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In particular, systemic infection underlying syndromes such as severe sepsis challenges the immune system by constant activation of its adaptive and innate components.
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Known disease sequelae in chronic inflammatory conditions can be explained by this constant activation of the SNS and HPA axis and the resultant catabolic state, like cachexia, high blood pressure, insulin resistance, and so on [ 93, 102].
Differentiation of B cells beyond the pre-B-cell stage requires dephosphorylation of STAT5, suggesting that the constant activation of STAT5 by BCR-ABL1 could potentially cause the block in B-cell differentiation seen in the BA mice.
This suggests that the suppression of SOCS-3 by miR-203 in psoriatic lesions would in turn lead to constant activation of STAT3.
However, recent studies showed that constant activation of BCR-regulated signaling pathways - as done by LMP2A - induces and maintains BCR unresponsiveness resulting in B cell anergy [ 12, 13].
N2a-Rα cells exhibited constant activation of the exogenous AhR.
Many cancers are strongly associated with constant activation of STATs, in particular Stat3 [ 3, 4].
Without protective mechanisms, this would lead to constant activation of immune and inflammatory reactions.
A key assumption in the proposed model is the constant activation of hypnozoites.
For N = 200 there is a near constant activation of hypnozoites (red and grey triangles).
Master curves were generated by shifting the data by hand and also using the constant activation energy of the glass transition relaxation to estimate the shift factors.
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