Wissenschaft und Deutsch (on Hiatus)
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

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

GREAT NEWS! Researchers have developed a new reconstructive procedure that uses lab-grown cartilage instead of borrowed cartilage from ribs or ears to reconstruct noses, and have performed the first reconstructive nasal surgery using engineered tissue. The method is less invasive and can also be used to engineer cartilage for eyelids or ear reconstruction procedures.Read more: http://bit.ly/P4s8A8 via Smithsonian MagazineImage: Department of Biomedicine at the University of Basel
text source

GREAT NEWS! Researchers have developed a new reconstructive procedure that uses lab-grown cartilage instead of borrowed cartilage from ribs or ears to reconstruct noses, and have performed the first reconstructive nasal surgery using engineered tissue. The method is less invasive and can also be used to engineer cartilage for eyelids or ear reconstruction procedures.

Read more: http://bit.ly/P4s8A8 via Smithsonian Magazine

Image: Department of Biomedicine at the University of Basel

text source

This watercolour shows the face of a man who was subject to very rapid post-mortem decomposition. It depicts his state in the hot summer of 1893, 36 hours after he fell to his death from a scaffold where one of the poles entered the rectum, causing rupture of the liver and other severe internal injuries. (By Leonard Mark from St Bartholomew’s Hospital Archives & Museum)
from the Irregular Anatomist 

This watercolour shows the face of a man who was subject to very rapid post-mortem decomposition. It depicts his state in the hot summer of 1893, 36 hours after he fell to his death from a scaffold where one of the poles entered the rectum, causing rupture of the liver and other severe internal injuries. 
(By Leonard Mark from St Bartholomew’s Hospital Archives & Museum)

from the Irregular Anatomist 

Pollution From Asia Makes Pacific Storms Stronger
Brian Clark Howard
National Geographic
PUBLISHED APRIL 14, 2014

What happens in Asia doesn’t stay in Asia, a new study warns. Pollution from booming economies in the Far East is causing stronger storms and changing weather patterns over the Pacific Ocean, which in turn is changing weather in North America, scientists report.

"Whether the weather [in North America] will change in a good direction or bad is hard to say at this time," says Renyi Zhang, a professor of atmospheric sciences at Texas A&M University in College Station. Zhang is a co-author, along with several scientists from the U.S. and China, of a study released in the Proceedings of the National Academy of Sciences on Monday.

The scientists say pollution from Asia is likely leading to strongercyclones in the midlatitudes of the Pacific, more precipitation, and a faster movement of heat from the tropics toward the North Pole. As a result of these changes, “it’s almost certain that weather in the U.S. is changing,” says Zhang.

Smaller Drops, Bigger Storms

Zhang and his colleagues used computer modeling to study the effects on the weather of aerosols, which are fine particles suspended in the air. The main natural aerosols over the Pacific are sea salt tossed up by waves and dust blown off the land.

But those natural particles are now increasingly outnumbered by human-made ones. According to Zhang, the most significant aerosols the team considered are sulfates, which are emitted primarily by coal-fired power plants. Other aerosol pollutants are released by vehicle emissions and industrial activities.

In the atmosphere, such aerosols scatter and absorb sunlight, and thus have both cooling and warming effects on climate. But they also affect the formation of clouds and precipitation—and the magnitude of that indirect effect on clouds is one of the biggest uncertainties hampering scientists’ ability to forecast climate change.

Clouds form when water vapor condenses around aerosol particles to form liquid droplets. Because pollution increases the number of particles, it leads to more water droplets—but smaller ones. Those smaller droplets in turn rise to greater heights in the atmosphere—and even form ice—before they precipitate back out.

In an earlier paper, Zhang and his colleagues used satellite data to show that the amount of “deep convective clouds,” including thunderstorms, had increased over the North Pacific between 1984 and 2005. The most likely reason, they concluded, was an increase in aerosol pollution from Asia. ”The intensified Pacific storm track likely has profound implications for climate,” they wrote.

Global Effects

In the recent study the scientists took a first stab at considering those global implications. Standard global climate models simulate the atmosphere at grid points that are too widely spaced to resolve the fine-scale processes involved in cloud formation—which is one reason clouds remain such a knotty problem for climate scientists. But the researchers found a way to embed a “cloud resolving model” into a conventional climate model.

They then used that “multiscale” model to compare the preindustrial atmosphere of 1850, when levels of aerosol pollution over the Pacific were low, with the present atmosphere.
read more from Nat Geo

Pollution From Asia Makes Pacific Storms Stronger

Brian Clark Howard

National Geographic

PUBLISHED APRIL 14, 2014

What happens in Asia doesn’t stay in Asia, a new study warns. Pollution from booming economies in the Far East is causing stronger storms and changing weather patterns over the Pacific Ocean, which in turn is changing weather in North America, scientists report.

"Whether the weather [in North America] will change in a good direction or bad is hard to say at this time," says Renyi Zhang, a professor of atmospheric sciences at Texas A&M University in College Station. Zhang is a co-author, along with several scientists from the U.S. and China, of a study released in the Proceedings of the National Academy of Sciences on Monday.

The scientists say pollution from Asia is likely leading to strongercyclones in the midlatitudes of the Pacific, more precipitation, and a faster movement of heat from the tropics toward the North Pole. As a result of these changes, “it’s almost certain that weather in the U.S. is changing,” says Zhang.

Smaller Drops, Bigger Storms

Zhang and his colleagues used computer modeling to study the effects on the weather of aerosols, which are fine particles suspended in the air. The main natural aerosols over the Pacific are sea salt tossed up by waves and dust blown off the land.

But those natural particles are now increasingly outnumbered by human-made ones. According to Zhang, the most significant aerosols the team considered are sulfates, which are emitted primarily by coal-fired power plants. Other aerosol pollutants are released by vehicle emissions and industrial activities.

In the atmosphere, such aerosols scatter and absorb sunlight, and thus have both cooling and warming effects on climate. But they also affect the formation of clouds and precipitation—and the magnitude of that indirect effect on clouds is one of the biggest uncertainties hampering scientists’ ability to forecast climate change.

Clouds form when water vapor condenses around aerosol particles to form liquid droplets. Because pollution increases the number of particles, it leads to more water droplets—but smaller ones. Those smaller droplets in turn rise to greater heights in the atmosphere—and even form ice—before they precipitate back out.

In an earlier paper, Zhang and his colleagues used satellite data to show that the amount of “deep convective clouds,” including thunderstorms, had increased over the North Pacific between 1984 and 2005. The most likely reason, they concluded, was an increase in aerosol pollution from Asia. ”The intensified Pacific storm track likely has profound implications for climate,” they wrote.

Global Effects

In the recent study the scientists took a first stab at considering those global implications. Standard global climate models simulate the atmosphere at grid points that are too widely spaced to resolve the fine-scale processes involved in cloud formation—which is one reason clouds remain such a knotty problem for climate scientists. But the researchers found a way to embed a “cloud resolving model” into a conventional climate model.

They then used that “multiscale” model to compare the preindustrial atmosphere of 1850, when levels of aerosol pollution over the Pacific were low, with the present atmosphere.

read more from Nat Geo

Don’t forget to look up during the lunar eclipse on April 15th! It’s the first of a rare tetrad of four total lunar eclipses that will occur around six months apart over the next two years. The total lunar eclipse is often called a “blood moon” because when the Moon passes through Earth’s shadow it has an eerie red glow. You’re likely to see a very bright Mars too. Start watching the skies.Find out more: http://bit.ly/1n0AdVu via Queensland University of Technology (QUT)
text and photo source

Don’t forget to look up during the lunar eclipse on April 15th! It’s the first of a rare tetrad of four total lunar eclipses that will occur around six months apart over the next two years. The total lunar eclipse is often called a “blood moon” because when the Moon passes through Earth’s shadow it has an eerie red glow. You’re likely to see a very bright Mars too. Start watching the skies.

Find out more: http://bit.ly/1n0AdVu via Queensland University of Technology (QUT)

text and photo source

Now that I fricking forgot what I was going to post before getting angry, here’s this:

The Boy Who Played With Fusion

Taylor Wilson always dreamed of creating a star. Now he’s become one

Dust Glints on Martian Dunes
High-flying winds on Mars lead to twin-toned dunes, seen in this Mars Reconnaissance Orbiter image released on April 9.
The HiRISE camera aboard the orbiter sees into the infrared spectrum, revealing the dual coloring of the dunes located in the Meridiani Terra region of Mars.
Rusty, light-colored dust coats the lower-lying folds of the dunes. That’s because they are left unmolested by fierce winds that flow at higher altitudes. 
Higher up on the dunes, the winds scour their surfaces, removing the dust and revealing the dark blue sands underlying the dune crests.
photo by NASA
text from Nat Geo

Dust Glints on Martian Dunes

High-flying winds on Mars lead to twin-toned dunes, seen in this Mars Reconnaissance Orbiter image released on April 9.

The HiRISE camera aboard the orbiter sees into the infrared spectrum, revealing the dual coloring of the dunes located in the Meridiani Terra region of Mars.

Rusty, light-colored dust coats the lower-lying folds of the dunes. That’s because they are left unmolested by fierce winds that flow at higher altitudes. 

Higher up on the dunes, the winds scour their surfaces, removing the dust and revealing the dark blue sands underlying the dune crests.

photo by NASA

text from Nat Geo

Scalp is the soft tissue layer covering the bony vault over the brain. It is usually described as having five layers:S: The skin on the head from which head hair grows. It contains numerous sabaeceous glands and hair folliclesC: Connective tissue. A thin layer of fat and fibrous tissue lies beneath the skin.A: The aponeurosis called epicranial aponeurosis (or galea aponeurotica) is the next layer. It is a tough layer of dense fibrous tissue which runs from the frontalis muscle anteriorly to the occipitalis posteriorly.L: The loose areolar connective tissue layer provides an easy plane of separation between the upper three layers and the pericranium.P: The pericranium is the periosteum of the skull bones and provides nutrition to the bone and the capacity for repair.Photo source: http://www.juniordentist.com/
text source

Scalp is the soft tissue layer covering the bony vault over the brain. It is usually described as having five layers:

S: The skin on the head from which head hair grows. It contains numerous sabaeceous glands and hair follicles

C: Connective tissue. A thin layer of fat and fibrous tissue lies beneath the skin.

A: The aponeurosis called epicranial aponeurosis (or galea aponeurotica) is the next layer. It is a tough layer of dense fibrous tissue which runs from the frontalis muscle anteriorly to the occipitalis posteriorly.

L: The loose areolar connective tissue layer provides an easy plane of separation between the upper three layers and the pericranium.

P: The pericranium is the periosteum of the skull bones and provides nutrition to the bone and the capacity for repair.

Photo source: http://www.juniordentist.com/

text source

8TH PLACE1983 PHOTOMICROGRAPHY COMPETITION
Du Boistesselin
Chu. La Pitie’Paris, France
Subject Matter:
Antique 19th century microscope slide featuring composition of mounted butterfly scales and diatoms (35x)
source

8TH PLACE
1983 PHOTOMICROGRAPHY COMPETITION

Du Boistesselin

Chu. La Pitie’
Paris, France

Subject Matter:

Antique 19th century microscope slide featuring composition of mounted butterfly scales and diatoms (35x)

source

A terrible disease and yet maybe a hope against osteroporosis?"Fibrodysplasia ossificans progressiva" (FOP) skeletonizes body tissue and makes the victim imprisoned in its own body.What you see in the photo is complete bone tissue.You might not think about your bones very often unless you break one. When you break a bone, the bone heals itself and begins to regrow. But, what if your muscles, tendons and ligaments turned to bone? What if you formed a skeleton on top of the one you already have? That’s what happens with Fibrodysplasia Ossificans Progressiva, or FOP.FOP patients’ bones fuse together, essentially forming a second skeleton out of the tendons, ligaments and muscles- a true metamorphosis. The skeleton is almost one solid piece, and sheets of bone exist where they should not.In FOP patients, extra bone formation almost always starts at the neck, spine and shoulders. Only then does it move to the other joints. Eventually, people with FOP will probably lose most of their mobility. Joints lock, and bones can twist into odd positions. Often, the jaw fuses together either spontaneously or as a result of an injection for dental work, which makes eating and brushing teeth extremely difficult. The skeleton will fuse into one position, and that is the position a person with FOP will stay in for the rest of his or her life. Any attempt to remove the extra bone only leads to more extra bone re-formation. Only 700 people worldwide are known to have FOP, which makes this disorder extremely rare. The reason for this disease seems to be a mutation in the gene encoding Activin receptor IA (ACVR1), that is important for the regulation of ossification (the production of bone tissue). This gene helps control bone morphogenetic proteins, or BMPs. In FOP, the gene is active without BMPs- operating like a leaky faucet. When BMPs are present, the faucet explodes with activity and lacks inhibition. So it initiates ossification processes that can’t be regulated anymore.However, the positive aspect of this syndrome is: This genetical clue might someday help scientists figure out how to make extra bone for people who need it, like people with osteoporosis.Article: http://tinyurl.com/nmjzlkyImage found on wikipedia
text source 

A terrible disease and yet maybe a hope against osteroporosis?
"Fibrodysplasia ossificans progressiva" (FOP) skeletonizes body tissue and makes the victim imprisoned in its own body.

What you see in the photo is complete bone tissue.

You might not think about your bones very often unless you break one. When you break a bone, the bone heals itself and begins to regrow. But, what if your muscles, tendons and ligaments turned to bone? What if you formed a skeleton on top of the one you already have? That’s what happens with Fibrodysplasia Ossificans Progressiva, or FOP.

FOP patients’ bones fuse together, essentially forming a second skeleton out of the tendons, ligaments and muscles- a true metamorphosis. The skeleton is almost one solid piece, and sheets of bone exist where they should not.

In FOP patients, extra bone formation almost always starts at the neck, spine and shoulders. Only then does it move to the other joints. Eventually, people with FOP will probably lose most of their mobility. Joints lock, and bones can twist into odd positions. Often, the jaw fuses together either spontaneously or as a result of an injection for dental work, which makes eating and brushing teeth extremely difficult. 

The skeleton will fuse into one position, and that is the position a person with FOP will stay in for the rest of his or her life. Any attempt to remove the extra bone only leads to more extra bone re-formation. Only 700 people worldwide are known to have FOP, which makes this disorder extremely rare. 

The reason for this disease seems to be a mutation in the gene encoding Activin receptor IA (ACVR1), that is important for the regulation of ossification (the production of bone tissue). This gene helps control bone morphogenetic proteins, or BMPs. 

In FOP, the gene is active without BMPs- operating like a leaky faucet. When BMPs are present, the faucet explodes with activity and lacks inhibition. So it initiates ossification processes that can’t be regulated anymore.

However, the positive aspect of this syndrome is: This genetical clue might someday help scientists figure out how to make extra bone for people who need it, like people with osteoporosis.

Article: http://tinyurl.com/nmjzlky
Image found on wikipedia

text source