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Abstract: Helping smokers quit is important as smoking is the number one preventable cause of death in the U.S. Smoking activates the mesolimbic dopamine reward system which is also responsible for pleasure associated with other behaviors, including engaging in novel, exciting and/or challenging (i.e., self-expanding) events. We hypothesized that the reward activation achieved by experiencing self-expanding events can supplant the reinforcement normally provided by smoking and can thus facilitate quitting. We investigated this hypothesis among 74 current and 66 former smokers who reported the self-expanding events they experienced for the 2months prior to their most successful or final, quit attempt, respectively. Former smokers, compared to current smokers, reported significantly more self-expanding events and that the events were more helpful to their quitting. For current smokers, there was a significant moderate-to-large positive correlation between number of self-expanding events and number of days subsequently abstained from smoking. The results support the proposition that experiencing self-expanding activities or events can be beneficial for smoking abstinence. [Copyright &y& Elsevier]

Background: Functions of astrocytes in the rehabilitation after ischemic stroke, especially their impacts on inflammatory processes, remain controversial. This study uncovered two phenotypes of astrocytes, of which one was helpful, and the other harmful to anoxic neurons after brain ischemia.Methods: We tested the levels of inflammatory factors including TNF-a, IL-6, IL-10, iNOS, IL-1beta, and CXCL10 in primary astrocytes at 0 h, 6 h, 12 h, 24 h, and 48 h after OGD, grouped the hypoxia astrocytes into iNOS-positive (iNOS(+)) and iNOS-negative (iNOS(-)) by magnetic bead sorting, and then co-cultured the two groups of cells with OGD-treated neurons for 24 h. We further verified the polarization of astrocytes in vivo by detecting the co-localization of iNOS, GFAP, and Iba-1 on MCAO brain sections. Lentivirus overexpressing LCN2 and LCN2 knockout mice (#024630. JAX, USA) were used to explore the role of LCN2 in the functional polarization of astrocytes. 7.0-T MRI scanning and the modified Neurological Severity Score (mNSS) were used to evaluate the neurological outcomes of the mice.Results: After oxygen-glucose deprivation (OGD), iNOS mRNA expression increased to the peak at 6 h in primary astrocytes, but keep baseline expression in LCN2-knockout astrocytes. In mice with transient middle cerebral artery occlusion (tMCAO), LCN2 was proved necessary for astrocyte classical activation. In LCN2 knockout mice with MCAO, no classically activated astrocytes were detected, and smaller infarct volumes and better neurological functions were observed.Conclusions: The results indicated a novel pattern of astrocyte activation after ischemic stroke and lipocalin-2 (LCN2) plays a key role in polarizing and activating astrocytes. [ABSTRACT FROM AUTHOR]