BPoD

Apr 23

[video]

Apr 22

22 April 2014
Nobel Nerves
Italian neurologist Rita Levi-Montalcini – born on this day in 1909 – received the 1986 Nobel Prize in Physiology and Medicine, along with Stanley Cohen, for their discovery that a protein called nerve growth factor plays a key role in the development of the nervous system. But particularly remarkable is how Levi-Montalcini managed to conduct her research at a time when Mussolini prevented non-Aryan Italian citizens from having academic careers. This impelled Levi-Montalcini to set up a laboratory in her bedroom at her family home in Turin. Following heavy bombing by English and American forces, she left Turin to rebuild her mini-laboratory in a cottage in the country. When the German army invaded Italy, she fled to Florence to work as a doctor for war refugees. After the war, she went to Washington University, St. Louis, USA, and remained there for thirty years. She died in December 2012 aged 103.
Written by Nick Kennedy
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Image courtesy of audrey_sel on Flickr Originally published under a Creative Commons Licence
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22 April 2014

Nobel Nerves

Italian neurologist Rita Levi-Montalcini – born on this day in 1909 – received the 1986 Nobel Prize in Physiology and Medicine, along with Stanley Cohen, for their discovery that a protein called nerve growth factor plays a key role in the development of the nervous system. But particularly remarkable is how Levi-Montalcini managed to conduct her research at a time when Mussolini prevented non-Aryan Italian citizens from having academic careers. This impelled Levi-Montalcini to set up a laboratory in her bedroom at her family home in Turin. Following heavy bombing by English and American forces, she left Turin to rebuild her mini-laboratory in a cottage in the country. When the German army invaded Italy, she fled to Florence to work as a doctor for war refugees. After the war, she went to Washington University, St. Louis, USA, and remained there for thirty years. She died in December 2012 aged 103.

Written by Nick Kennedy

Image courtesy of audrey_sel on Flickr
Originally published under a Creative Commons Licence

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Apr 21

21 April 2014
Crypt Cell Alchemy
In people with type-1 diabetes, beta cells in the pancreas don’t produce a hormone called insulin, leading to increased glucose levels in the blood. To control the problem, patients inject themselves with insulin. In the search for a better way to tackle diabetes, researchers have used stem cells to make new beta cells. Now, they may have a simpler strategy. By delivering three transcription factors – proteins that control gene activity – into mice, they transformed intestinal cells called crypt cells (stained green) into insulin-producing cells (red). The same combination of proteins turned human intestine cells grown in the dish into beta-like cells. So, if researchers can perfect this cellular alchemy to produce higher-quality beta-like cells, the intestines of diabetes patients could provide a ready supply of insulin-producing cells. These cells could then be given back to patients to regulate blood-sugar levels without the need for regular injections.
Written by Daniel Cossins
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Image courtesy of Ben Stanger and colleagues Perelman School of Medicine, University of Pennsylvania, USA Copyright held by original authors Research published in Cell, March 2014
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21 April 2014

Crypt Cell Alchemy

In people with type-1 diabetes, beta cells in the pancreas don’t produce a hormone called insulin, leading to increased glucose levels in the blood. To control the problem, patients inject themselves with insulin. In the search for a better way to tackle diabetes, researchers have used stem cells to make new beta cells. Now, they may have a simpler strategy. By delivering three transcription factors – proteins that control gene activity – into mice, they transformed intestinal cells called crypt cells (stained green) into insulin-producing cells (red). The same combination of proteins turned human intestine cells grown in the dish into beta-like cells. So, if researchers can perfect this cellular alchemy to produce higher-quality beta-like cells, the intestines of diabetes patients could provide a ready supply of insulin-producing cells. These cells could then be given back to patients to regulate blood-sugar levels without the need for regular injections.

Written by Daniel Cossins

Image courtesy of Ben Stanger and colleagues
Perelman School of Medicine, University of Pennsylvania, USA
Copyright held by original authors
Research published in Cell, March 2014

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Apr 20

20 April 2014
Nuclear Deterioration
In the long-running investigation into the causes of Parkinson’s disease, scientists have a new lead: defects in the nuclei of brain-cell precursors. Post-mortem analysis of brain tissue from Parkinson’s patients revealed a high proportion of neurons [nerve cells] with deformed nuclei, suggesting nuclear deterioration plays a role in the disease. Researchers suspect the distortion might be caused by mutation in the LRRK2 gene that correlates with Parkinson’s, so they put the theory to the test. As induced pluripotent stem cells derived from patients became brain-cell precursors, nuclear architecture slowly deteriorated until they were clearly misshapen (pictured right) compared to healthy controls (left). The mutant cells also failed to mature into neurons. When the LRRK2 mutation was corrected, however, nuclei developed normally. Treating the brain-cell precursors with a particular compound achieved the same result, raising the possibility of a drug to reverse the problem and treat the disease.
Written by Daniel Cossins
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Image courtesy of Juan Carlos Izpisua Belmonte and colleaguesThe Salk Institute for Biological Studies, USA Copyright held by original authors Research published in Nature, November 2012
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20 April 2014

Nuclear Deterioration

In the long-running investigation into the causes of Parkinson’s disease, scientists have a new lead: defects in the nuclei of brain-cell precursors. Post-mortem analysis of brain tissue from Parkinson’s patients revealed a high proportion of neurons [nerve cells] with deformed nuclei, suggesting nuclear deterioration plays a role in the disease. Researchers suspect the distortion might be caused by mutation in the LRRK2 gene that correlates with Parkinson’s, so they put the theory to the test. As induced pluripotent stem cells derived from patients became brain-cell precursors, nuclear architecture slowly deteriorated until they were clearly misshapen (pictured right) compared to healthy controls (left). The mutant cells also failed to mature into neurons. When the LRRK2 mutation was corrected, however, nuclei developed normally. Treating the brain-cell precursors with a particular compound achieved the same result, raising the possibility of a drug to reverse the problem and treat the disease.

Written by Daniel Cossins

Image courtesy of Juan Carlos Izpisua Belmonte and colleagues
The Salk Institute for Biological Studies, USA
Copyright held by original authors
Research published in Nature, November 2012

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Apr 19

19 April 2014
BRCA1 Shapes Brains
BRCA1, is a gene most will have heard of in relation to breast and ovarian cancer – BRCA1 mutations are associated with inherited susceptibility to these diseases. However, normal BRCA1 plays an important role in neurodevelopment. Researchers ‘knocked out’ the gene in the mouse central nervous system to find out what its function is there. They noted that among other widespread neural defects in the mutant mice the brain region called the cerebellum (right panel) is at least 50% smaller than that of normal mice (left). And the cells that make up the cerebellum are also very disorganised. Rare cases of similar brain abnormalities have been observed in people with mutated BRCA1. Thus, results generated from such studies of mice are likely to enhance our understanding of human brain development and gene defects associated with neural pathologies.
Written by Rhiannon Grant
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Image by Carlos Perez-Garcia and colleaguesThe Salk Institute for Biological Studies, USA Copyright held by original authors Research published in PNAS, April 2014
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19 April 2014

BRCA1 Shapes Brains

BRCA1, is a gene most will have heard of in relation to breast and ovarian cancer – BRCA1 mutations are associated with inherited susceptibility to these diseases. However, normal BRCA1 plays an important role in neurodevelopment. Researchers ‘knocked out’ the gene in the mouse central nervous system to find out what its function is there. They noted that among other widespread neural defects in the mutant mice the brain region called the cerebellum (right panel) is at least 50% smaller than that of normal mice (left). And the cells that make up the cerebellum are also very disorganised. Rare cases of similar brain abnormalities have been observed in people with mutated BRCA1. Thus, results generated from such studies of mice are likely to enhance our understanding of human brain development and gene defects associated with neural pathologies.

Written by Rhiannon Grant

Image by Carlos Perez-Garcia and colleagues
The Salk Institute for Biological Studies, USA
Copyright held by original authors
Research published in PNAS, April 2014

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Apr 18

[video]

Apr 17

17 April 2014
Splitting the Egg
We start life as a single cell, created when dad’s sperm meets mum’s egg cell. The fertilised egg has a complete set of DNA, half from mum and half from dad. In order to create eggs and sperm that carry only half a set of DNA, specialised germ cells go through a process called meiosis. Here, a female mouse germ cell is in the final stage of meiosis. Shown in pink, the DNA is about to be divided to create a large egg cell and a much smaller cell called a polar body, which sticks to the side of the egg and plays no part in making a baby. This uneven division ensures that the cell destined to be the egg gets the biggest share of nutrients, to fuel the early stages of development. Researchers are studying how this process is controlled, to gain insights into the earliest stages of life.
Written by Kat Arney
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Image courtesy of Melina Schuh and colleagues MRC Laboratory of Molecular Biology  Copyright held by original authors Research published in PLOS Biology, February 2014
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17 April 2014

Splitting the Egg

We start life as a single cell, created when dad’s sperm meets mum’s egg cell. The fertilised egg has a complete set of DNA, half from mum and half from dad. In order to create eggs and sperm that carry only half a set of DNA, specialised germ cells go through a process called meiosis. Here, a female mouse germ cell is in the final stage of meiosis. Shown in pink, the DNA is about to be divided to create a large egg cell and a much smaller cell called a polar body, which sticks to the side of the egg and plays no part in making a baby. This uneven division ensures that the cell destined to be the egg gets the biggest share of nutrients, to fuel the early stages of development. Researchers are studying how this process is controlled, to gain insights into the earliest stages of life.

Written by Kat Arney

Image courtesy of Melina Schuh and colleagues
MRC Laboratory of Molecular Biology
Copyright held by original authors
Research published in PLOS Biology, February 2014

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Apr 16

16 April 2014
Sticking Local
Like people in close-knit communities, neighbouring cells in our body need to stick together and talk to each other. So-called focal adhesions (coloured green) are one of the structures that allow cells to do this. Recent research has re-emphasized just how important these complexes are not just for maintaining the body, but also for building it to begin with. When scientists deleted a gene that’s necessary for these particular focal adhesions to form, the bellies of mouse embryos did not close fully, leaving the gut to protrude out of the body. Besides providing insights into the basic workings of cells, this discovery might also be of use in human medicine. About 1 in every 4000 babies born suffers from a similar condition called omphalocoele. This birth defect is very dangerous, and finding mechanisms that cause it could be a first step in the long road to specific treatments.
Written by Emma Bornebroek
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Image courtesy of Naveenan Navaratnam and colleagues MRC Clinical Sciences Centre  Copyright held by original authors Research by Cellular Stress Group, MRC Clinical Sciences Centre
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16 April 2014

Sticking Local

Like people in close-knit communities, neighbouring cells in our body need to stick together and talk to each other. So-called focal adhesions (coloured green) are one of the structures that allow cells to do this. Recent research has re-emphasized just how important these complexes are not just for maintaining the body, but also for building it to begin with. When scientists deleted a gene that’s necessary for these particular focal adhesions to form, the bellies of mouse embryos did not close fully, leaving the gut to protrude out of the body. Besides providing insights into the basic workings of cells, this discovery might also be of use in human medicine. About 1 in every 4000 babies born suffers from a similar condition called omphalocoele. This birth defect is very dangerous, and finding mechanisms that cause it could be a first step in the long road to specific treatments.

Written by Emma Bornebroek

Image courtesy of Naveenan Navaratnam and colleagues
MRC Clinical Sciences Centre
Copyright held by original authors
Research by Cellular Stress Group, MRC Clinical Sciences Centre

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Apr 15

15 April 2014
Germs Go-Slow
Most people who catch a dose of the food poisoning bacteria Salmonella just suffer a nasty bout of diarrhoea. But if the bacteria spread through the body, which can occasionally happen in young children and the elderly, this ‘tummy bug’ can be life-threatening. Treatment with antibiotics often works, but sometimes the infection comes back with a vengeance when the drugs stop. To discover why, researchers are studying mice that suffer from Salmonella infections in the same way we do. They’ve found that the bacteria ‘hide out’ in special immune cells called dendritic cells – highlighted green in this image of an infected mouse’s lymph node – and slow down their growth. This enables them to lay low and resist antibiotic treatment, so they can grow again afterwards. Stimulating the immune system helps to flush out these sneaky bugs, which could be a new approach for treating severe infections in future.
Written by Kat Arney
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Image courtesy of Wolf-Dietrich Hardt and colleagues ETH, Zurich, Switzerland Copyright held by original authors Research published in PLOS Biology, February 2014
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15 April 2014

Germs Go-Slow

Most people who catch a dose of the food poisoning bacteria Salmonella just suffer a nasty bout of diarrhoea. But if the bacteria spread through the body, which can occasionally happen in young children and the elderly, this ‘tummy bug’ can be life-threatening. Treatment with antibiotics often works, but sometimes the infection comes back with a vengeance when the drugs stop. To discover why, researchers are studying mice that suffer from Salmonella infections in the same way we do. They’ve found that the bacteria ‘hide out’ in special immune cells called dendritic cells – highlighted green in this image of an infected mouse’s lymph node – and slow down their growth. This enables them to lay low and resist antibiotic treatment, so they can grow again afterwards. Stimulating the immune system helps to flush out these sneaky bugs, which could be a new approach for treating severe infections in future.

Written by Kat Arney

Image courtesy of Wolf-Dietrich Hardt and colleagues
ETH, Zurich, Switzerland
Copyright held by original authors
Research published in PLOS Biology, February 2014

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Apr 14

14 April 2014
Surrounded in Science
Imagine being able to walk through a database of research: computer-assisted automatic virtual environments (CAVEs) – rooms enclosed by high-resolution display panels – allow users to do precisely that. In these chambers, scientists are able to submerge themselves in large volumes of data, exploring structures in three-dimensional space. Viewing data in this way provides a different perspective, it allows patterns to be more easily identified, and overcomes the difficulty of visualising and comprehending large, complex molecules on 2D monitors. CAVEs have already been implemented at some universities and credited with a number of results, including a breakthrough in our understanding of how cocaine interacts with the brain – shedding light on how to best combat its addictive properties. This technology has also been instrumental in identifying specific genes responsible for the development of mouth cancer, and for studying activation patterns in the brains of zebrafish (pictured).
Written by Helen Thomas
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Christie Digital Systems, Weill Cornell Medical College, New York Weill Cornell Medical College, New YorkCopyright held by original authors Originally published in Nature Medicine, March 2014
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14 April 2014

Surrounded in Science

Imagine being able to walk through a database of research: computer-assisted automatic virtual environments (CAVEs) – rooms enclosed by high-resolution display panels – allow users to do precisely that. In these chambers, scientists are able to submerge themselves in large volumes of data, exploring structures in three-dimensional space. Viewing data in this way provides a different perspective, it allows patterns to be more easily identified, and overcomes the difficulty of visualising and comprehending large, complex molecules on 2D monitors. CAVEs have already been implemented at some universities and credited with a number of results, including a breakthrough in our understanding of how cocaine interacts with the brain – shedding light on how to best combat its addictive properties. This technology has also been instrumental in identifying specific genes responsible for the development of mouth cancer, and for studying activation patterns in the brains of zebrafish (pictured).

Written by Helen Thomas

Christie Digital Systems, Weill Cornell Medical College, New York
Weill Cornell Medical College, New York
Copyright held by original authors
Originally published in Nature Medicine, March 2014

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