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This happens to a lot of scientific publications that get picked up by the media. There’s even a PhD comic about it.

Pop neuroscience makes an easy target, we know. Yet we invoke it because these studies garner a disproportionate amount of media coverage and shape public perception of what brain imaging can tell us. Skilled science journalists cringe when they read accounts claiming that scans can capture the mind itself in action. Serious science writers take pains to describe quality neuroscience research accurately. Indeed, an eddy of discontent is already forming. “Neuromania,” “neurohubris,” and “neurohype”—“neurobollocks,” if you’re a Brit—are just some of the labels that have been brandished, sometimes by frustrated neuroscientists themselves. But in a world where university press releases elbow one another for media attention, it’s often the study with a buzzy storyline (“Men See Bikini-Clad Women as Objects, Psychologists Say”) that gets picked up and dumbed down. 
The problem with such mindless neuroscience is not neuroscience itself. The field is one of the great intellectual achievements of modern science. Its instruments are remarkable. The goal of brain imaging is enormously important and fascinating: to bridge the explanatory gap between the intangible mind and the corporeal brain. But that relationship is extremely complex and incompletely understood. Therefore, it is vulnerable to being oversold by the media, some overzealous scientists, and neuroentrepreneurs who tout facile conclusions that reach far beyond what the current evidence warrants— fits of “premature extrapolation,” as British neuroskeptic Steven Poole calls them. When it comes to brain scans, seeing may be believing, but it isn’t necessarily understanding. (read the entire story at the link below)

BY SALLY SATEL AND SCOTT O. LILIENFELD (via Pop neuroscience is bunk! - Salon.com)

This happens to a lot of scientific publications that get picked up by the media. There’s even a PhD comic about it.

Pop neuroscience makes an easy target, we know. Yet we invoke it because these studies garner a disproportionate amount of media coverage and shape public perception of what brain imaging can tell us. Skilled science journalists cringe when they read accounts claiming that scans can capture the mind itself in action. Serious science writers take pains to describe quality neuroscience research accurately. Indeed, an eddy of discontent is already forming. “Neuromania,” “neurohubris,” and “neurohype”—“neurobollocks,” if you’re a Brit—are just some of the labels that have been brandished, sometimes by frustrated neuroscientists themselves. But in a world where university press releases elbow one another for media attention, it’s often the study with a buzzy storyline (“Men See Bikini-Clad Women as Objects, Psychologists Say”) that gets picked up and dumbed down.

The problem with such mindless neuroscience is not neuroscience itself. The field is one of the great intellectual achievements of modern science. Its instruments are remarkable. The goal of brain imaging is enormously important and fascinating: to bridge the explanatory gap between the intangible mind and the corporeal brain. But that relationship is extremely complex and incompletely understood. Therefore, it is vulnerable to being oversold by the media, some overzealous scientists, and neuroentrepreneurs who tout facile conclusions that reach far beyond what the current evidence warrants— fits of “premature extrapolation,” as British neuroskeptic Steven Poole calls them. When it comes to brain scans, seeing may be believing, but it isn’t necessarily understanding. (read the entire story at the link below)

BY  AND  (via Pop neuroscience is bunk! - Salon.com)

The Google doodle today celebrates Julius Richard Petri’s 161st birthday. It starts with blank petri dishes and when you hit play, they are swabbed and grow. If you scroll over each, a graphic pops up telling you where the culture is from.

The Google doodle today celebrates Julius Richard Petri’s 161st birthday. It starts with blank petri dishes and when you hit play, they are swabbed and grow. If you scroll over each, a graphic pops up telling you where the culture is from.


Using infrared cameras, surgically implanted electrocardiograms, and radio transmitters, Barnes and his team monitored hibernating black bears (Ursus americanus) for three years. Think of it as CBS’s Big Brother—except someone actually cared about the bear feeds. Their research showed that bears can drop their heart rate from 55 to 9 beats per minute and reduce their metabolism by an incredible 53 percent. They accomplish this without compromising much on body temperature, a crucial fact that allows bears to be more alert than true hibernators. (Those fancy squirrels can require hours to thaw out.)
Higher body temperatures also allow hibernating bears to keep newborn cubs warm. During a period when most animals are locked in hand-to-hand combat with the bony fists of Death, bears perform the miracle of Life. Bear reproduction is actually sort of a boring story though, so let’s move on to …
I’m kidding, of course. Bear reproduction is all kinds of curious. The coitus occurs in spring or summer, when many animals are already giving birth. The male is aided by a penis bone called a baculum, which is not attached to the rest of the skeleton. (Baculi are rather common among mammals, from walruses and chimps to cats and bats. Because the Internet is a wonderful, horrible place, you can purchase baculi online, where they are marketed improbably as Mountain Man Toothpicks. Humans do not have penis bones, alas. Just the euphemism.)
After bears rock it in the usual way, the reproductive process takes a hard left from everything you learned in that sex-ed class taught by the school gym teacher. Following fertilization, the baby bears stop growing after becoming multicelled blastocysts. For a few months, they just float around in a state of arrested development known as delayed implantation. Should the female bear fail to fatten up enough over the course of the year, her body can put the kibosh on pregnancy in an act of self-preservation. Conversely, if times are good, her body will allow more blastocysts to develop and implant in her womb—adjusting the number of cubs created based on fat stores. 
Even though the deed is done months ahead of time, active gestation is surprisingly short—just 60 days in polar bears—and this results in helpless, underdeveloped cubs that are usually born between November and February, depending on the species and climate. Super-rich milk ensures that by the time spring comes, the cubs are ready to hit the ground running in a life-or-death race to rotundness. Polar bear milk contains up to 46 percent fat and tastes like the chalky cream of a fishy cow. And how do we know what it tastes like? Well, because polar bear scientists like Andrew Derocher are absurdly dedicated dudes. (click through to read the whole thing)

Photo by Kaisa Siren/AFP/Getty Images(via Do bears hibernate: Polar bear, black bear, grizzly bear sex and torpor. - Slate Magazine)

Using infrared cameras, surgically implanted electrocardiograms, and radio transmitters, Barnes and his team monitored hibernating black bears (Ursus americanus) for three years. Think of it as CBS’s Big Brother—except someone actually cared about the bear feeds. Their research showed that bears can drop their heart rate from 55 to 9 beats per minute and reduce their metabolism by an incredible 53 percent. They accomplish this without compromising much on body temperature, a crucial fact that allows bears to be more alert than true hibernators. (Those fancy squirrels can require hours to thaw out.)

Higher body temperatures also allow hibernating bears to keep newborn cubs warm. During a period when most animals are locked in hand-to-hand combat with the bony fists of Death, bears perform the miracle of Life. Bear reproduction is actually sort of a boring story though, so let’s move on to …

I’m kidding, of course. Bear reproduction is all kinds of curious. The coitus occurs in spring or summer, when many animals are already giving birth. The male is aided by a penis bone called a baculum, which is not attached to the rest of the skeleton. (Baculi are rather common among mammals, from walruses and chimps to cats and bats. Because the Internet is a wonderful, horrible place, you can purchase baculi online, where they are marketed improbably as Mountain Man Toothpicks. Humans do not have penis bones, alas. Just the euphemism.)

After bears rock it in the usual way, the reproductive process takes a hard left from everything you learned in that sex-ed class taught by the school gym teacher. Following fertilization, the baby bears stop growing after becoming multicelled blastocysts. For a few months, they just float around in a state of arrested development known as delayed implantation. Should the female bear fail to fatten up enough over the course of the year, her body can put the kibosh on pregnancy in an act of self-preservation. Conversely, if times are good, her body will allow more blastocysts to develop and implant in her womb—adjusting the number of cubs created based on fat stores.

Even though the deed is done months ahead of time, active gestation is surprisingly short—just 60 days in polar bears—and this results in helpless, underdeveloped cubs that are usually born between November and February, depending on the species and climate. Super-rich milk ensures that by the time spring comes, the cubs are ready to hit the ground running in a life-or-death race to rotundness. Polar bear milk contains up to 46 percent fat and tastes like the chalky cream of a fishy cow. And how do we know what it tastes like? Well, because polar bear scientists like Andrew Derocher are absurdly dedicated dudes. (click through to read the whole thing)

Photo by Kaisa Siren/AFP/Getty Images(via Do bears hibernate: Polar bear, black bear, grizzly bear sex and torpor. - Slate Magazine)

a-a-a-a-a-a-a-a-a:

(Photo from Scientific American, click through to read the story)
From Scientific American, an article about a real life Bones and MacArthur genius grant recipient- Mercedes Doretti. An Argentinian anthropologist who got her start in forensic anthropology following the collapse of the Argentinian dictatorship in 1982, she’s now working to find answers for families of migrants who have disappeared. In her words:

What we are trying to do with the Missing Migrants program that we started in 2009 is improve the search of missing migrants among unidentified remains by creating a regional exchange system. 

a-a-a-a-a-a-a-a-a:

(Photo from Scientific American, click through to read the story)

From Scientific American, an article about a real life Bones and MacArthur genius grant recipient- Mercedes Doretti. An Argentinian anthropologist who got her start in forensic anthropology following the collapse of the Argentinian dictatorship in 1982, she’s now working to find answers for families of migrants who have disappeared. In her words:

What we are trying to do with the Missing Migrants program that we started in 2009 is improve the search of missing migrants among unidentified remains by creating a regional exchange system. 

(Source: aaniaa)

Amanda, I think the circular areas in the kidney pancake were meant to represent the medulla, which has a somewhat triangular/pyramidal shape in the human kidney.

Amanda, I think the circular areas in the kidney pancake were meant to represent the medulla, which has a somewhat triangular/pyramidal shape in the human kidney.

This 2 hour special about the periodic table and the elements is airing tonight on PBS (9 p.m EDT).
A SHOUT OUT TO -periodic-meltdowns- ESPECIALLY!


Where do nature’s building blocks, called the elements, come from? They’re the hidden ingredients of everything in our world, from the carbon in our bodies to the metals in our smartphones. To unlock their secrets, David Pogue, the lively host of NOVA’s popular “Making Stuff” series and technology correspondent ofThe New York Times, spins viewers through the world of weird, extreme chemistry: the strongest acids, the deadliest poisons, the universe’s most abundant elements, and the rarest of the rare—substances cooked up in atom smashers that flicker into existence for only fractions of a second.
Why are some elements like platinum or gold inert while others like phosphorus or potassium violently explosive? Why are some vital to every breath we take while others are lethal toxins that killed off their discoverers such as Marie Curie? As he digs for answers, Pogue reveals the story of the elements to be a rich stew simmering with passion, madness, and obsessive scientific rivalry. Punctuated by surprising and often alarming experiments, this program takes NOVA on a roller-coaster ride through nature’s hidden lab and the compelling stories of discovery that revealed its secrets.



(via NOVA | Hunting the Elements)

This 2 hour special about the periodic table and the elements is airing tonight on PBS (9 p.m EDT).

A SHOUT OUT TO -periodic-meltdowns- ESPECIALLY!

Where do nature’s building blocks, called the elements, come from? They’re the hidden ingredients of everything in our world, from the carbon in our bodies to the metals in our smartphones. To unlock their secrets, David Pogue, the lively host of NOVA’s popular “Making Stuff” series and technology correspondent ofThe New York Times, spins viewers through the world of weird, extreme chemistry: the strongest acids, the deadliest poisons, the universe’s most abundant elements, and the rarest of the rare—substances cooked up in atom smashers that flicker into existence for only fractions of a second.

Why are some elements like platinum or gold inert while others like phosphorus or potassium violently explosive? Why are some vital to every breath we take while others are lethal toxins that killed off their discoverers such as Marie Curie? As he digs for answers, Pogue reveals the story of the elements to be a rich stew simmering with passion, madness, and obsessive scientific rivalry. Punctuated by surprising and often alarming experiments, this program takes NOVA on a roller-coaster ride through nature’s hidden lab and the compelling stories of discovery that revealed its secrets.

(via NOVA | Hunting the Elements)

mabelmoments:

Photograph: Courtesy of Emiko Paul and Quade Paul/ Echo Medical Media; Ron Gamble/UAB Insight/Science. 2011 International Science & Engineering Visual Challenge
Tumour death-cell receptors on breast cancer cell (Illustration – Honorable Mention). This artist’s illustration shows a monoclonal antibody (green) developed by scientists at the University of Alabama binding to a ‘death cell receptor’ on a cancer cell (top left). This triggers the cell’s inbuilt suicide program (apoptosis).

It looks like a setting for a sci-fi movie.
(I wish those monoclonal antibodies were as super specific as the researchers would like them to be. They seem to end up hitting receptors on cells you don’t want taken out.)

mabelmoments:

Photograph: Courtesy of Emiko Paul and Quade Paul/ Echo Medical Media; Ron Gamble/UAB Insight/Science. 2011 International Science & Engineering Visual Challenge

Tumour death-cell receptors on breast cancer cell (Illustration – Honorable Mention). This artist’s illustration shows a monoclonal antibody (green) developed by scientists at the University of Alabama binding to a ‘death cell receptor’ on a cancer cell (top left). This triggers the cell’s inbuilt suicide program (apoptosis).

It looks like a setting for a sci-fi movie.

(I wish those monoclonal antibodies were as super specific as the researchers would like them to be. They seem to end up hitting receptors on cells you don’t want taken out.)

Desertmar asked about the big spider trees and the reduction of malaria. I’m filching the nice caption explaining the life cycle of the organisms that cause malaria, Plasmodium spp. Plasmodium is a protozoa that requires mosquitoes to be vectors to spread the organism and needs them (as well as the human) to go through the life cycle and multiply.  Mosquito nets can be extremely helpful in areas with malaria to reduce exposure to mosquitoes.  I also remember when we learned about sickle cell anemia in various classes in vet school that sickle cell anemia is prevalent in people who live in areas (or have ancestry) where malaria is prevalent.  The Plasmodium organism can’t live in a sickled red blood cell and I remember hearing about it being an adaptation (albeit not a good adaptation) to the disease.  That kind of not so great adaptation is thought to be behind cystic fibrosis which is a mutation of a chloride channel in the cell (and is prevalent in people who live or have ancestry in places where cholera is/was endemic). I could say more but then I’ll never publish this post and instead frantically keep trying to edit the draft and then finally give up.
Here’s lots of info about malaria at the CDC website.
(I can’t really help with the spider thing - *shudder*)
The P.vivax life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host (1). Sporozoites infect liver cells (2) and either enter a dormant hypnozoite state or mature into schizonts (3), which rupture and release merozoites (4). After this initial replication in the liver (exo-erythrocytic schizogony A), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony B). Merozoites infect red blood cells (5). The ring stage trophozoites mature into schizonts, which rupture releasing merozoites (6). Some parasites differentiate into sexual erythrocytic stages (gametocytes) (7). Blood stage parasites are responsible for the clinical manifestations of the disease.
The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal (8). The parasites’ multiplication in the mosquito is known as the sporogonic cycle (C). While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes (9). The zygotes in turn become motile and elongated (ookinetes) (10) which invade the midgut wall of the mosquito where they develop into oocysts (11). The oocysts grow, rupture, and release sporozoites (12), which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites (1) into a new human host perpetuates the malaria life cycle. (via Plasmodium vivax)

Desertmar asked about the big spider trees and the reduction of malaria. I’m filching the nice caption explaining the life cycle of the organisms that cause malaria, Plasmodium spp. Plasmodium is a protozoa that requires mosquitoes to be vectors to spread the organism and needs them (as well as the human) to go through the life cycle and multiply.  Mosquito nets can be extremely helpful in areas with malaria to reduce exposure to mosquitoes.  I also remember when we learned about sickle cell anemia in various classes in vet school that sickle cell anemia is prevalent in people who live in areas (or have ancestry) where malaria is prevalent.  The Plasmodium organism can’t live in a sickled red blood cell and I remember hearing about it being an adaptation (albeit not a good adaptation) to the disease.  That kind of not so great adaptation is thought to be behind cystic fibrosis which is a mutation of a chloride channel in the cell (and is prevalent in people who live or have ancestry in places where cholera is/was endemic). I could say more but then I’ll never publish this post and instead frantically keep trying to edit the draft and then finally give up.

Here’s lots of info about malaria at the CDC website.

(I can’t really help with the spider thing - *shudder*)

The P.vivax life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host (1). Sporozoites infect liver cells (2) and either enter a dormant hypnozoite state or mature into schizonts (3), which rupture and release merozoites (4). After this initial replication in the liver (exo-erythrocytic schizogony A), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony B). Merozoites infect red blood cells (5). The ring stage trophozoites mature into schizonts, which rupture releasing merozoites (6). Some parasites differentiate into sexual erythrocytic stages (gametocytes) (7). Blood stage parasites are responsible for the clinical manifestations of the disease.

The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal (8). The parasites’ multiplication in the mosquito is known as the sporogonic cycle (C). While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes (9). The zygotes in turn become motile and elongated (ookinetes) (10) which invade the midgut wall of the mosquito where they develop into oocysts (11). The oocysts grow, rupture, and release sporozoites (12), which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites (1) into a new human host perpetuates the malaria life cycle. (via Plasmodium vivax)

When we honestly ask ourselves which person in our lives mean the most to us, we often find that it is those who, instead of giving advice, solutions, or cures, have chosen rather to share our pain and touch our wounds with a warm and tender hand.

- Henri Nouwen

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