Investigating the Relationship between Sociodemographic Factors and Bird Identification by Landowners Across a Rural-to-Urban Gradient.

Social, cultural, and economic differences have been shown to influence ecological knowledge. Given the importance of ecological knowledge for appreciation and protection of nature, we sought to investigate the relationship between landowners' sociodemographic attributes and the number of birds listed by landowners on their property across a rural-to-urban gradient. We hypothesized that: (1) age and education would be positively related to the number of birds an individual listed, while gender would be unrelated to the number of birds an individual listed; (2) rural landowners would list a larger number of bird species due to their increased level of exposure to nature and place-based knowledge; and (3) the number of years spent living on a property would positively impact the number of birds an individual listed by increasing the amount of time possible to interact with nature. To test these hypotheses, we conducted a survey of ~1700 landowners (with 59% responding) across a rural-to-urban gradient in southeastern Michigan that asked questions pertaining to age, gender, education, property size, years lived on property, and bird identification. Age, education, and years on property were positively associated with the number of birds listed by landowner. However, sociodemographic factors interacted with the rural-to-urban gradient to determine how such factors influenced landowner listing ability. For example, females listed more birds than males on suburban routes, but not on urban or rural routes. Ultimately, sociodemographic factors were indicators of a person's ability to list bird species on their property.

Regulation of inflammatory responses by neuregulin-1 in brain ischemia and microglial cells in vitro involves the NF-kappa B pathway.

BACKGROUND: We previously demonstrated that neuregulin-1 (NRG-1) was neuroprotective in rats following ischemic stroke. Neuroprotection by NRG-1 was associated with the suppression of pro-inflammatory gene expression in brain tissues. Over-activation of brain microglia can induce pro-inflammatory gene expression by activation of transcriptional regulators following stroke. Here, we examined how NRG-1 transcriptionally regulates inflammatory gene expression by computational bioinformatics and in vitro using microglial cells. METHODS: To identify transcriptional regulators involved in ischemia-induced inflammatory gene expression, rats were sacrificed 24 h after middle cerebral artery occlusion (MCAO) and NRG-1 treatment. Gene expression profiles of brain tissues following ischemia and NRG-1 treatment were examined by microarray technology. The Conserved Transcription Factor-Binding Site Finder (CONFAC) bioinformatics software package was used to predict transcription factors associated with inflammatory genes induced following stroke and suppressed by NRG-1 treatment. NF-kappa B (NF-kB) was identified as a potential transcriptional regulator of NRG-1-suppressed genes following ischemia. The involvement of specific NF-kB subunits in NRG-1-mediated inflammatory responses was examined using N9 microglial cells pre-treated with NRG-1 (100 ng/ml) followed by lipopolysaccharide (LPS; 10 µg/ml) stimulation. The effects of NRG-1 on cytokine production were investigated using Luminex technology. The levels of the p65, p52, and RelB subunits of NF-kB and IkB-α were determined by western blot analysis and ELISA. Phosphorylation of IkB-α was investigated by ELISA. RESULTS: CONFAC identified 12 statistically over-represented transcription factor-binding sites (TFBS) in our dataset, including NF-kBP65. Using N9 microglial cells, we observed that NRG-1 significantly inhibited LPS-induced TNFα and IL-6 release. LPS increased the phosphorylation and degradation of IkB-α which was blocked by NRG-1. NRG-1 also prevented the nuclear translocation of the NF-kB p65 subunit following LPS administration. However, NRG-1 increased production of the neuroprotective cytokine granulocyte colony-stimulating factor (G-CSF) and the nuclear translocation of the NF-kB p52 subunit, which is associated with the induction of anti-apoptotic and suppression of pro-inflammatory gene expression. CONCLUSIONS: Neuroprotective and anti-inflammatory effects of NRG-1 are associated with the differential regulation of NF-kB signaling pathways in microglia. Taken together, these findings suggest that NRG-1 may be a potential therapeutic treatment for treating stroke and other neuroinflammatory disorders.