ABSTRACT
BACKGROUND: There is an urgent need to assess the role of schools in the spread of SARS-CoV-2 in Canada to inform public health measures. We describe the epidemiology of SARS-CoV-2 infection among students and staff in the Vancouver Coastal Health (VCH) region in the first 3 months of the 2020/2021 academic year, and examine the extent of transmission in schools. METHODS: This descriptive epidemiologic study using contact tracing data included individuals aged 5 years and older with SARS-CoV-2 infection, reported between Sept. 10 and Dec. 18, 2020, who worked in or attended kindergarten to grade 12 (K-12) schools in person in the VCH region. We described case and cluster characteristics and reported the number of school-based transmissions. RESULTS: During the study period, 699 cases of SARS-CoV-2 infection were reported (55 cases per 10 000 VCH school population). Among cases in VCH resident staff and students, 52.5% (354/674) were linked to a household case or cluster; less than 1.5% (< 10) of infected individuals were hospitalized and none died. Out of 699 cases present at school, 26 clusters with school-based transmission resulted in 55 secondary cases. Staff members accounted for 53.8% of index cases (14/26) while making up 14.3% of the school population (17 742/123 647). Among clusters, 88.5% (23) had fewer than 4 secondary cases. INTERPRETATION: In our population during the study period, there were no deaths and severe disease was rare; furthermore, school-based SARS-CoV-2 transmissions were uncommon and clusters were small. Our results, which relate primarily to symptomatic disease, support the growing body of evidence that schools likely did not play a major role in SARS-CoV-2 spread in 2020.
Subject(s)
COVID-19 , Schools , Adolescent , COVID-19/transmission , Child , Child, Preschool , Contact Tracing , Epidemiologic Studies , Female , Humans , Male , Public HealthABSTRACT
BACKGROUND: Metformin has been shown to have a strong anti-proliferative effect in many breast cancer cell lines, mainly due to the activation of the energy sensing kinase, AMP-activated protein kinase (AMPK). MDA-MB-231 cells are aggressive and invasive breast cancer cells that are known to be resistant to several anti-cancer agents as well as to the anti-proliferative effect of metformin. As metformin is a glucose lowering drug, we hypothesized that normoglycemia will sensitize MDA-MB-231 cells to the anti-proliferative effect of metformin. METHODS: MDA-MB-231 cells were treated with increasing metformin concentrations in hyperglycemic or normoglycemic conditions. The growth inhibitory effect of metformin was assessed by MTT assay. The expression of several proteins involved in cell proliferation was measured by Western blotting. RESULTS: In agreement with previous studies, treatment with metformin did not inhibit the growth of MDA-MB-231 cells cultured in hyperglycemic conditions. However, metformin significantly inhibited MDA-MB-231 growth when the cells were cultured in normoglycemic conditions. In addition, we show that metformin-treatment of MDA-MB-231 cells cultured in normoglycemic conditions and not in hyperglycemic conditions caused a striking activation of AMPK, and an AMPK-dependent inhibition of multiple molecular signaling pathways known to control protein synthesis and cell proliferation. CONCLUSION: Our data show that normoglycemia sensitizes the triple negative MDA-MB-231 breast cancer cells to the anti-proliferative effect of metformin through an AMPK-dependent mechanism. GENERAL SIGNIFICANCE: These findings suggest that tight normoglycemic control may enhance the anti-proliferative effect of metformin in diabetic cancer patients.
