Unsupervised hierarchical clustering of samples indicated an effect of a short exposure to PL, besides a strong effect of a prolonged exposure to TNF. We applied stringent statistical analyses to identify genes differentially expressed between the experimental conditions, and we searched for over-representation of functional annotations to identify pathways involved. Since the b-amyloid protein has been also detected in brains during human and mouse CM, our results suggest that TNF inhibits the capacity of HBEC to eliminate the b-amyloid protein from brain. This further supports the hypothesis that CM and Alzheimer�� disease share some common mechanisms of pathogenesis. Here we show that platelets dramatically modulate the expression of genes involved in inflammation and apoptosis. The analysis of canonical pathways revealed the effect of PL on cytokine-, chemokine-, TGFb-, death-receptor-, apoptosis-, erythropoietin-, and TREM1-signaling. These observations are in line with evidence that i) TGFb participates in HBEC ARRY-142886 apoptosis induced by PL, ii) erythropoietin promotes endothelial cell integrity and angiogenesis and has been associated with resistance against CM in humans and mice, iii) TREM-1, which is expressed on myeloid and endothelial cells, has been shown to be involved in the innate inflammatory response and sepsis, and its ligand is expressed on human PL. All together, these data support the hypothesis that PL induce HBEC gene expression changes affecting the outcome of malaria infection. It should be stressed that we used platelets from one single donor, and that this is a limitation in our approach. However, those platelets did not show any abnormalities in term of reactivity and probably induced a typical response of HBEC. Cryo-EM analyses show that empty ribosomes, such as were used in the current study, are AbMole BioScience thermodynamically unconstrained at physiological temperature and can freely assume,50 distinct ribosomal conformations. The intersubunit ratcheting process that occurs during translocation results in the most dynamic changes in ribosome structure, with the head of the SSU and the central protuberance of the LSU undergoing the largest conformational changes. The B1b/c bridge, which is formed by L11 and S18, is at the center of this structural rearrangement, and we hypothesize that this bridge may serve as a conduit for the exchange of information among different functional centers in both subunits. The L11 mutants analyzed in the current study are useful not only for testing the hypothesis that the bridge functions as a molecular yardstick by restricting the B1b/c bridge movements to a 30A�� conformational adjustment, but also to map the allosteric information transmission pathways within the ribosome. Inspection of Figure 1A reveals that H84 of the LSU is nestled in between two distinct structural elements of L11: the ����L11 P-site loop,���� which helps the ribosome monitor the tRNA occupancy status of the P-site, and the intersubunit bridge region.