Project description:Transcriptomes of 24 clinical strains of E. coli O157:H7 that differ phylogenetically and by Shiga toxin profiles were compared after 30 min co-incubation with epithelial cells.
Project description:Hemorphins are short peptides generated during cleavage of the hemoglobin chains but alpha chain, with various functions in different systems and tissues in both physiology and pathophysiology. The main purpose of this study was to establish the role of LVV-H7 in the mechanism of alcohol dependence. LVV-hemorphin 7 (LVV-H7) is released at higher concentrations in the presence of alcohol in vitro. Therefore, we predicted that alcohol intake can change the level of LVV-H7. We have accomplished behavioral tests in animal studies, along with proteomic analysis of the CNS tissues of alcohol addicted rats to verify the correlation of LVV-H7 level and ethanol dependence. We have also confirmed the BBB permeability of synthesized LVV-H7, as well as an inhibitor of its releasing enzyme- pepstatin using fluorescent microscopy. We have found a dose-dependent correlation between LVV-H7 and the time spent by rats in the drug-associated compartment using CPP test. Utilizing mass spectrometry-based methods we identified protein binding targets of LVV-H7 in the CNS tissue of addicted rats, along with the LVV-H7 degrading enzymes. The interpretation of the obtained results reveals the substantial role of LVV-H7 in the mechanism of alcohol dependence.
Project description:To determine if genetic background can modulate severity of an infection, we studied the host responses to influenza infections in the eight genetically highly diverse Collaborative Cross (CC) founder mice. The CC founder (C57BL/6J, 129S1/SvlmJ, CAST/EiJ, PWK/PhJ) were intranasally infected with influenza A/HK/01/68 (H3N2) with 20μl virus solution (1x101 ffu) or mock infected (with PBS). After infection lung was collected at different time points (mock_d3), d3, d5).
Project description:To determine if genetic background can modulate severity of an infection, we studied the host responses to influenza infections in the eight genetically highly diverse Collaborative Cross (CC) founder mice. The CC founder (C57BL/6J, 129S1/SvlmJ, CAST/EiJ, PWK/PhJ) were intranasally infected with influenza A/HK/01/68 (H3N2) with 20μl virus solution (1x101 ffu) or mock infected (with PBS). After infection lung was collected at different time points (mock_d3), d3, d5).