Magnified World


When I looked through my first microscope at the age of eight, I didn't just see tiny swimming microbes from our bird bath. I saw the complete and total beauty of the world in the tiniest details. Here I post what we pass every day because we cannot see it. I hope you can see the beauty as I do.
heythereuniverse:

Nano Coral Reef | FEI Company
The silicon nanopillars are fabricated through combining two techniques, a gold mask made by nanosphere lithography and a Metal-Assisted Chemical Etching of Silicon.
The structures shown in the imagen look like an amazing coral reef, but at the nanoscale

heythereuniverse:

Nano Coral Reef | FEI Company

The silicon nanopillars are fabricated through combining two techniques, a gold mask made by nanosphere lithography and a Metal-Assisted Chemical Etching of Silicon.

The structures shown in the imagen look like an amazing coral reef, but at the nanoscale

science-junkie:

How plankton gets jet lagged
A hormone that governs sleep and jet lag in humans may also drive the mass migration of plankton in the ocean, scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have found. The molecule in question, melatonin, is essential to maintain our daily rhythm, and the European scientists have now discovered that it governs the nightly migration of a plankton species from the surface to deeper waters. The findings, published online today in Cell, indicate that melatonin’s role in controlling daily rhythms probably evolved early in the history of animals, and hold hints to how our sleep patterns may have evolved.[…]
[The researchers] discovered a group of specialised motor neurons that respond to melatonin. Using modern molecular sensors, [they were] able to visualise the activity of these neurons in the larva’s brain, and found that it changes radically from day to night. The night-time production of melatonin drives changes in these neurons’ activity, which in turn cause the larva’s cilia to take long pauses from beating. Thanks to these extended pauses, the larva slowly sinks down. During the day, no melatonin is produced, the cilia pause less, and the larva swims upwards.
“Step by step we can elucidate the evolutionary origin of key functions of our brain. The fascinating picture emerges that human biology finds its roots in some deeply conserved, fundamental aspects of ocean ecology that dominated life on Earth since ancient evolutionary times”
Read more @EMBL

science-junkie:

How plankton gets jet lagged

A hormone that governs sleep and jet lag in humans may also drive the mass migration of plankton in the ocean, scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have found. The molecule in question, melatonin, is essential to maintain our daily rhythm, and the European scientists have now discovered that it governs the nightly migration of a plankton species from the surface to deeper waters. The findings, published online today in Cell, indicate that melatonin’s role in controlling daily rhythms probably evolved early in the history of animals, and hold hints to how our sleep patterns may have evolved.[…]

[The researchers] discovered a group of specialised motor neurons that respond to melatonin. Using modern molecular sensors, [they were] able to visualise the activity of these neurons in the larva’s brain, and found that it changes radically from day to night. The night-time production of melatonin drives changes in these neurons’ activity, which in turn cause the larva’s cilia to take long pauses from beating. Thanks to these extended pauses, the larva slowly sinks down. During the day, no melatonin is produced, the cilia pause less, and the larva swims upwards.

Step by step we can elucidate the evolutionary origin of key functions of our brain. The fascinating picture emerges that human biology finds its roots in some deeply conserved, fundamental aspects of ocean ecology that dominated life on Earth since ancient evolutionary times

Read more @EMBL

currentsinbiology:

Gut Bacteria May Play a Role in Autism (Scientific American) 
Autism is primarily a disorder of the brain, but research suggests that as many as nine out of 10 individuals with the condition also suffer from gastrointestinal problems such as inflammatory bowel disease and “leaky gut.” The latter condition occurs when the intestines become excessively permeable and leak their contents into the bloodstream. Scientists have long wondered whether the composition of bacteria in the intestines, known as the gut microbiome, might be abnormal in people with autism and drive some of these symptoms. Now a spate of new studies supports this notion and suggests that restoring proper microbial balance could alleviate some of the disorder’s behavioral symptoms.
At the annual meeting of the American Society for Microbiology held in May in Boston, researchers at Arizona State University reported the results of an experiment in which they measured the levels of various microbial by-products in the feces of children with autism and compared them with those found in healthy children. The levels of 50 of these substances, they found, significantly differed between the two groups. And in a 2013 study published in PLOS ONE, Italian researchers reported that, compared with healthy kids, those with autism had altered levels of several intestinal bacterial species, including fewer Bifidobacterium, a group known to promote good intestinal health.
One open question is whether these microbial differences drive the development of the condition or are instead a consequence of it. A study published in December 2013 in Cell supports the former idea. When researchers at the California Institute of Technology incited autismlike symptoms in mice using an established paradigm that involved infecting their mothers with a viruslike molecule during pregnancy, they found that after birth, the mice had altered gut bacteria compared with healthy mice. By treating the sick rodents with a health-promoting bacterium called Bacteroides fragilis, the researchers were able to attenuate some, but not all, of their behavioral symptoms. The treated mice had less anxious and stereotyped behaviors and became more vocally communicative.
Bacteroides fragilis Credit: CNRI/SCIENCE SOURCE

currentsinbiology:

Gut Bacteria May Play a Role in Autism (Scientific American)

Autism is primarily a disorder of the brain, but research suggests that as many as nine out of 10 individuals with the condition also suffer from gastrointestinal problems such as inflammatory bowel disease and “leaky gut.” The latter condition occurs when the intestines become excessively permeable and leak their contents into the bloodstream. Scientists have long wondered whether the composition of bacteria in the intestines, known as the gut microbiome, might be abnormal in people with autism and drive some of these symptoms. Now a spate of new studies supports this notion and suggests that restoring proper microbial balance could alleviate some of the disorder’s behavioral symptoms.

At the annual meeting of the American Society for Microbiology held in May in Boston, researchers at Arizona State University reported the results of an experiment in which they measured the levels of various microbial by-products in the feces of children with autism and compared them with those found in healthy children. The levels of 50 of these substances, they found, significantly differed between the two groups. And in a 2013 study published in PLOS ONE, Italian researchers reported that, compared with healthy kids, those with autism had altered levels of several intestinal bacterial species, including fewer Bifidobacterium, a group known to promote good intestinal health.

One open question is whether these microbial differences drive the development of the condition or are instead a consequence of it. A study published in December 2013 in Cell supports the former idea. When researchers at the California Institute of Technology incited autismlike symptoms in mice using an established paradigm that involved infecting their mothers with a viruslike molecule during pregnancy, they found that after birth, the mice had altered gut bacteria compared with healthy mice. By treating the sick rodents with a health-promoting bacterium called Bacteroides fragilis, the researchers were able to attenuate some, but not all, of their behavioral symptoms. The treated mice had less anxious and stereotyped behaviors and became more vocally communicative.

Bacteroides fragilis
Credit: CNRI/SCIENCE SOURCE

Scientists Discover Strange New Brain Cell Shape | IFLScience

bpod-mrc:

27 May 2014
Hint Hunting
Researchers are looking for clues to help unravel the mystery of how some muscles become damaged by genetic disease. Charcot-Marie-Tooth (CMT) is the most common solely inherited disease. It’s caused by mutations in genes that make the proteins that are the building blocks of our muscles. CMT patients suffer from weakness and numbness of the arms, legs and feet. However, there are few treatments beyond physical therapy. Looking at the muscles of a type of mouse that will develop CMT, the team found that neuromuscular junctions (pictured) in the feet weren’t developing properly. These are relay stations for nerve fibres (in green) carrying information from the brain to receptors in the muscle (shown in red). Since the mice were not yet showing symptoms of CMT, this growth defect could be an early sign of the disease. Future drug therapies could target this region to help prevent eventual muscle damage.
Written by Gaëlle Coullon
—
Image by Zameel Cader and colleagues University of Oxford, UKCopyright held by original authors Research published in Human Molecular Genetics, December 2013
—
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bpod-mrc:

27 May 2014

Hint Hunting

Researchers are looking for clues to help unravel the mystery of how some muscles become damaged by genetic disease. Charcot-Marie-Tooth (CMT) is the most common solely inherited disease. It’s caused by mutations in genes that make the proteins that are the building blocks of our muscles. CMT patients suffer from weakness and numbness of the arms, legs and feet. However, there are few treatments beyond physical therapy. Looking at the muscles of a type of mouse that will develop CMT, the team found that neuromuscular junctions (pictured) in the feet weren’t developing properly. These are relay stations for nerve fibres (in green) carrying information from the brain to receptors in the muscle (shown in red). Since the mice were not yet showing symptoms of CMT, this growth defect could be an early sign of the disease. Future drug therapies could target this region to help prevent eventual muscle damage.

Written by Gaëlle Coullon

Image by Zameel Cader and colleagues
University of Oxford, UK
Copyright held by original authors
Research published in Human Molecular Genetics, December 2013

You can also follow BPoD on Twitter and Facebook

(via fyeahmedlab)