Historical Roots of Canadian Aboriginal and Non-Aboriginal Maple Practices

This research is concerned with developing a historical baseline of Canadian Aboriginal and non-Aboriginal maple practices and the contribution of these activities to the well-being (WB) of communities up to approximately 1950. This research measures WB using two unique frameworks developed for Aboriginal and non-Aboriginal communities associated with maple products and practices. In order to describe WB in historical contexts the research used archival data obtained primarily from Library and Archives Canada (LAC) and Early Canadiana Online (ECO). Results from the research showed that in Aboriginal communities, dynamics related to emotional, physical and mental WB were referenced the most often among results. In non-Aboriginal communities economic and social dynamics of WB were identified as important influences of WB. Dynamics related to resilience were also found in the non-Aboriginal results. Furthermore, the research identified dynamics related to governance as important pieces of the historical contexts of maple products within Aboriginal and non-Aboriginal communities. The role of early government rules and regulations associated with maple products and the impacts of the Indian Act on Aboriginal maple producers are further explored and discussed. This research concludes by outlining the areas where more research remains to be completed

Neutrophils resist ferroptosis and promote breast cancer metastasis through aconitate decarboxylase 1

Metastasis causes breast cancer-related mortality. Tumor-infiltrating neutrophils (TINs) inflict immunosuppression and promote metastasis. Therapeutic debilitation of TINs may enhance immunotherapy, yet it remains a challenge to identify therapeutic targets highly expressed and functionally essential in TINs but under-expressed in extra-tumoral neutrophils. Here, using single-cell RNA sequencing to compare TINs and circulating neutrophils in murine mammary tumor models, we identified aconitate decarboxylase 1 (Acod1) as the most upregulated metabolic enzyme in mouse TINs and validated high Acod1 expression in human TINs. Activated through the GM-CSF-JAK/STAT5-C/EBPβ pathway, Acod1 produces itaconate, which mediates Nrf2-dependent defense against ferroptosis and upholds the persistence of TINs. Acod1 ablation abates TIN infiltration, constrains metastasis (but not primary tumors), bolsters antitumor T cell immunity, and boosts the efficacy of immune checkpoint blockade. Our findings reveal how TINs escape from ferroptosis through the Acod1-dependent immunometabolism switch and establish Acod1 as a target to offset immunosuppression and improve immunotherapy against metastasis.</p