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Balls and Sticks
Biology is applied chemistry, chemistry is applied physics, and physics is applied maths. But nature cares little for the traditional lines separating the disciplines. And cutting-edge laboratories reflect this increasingly by encouraging researchers to work in interdisciplinary teams. For example, biophysicists discovered that by mutating four genes associated with an enzyme found in all our cells (CGI of the protein, in red and blue, pictured), they disturbed the finely-tuned electrostatic field (represented by white lines) that surrounds the molecule and controls its shape, and how it attracts vital chemicals. Because even mild defects in the enzyme can cause a rare mental disability called Snyder-Robinson syndrome, it’s critical that biologists explain how complex molecules work in as much detail as possible. For that, they need to understand physics and even quantum mechanics. Ball-and-stick models won’t do anymore.
Written by Tristan Farrow
—

Yoshihiko Ikeguchi, Josai University, Japan 
Emil Alexov, Clemson University, USA
Originally published under a Creative Commons Attribution license
Published in PLoS Computational Biology 9(2): e1002924
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Balls and Sticks

Biology is applied chemistry, chemistry is applied physics, and physics is applied maths. But nature cares little for the traditional lines separating the disciplines. And cutting-edge laboratories reflect this increasingly by encouraging researchers to work in interdisciplinary teams. For example, biophysicists discovered that by mutating four genes associated with an enzyme found in all our cells (CGI of the protein, in red and blue, pictured), they disturbed the finely-tuned electrostatic field (represented by white lines) that surrounds the molecule and controls its shape, and how it attracts vital chemicals. Because even mild defects in the enzyme can cause a rare mental disability called Snyder-Robinson syndrome, it’s critical that biologists explain how complex molecules work in as much detail as possible. For that, they need to understand physics and even quantum mechanics. Ball-and-stick models won’t do anymore.

Written by Tristan Farrow

—

  • Yoshihiko Ikeguchi, Josai University, Japan
  • Emil Alexov, Clemson University, USA
  • Originally published under a Creative Commons Attribution license
  • Published in PLoS Computational Biology 9(2): e1002924

Source: bpod.mrc.ac.uk

    • #science
    • #maths
    • #biology
    • #computational
    • #simulation
    • #netweos
    • #biophysics
    • #chemistry
    • #electrostatic
    • #snyder-robinson
    • #ball and stick
  • 2 months ago
  • 159
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Virtual Immunity
A dandelion head is more than a jumble of its parts. It has order brought about by a natural organisation sometimes called emergence. But this picture is not of a seed head, it’s a visual representation of a database for the innate immune system – our body’s first line of defence against bacteria but which, when it goes wrong, can lead to allergies, asthma and inflammation. Scientists investigating these common diseases painstakingly recorded over 18,000 connections between elements of the system that had been published in the scientific literature. The colours represent when the data were added: 2008-2010 in white and 2011-2012 in red. Computational biologists are using this resource as more than just a library, they’re analysing it for patterns of emergent organisation that could help identify therapeutic targets and bring about widespread improvements for these ailments.
Written by Julie Webb
—

David Lynn
Teagasc, Ireland
Originally published under a Creative Commons Attribution license (CC-BY-NC 3.0)
Published in Nucleic Acids Research 41(D1): D1228-D1233
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Virtual Immunity

A dandelion head is more than a jumble of its parts. It has order brought about by a natural organisation sometimes called emergence. But this picture is not of a seed head, it’s a visual representation of a database for the innate immune system – our body’s first line of defence against bacteria but which, when it goes wrong, can lead to allergies, asthma and inflammation. Scientists investigating these common diseases painstakingly recorded over 18,000 connections between elements of the system that had been published in the scientific literature. The colours represent when the data were added: 2008-2010 in white and 2011-2012 in red. Computational biologists are using this resource as more than just a library, they’re analysing it for patterns of emergent organisation that could help identify therapeutic targets and bring about widespread improvements for these ailments.

Written by Julie Webb

—

  • David Lynn
  • Teagasc, Ireland
  • Originally published under a Creative Commons Attribution license (CC-BY-NC 3.0)
  • Published in Nucleic Acids Research 41(D1): D1228-D1233

Source: bpod.mrc.ac.uk

    • #science
    • #emergency
    • #computation
    • #biology
    • #medicine
    • #immune
    • #allergies
    • #simulation
    • #computational biology
  • 3 months ago
  • 151
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Hostile Takeover
Viruses thrive by exploiting host cells to replicate themselves – with potentially devastating effects on host health. A case in point, Simian Virus 40 (pictured here as a computer simulation) hijacks its host cell’s replication machinery, and causes uncontrolled cell division and tumour formation. SV40 was famously discovered in 1960 by researchers using macaque monkey cells to produce a vaccine against poliomyelitis. This sparked fears that it might cause cancer in vaccinated patients. So far only ‘footprints’ from SV40 have been found in human tumours. Antibodies that detect an SV40 protein (shown in red) do ‘light up’ tumours from some patients suffering from chest cancers caused by exposure to asbestos. But despite this tantalising sign, a clear causal link remains to be unearthed, and more work is needed to understand the impact of SV40 on humans.
Written by Emmanuelle Briolat
—

Mauro Tognon, Fernanda Martini
Cell Biology and Molecular Genetics, University of Ferrara, Italy
Published in PNAS 109(44): 18066-18071 
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Hostile Takeover

Viruses thrive by exploiting host cells to replicate themselves – with potentially devastating effects on host health. A case in point, Simian Virus 40 (pictured here as a computer simulation) hijacks its host cell’s replication machinery, and causes uncontrolled cell division and tumour formation. SV40 was famously discovered in 1960 by researchers using macaque monkey cells to produce a vaccine against poliomyelitis. This sparked fears that it might cause cancer in vaccinated patients. So far only ‘footprints’ from SV40 have been found in human tumours. Antibodies that detect an SV40 protein (shown in red) do ‘light up’ tumours from some patients suffering from chest cancers caused by exposure to asbestos. But despite this tantalising sign, a clear causal link remains to be unearthed, and more work is needed to understand the impact of SV40 on humans.

Written by Emmanuelle Briolat

—

  • Mauro Tognon, Fernanda Martini
  • Cell Biology and Molecular Genetics, University of Ferrara, Italy
  • Published in PNAS 109(44): 18066-18071 

Source: bpod.mrc.ac.uk

    • #science
    • #SV40
    • #virus
    • #disease
    • #simian virus
    • #simulation
    • #poliomyelitis
    • #vaccine
    • #vaccination
    • #safety
    • #cancer
    • #tumour
    • #medicine
  • 3 months ago
  • 11
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Mock-up in Red
The upper chambers of the heart (the atria) are crucial compartments in our body’s blood-pumping device. Electrical signals fired off within their walls drive each heartbeat, pumping blood through the heart and onwards around the body. Physicists and biologists keen to understand what happens when the heart misfires in a common heart condition called atrial fibrilation (AF) have built a virtual heart to test the ‘circuits’. Using computer programming, the team welded together thousands of images of slices through a sheep’s heart to build a 3D replica of the atria (pictured). Multi-coloured flecks show how muscle fibres arrange within the atrial walls. To mimic AF, scientists sent simulated erratic electrical signals through the mock-up. They found that where complex fibres around the pulmonary vein (opening on upper right hand side), connect with neatly aligned fibres below, electrical signals struggle to flow, leading them to the faults caused by AF.
Written by Caroline Cross
—

Today is ‘Rock up in Red’ day, organised by the British Heart Foundation
Henggui Zhang
The University of Manchester, UK
Research published in Interface Focus
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Mock-up in Red

The upper chambers of the heart (the atria) are crucial compartments in our body’s blood-pumping device. Electrical signals fired off within their walls drive each heartbeat, pumping blood through the heart and onwards around the body. Physicists and biologists keen to understand what happens when the heart misfires in a common heart condition called atrial fibrilation (AF) have built a virtual heart to test the ‘circuits’. Using computer programming, the team welded together thousands of images of slices through a sheep’s heart to build a 3D replica of the atria (pictured). Multi-coloured flecks show how muscle fibres arrange within the atrial walls. To mimic AF, scientists sent simulated erratic electrical signals through the mock-up. They found that where complex fibres around the pulmonary vein (opening on upper right hand side), connect with neatly aligned fibres below, electrical signals struggle to flow, leading them to the faults caused by AF.

Written by Caroline Cross

—

  • Today is ‘Rock up in Red’ day, organised by the British Heart Foundation
  • Henggui Zhang
  • The University of Manchester, UK
  • Research published in Interface Focus

Source: bpod.mrc.ac.uk

    • #science
    • #british heart foundation
    • #heart
    • #biology
    • #research
    • #simulation
    • #atrial fibrilation
    • #virtual
    • #computational biology
    • #3d
  • 4 months ago
  • 17
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