Magic™ Anti-LCN2 monoclonal antibody, clone N92667-C [Biotin]

The spatiotemporal analysis of brain activation during the execution of easy analogy (EA) and difficult analogy (DA) tasks was investigated using high-density event-related brain potentials (ERPs). Results showed that reasoning tasks (schema induction) elicited a more negative ERP deflection (N500-1000) than did the baseline task (BS) between 500 and 1000 ms. Dipole source analysis of difference waves (EA-BS and DA-BS) indicated that the negative components were both localized near the left thalamus, possibly associated with the retrieval of alphabetical information. Furthermore, DA elicited more positive ERP component (P600-1000) than did EA in the same time window. Two generators of P600-1000 were located in the medial prefrontal cortex (BA10) and the left frontal cortex (BA6)which was possibly involved in integrating information in schema abstraction. In the stage of analogy mapping, a greater negativity (N400-600) in the reasoning tasks as compared to BS was found over fronto-central scalp regions. A generator of this effect was located in the left fusiform gyrus and was possibly related to associative memory and activation of schema. Then, a greater negativity in the reasoning tasks, in comparison to BS task, developed between 900-1200 ms (LNC1) and 2000-2500 ms (LNC2). Dipole source analysis (EA-BS) localized the generator of LNC1 in the left prefrontal cortex (BA 10) which was possibly related to mapping the schema to the target problem, and the generator of LNC2 in the left prefrontal cortex (BA 9) which was possibly related to deciding whether a conclusion Correctly follows from the schema. (C) 2008 Elsevier Ltd. All rights reserved.

Lipocalin 2 (Lcn2) is an important innate immunity component against bacterial pathogens. In this study, we report that Lcn2 is induced by Brucella (B.) abortus infection and significantly contributes to the restriction of intracellular survival of Brucella in macrophages. We found that Lcn2 prevented iron uptake by B.abortus through two distinct mechanisms. First, Lcn2 is secreted to capture bacterial siderophore(s) and abrogate iron import by Brucella. Second, Lcn2 decreases the intracellular iron levels during Brucella infection, which probably deprives the invading Brucella of the iron source needed for growth. Suppression of Lcn2 signalling resulted in a marked induction of anti-inflammatory cytokine, interleukin 10, which was shown to play a major role in Lcn2-induced antibrucella immunity. Similarly, interleukin 6 was also found to be increased when Lcn2 signalling is abrogated; however, this induction was thought to be an alternative pathway that rescues the cell from infection when the effective Lnc2 pathway is repressed. Furthermore, Lcn2 deficiency also caused a marked decrease in brucellacidal effectors, such as reactive oxygen species and nitric oxide but not the phagolysosome fusion. Taken together, our results indicate that Lcn2 is required for the efficient restriction of intracellular B.abortus growth that is through limiting iron acquisition and shifting cells to pro-inflammatory brucellacidal activity in murine macrophages.