BPoD

Sep 02

02 September 2014
Death Star
C. elegans – a worm used as a model for many aspects of mammalian biology – has been seen moving in a new and mysterious way in the presence of a worm disease-causing bacterium. Worms swim singly in liquid until a type of Leucobacter is added, then they wriggle into a ‘worm-star’ formation (pictured). Once infected, their tails stick together and become knotted. Any adult worms trapped in the worm-star are unable to move and die, allowing growth of the infecting bacteria; however, baby worms occasionally make a quick get-away (bottom right) by autotomy or self-amputation, splitting their body in half. This is the first time that this mode of attack has been reported, and its mechanism of action is unknown. Discovering how this worm-trapping trickery works could provide insight into beating bacterial infection in humans.
Written by Katie Panteli
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Image by Jonathan Hodgkin and colleaguesUniversity of Oxford, UKCopyright Elsevier 2014Research published in Current Biology, November 2013
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02 September 2014

Death Star

C. elegans – a worm used as a model for many aspects of mammalian biology – has been seen moving in a new and mysterious way in the presence of a worm disease-causing bacterium. Worms swim singly in liquid until a type of Leucobacter is added, then they wriggle into a ‘worm-star’ formation (pictured). Once infected, their tails stick together and become knotted. Any adult worms trapped in the worm-star are unable to move and die, allowing growth of the infecting bacteria; however, baby worms occasionally make a quick get-away (bottom right) by autotomy or self-amputation, splitting their body in half. This is the first time that this mode of attack has been reported, and its mechanism of action is unknown. Discovering how this worm-trapping trickery works could provide insight into beating bacterial infection in humans.

Written by Katie Panteli

Image by Jonathan Hodgkin and colleagues
University of Oxford, UK
Copyright Elsevier 2014
Research published in Current Biology, November 2013

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Sep 01

01 September 2014
Gimme a C!
There is some truth in the old saying, “an apple a day keeps the doctor away”. Vitamin C – pictured here in crystalline form – is produced in the liver of many animals, but not humans. Keeping ourselves topped up is essential – vitamin C (also known as L-ascorbic acid) has several important roles in the body and is hard at work inside every cell in the brain. It’s a very effective anti-oxidant, able to ‘mop up’ volatile molecules produced in energetic brain regions such as the hippocampus. Recent research suggests that as well as having this protective role, vitamin C is directly involved in producing energy inside nerve cells and may reduce the risk of epileptic seizures. So “an apple a day” is good advice, but a couple of strawberries would be even better – they contain up to ten-times as much of this vital vitamin.
Written by John Ankers
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Image by Spike Walker from the Wellcome Image Awards 2014Originally published under a Creative Commons Licence (BY 4.0)Research published in Journal of Neurochemistry, February 2014
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01 September 2014

Gimme a C!

There is some truth in the old saying, “an apple a day keeps the doctor away”. Vitamin C – pictured here in crystalline form – is produced in the liver of many animals, but not humans. Keeping ourselves topped up is essential – vitamin C (also known as L-ascorbic acid) has several important roles in the body and is hard at work inside every cell in the brain. It’s a very effective anti-oxidant, able to ‘mop up’ volatile molecules produced in energetic brain regions such as the hippocampus. Recent research suggests that as well as having this protective role, vitamin C is directly involved in producing energy inside nerve cells and may reduce the risk of epileptic seizures. So “an apple a day” is good advice, but a couple of strawberries would be even better – they contain up to ten-times as much of this vital vitamin.

Written by John Ankers

Image by Spike Walker from the Wellcome Image Awards 2014
Originally published under a Creative Commons Licence (BY 4.0)
Research published in Journal of Neurochemistry, February 2014

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Aug 31

31 August 2014
Lessons from Lizards
Lizards can lose their tails. The idea is that reptile-guzzling predators are distracted by the abandoned appendage while the lizard scarpers to safety. And then the lizard’s tail grows back. This ability to regenerate body parts has long interested scientists, who hope to mimic it in humans. As the most closely related animals to humans (who sometimes regrow lost fingertips) that can regenerate entire body parts we and lizards share the same toolbox of genes for the job. Researchers have now carried out the first genome analysis of tail regeneration in the green anole (pictured), which revealed that during tail regrowth lizards turn on 326 genes, including those involved in embryonic development, response to hormone signals and wound healing. By following the lizard’s genetic recipe for regeneration, then harnessing those genes in humans, it may be possible to regrow new cartilage, muscle or spinal cord in the future.
Written by Nick Kennedy
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Image by Piccolo NamekOriginally published under a Creative Commons Licence (BY 3.0)Research published in PLOS One, August 2014
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31 August 2014

Lessons from Lizards

Lizards can lose their tails. The idea is that reptile-guzzling predators are distracted by the abandoned appendage while the lizard scarpers to safety. And then the lizard’s tail grows back. This ability to regenerate body parts has long interested scientists, who hope to mimic it in humans. As the most closely related animals to humans (who sometimes regrow lost fingertips) that can regenerate entire body parts we and lizards share the same toolbox of genes for the job. Researchers have now carried out the first genome analysis of tail regeneration in the green anole (pictured), which revealed that during tail regrowth lizards turn on 326 genes, including those involved in embryonic development, response to hormone signals and wound healing. By following the lizard’s genetic recipe for regeneration, then harnessing those genes in humans, it may be possible to regrow new cartilage, muscle or spinal cord in the future.

Written by Nick Kennedy

Image by Piccolo Namek
Originally published under a Creative Commons Licence (BY 3.0)
Research published in PLOS One, August 2014

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Aug 30

30 August 2014
Glowing Health
Changes to blood circulation in the brain can be a symptom of migraine, a stroke or even Alzheimer’s but can’t easily be seen with X-rays or magnetic resonance scanning. Sharper and more detailed 3D images – and even video sequences – can be obtained by scanning with near infrared light, although a major drawback is that only a few millimetres of surface tissue can be penetrated. To get around this problem, scientists injected a mouse with carbon nanotubes, which fluoresce strongly in near infrared light, before scanning its brain. This experiment produced high quality images of blood vessels near the surface of the brain, like the one shown here, without the need to remove part of the animal’s skull. The technique will aid research on animals into brain diseases and could in theory be used for diagnosis in humans, although proof would be required that the procedure is safe.
Written by Mick Warwicker
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Image by Hongjie Dai and colleaguesStanford University, USACopyright held by Nature Publishing GroupResearch published in Nature Photonics, August 2014
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30 August 2014

Glowing Health

Changes to blood circulation in the brain can be a symptom of migraine, a stroke or even Alzheimer’s but can’t easily be seen with X-rays or magnetic resonance scanning. Sharper and more detailed 3D images – and even video sequences – can be obtained by scanning with near infrared light, although a major drawback is that only a few millimetres of surface tissue can be penetrated. To get around this problem, scientists injected a mouse with carbon nanotubes, which fluoresce strongly in near infrared light, before scanning its brain. This experiment produced high quality images of blood vessels near the surface of the brain, like the one shown here, without the need to remove part of the animal’s skull. The technique will aid research on animals into brain diseases and could in theory be used for diagnosis in humans, although proof would be required that the procedure is safe.

Written by Mick Warwicker

Image by Hongjie Dai and colleagues
Stanford University, USA
Copyright held by Nature Publishing Group
Research published in Nature Photonics, August 2014

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Aug 29

29 August 2014
Blood and Gold
One of the biggest hopes for nanotechnology is the design of molecules to support living processes. Pictured here, tiny gold ‘nanorods’ cover the surface of red blood cells – a snapshot of biotechnology in action, fixed in time with a blue chemical agent. Each gold nanorod holds tiny ‘pockets’, called aptamers, filled with a blood thinning chemical called thrombin. Firing a laser at these harmless specks of gold causes them to melt just enough to release the thrombin, preventing blood from clotting. The process can be reversed by triggering the release of a different chemical which counteracts the thrombin, allowing the blood to clot naturally. Intravenous injections of chemicals like heparin are currently used all over the world to prevent dangerous blood clots after operations. In the future, nanotechnology could be used instead, with the advantage of controllable clotting at the flick of a laser switch.
Written by John Ankers
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Image by Helena de PuigMassachusetts Institute of Technology, USAOriginally published under a Creative Commons Licence (BY 4.0)Research published in PLOS One, July 2014
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29 August 2014

Blood and Gold

One of the biggest hopes for nanotechnology is the design of molecules to support living processes. Pictured here, tiny gold ‘nanorods’ cover the surface of red blood cells – a snapshot of biotechnology in action, fixed in time with a blue chemical agent. Each gold nanorod holds tiny ‘pockets’, called aptamers, filled with a blood thinning chemical called thrombin. Firing a laser at these harmless specks of gold causes them to melt just enough to release the thrombin, preventing blood from clotting. The process can be reversed by triggering the release of a different chemical which counteracts the thrombin, allowing the blood to clot naturally. Intravenous injections of chemicals like heparin are currently used all over the world to prevent dangerous blood clots after operations. In the future, nanotechnology could be used instead, with the advantage of controllable clotting at the flick of a laser switch.

Written by John Ankers

Image by Helena de Puig
Massachusetts Institute of Technology, USA
Originally published under a Creative Commons Licence (BY 4.0)
Research published in PLOS One, July 2014

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Aug 28

28 August 2014
Space Invaders
Cancer starts when our own cells start growing out of control, forming a tumour. If detected early and removed with surgery, the chances of survival are usually good. But if cancer cells go on the move, invading the tissue around them and spreading through the body, it can be much harder to treat effectively. To understand how cancer cells spread, researchers are putting them through their paces in ‘obstacle courses’ like the one shown here – a labyrinth of microscopic pillars (black dots) which the blue, green and red-stained cancer cells have to navigate around. The green cells like to stick together, moving slowly as a group. While the red cells, which have different molecular characteristics prefer to go it alone. Figuring out how cells switch between these behaviours could reveal new ways of preventing cancer from spreading and treating it more effectively.
Written by Kat Arney
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Image by Ian Wong Brown University, USAOriginally published under a Creative Commons LicenceResearch published in Nature Materials, August 2014
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28 August 2014

Space Invaders

Cancer starts when our own cells start growing out of control, forming a tumour. If detected early and removed with surgery, the chances of survival are usually good. But if cancer cells go on the move, invading the tissue around them and spreading through the body, it can be much harder to treat effectively. To understand how cancer cells spread, researchers are putting them through their paces in ‘obstacle courses’ like the one shown here – a labyrinth of microscopic pillars (black dots) which the blue, green and red-stained cancer cells have to navigate around. The green cells like to stick together, moving slowly as a group. While the red cells, which have different molecular characteristics prefer to go it alone. Figuring out how cells switch between these behaviours could reveal new ways of preventing cancer from spreading and treating it more effectively.

Written by Kat Arney

Image by Ian Wong
Brown University, USA
Originally published under a Creative Commons Licence
Research published in Nature Materials, August 2014

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Aug 27

27 August 2014
Brain Scene Investigation
Piecing together the progression of deadly diseases from autopsy samples is a challenge often met by biomedical scientists. This brain tissue – from a rhesus monkey – is infected with the Japanese encephalitis virus (JEV), the cause of over 10,000 human deaths per year. On the left, JEV (stained in orange) has infected several neurons [nerve cells]. The neurons look healthy, but JEV is a slow-acting and devious virus. It hijacks the neurons’ chemical signals, sending out cytokines that turn inflammation, the brain’s natural protective process, against itself. On the right, the brain’s own immune defenders, microglial cells, have swarmed to attack infected neurons, leaving them shrivelled. There is currently no treatment for JEV, which, aside from many deaths, causes brain damage in many thousands of patients. Cultural constraints on autopsies in the Western Pacific, where Japanese encephalitis predominantly occurs, make this evidence for the timeline of JEV both rare and valuable.
Written by John Ankers
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Image by Tom Solomon and colleaguesUniversity of Liverpool, UKOriginally published under a Creative Commons Licence (BY 4.0)Research published in PLOS Neglected Tropical Diseases, August 2014
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27 August 2014

Brain Scene Investigation

Piecing together the progression of deadly diseases from autopsy samples is a challenge often met by biomedical scientists. This brain tissue – from a rhesus monkey – is infected with the Japanese encephalitis virus (JEV), the cause of over 10,000 human deaths per year. On the left, JEV (stained in orange) has infected several neurons [nerve cells]. The neurons look healthy, but JEV is a slow-acting and devious virus. It hijacks the neurons’ chemical signals, sending out cytokines that turn inflammation, the brain’s natural protective process, against itself. On the right, the brain’s own immune defenders, microglial cells, have swarmed to attack infected neurons, leaving them shrivelled. There is currently no treatment for JEV, which, aside from many deaths, causes brain damage in many thousands of patients. Cultural constraints on autopsies in the Western Pacific, where Japanese encephalitis predominantly occurs, make this evidence for the timeline of JEV both rare and valuable.

Written by John Ankers

Image by Tom Solomon and colleagues
University of Liverpool, UK
Originally published under a Creative Commons Licence (BY 4.0)
Research published in PLOS Neglected Tropical Diseases, August 2014

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Aug 26

26 August 2014
Explained Mysteries
Charles Richet was a Parisian physiologist, who was born on this day in 1850. There scarcely seems an area of science – actually, life in general – that he didn’t delve into. His research roved between disciplines and interests, from hydrochloric acid in gastric juices to aviation, from heat regulation in mammals to spiritualism. But it was for his work on anaphylaxis that he was awarded the Nobel Prize in Physiology or Medicine 1913. Anaphylaxis is a massive, life-threatening allergic reaction, which occurs when the immune system overreacts to an otherwise harmless substance – like a peanut. Richet injected poison from the Portuguese man-of-war jellyfish into dogs on two occasions. He found that dogs that survived the first injection without any distress, when given a second injection three weeks later, had a violent reaction and died within 25 minutes. His work explained a host of previously misunderstood cases of intoxication and sudden death.
Written by Nick Kennedy
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Image by Agence de presse MeurisseBibliothèque nationale de FranceOriginally published under a Creative Commons Licence (BY 4.0)
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26 August 2014

Explained Mysteries

Charles Richet was a Parisian physiologist, who was born on this day in 1850. There scarcely seems an area of science – actually, life in general – that he didn’t delve into. His research roved between disciplines and interests, from hydrochloric acid in gastric juices to aviation, from heat regulation in mammals to spiritualism. But it was for his work on anaphylaxis that he was awarded the Nobel Prize in Physiology or Medicine 1913. Anaphylaxis is a massive, life-threatening allergic reaction, which occurs when the immune system overreacts to an otherwise harmless substance – like a peanut. Richet injected poison from the Portuguese man-of-war jellyfish into dogs on two occasions. He found that dogs that survived the first injection without any distress, when given a second injection three weeks later, had a violent reaction and died within 25 minutes. His work explained a host of previously misunderstood cases of intoxication and sudden death.

Written by Nick Kennedy

Image by Agence de presse Meurisse
Bibliothèque nationale de France
Originally published under a Creative Commons Licence (BY 4.0)

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Aug 25

[video]

Aug 24

24 August 2014
The High Life
When people live at high altitude, where oxygen is limited, their bodies usually produce a higher number of red blood cells. The more red blood cells present, the more oxygen can be lugged around the body… up to a point. This response can cause the blood to become thick and sticky with oxygen-carrying red blood cells, which can increase the risk of heart failure. A study has found that highland inhabitants of the Tibetan plateau (pictured) possess a unique genetic variant that enables them to survive in the oxygen-thin air. The researchers believe that this EGLN1 gene, which entered the Tibetan population 8,000 years ago, serves to protect highland Tibetans against an over-eager response to low oxygen levels. Because oxygen plays a central role in disease, a deep understanding of how high altitude adaptations work may lead to novel treatments for various diseases, including cancer.
Written by Nick Kennedy
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Image by NASA’s Marshall Space Flight Center on FlickrNASAOriginally published under a Creative Commons Licence (BY 2.0)Research published in Nature Genetics, August 2014
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24 August 2014

The High Life

When people live at high altitude, where oxygen is limited, their bodies usually produce a higher number of red blood cells. The more red blood cells present, the more oxygen can be lugged around the body… up to a point. This response can cause the blood to become thick and sticky with oxygen-carrying red blood cells, which can increase the risk of heart failure. A study has found that highland inhabitants of the Tibetan plateau (pictured) possess a unique genetic variant that enables them to survive in the oxygen-thin air. The researchers believe that this EGLN1 gene, which entered the Tibetan population 8,000 years ago, serves to protect highland Tibetans against an over-eager response to low oxygen levels. Because oxygen plays a central role in disease, a deep understanding of how high altitude adaptations work may lead to novel treatments for various diseases, including cancer.

Written by Nick Kennedy

Image by NASA’s Marshall Space Flight Center on Flickr
NASA
Originally published under a Creative Commons Licence (BY 2.0)
Research published in Nature Genetics, August 2014

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