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Vasodilatation could be an essential trigger, but only in conjunction with other unknown factors.
Inflammation/immune response at the site of nerve lesion is known to be an essential trigger of the pathological changes that have a critical impact on nerve repair and regeneration.
Extracellular ATP had already been suggested to be an essential trigger for activation of the IL-1 β producing caspase-1 in the multiprotein inflammasome complex in macrophages, but our current results clearly show that in an in vivo setting ATP signaling is involved in the production of other cytokines as well.
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During the evolution of nociception the concentration of PACAP-38 can increase and it exerts vasodilation, which is an essential trigger in conjunction with other unknown factors to the development of pain.
IL-4 is an essential trigger for Th2 lymphocyte differentiation, and both IL-4 and IL-13 can induce IgE class switching in B lymphocytes.
Stimulated influx of Ca2+ across the plasma membrane of T lymphocytes is an essential triggering signal for T-cell activation by antigen.
Feedback is also an essential trigger for flow.
This may be an essential factor in the triggering of attacks or may reflect generally altered function of central autonomic command.
As mentioned in the introduction, these concentrations have been proven to modulate the local neuron excitability and this feedback has been identified in recent studies [1] to be an essential mechanism of several pathologies triggered by astrocytic uptake deficiencies.
In agreement with previous experiments, strains defective in these two proteins were unable to form fruiting bodies, showing that blue light is an essential environmental trigger of mushroom development [ 16].
CREB phosphorylation at Ser133 has been identified as an essential trigger for CREB activation, which leads to the transcription of a number of immediate early genes, including those coding for the important pain-related proteins c-Fos and cyclooxygenase-2 [ 10].
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