Neuroscience: The brain in glorious Technicolor
With a combination of genetic tricks and fancy proteins, researchers have colourfully labelled hundreds of individual neurons with distinctive hues to create a ‘Brainbow’. The research, takes mapping to a new level, and results in the labelling of neurons with approximately 90 different colour combinations.
Over a hundred years ago, Ramon Y Cajal’s use of Golgi staining on nerve cells opened the gates to modern neuroscience, but until now it has been tough to map out individual cells in each neuronal circuit. Jeff Lichtman and colleagues have developed the Technicolor version of Golgi staining, Brainbow, allowing more detailed reconstructions of brain circuits. This provides a key step towards modelling how the nervous system works normally and in diseased brains.
CONTACT
Jeff Lichtman (Harvard University, Cambridge, Ma, USA)
Tel: +1 617 496 8943; E-mail: jeff@mcb.harvard.edu
Showing posts with label MA. Show all posts
Showing posts with label MA. Show all posts
Thursday, November 01, 2007
Monday, October 29, 2007
Responding to sepsis
How quickly key receptors are activated on blood vessel cells can determine whether one survives or succumbs to sepsis.
Sepsis, a potentially life-threatening immune response to blood-borne infections, leads to loss of blood vessel function, resulting in shock and multiorgan failure. Athan Kuliopulos and colleagues looked to see if inhibition or activation of a receptor called PAR1 could limit the severity of sepsis. Mice injected with bacteria directly into the bloodstream developed sepsis and died; however, these mice were protected if given a PAR1 inhibitor within 4 hours.
The surprise came if PAR1 was inhibited at later times, as this failed to protect these mice; rather, activation of PAR1 at these later times ‘protected’ mice from toxic shock. The authors show this ‘late’ activation of PAR1 induces another PAR receptor to become activated. This establishes a protective effect by instructing cells lining the blood vessel to maintain tight junctions and averting the widespread edema and intravascular blood clotting that accompanies shock.
These findings might lead to successful therapies for patients with sepsis and other systemic inflammatory responses.
Author contact:
Athan Kuliopulos (Tufts-New England Medical Center, Boston, MA, USA)
Tel: +1 617 636 8482; E-mail: athan.kuliopulos@tufts.edu
How quickly key receptors are activated on blood vessel cells can determine whether one survives or succumbs to sepsis.
Sepsis, a potentially life-threatening immune response to blood-borne infections, leads to loss of blood vessel function, resulting in shock and multiorgan failure. Athan Kuliopulos and colleagues looked to see if inhibition or activation of a receptor called PAR1 could limit the severity of sepsis. Mice injected with bacteria directly into the bloodstream developed sepsis and died; however, these mice were protected if given a PAR1 inhibitor within 4 hours.
The surprise came if PAR1 was inhibited at later times, as this failed to protect these mice; rather, activation of PAR1 at these later times ‘protected’ mice from toxic shock. The authors show this ‘late’ activation of PAR1 induces another PAR receptor to become activated. This establishes a protective effect by instructing cells lining the blood vessel to maintain tight junctions and averting the widespread edema and intravascular blood clotting that accompanies shock.
These findings might lead to successful therapies for patients with sepsis and other systemic inflammatory responses.
Author contact:
Athan Kuliopulos (Tufts-New England Medical Center, Boston, MA, USA)
Tel: +1 617 636 8482; E-mail: athan.kuliopulos@tufts.edu
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