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Neutrophils are recognized as major cellular mediators of inflammation. They contain specific and highly regulated mechanisms for controlling the expression of adhesion molecules that allow for their tethering and migration into inflammatory sites. These adhesion molecules not only are activated by exogenous pollutants but are regulated by endothelial and epithelial cell signals. Lipid mediators, such as platelet-activating factor, reactive oxygen and nitrogen species, and cytokines from airway epithelial cells, further control neutrophil functions such as infiltration and activation resulting in an increase in respiratory burst activity and release of granule enzymes, such as elastase. Furthermore, virus and bacteria products affect inflammation by increasing secondary epithelial mediators. However, once the endogenous or exogenous agents are expelled, neutrophil populations are programmed to die and are cleared by macrophage phagocytosis.

Protection of biodiversity, human assets, and cultural heritage pose significant challenges to contemporary planning of bushfire mitigation activities. Current mitigation approaches are not always appropriate, and mismanagement is a source of distress for Indigenous peoples. Increased understanding of Indigenous fire knowledge and increased Indigenous participation may provide insight into more appropriate and inclusive land management for fire mitigation. We analysed contemporary Noongar and Western fire practitioner approaches within an Indigenous fire knowledge (IFK) framework to explore knowledge and aspirations for small reserves in the Southwest Australian Floristic Region (SWAFR) global biodiversity hotspot. We recorded an extensive knowledge base, characterised by a highly nuanced approach to burning, held by the Noongar coauthors. We explore potential approaches to applying this knowledge to build collaborative fire mitigation strategies with mutually beneficial outcomes for biodiversity, cultural heritage, and human assets.

The ovalbumin (OVA)-sensitized guinea pig is often used as an animal model of asthma and airway hyperreactivity. A characteristic lesion of asthma is excessive production of mucin in the airways. Mechanistic studies of this lesion in guinea pigs have been limited due to lack of mucin gene probes for this species. The aim of the present study was to clone the cDNAs encoding two major airway mucins (Muc2 and Muc5ac) from the guinea pig, and investigate mucin gene expression in lungs of sensitized animals in response to antigen challenge. We isolated and sequenced two cDNA fragments coding for the sequences located within the carboxyl-terminal cysteine-rich region of guinea pig Muc2 and Muc5ac mucins. Comparison of cloned cDNAs with those from other species revealed high degrees of sequence identity and conservation of all cysteine residues in deduced primary sequences. Based on the resultant sequence information, we also designed oligonucleotide primers for specific detection of guinea-pig Muc2 and Muc5ac steady-state mRNA levels via reverse transcriptase/ polymerase chain reaction (RT-PCR). Levels of both Muc2 and Muc5ac mRNA in lungs of OVA-sensitized guinea pigs increased significantly by 30 min after an acute exposure to 0.3% OVA. In addition, levels of eotaxin mRNA also increased in these tissues, but the increases were not significant until 2 h after challenge. Correspondingly, the number of eosinophils in bronchoalveolar lavage fluid did not increase until 4 h postchallenge. Results of these studies suggest that the OVA-sensitized guinea pig responds to allergic challenge with enhanced expression of genes (e.g., eotaxin, Muc2, and Muc5ac) that likely play a role in increased airway inflammation and mucin overproduction, and enhanced mucin gene expression appears to occur before eosinophil infiltration.

Through a lens of Human Niche Construction theory, we examineNoongar(an indigenous people of south western Australia) relationships with southwestern Australian flora and suggest influences of these relationships on contemporary botanical patterns in this global biodiversity hotspot. By conducting a review of historical and contemporary literature and drawing upon the contemporary knowledge ofNoongarElders, we examine the merits of five key hypotheses of human niche construction theory in relation to this large cultural group. We find compelling evidence that supportsNoongarniche construction, but caution that further research is required to test its likely ecological and evolutionary outcomes. We suggest that further collaborative, multi-disciplinary research that appliesNoongarand Western science will lead to a greater understanding of the biological assets of southwestern Australia.

Neutrophils are recognized as major cellular mediators of inflammation. They contain specific and highly regulated mechanisms for controlling the expression of adhesion molecules that allow for their tethering and migration into inflammatory sites. These adhesion molecules not only are activated by exogenous pollutants but are regulated by endothelial and epithelial cell signals. Lipid mediators, such as platelet-activating factor, reactive oxygen and nitrogen species, and cytokines from airway epithelial cells, further control neutrophil functions such as infiltration and activation resulting in an increase in respiratory burst activity and release of granule enzymes, such as elastase. Furthermore, virus and bacteria products affect inflammation by increasing secondary epithelial mediators. However, once the endogenous or exogenous agents are expelled, neutrophil populations are programmed to die and are cleared by macrophage phagocytosis.