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The stress memory response showed a strong dependence on the loading/unloading strain rate which cannot be predicted by linear viscoelasticity and also provides a significant challenge to a current nonlinear constitutive models.
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Additionally, the memory responses shown in our work are both durable and specific because they persist without the need to boost or reprime the immune system.
Multivariate logistic analysis incorporating age and CS response showed that cultured memory T cell responses against TRAP were associated with a significantly reduced incidence of malaria (p = 0.028).
An enhanced memory response was shown after polysaccharide challenge.
All memory subtypes in the later phase of the response showed low levels of active caspase-3.
The sustained response showed phenotypic features typical of effector memory and was enriched in tissues, whereas the reverse was true for the contracting response.
These authors have shown that Bz-induced cure drives conversion of the immune response to a stable and protective CD8+ T-cell central memory response, capable of showing effector function and providing protective immunity upon re-challenge [ 21, 34].
Contextual fear response shows a reduced immobility (freezing) at day three, revealing and hippocampal-dependent memory impairment.
Thus, mice vaccinated first with a mixture of purified N1 and N2 proteins and subsequently boosted with the individual antigens showed a small memory response also against the heterologous subtype (40).
Tracking of the CD4 T cell memory response with MHC class II tetramers shows no impairment of the primary clonal expansion, or long-term survival, but does show impaired secondary expansion.
This "memory inflation" is in contrast to the immunodominant epitope-specific CD8+ T-cell response from the acute phase (M45) that shows a classical memory response and a "central memory" phenotype.
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