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As you can see, the arachnoid membrane contains a lot of venes laying on top of brain’s surface (cortex) in order to guarantee a good blood circulation in the brain region. Also, it plays a large role for the cerebrospinal fluid.Cerebrospinal fluid circulates in the subarachnoid space (between arachnoid and pia mater). It is produced by the choroid plexus (inside the ventricles of the brain, which are in direct communication with the subarachnoid space so the fluid can flow freely through the nervous system).Cerebrospinal fluid is a transparent, colourless fluid and it is produced at about 500 ml/day. Its electrolyte levels, glucose levels, and pH are very similar to those in plasma, but the presence of blood in cerebrospinal fluid is always abnormal.The arachnoid mater is named after the Greek words “Arachne” (“spider”) and suffix “-oid” (“in the image of”), and “mater” (the Latin word for mother), because of the fine spider web-like appearance of the delicate fibres of the arachnoid which extend down through the subarachnoid space and attach to the pia mater.Image found on mr-friendly-awesomesauce.tumblr.com (if you go to this page, there are NSFW photos)
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As you can see, the arachnoid membrane contains a lot of venes laying on top of brain’s surface (cortex) in order to guarantee a good blood circulation in the brain region. Also, it plays a large role for the cerebrospinal fluid.

Cerebrospinal fluid circulates in the subarachnoid space (between arachnoid and pia mater). It is produced by the choroid plexus (inside the ventricles of the brain, which are in direct communication with the subarachnoid space so the fluid can flow freely through the nervous system).

Cerebrospinal fluid is a transparent, colourless fluid and it is produced at about 500 ml/day. Its electrolyte levels, glucose levels, and pH are very similar to those in plasma, but the presence of blood in cerebrospinal fluid is always abnormal.

The arachnoid mater is named after the Greek words “Arachne” (“spider”) and suffix “-oid” (“in the image of”), and “mater” (the Latin word for mother), because of the fine spider web-like appearance of the delicate fibres of the arachnoid which extend down through the subarachnoid space and attach to the pia mater.

Image found on mr-friendly-awesomesauce.tumblr.com (if you go to this page, there are NSFW photos)

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What you can see here is a resin cast of pancreatic blood vessels. The fine network of smaller vessels that branches off from the main vessels infiltrates the tissue, supplying it with blood. Gases and nutrients are exchanged between the blood and surrounding tissues through the permeable walls of capillaries, the smallest blood vessels. The pancreas produces the hormones insulin and glucagon, which regulate blood glucose levels. It also secretes digestive enzymes. The cast was made by injecting resin into the blood vessels, followed by chemical digestion of surrounding tissues. Even on this microscopic image with 30x magnification, the network of blood vessels is sheer endless, our body is a miracle of architectural compactness 
Image by Susumu Nishinaga
text source

What you can see here is a resin cast of pancreatic blood vessels. The fine network of smaller vessels that branches off from the main vessels infiltrates the tissue, supplying it with blood. Gases and nutrients are exchanged between the blood and surrounding tissues through the permeable walls of capillaries, the smallest blood vessels. 

The pancreas produces the hormones insulin and glucagon, which regulate blood glucose levels. It also secretes digestive enzymes. The cast was made by injecting resin into the blood vessels, followed by chemical digestion of surrounding tissues. 

Even on this microscopic image with 30x magnification, the network of blood vessels is sheer endless, our body is a miracle of architectural compactness 

Image by Susumu Nishinaga

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How to: Improve your Memory

Nearly everyone wants a better memory, or could just use a better memory. To just be able to remember the last item on a shopping list, or where they put their car keys. But most importantly, remember all the information for exams. This video has tips and tricks to improving your memory in all kinds of ways.

Impressive example of Pneumococcal meningitis!Meningitis is a clinical syndrome characterized by inflammation of the meninges, the 3 layers of membranes that enclose the brain and spinal cord. These layers consist of the following:Dura - A tough outer membraneArachnoid - A lacy, weblike middle membraneSubarachnoid space - A delicate, fibrous inner layer that contains many of the blood vessels that feed the brain and spinal cordThe inflammation may be caused by infection with viruses, bacteria, or other microorganisms.Meningitis can be life-threatening because of the inflammation’s proximity to the brain and spinal cord; therefore, the condition is classified as a medical emergency.Pneumococcal meningitis occurs when the bacteria that have invaded the bloodstream move across to infect the meninges.The meninges are filled with a liquid called cerebrospinal fluid (CSF), which is there to bathe the brain and cushion it against physical damage.Bacteria can multiply freely in CSF, and there they release poisons, causing inflammation and swelling in the meninges and the brain tissue itself.This increases pressure on the brain, producing symptoms of meningitis such as headache, stiff neck and dislike of bright lights.Risk factors: -Extremes of age (< 5 or >60 years)-Diabetes mellitus, renal or adrenal insufficiency, hypoparathyroidism, or cystic fibrosis-HIV infection-Splenectomy and sickle cell disease-Alcoholism and cirrhosis-Recent exposure to others with meningitis-Contiguous infection (eg, sinusitis)-Intravenous (IV) drug abuse-Some cranial congenital deformitiesRead more: www.bit.ly/1j1XDUQwww.bit.ly/1j28BsfPhoto credits: Dr. Edwin P. Ewing, Jr.
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Impressive example of Pneumococcal meningitis!

Meningitis is a clinical syndrome characterized by inflammation of the meninges, the 3 layers of membranes that enclose the brain and spinal cord. These layers consist of the following:

Dura - A tough outer membrane
Arachnoid - A lacy, weblike middle membrane
Subarachnoid space - A delicate, fibrous inner layer that contains many of the blood vessels that feed the brain and spinal cord

The inflammation may be caused by infection with viruses, bacteria, or other microorganisms.

Meningitis can be life-threatening because of the inflammation’s proximity to the brain and spinal cord; therefore, the condition is classified as a medical emergency.

Pneumococcal meningitis occurs when the bacteria that have invaded the bloodstream move across to infect the meninges.

The meninges are filled with a liquid called cerebrospinal fluid (CSF), which is there to bathe the brain and cushion it against physical damage.

Bacteria can multiply freely in CSF, and there they release poisons, causing inflammation and swelling in the meninges and the brain tissue itself.

This increases pressure on the brain, producing symptoms of meningitis such as headache, stiff neck and dislike of bright lights.

Risk factors: -Extremes of age (< 5 or >60 years)
-Diabetes mellitus, renal or adrenal insufficiency, hypoparathyroidism, or cystic fibrosis
-HIV infection
-Splenectomy and sickle cell disease
-Alcoholism and cirrhosis
-Recent exposure to others with meningitis
-Contiguous infection (eg, sinusitis)
-Intravenous (IV) drug abuse
-Some cranial congenital deformities

Read more: www.bit.ly/1j1XDUQ
www.bit.ly/1j28Bsf

Photo credits: Dr. Edwin P. Ewing, Jr.

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Today is cool news:
Find out more: http://bit.ly/1i4V0FA via Science Unraveled
source 

Today is cool news:

Find out more: http://bit.ly/1i4V0FA via Science Unraveled

source 

sixpenceee:

Another oddity museum for all the bizarre lovers!

The Musée Fragonard d’Alfort is a museum of anatomical oddities.

It opened to the public in 1991, and today consists of three rooms containing a large collection of anatomical oddities and dissections, most of which date from the 19th and early 20th centuries.

In addition to animal skeleton and dissections such as a piglet displayed in cross-section, the museum contains a substantial collection of monstrosities Siamese twin lambs, a two-headed calf, a 10-legged sheep, and a colt with one huge eye.

The museum’s most astonishing items are the famous “écorchés” (flayed figures) prepared by Honoré Fragonard.

His speciality was the preparation and preservation of skinned cadavers, of which he prepared some 700 examples. Only 21 remain; all are on display in the museum’s final room

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ANOTHER ODDITY MUESEUM

The cervical spinal cordBy removing the rear arches of the neck (cervical) vertebra and the fibrous covering (dura) over the spinal cord one sees the cervical spinal cord and its nerves. The blood vessels nourishing the cord and vertebral column and the origin of the cord from the brain are clearly shown.Read more: http://bit.ly/1le0rnD
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The cervical spinal cord

By removing the rear arches of the neck (cervical) vertebra and the fibrous covering (dura) over the spinal cord one sees the cervical spinal cord and its nerves. The blood vessels nourishing the cord and vertebral column and the origin of the cord from the brain are clearly shown.

Read more: http://bit.ly/1le0rnD

source 

Dolphins play it safe and monitor their environment all the time.Read more: http://bit.ly/1gOkhSz via LiveScience
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Dolphins play it safe and monitor their environment all the time.

Read more: http://bit.ly/1gOkhSz via LiveScience

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Kilauea&#8217;s Halemaʻumaʻu CraterHalema’uma’u Crater is the center of activity at Hawaii’s Kilauea Volcano. From 1820—when visiting scientists began recording their observations—until 1924, Halema’uma’u and much of Kilauea Caldera was usually filled with a lava lake. In 1924, lava drained suddenly, vaporizing groundwater deep beneath the caldera. A series of violent steam explosions followed, sculpting Halema’uma’u into its current shape. For the rest of the 20th Century, Halema’uma’u occasionally filled with lava, but quickly drained again. Most of the time the crater floor was solid. The pattern ended in March 2008, when a new pit formed along the eastern edge of Halema’uma’u; deep within the new pit crater was a lava lake. Since the pit crater formed, it has slowly expanded and is now about 160 meters (520 ft) across. The level of the lava fluctuates as magma moves from beneath the summit to the ongoing eruption in Kilauea’s East Rift Zone. This U.S. Geological Survey photograph of the lava lake was taken from the rim of Halemaʻumaʻu Crater on February 1, 2014. The level had dropped slightly from the previous day, leaving a black veneer of lava on the crater walls just above the surface of the lava and easily visible in this photograph.See the image and read more from the U.S. Geological Survey athttps://www.flickr.com/photos/usgeologicalsurvey/12792432484/See the Halemaʻumaʻu Crater from space at http://earthobservatory.nasa.gov/NaturalHazards/view.php?id=81781&amp;src=fbSee more satellite imagery of the Halemaʻumaʻu Crater athttp://earthobservatory.nasa.gov/NaturalHazards/event.php?id=36090&amp;src=fb
photo and text from NASA

Kilauea’s Halemaʻumaʻu Crater

Halema’uma’u Crater is the center of activity at Hawaii’s Kilauea Volcano. From 1820—when visiting scientists began recording their observations—until 1924, Halema’uma’u and much of Kilauea Caldera was usually filled with a lava lake. In 1924, lava drained suddenly, vaporizing groundwater deep beneath the caldera. A series of violent steam explosions followed, sculpting Halema’uma’u into its current shape. For the rest of the 20th Century, Halema’uma’u occasionally filled with lava, but quickly drained again. Most of the time the crater floor was solid. The pattern ended in March 2008, when a new pit formed along the eastern edge of Halema’uma’u; deep within the new pit crater was a lava lake. Since the pit crater formed, it has slowly expanded and is now about 160 meters (520 ft) across. The level of the lava fluctuates as magma moves from beneath the summit to the ongoing eruption in Kilauea’s East Rift Zone. This U.S. Geological Survey photograph of the lava lake was taken from the rim of Halemaʻumaʻu Crater on February 1, 2014. The level had dropped slightly from the previous day, leaving a black veneer of lava on the crater walls just above the surface of the lava and easily visible in this photograph.

See the image and read more from the U.S. Geological Survey at
https://www.flickr.com/photos/usgeologicalsurvey/12792432484/

See the Halemaʻumaʻu Crater from space at 
http://earthobservatory.nasa.gov/NaturalHazards/view.php?id=81781&src=fb

See more satellite imagery of the Halemaʻumaʻu Crater at
http://earthobservatory.nasa.gov/NaturalHazards/event.php?id=36090&src=fb

photo and text from NASA

How Harmless Bacteria Quickly Turned Into a Flesh-Eating Monster

Just four changes gave Streptococcus the ability to cause deadly disease
Susan Brink
for National Geographic
PUBLISHED APRIL 15, 2014

By examining decades&#8217; worth of stored bacteria samples, researchers have determined how a benign organism evolved into a deadly pathogen that causes necrotizing fasciitis, commonly known as flesh-eating bacteria disease.
Using genetic sequences from more than 3,600 strains of bacteria, scientists were able to see that it took only four steps to create the unusual microbe that spreads rapidly and destroys the body&#8217;s soft tissue. Their report was published Monday in the Proceedings of the National Academy of Sciences.
Necrotizing fasciitis is caused by several types of bacteria, most commonly group A Streptococcus. (See images of Streptococcus and other microbes in the &#8220;Small, Small World&#8221; photo gallery.) An international group of researchers sequenced the genomes of group A strep bacteria in samples that had been collected from as early as the 1920s. Those sequences revealed that sometime in the past, group A strep was infected with first one virus and then soon after with another. With each infection, the bacterium gained viral genes that made group A strep more likely to cause disease.
"The third event was a mutation of a single letter of the genome of the organism to create an even more virulent form," said the study&#8217;s main author, James Musser, director of the Center for Molecular and Translational Human Infectious Diseases Research at the Houston Methodist Research Institute in Texas. That mutation probably occurred in the late 1960s.
Then, in the early 1980s, the bacterium acquired another piece of foreign DNA, which carried the code for two toxins that cause necrotizing fasciitis&#8217;s worst effects. &#8220;We were off and running with a strain that had increased ability to spread in humans and to cause a more severe form of disease,&#8221; Musser said.
A Long Search for Answers
The new research would not have been possible without the foresight of several international collaborators who saved comprehensive samples of this kind of bacteria for many decades. That let scientists study how the organism evolved over all that time.
"If you simply sequenced the samples from today, you really wouldn&#8217;t understand how and when it flipped from a bad pathogen to a really bad pathogen," Musser said.
Musser has been gripped with curiosity about the flesh-eating disease since Muppets creator Jim Henson died of the infection in 1990. At that time a new field of research—bacterial population genetics—was just beginning. &#8220;This has been my white whale for almost 25 years,&#8221; Musser said.
Today about 650 to 800 Americans become infected with flesh-eating bacteria each year, according to the Centers for Disease Control and Prevention. The bacteria infect layers of membranes and connective tissue around muscle, nerves, fat, and blood vessels. The toxins made by the bacteria destroy the tissue they infect, causing it to die.
Healthy people with strong immune systems who carefully clean and care for cuts, scrapes, and insect bites are usually able to fight off the bacteria. But people with compromised immune systems or with conditions such as diabetes, kidney disease, or cancer are more vulnerable.
Jacqueline Roemmele was one such unlucky person. She became infected in 1994 after the cesarean section birth of her twins. &#8220;Before they found what it was, my flesh was falling off in the nurses&#8217; hands,&#8221; she said. Roemmele survived and went on to found, with Donna Batdorff, the National Necrotizing Fasciitis Foundation.
The new discovery &#8220;is very exciting,&#8221; Roemmele said. &#8220;This is the first time I&#8217;ve heard of science ripping apart how this actually happens to explain: Why did this become a supercharged bacteria? &#8230;This gives us greater insight into why it happens.&#8221;
There is still a lot of work that needs to be done toward finding methods to prevent, treat, and cure necrotizing fasciitis. But this study shows that analyzing the timing of the molecular events that lead to global epidemics can help to monitor and predict the emergence of deadly infectious diseases.
"This is the first time we&#8217;ve been able to sort out the precise events that give rise to bacterial epidemics," said Musser. "We need to understand the general rules in order to understand epidemics. This is the first understanding of that."
text and photo from Nat Geo

How Harmless Bacteria Quickly Turned Into a Flesh-Eating Monster

Just four changes gave Streptococcus the ability to cause deadly disease

Susan Brink

for National Geographic

PUBLISHED APRIL 15, 2014

By examining decades’ worth of stored bacteria samples, researchers have determined how a benign organism evolved into a deadly pathogen that causes necrotizing fasciitis, commonly known as flesh-eating bacteria disease.

Using genetic sequences from more than 3,600 strains of bacteria, scientists were able to see that it took only four steps to create the unusual microbe that spreads rapidly and destroys the body’s soft tissue. Their report was published Monday in the Proceedings of the National Academy of Sciences.

Necrotizing fasciitis is caused by several types of bacteria, most commonly group A Streptococcus. (See images of Streptococcus and other microbes in the “Small, Small World” photo gallery.) An international group of researchers sequenced the genomes of group A strep bacteria in samples that had been collected from as early as the 1920s. Those sequences revealed that sometime in the past, group A strep was infected with first one virus and then soon after with another. With each infection, the bacterium gained viral genes that made group A strep more likely to cause disease.

"The third event was a mutation of a single letter of the genome of the organism to create an even more virulent form," said the study’s main author, James Musser, director of the Center for Molecular and Translational Human Infectious Diseases Research at the Houston Methodist Research Institute in Texas. That mutation probably occurred in the late 1960s.

Then, in the early 1980s, the bacterium acquired another piece of foreign DNA, which carried the code for two toxins that cause necrotizing fasciitis’s worst effects. “We were off and running with a strain that had increased ability to spread in humans and to cause a more severe form of disease,” Musser said.

A Long Search for Answers

The new research would not have been possible without the foresight of several international collaborators who saved comprehensive samples of this kind of bacteria for many decades. That let scientists study how the organism evolved over all that time.

"If you simply sequenced the samples from today, you really wouldn’t understand how and when it flipped from a bad pathogen to a really bad pathogen," Musser said.

Musser has been gripped with curiosity about the flesh-eating disease since Muppets creator Jim Henson died of the infection in 1990. At that time a new field of research—bacterial population genetics—was just beginning. “This has been my white whale for almost 25 years,” Musser said.

Today about 650 to 800 Americans become infected with flesh-eating bacteria each year, according to the Centers for Disease Control and Prevention. The bacteria infect layers of membranes and connective tissue around muscle, nerves, fat, and blood vessels. The toxins made by the bacteria destroy the tissue they infect, causing it to die.

Healthy people with strong immune systems who carefully clean and care for cuts, scrapes, and insect bites are usually able to fight off the bacteria. But people with compromised immune systems or with conditions such as diabetes, kidney disease, or cancer are more vulnerable.

Jacqueline Roemmele was one such unlucky person. She became infected in 1994 after the cesarean section birth of her twins. “Before they found what it was, my flesh was falling off in the nurses’ hands,” she said. Roemmele survived and went on to found, with Donna Batdorff, the National Necrotizing Fasciitis Foundation.

The new discovery “is very exciting,” Roemmele said. “This is the first time I’ve heard of science ripping apart how this actually happens to explain: Why did this become a supercharged bacteria? …This gives us greater insight into why it happens.”

There is still a lot of work that needs to be done toward finding methods to prevent, treat, and cure necrotizing fasciitis. But this study shows that analyzing the timing of the molecular events that lead to global epidemics can help to monitor and predict the emergence of deadly infectious diseases.

"This is the first time we’ve been able to sort out the precise events that give rise to bacterial epidemics," said Musser. "We need to understand the general rules in order to understand epidemics. This is the first understanding of that."

text and photo from Nat Geo