Publications by authors named "Mikaela Eng"

Background: Sepsis, the life-threatening host response to infection, is a major cause of mortality. Obesity increases vulnerability to sepsis; however, some degree of obesity may be protective, called the "obesity paradox". This scoping review systematically maps the literature on outcomes associated with diet-induced obesity and sepsis-induced organ injury, focusing on non-transgenic murine models.

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Background: Preclinical sepsis models have been criticized for their inability to recapitulate human sepsis and suffer from methodological shortcomings that limit external validity and reproducibility. The National Preclinical Sepsis Platform (NPSP) is a consortium of basic science researchers, veterinarians, and stakeholders in Canada undertaking standardized multi-laboratory sepsis research to increase the efficacy and efficiency of bench-to-bedside translation. In this study, we aimed to develop and characterize a 72-h fecal-induced peritonitis (FIP) model of murine sepsis conducted in two independent laboratories.

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Unlabelled: Preclinical studies provide an opportunity to evaluate the relationship between sex and sepsis, and investigate underlying mechanisms in a controlled experimental environment. The objective of our systematic review was to assess the impact of biological sex on treatment response to fluid and antibiotic therapy in animal models of sepsis. Furthermore, we provide a narrative elaboration of sex-dependent differences in preclinical models of sepsis.

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Article Synopsis
  • Inactivation of mTORC1 enhances the nuclear levels of certain transcription factors involved in metabolism and cell death, particularly STAT1, which requires the mTORC1-associated protein KPNA1 for its nuclear import.
  • The study identifies a specific TOS motif in protein kinase C delta (PKCδ) that facilitates its interaction with mTORC1, suggesting that PKCδ's regulation is influenced by mTORC1 activity.
  • Disruption of this TOS motif leads to increased nuclear PKCδ levels, heightening STAT1 activity and apoptosis, indicating that mTORC1 plays a role in controlling the nuclear entry of PKCδ and consequently affects apoptosis signaling pathways.
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