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Lehmann, S., Costa, A

Using this mechanistic model of bile acids, we explain how abnormal bile acid physiology drives disease pathogenesis, emphasizing how ceramide synthesis may serve as a unifying pathogenic feature for cardiometabolic diseases

Choi SM, Lee KM, Ryu SB, Park YJ, Hwang YG, Baek D, Choi Y, Park KH, Park KD, Lee JW

Anabel AS, Eduardo PC, Pedro Antonio HC, Carlos SM, Juana NM, Honorio TA, et al
Concerning the TLRs pathways, the stimulus with different BCG loads (MOI 5, 10, 20, and 40) or with the specific agonists for TLR2 (Pam3CSK4), TLR4 (ultrapure LPS), or TLR9 (CpG 1826) were not able to induce B16-F10 cells to secrete inflammatory cytokines such as TNF-a ( Figure 2C ), IL-6 ( Figure 2D ) or IL-12 ( Figure 2E )

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