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Neglected Siege Tactics
Sieges are a tried and tested tactic in war: if you can stop supplies passing through a city’s gates, it won’t be long before it surrenders. This principle also works on a microscopic scale, and could be important in the fight against sleeping sickness. The parasite that causes the disease has only one pathway to absorb and excrete chemicals, located in an area called the flagellar pocket. Using a nanoparticle, which attaches itself to the parasite’s surface, scientists can disrupt this vital gateway and stop the free movement of substances. The pocket (stained brighter green) of parasites exposed to this nanoparticle (third and forth columns) becomes swollen and distended, compared to those covered in a similar, but inert molecule (first and second column). With its supply line cut, the parasite quickly dies, offering hope to 30,000 sufferers across Africa at risk of coma and death from the disease.
Written by Jan Piotrowski
—

Benoît Stijlemans
VIB, Belgium
Originally published under a Creative Commons Attribution license
Published in PLOS Pathogens 7(6): e1002072
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Neglected Siege Tactics

Sieges are a tried and tested tactic in war: if you can stop supplies passing through a city’s gates, it won’t be long before it surrenders. This principle also works on a microscopic scale, and could be important in the fight against sleeping sickness. The parasite that causes the disease has only one pathway to absorb and excrete chemicals, located in an area called the flagellar pocket. Using a nanoparticle, which attaches itself to the parasite’s surface, scientists can disrupt this vital gateway and stop the free movement of substances. The pocket (stained brighter green) of parasites exposed to this nanoparticle (third and forth columns) becomes swollen and distended, compared to those covered in a similar, but inert molecule (first and second column). With its supply line cut, the parasite quickly dies, offering hope to 30,000 sufferers across Africa at risk of coma and death from the disease.

Written by Jan Piotrowski

—

  • Benoît Stijlemans
  • VIB, Belgium
  • Originally published under a Creative Commons Attribution license
  • Published in PLOS Pathogens 7(6): e1002072

Source: bpod.mrc.ac.uk

    • #science
    • #neglected diseases
    • #ntd
    • #sleeping sickness
    • #medicine
    • #tropical
    • #africa
    • #nanotechnology
    • #biology
    • #development
  • 3 months ago
  • 13
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On the Run
Life as a parasite is a constant race to evade host defences. For African trypanosomes (pictured) – responsible for diseases such as sleeping sickness – staying ahead means they have to keep moving. Each is a single cell with a long hair-like structure, or flagellum, anchored to the cell body and rotating to propel it through vertebrate bloodstreams, as shown here by 3D imaging. The host immune system detects threats using antibodies, molecules that recognise and bind to specific proteins on the surface of the parasite, marking it out for destruction. Rapid swimming generates a strong enough current to drag these antibodies to the base of the flagellum, where the cell can absorb them, thus allowing trypanosomes to go unnoticed. However, this swimming behaviour could ultimately be their downfall, as research into the mechanisms of trypanosome motion and its molecular underpinnings may reveal new targets for treatment.
Written by Emmanuelle Briolat
—

Markus Engstler
University of Würzburg, Germany
Originally published under a Creative Commons Attribution license
Published in PLOS Pathogens 8(11): e1003023
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On the Run

Life as a parasite is a constant race to evade host defences. For African trypanosomes (pictured) – responsible for diseases such as sleeping sickness – staying ahead means they have to keep moving. Each is a single cell with a long hair-like structure, or flagellum, anchored to the cell body and rotating to propel it through vertebrate bloodstreams, as shown here by 3D imaging. The host immune system detects threats using antibodies, molecules that recognise and bind to specific proteins on the surface of the parasite, marking it out for destruction. Rapid swimming generates a strong enough current to drag these antibodies to the base of the flagellum, where the cell can absorb them, thus allowing trypanosomes to go unnoticed. However, this swimming behaviour could ultimately be their downfall, as research into the mechanisms of trypanosome motion and its molecular underpinnings may reveal new targets for treatment.

Written by Emmanuelle Briolat

—

  • Markus Engstler
  • University of Würzburg, Germany
  • Originally published under a Creative Commons Attribution license
  • Published in PLOS Pathogens 8(11): e1003023

Source: bpod.mrc.ac.uk

    • #science
    • #parasite
    • #trypanosomes
    • #sleeping sickness
    • #flagellum
    • #antibodies
    • #3d
    • #biology
    • #medicine
  • 5 months ago
  • 53
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Divide and Conquer

‘Sleeping sickness’ really doesn’t effectively describe the severity of the disease caused by Trypanosoma brucei. The parasite is injected into the bloodstream by a biting insect.Anaemia soon results before T. Brucei spreads to the central nervous system, disrupting brain function and sleeping patterns. While it is a single-celled organism, the parasite shares many aspects of cell division with multicellular organisms like us. Here it is shown at different stages of a ‘hybrid’ cell division. DNA (orange spots) is found in two locations within the trypanosome. As with our cells, most of the DNA is wrapped up in the cell’s nucleus (large orange spots), but a few genes (small orange spots) are also found in energy generating structures – mitochondria. The parallels between host and parasite biology may be relevant to the design of therapies for the potentially fatal sleeping sickness.
Written by John Ankers
—
Image created by Dr Helen Farr
First published in the Oxford University Biochemical Society magazine, Phenotype
Winning image of Oxford University Press sponsored competition Snapshot
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Divide and Conquer

‘Sleeping sickness’ really doesn’t effectively describe the severity of the disease caused by Trypanosoma brucei. The parasite is injected into the bloodstream by a biting insect.Anaemia soon results before T. Brucei spreads to the central nervous system, disrupting brain function and sleeping patterns. While it is a single-celled organism, the parasite shares many aspects of cell division with multicellular organisms like us. Here it is shown at different stages of a ‘hybrid’ cell division. DNA (orange spots) is found in two locations within the trypanosome. As with our cells, most of the DNA is wrapped up in the cell’s nucleus (large orange spots), but a few genes (small orange spots) are also found in energy generating structures – mitochondria. The parallels between host and parasite biology may be relevant to the design of therapies for the potentially fatal sleeping sickness.

Written by John Ankers

—

  • Image created by Dr Helen Farr
  • First published in the Oxford University Biochemical Society magazine, Phenotype
  • Winning image of Oxford University Press sponsored competition Snapshot

Source: bpod.mrc.ac.uk

    • #science
    • #dna
    • #sleeping sickness
    • #trypanosome
    • #picture
    • #design
    • #medical
  • 1 year ago
  • 3
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