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Furthermore, in the isoprenaline-treated rats, the implementation of NO system blockade (L-NAME), NO system over-stimulation (L-arginine) and NO system immobilization (L-NAME + L-arginine) would fully consider the role of the NO system as an endogenous cardioprotectant [38] (i.e., in rats and mice, doxorubicin congestive heart failure therapy with BPC 157 resulted in the normalization of NO system functioning due to the induced normalization of the increased endothelin-1 values [5])

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Since mTORC1 activation trigger M1 polarization, our data suggest that TLR9 signaling during fatal Ehrlichia infection induces M1 polarization

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