BPoD

Sep 21

21 September 2014
Faulty Plumbing
We need perfect plumbing to carry blood, food, air and waste products to the right places in our body. How our tubes remain the right length when we’re changing shape as we grow is a puzzle that we’re just beginning to understand. In a recent study of fruit fly embryos, some were found to have a trachea [windpipe], that had grown too long, causing the kinks and bends we see in this highly magnified, false-coloured picture. Scientists discovered that a faulty gene had disturbed a natural balance between two forces – the growth of the membrane lining the inner surface of the trachea, which tends to stretch it lengthways, and resistance to this stretching action from the extracellular matrix, the springy structure between cells. The gradual adjustment of these balancing forces is believed to be how nature ‘precision engineers’ our tubes so that they grow with our bodies.
Written by Mick Warwicker
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Image by Shigeo Hayashi, Edouard Hannezo and Bo DongRIKEN Center for Developmental Biology, JapanOriginally published under a Creative Commons Licence (BY 3.0)Research published in Cell Reports, May 2014
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21 September 2014

Faulty Plumbing

We need perfect plumbing to carry blood, food, air and waste products to the right places in our body. How our tubes remain the right length when we’re changing shape as we grow is a puzzle that we’re just beginning to understand. In a recent study of fruit fly embryos, some were found to have a trachea [windpipe], that had grown too long, causing the kinks and bends we see in this highly magnified, false-coloured picture. Scientists discovered that a faulty gene had disturbed a natural balance between two forces – the growth of the membrane lining the inner surface of the trachea, which tends to stretch it lengthways, and resistance to this stretching action from the extracellular matrix, the springy structure between cells. The gradual adjustment of these balancing forces is believed to be how nature ‘precision engineers’ our tubes so that they grow with our bodies.

Written by Mick Warwicker

Image by Shigeo Hayashi, Edouard Hannezo and Bo Dong
RIKEN Center for Developmental Biology, Japan
Originally published under a Creative Commons Licence (BY 3.0)
Research published in Cell Reports, May 2014

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Sep 20

20 September 2014
Turn it Down
Whether it’s a distant bird call, a whispered conversation or a suspicious sound in the house, we all behave in the same way when straining to hear something: stand stock still and be as quiet as possible. Unbeknownst to us, an equivalent correction is constantly taking place within the brain, keeping us responsive to sound throughout our many noisy activities. This is achieved by neurons [nerve cells], shown in green (in a section of mouse brain) which project from the motor cortex, an area responsible for controlling movement, to the auditory cortex, which processes signals from our ears. When mice are grooming, running or feeding, these neurons send signals to inhibit other cells in the auditory cortex, dampening their response to sound. By reducing sensitivity to the sounds of our own body, this mechanism is thought to maintain our ability to detect other, more important noises in the environment.
Written by Emmanuelle Briolat
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Image by Anders NelsonDuke University, USAOriginally published under a Creative Commons LicenceResearch published in Nature, August 2014
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20 September 2014

Turn it Down

Whether it’s a distant bird call, a whispered conversation or a suspicious sound in the house, we all behave in the same way when straining to hear something: stand stock still and be as quiet as possible. Unbeknownst to us, an equivalent correction is constantly taking place within the brain, keeping us responsive to sound throughout our many noisy activities. This is achieved by neurons [nerve cells], shown in green (in a section of mouse brain) which project from the motor cortex, an area responsible for controlling movement, to the auditory cortex, which processes signals from our ears. When mice are grooming, running or feeding, these neurons send signals to inhibit other cells in the auditory cortex, dampening their response to sound. By reducing sensitivity to the sounds of our own body, this mechanism is thought to maintain our ability to detect other, more important noises in the environment.

Written by Emmanuelle Briolat

Image by Anders Nelson
Duke University, USA
Originally published under a Creative Commons Licence
Research published in Nature, August 2014

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Sep 19

19 September 2014
Immortal Souls
This is an aquatic flatworm called a planarian with a bellyful of green fluorescent bacteria. Planarians posses a truly enviable trait: immortality. Astonishingly, they can’t die of old age because of an extraordinary ability to regenerate. Not only that, they can resist bacteria that are harmful, even fatal, to humans. Striving to understand the planarian’s impressive immune defence, researchers have infected the planarian with bacteria that are dangerous in humans, such as the species that causes tuberculosis, and studied the genes the worm activated. They identified 18 genes that make it resistant to these harmful organisms and focused on one gene in particular, MORN2. Later, the team switched on this MORN2 gene in a type of human white blood cell (a macrophage). These white blood cells could efficiently eliminate the TB-bacteria, bringing the possibility of new ammunition to fight against bacteria-borne diseases. But oh, to be a planarian!
Written by Nick Kennedy
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Image by Eric Ghigo and Sophie PagnottaAix-Marseille UniversityOriginally published under a Creative Commons Licence (BY 4.0)Research published in Cell Host and Microbe, September 2014
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19 September 2014

Immortal Souls

This is an aquatic flatworm called a planarian with a bellyful of green fluorescent bacteria. Planarians posses a truly enviable trait: immortality. Astonishingly, they can’t die of old age because of an extraordinary ability to regenerate. Not only that, they can resist bacteria that are harmful, even fatal, to humans. Striving to understand the planarian’s impressive immune defence, researchers have infected the planarian with bacteria that are dangerous in humans, such as the species that causes tuberculosis, and studied the genes the worm activated. They identified 18 genes that make it resistant to these harmful organisms and focused on one gene in particular, MORN2. Later, the team switched on this MORN2 gene in a type of human white blood cell (a macrophage). These white blood cells could efficiently eliminate the TB-bacteria, bringing the possibility of new ammunition to fight against bacteria-borne diseases. But oh, to be a planarian!

Written by Nick Kennedy

Image by Eric Ghigo and Sophie Pagnotta
Aix-Marseille University
Originally published under a Creative Commons Licence (BY 4.0)
Research published in Cell Host and Microbe, September 2014

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Sep 18

18 September 2014
Smiley Giant
This happy face belongs to a giant cell, formed when several immune cells (known as macrophages) team up and fuse together. Although they may look like eyes and a mouth, the dark spots are actually the cells’ nuclei – the ‘control centres’ containing their DNA. These unusual cells are created in certain illnesses where the immune system runs out of control and causes inflammation such as arthritis, which affects the joints, or the kidney disease glomerulonephritis. A molecule on the surface of macrophages, called KCNN4, directs this biological get-together in mice and humans by orchestrating a complex interacting network of cellular signals. KCNN4 has previously been implicated in other types of over-enthusiastic immune response, and drugs that block it are already being tested in clinical trials for immune system-related conditions such as inflammatory bowel disease and asthma. So maybe they could be useful for treating other illnesses too.
Written by Kat Arney
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Image by Enrico PetrettoMRC Clinical Sciences Centre Copyright held by original authorsResearch published in Cell Reports, August 2014
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18 September 2014

Smiley Giant

This happy face belongs to a giant cell, formed when several immune cells (known as macrophages) team up and fuse together. Although they may look like eyes and a mouth, the dark spots are actually the cells’ nuclei – the ‘control centres’ containing their DNA. These unusual cells are created in certain illnesses where the immune system runs out of control and causes inflammation such as arthritis, which affects the joints, or the kidney disease glomerulonephritis. A molecule on the surface of macrophages, called KCNN4, directs this biological get-together in mice and humans by orchestrating a complex interacting network of cellular signals. KCNN4 has previously been implicated in other types of over-enthusiastic immune response, and drugs that block it are already being tested in clinical trials for immune system-related conditions such as inflammatory bowel disease and asthma. So maybe they could be useful for treating other illnesses too.

Written by Kat Arney

Image by Enrico Petretto
MRC Clinical Sciences Centre
Copyright held by original authors
Research published in Cell Reports, August 2014

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Sep 17

17 September 2014
Stiff Blood Cells
When you give blood, your red blood cells are separated and banked until they’re needed for a transfusion. During storage, those cells undergo biochemical and structural changes, but for the most part appear like new. Now, researchers have used a special microscopy technique to look closely at how storage affects the performance of red blood cells. Taking time-lapse images of the cells to chart nanoscale fluctuations in the cell membrane (pictured) over time, the researchers found that red blood cell membranes get stiffer during storage, which impairs their ability to carry oxygen around the body. Stiffened cells look fine and retain normal levels of oxygen-carrying haemoglobin, but they’re not flexible enough to squeeze through narrow capillaries – in the brain, for example – which could cause serious problems in transfusion recipients. Potentially, doctors could use this imaging method to check red blood cells before they’re given to patients.
Written by Daniel Cossins
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Image by Gabriel PopescuUniversity of Illinois at Urbana-Champaign, USACopyright held by Nature Publishing GroupResearch published in Nature, September 2014
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17 September 2014

Stiff Blood Cells

When you give blood, your red blood cells are separated and banked until they’re needed for a transfusion. During storage, those cells undergo biochemical and structural changes, but for the most part appear like new. Now, researchers have used a special microscopy technique to look closely at how storage affects the performance of red blood cells. Taking time-lapse images of the cells to chart nanoscale fluctuations in the cell membrane (pictured) over time, the researchers found that red blood cell membranes get stiffer during storage, which impairs their ability to carry oxygen around the body. Stiffened cells look fine and retain normal levels of oxygen-carrying haemoglobin, but they’re not flexible enough to squeeze through narrow capillaries – in the brain, for example – which could cause serious problems in transfusion recipients. Potentially, doctors could use this imaging method to check red blood cells before they’re given to patients.

Written by Daniel Cossins

Image by Gabriel Popescu
University of Illinois at Urbana-Champaign, USA
Copyright held by Nature Publishing Group
Research published in Nature, September 2014

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Sep 16

16 September 2014
Sensors for Senses
Chemicals control our thoughts. Calcium, for example, regulates the signals that zip along miles of nerve cells – neurons – to and from the brain. ‘Waves’ of calcium signalling are tell-tale signs of healthy brain activity, but they’re often difficult to detect inside living tissues. Pictured here, neurons in a mouse brain are lit up with a fluorescent calcium sensor (green) – the result of a type of genetic modification, inserting manmade DNA into the mouse’s genome without harming the rest of its genes. As the healthy mouse develops, the fluorescent sensor (together with a red marker) can be used to map activity in important brain regions like the hippocampus (pictured). Calcium measurements in different parts of the brain also reveal details about how mammalian senses work – such as inside the olfactory bulb, where neurons fizzle into life in response to smells from the outside world.
Written by John Ankers
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Image by John White and colleaguesUniversity of Utah, USAOriginally published under a Creative Commons LicenceResearch published in Neuron, August 2014
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16 September 2014

Sensors for Senses

Chemicals control our thoughts. Calcium, for example, regulates the signals that zip along miles of nerve cells – neurons – to and from the brain. ‘Waves’ of calcium signalling are tell-tale signs of healthy brain activity, but they’re often difficult to detect inside living tissues. Pictured here, neurons in a mouse brain are lit up with a fluorescent calcium sensor (green) – the result of a type of genetic modification, inserting manmade DNA into the mouse’s genome without harming the rest of its genes. As the healthy mouse develops, the fluorescent sensor (together with a red marker) can be used to map activity in important brain regions like the hippocampus (pictured). Calcium measurements in different parts of the brain also reveal details about how mammalian senses work – such as inside the olfactory bulb, where neurons fizzle into life in response to smells from the outside world.

Written by John Ankers

Image by John White and colleagues
University of Utah, USA
Originally published under a Creative Commons Licence
Research published in Neuron, August 2014

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Sep 15

15 September 2014
Refusing to Fuse
Our skull may look and feel solid but it’s actually made up of 28 separate bones that fuse together during development. Having multiple junctions allows the skull to squeeze through the birth canal and then keep up with rapid brain growth. If this process is not perfectly orchestrated, however, children can be born with serious deformations. Cleft palates, which affect one in 700 newborns, are a case in point, caused when the two arch-like plates in the roof of their mouth fail to come together in the womb. Left with a hole in their palate, children can develop speech and feeding problems. The central pin-shaped blue region shows this gap in the skull of a mouse lacking a specific protein implicated in palate formation. In healthy animals with this protein, this space does not exist as the surrounding bones (coloured in pink) close in and fuse together before birth.
Written by Jan Piotrowski
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Image by Juhee Jeong and colleaguesNew York University College of Dentistry, USAOriginally published under a Creative Commons Licence (BY 2.0)Research published in BMC Developmental Biology, August 2014
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15 September 2014

Refusing to Fuse

Our skull may look and feel solid but it’s actually made up of 28 separate bones that fuse together during development. Having multiple junctions allows the skull to squeeze through the birth canal and then keep up with rapid brain growth. If this process is not perfectly orchestrated, however, children can be born with serious deformations. Cleft palates, which affect one in 700 newborns, are a case in point, caused when the two arch-like plates in the roof of their mouth fail to come together in the womb. Left with a hole in their palate, children can develop speech and feeding problems. The central pin-shaped blue region shows this gap in the skull of a mouse lacking a specific protein implicated in palate formation. In healthy animals with this protein, this space does not exist as the surrounding bones (coloured in pink) close in and fuse together before birth.

Written by Jan Piotrowski

Image by Juhee Jeong and colleagues
New York University College of Dentistry, USA
Originally published under a Creative Commons Licence (BY 2.0)
Research published in BMC Developmental Biology, August 2014

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Sep 14

14 September 2014
Blood Cleaner
Microbial pathogens in the bloodstream can lead to sepsis, when the immune system goes wild in response to the infection, often causing organ failure and death. It usually takes days to identify the culprit, so doctors use broad-spectrum antibiotics, which are not very effective. Now, though, researchers have debuted a potential solution: an external device that removes pathogens and toxins from blood. As infected blood passes through the device, it’s mixed with magnetic nanobeads coated with engineered proteins that bind to a range of nasties. Pictured is a protein-coated magnetic bead (blue) binding to Escherichia coli. The bead-bound invaders are then pulled from the flowing blood by a magnet, before the cleansed blood is returned to the patient. When tested in infected rats, the device worked well: the cleansed blood brought down the number of inflammatory proteins and reduced the impact on the rats’ vital organs.
Written by Daniel Cossins
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Image by Donald Ingber and colleaguesWyss Institute at Harvard, USACopyright held by Nature Publishing GroupResearch published in Nature Medicine, September 2014
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14 September 2014

Blood Cleaner

Microbial pathogens in the bloodstream can lead to sepsis, when the immune system goes wild in response to the infection, often causing organ failure and death. It usually takes days to identify the culprit, so doctors use broad-spectrum antibiotics, which are not very effective. Now, though, researchers have debuted a potential solution: an external device that removes pathogens and toxins from blood. As infected blood passes through the device, it’s mixed with magnetic nanobeads coated with engineered proteins that bind to a range of nasties. Pictured is a protein-coated magnetic bead (blue) binding to Escherichia coli. The bead-bound invaders are then pulled from the flowing blood by a magnet, before the cleansed blood is returned to the patient. When tested in infected rats, the device worked well: the cleansed blood brought down the number of inflammatory proteins and reduced the impact on the rats’ vital organs.

Written by Daniel Cossins

Image by Donald Ingber and colleagues
Wyss Institute at Harvard, USA
Copyright held by Nature Publishing Group
Research published in Nature Medicine, September 2014

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Sep 13

13 September 2014
Vermicular Vomiting
This is a schistosome, a parasitic flatworm that infects more than 200 million people worldwide, causing a debilitating disease called schistosomiasis. Adult worms spend their lives bathed in blood in the veins of the bladder or intestine. In a recent study scientists have shed light on the schistosome’s complex feeding habits, which could have major implications for developing drugs against them. The study shows that even within the weird world of worm parasites, schistosomes are odd. Unlike other worm parasites, they take up food in two ways. They either ‘feed’ by absorbing nutrients directly across the body surface (here, dyed green) or by drinking up blood through a mouth. Stranger still, they don’t have a bottom, or to use scientific speak, ‘schistosomes lack an anus.’ So as they lap up human blood with vampiric zeal, they later vomit up a toxic substance called heme that accumulates in their gut.
Written by Nick Kennedy
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Image by Patrick Skelly and colleaguesTufts University, USAOriginally published under a Creative Commons Licence (BY 4.0)Research published in PLOS Pathogens, August 2014
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13 September 2014

Vermicular Vomiting

This is a schistosome, a parasitic flatworm that infects more than 200 million people worldwide, causing a debilitating disease called schistosomiasis. Adult worms spend their lives bathed in blood in the veins of the bladder or intestine. In a recent study scientists have shed light on the schistosome’s complex feeding habits, which could have major implications for developing drugs against them. The study shows that even within the weird world of worm parasites, schistosomes are odd. Unlike other worm parasites, they take up food in two ways. They either ‘feed’ by absorbing nutrients directly across the body surface (here, dyed green) or by drinking up blood through a mouth. Stranger still, they don’t have a bottom, or to use scientific speak, ‘schistosomes lack an anus.’ So as they lap up human blood with vampiric zeal, they later vomit up a toxic substance called heme that accumulates in their gut.

Written by Nick Kennedy

Image by Patrick Skelly and colleagues
Tufts University, USA
Originally published under a Creative Commons Licence (BY 4.0)
Research published in PLOS Pathogens, August 2014

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Sep 12

12 September 2014
Fever-fighting Fit
As it sweeps across West Africa, Ebola has become the virus to fear, its deadly haemorrhagic fevers claiming around 1500 lives to date. The closely-related Marburg virus, pictured, causes similar severe symptoms; in one outbreak, 90% of infected patients succumbed to the disease. Both Ebola and Marburg are notoriously difficult to cure, and to be effective most potential treatments need to be administered very soon after infection before symptoms appear. However, recent tests on Rhesus monkeys suggest a solution could be at hand. Monkeys infected with Marburg were injected with a small RNA molecule, which interferes with the synthesis of one of the virus’ proteins; all the animals recovered, even if the treatment was given three days after infection. While further tests are needed, this study raises the possibility of extending the treatment window for these diseases, a major step towards improving the likelihood of survival.
Written by Emmanuelle Briolat
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Image by Science SourceScience Photo LibraryAny re-use of this image must be authorised by Science Photo LibraryResearch published in Science Translational Medicine, August 2014
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12 September 2014

Fever-fighting Fit

As it sweeps across West Africa, Ebola has become the virus to fear, its deadly haemorrhagic fevers claiming around 1500 lives to date. The closely-related Marburg virus, pictured, causes similar severe symptoms; in one outbreak, 90% of infected patients succumbed to the disease. Both Ebola and Marburg are notoriously difficult to cure, and to be effective most potential treatments need to be administered very soon after infection before symptoms appear. However, recent tests on Rhesus monkeys suggest a solution could be at hand. Monkeys infected with Marburg were injected with a small RNA molecule, which interferes with the synthesis of one of the virus’ proteins; all the animals recovered, even if the treatment was given three days after infection. While further tests are needed, this study raises the possibility of extending the treatment window for these diseases, a major step towards improving the likelihood of survival.

Written by Emmanuelle Briolat

Image by Science Source
Science Photo Library
Any re-use of this image must be authorised by Science Photo Library
Research published in Science Translational Medicine, August 2014

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