The Experts below are selected from a list of 10488 Experts worldwide ranked by ideXlab platform

Stephen R. Bolsover - One of the best experts on this subject based on the ideXlab platform.

  • CAMs and FGF cause a local subMembrane calcium signal promoting axon outgrowth without a rise in bulk calcium concentration
    European Journal of Neuroscience, 1999
    Co-Authors: Fabienne Archer, Patrick Doherty, Dominic Collins, Stephen R. Bolsover
    Abstract:

    Binding of basic fibroblast growth factor (bFGF) and Cell adhesion molecules to the Nerve Cell Membrane promotes axon outgrowth. This response can be blocked by antagonists of voltage-gated calcium channels, yet no change of cytosolic calcium concentration in the growth cone can be detected upon binding of the growth factor bFGF or the Cell adhesion molecule L1. Using barium as a charge carrier, we show that bFGF and L1 open a calcium influx pathway in growth cones of rat sensory neurons without changing the Membrane voltage. L1 does not activate influx in Cells expressing a dominant negative mutant of the fibroblast growth factor receptor (FGFR) tyrosine kinase. FGFR-activated influx is blocked by specific antagonists of L- and N-type voltage-gated calcium channels and by an inhibitor of diacylglycerol lipase. We propose that both L1 and bFGF act via the FGFR to generate polyunsaturated fatty acids which in turn cause calcium channels to flicker open and shut. Short-lived domains of raised calcium at the cytosolic mouth of open channels activate axon outgrowth without raising bulk cytosolic calcium concentration. In confirmation of this model, the rapidly-acting calcium buffer BAPTA is significantly more effective at blocking FGF-induced axon outgrowth when compared with the slower buffer EGTA. Generation of short-lived calcium domains may provide a crucial mechanism for axon guidance during development and for promoting regeneration of damaged axons.

Shanastasia Swastila - One of the best experts on this subject based on the ideXlab platform.

  • review of phytosome potential of gotu kola centella asiatica extract to restore Nerve Cell Membrane and improve cognitive function
    Social Science Research Network, 2020
    Co-Authors: Shanastasia Swastila
    Abstract:

    One of the herbs in Indonesia, Gotu Kola (Centella asiatica) contains triterpenoid glycosides, which are ethnomedicine used as neuroprotectors. Phytochemical components of Gotu Kola extract tend to be polar, so it needs an approach to modify the polarity of the extract. The method is to formulate an extract in the form of phytosome as an herbal delivery system so that it can increase the absorption and bioavailability of the active substance. It is suitable for the delivery system of active compounds from plants because it can carry hydrophilic and lipophilic compounds from plants. This paper specifically reviews the potential of the plant extracts for the recovery of Nerve Cell Membranes and improving one's cognitive function.

Fabienne Archer - One of the best experts on this subject based on the ideXlab platform.

  • CAMs and FGF cause a local subMembrane calcium signal promoting axon outgrowth without a rise in bulk calcium concentration
    European Journal of Neuroscience, 1999
    Co-Authors: Fabienne Archer, Patrick Doherty, Dominic Collins, Stephen R. Bolsover
    Abstract:

    Binding of basic fibroblast growth factor (bFGF) and Cell adhesion molecules to the Nerve Cell Membrane promotes axon outgrowth. This response can be blocked by antagonists of voltage-gated calcium channels, yet no change of cytosolic calcium concentration in the growth cone can be detected upon binding of the growth factor bFGF or the Cell adhesion molecule L1. Using barium as a charge carrier, we show that bFGF and L1 open a calcium influx pathway in growth cones of rat sensory neurons without changing the Membrane voltage. L1 does not activate influx in Cells expressing a dominant negative mutant of the fibroblast growth factor receptor (FGFR) tyrosine kinase. FGFR-activated influx is blocked by specific antagonists of L- and N-type voltage-gated calcium channels and by an inhibitor of diacylglycerol lipase. We propose that both L1 and bFGF act via the FGFR to generate polyunsaturated fatty acids which in turn cause calcium channels to flicker open and shut. Short-lived domains of raised calcium at the cytosolic mouth of open channels activate axon outgrowth without raising bulk cytosolic calcium concentration. In confirmation of this model, the rapidly-acting calcium buffer BAPTA is significantly more effective at blocking FGF-induced axon outgrowth when compared with the slower buffer EGTA. Generation of short-lived calcium domains may provide a crucial mechanism for axon guidance during development and for promoting regeneration of damaged axons.

Anette Saljo - One of the best experts on this subject based on the ideXlab platform.

  • neck injuries in car collisions a review covering a possible injury mechanism and the development of a new rear impact dummy
    Accident Analysis & Prevention, 2000
    Co-Authors: Mats Y. Svensson, Ola Bostrom, A Suneson, Yngve Haland, Johan Davidsson, Per Lövsund, Hans -arne Hansson, Anette Saljo
    Abstract:

    A review of a few Swedish research projects on soft tissue neck injuries in car collisions is presented together with some new results. Efforts to determine neck injury mechanisms was based on a hypothesis stating that injuries to the Nerve root region in the cervical spine are a result of transient pressure gradients in the spinal canal during rapid neck bending. In experimental neck trauma research on animals, pressure gradients were observed and indications of Nerve Cell Membrane dysfunction were found in the cervical spinal ganglia. The experiments covered neck extension, flexion and lateral bending. A theoretical model in which fluid flow was predicted to cause the transient pressure gradients was developed and a neck injury criterion based on Navier-Stokes Equations was applied on the flow model. The theory behind the Neck Injury Criterion indicates that the neck injury occurs early on in the rearward motion of the head relative to the torso in a rear-end collision. Thus the relative horizontal acceleration and velocity between the head and the torso should be restricted during the early head-neck motion to avoid neck injury. A Bio-fidelic Rear Impact Dummy (BioRID) was developed in several steps and validated against volunteer test results. The new dummy was partly based on the Hybrid III dummy. It had a new articulated spine with curvature and range of motion resembling that of a human being. A new crash dummy and a neck injury criterion will be very important components in a future rear-impact crash test procedure.

Dominic Collins - One of the best experts on this subject based on the ideXlab platform.

  • CAMs and FGF cause a local subMembrane calcium signal promoting axon outgrowth without a rise in bulk calcium concentration
    European Journal of Neuroscience, 1999
    Co-Authors: Fabienne Archer, Patrick Doherty, Dominic Collins, Stephen R. Bolsover
    Abstract:

    Binding of basic fibroblast growth factor (bFGF) and Cell adhesion molecules to the Nerve Cell Membrane promotes axon outgrowth. This response can be blocked by antagonists of voltage-gated calcium channels, yet no change of cytosolic calcium concentration in the growth cone can be detected upon binding of the growth factor bFGF or the Cell adhesion molecule L1. Using barium as a charge carrier, we show that bFGF and L1 open a calcium influx pathway in growth cones of rat sensory neurons without changing the Membrane voltage. L1 does not activate influx in Cells expressing a dominant negative mutant of the fibroblast growth factor receptor (FGFR) tyrosine kinase. FGFR-activated influx is blocked by specific antagonists of L- and N-type voltage-gated calcium channels and by an inhibitor of diacylglycerol lipase. We propose that both L1 and bFGF act via the FGFR to generate polyunsaturated fatty acids which in turn cause calcium channels to flicker open and shut. Short-lived domains of raised calcium at the cytosolic mouth of open channels activate axon outgrowth without raising bulk cytosolic calcium concentration. In confirmation of this model, the rapidly-acting calcium buffer BAPTA is significantly more effective at blocking FGF-induced axon outgrowth when compared with the slower buffer EGTA. Generation of short-lived calcium domains may provide a crucial mechanism for axon guidance during development and for promoting regeneration of damaged axons.