based on a concept of perceptual learning and Bayesian perceptual inference, we developed the first neurophysiological model of cutaneous wetness sensitivity centered on the multisensory integration of cold-sensitive and mechanosensitive skin afferents,” the research team wrote. “Our results provide evidence for the existence of a specific information processing model that underpins the neural representation of a typical wet stimulus.”

The article “Why wet feels wet? A neurophysiological model of human cutaneous wetness sensitivity” is published in the Journal of Neurophysiology.

(Image credit)