Andragogy: The Common Thread In The Teaching Of Adults in Colleges of Education, Criminal Justice, and Health Management

The Covid-19 pandemic has brought dramatic changes to higher education. Students and educators face challenges never anticipated, including switching classes from on-ground to online and back again, mental fatigue, stress, and burnout. Faculty across disciplines may turn to Andragogy to best teach college students to inform their teaching practices. This paper demonstrates how professors from education, criminal justice, and healthcare management have used andragogical techniques in their classrooms

Role of Neutrophils and Macrophages in the Pathogenesis of Necrotizing Enterocolitis Caused by Cronobacter sakazakii

BACKGROUND: Cronobacter sakazakii (CS) is a highly virulent gram-negative opportunistic pathogen that has been implicated in clinical outbreaks of necrotizing enterocolitis (NEC). The role of mucosal immune cells in CS infection is not well understood. In this study, we sought to elucidate the role of neutrophils (polymorphonuclear leukocytes; PMNs) and macrophages in the pathogenesis of NEC induced by CS using a novel newborn mouse model. MATERIALS AND METHODS: PMNs and macrophages were depleted in newborn mice using Gr-1 antibody and carrageenan respectively, and then infected with 10(3) CFU of CS. The development of NEC in these mice was assessed by a pathologist based on the morphological changes in the intestine. Cytokine production was determined in the serum and intestinal homogenates of infected mice by ELISA. Inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production was determined by flow cytometry and Greiss method, respectively. RESULTS: Depletion of PMNs and macrophages in newborn mice led to increased recruitment of dendritic cells (DCs) in the intestine compared to wild-type mice upon infection with CS. PMN- and macrophage-depleted mice showed increased bacterial load, production of pro-inflammatory cytokines, iNOS expression and NO production in the intestines in comparison to wild-type mice fed with CS. In addition, depletion of PMNs and macrophages prior to infection in mice resulted in severe inflammation, villus destruction and enhanced enterocyte apoptosis in the intestines compared to CS-infected wild-type mice. CONCLUSIONS: Our data suggest that depletion of PMNs and macrophages from the lamina propria (LP) exacerbates experimental NEC, indicating that both of these immunocytes play an important role in the clearance of CS during the initial stages of infection. The increased mucosal cytokine response and NO production in the absence of these immunocytes may be responsible for the observed increase in mucosal injury. Understanding how CS manipulates these cells employing novel mouse model of NEC reported in this study will provide significant insights for the development of novel therapeutic and preventive strategies to combat NEC