Antimicrobial resistance (AMR) is a growing public health concern, with water treatment plants serving as environments where antibiotic-resistant bacteria (ARB) can persist and spread. This study quantified total and cefotaxime-resistant Escherichia coli in the influent and final UV-disinfected effluent of the Portage Lake Water & Sewage Authority (PLWSA) in Houghton, Michigan, over three months from February to April 2026. Wastewater influent and effluent samples were processed using a membrane filtration method adapted from the WHO GLASS-AMR surveillance protocol. Tryptone bile x-glucuronide (TBX) agar was used for total E. coli enumeration, and TBX supplemented with cefotaxime (TBX+CTX) was used for resistant E. coli enumeration. Samples were filtered at various volumes, plated, and incubated before colony enumeration and data analysis. Results indicate that influent total E. coli concentrations ranged from 9.13 × 10⁵ to 9.80 × 10⁷ CFU/100 mL, while CTX-resistant E. coli concentrations ranged from 6.60 × 10² to 4.83 × 10⁵ CFU/100 mL. The PLWSA treatment processes achieved 2–5 log reductions in total E. coli and 2–6 log reductions in CTX-resistant E. coli. These results indicate that the PLWSA treatment process is effective at reducing CTX-resistant E. coli to low or undetectable levels in final effluent. This work contributes to the growing body of evidence supporting wastewater-based surveillance as a tool for monitoring AMR in municipal systems.

Breast cancer is one of the most common cancers affecting women, with approximately one in eight women in the United States expected to develop invasive breast cancer during their lifetime. Clinical subtypes are commonly defined by receptor status, including ER+, ER-, HER2+, and triple-negative breast cancer. These categories influence treatment options and therapeutic response. Although triple-negative breast cancer is classified as ER-, estrogen may still be present in the tumor environment and influence cellular behavior through non-classical receptors such as GPER1. GPER1 is a membrane-associated estrogen receptor that can activate non-classical signaling pathways by a G-1 agonist. A scratch wound assay has previously been conducted to evaluate how G-1 treatment affects breast cancer cell migration across different cell lines. This research examines GPER1 expression and G-1 response in breast cancer cell lines, with a focus on whether triple-negative 4T1 mouse mammary cancer cells express GPER1 and whether G-1 treatment alters signaling, migration, and cellular behavior. Preliminary findings detected GPER1 expression in the triple-negative breast cancer MDA-MB-231 cell line, but not in ER+ TC-11 cells, while GPER1 status in 4T1 cells remains unknown. To confirm GPER1 expression in 4T1 cells, protein and RNA samples will be analyzed by western blotting and qPCR. Future studies will assess GPER1-dependent signaling cascades, including SRC/FAK, ERK/MAPK, and CREB activation, using western blotting and immunofluorescence. Defining these responses may clarify how GPER1 activation influences breast cancer cell signaling, migration, exosome secretion, and cell communication in models with distinct receptor expression patterns.