Waste not want not: piloting a clinical waste audit at a United States university veterinary teaching hospital.

Biomedical waste is a well-recognized environmental problem, yet less is known about the waste generated in the delivery of veterinary care compared to human medicine. The objective of this project was to develop and pilot a waste audit protocol for veterinary medicine that could inform waste management at a US university veterinary teaching hospital and the broader veterinary community. We conducted a multi-day review of the Colorado State University Veterinary Teaching Hospital's small animal surgery and anesthesia units to measure the types and amounts of waste generated during routine surgeries. Metrics included total weight, number of bags, and individual counts for specific items of concern and items with sustainable alternatives. We calculated frequencies and percentages of waste by waste audit material category and noted any erroneous materials sorted. Despite waste being a prioritized sustainability issue in veterinary medicine, this work highlighted opportunities for better education on managing and optimizing existing resources through behavior modification. This article explores ways the 5Rs (Rethink, Reduce, Reuse, Recycle, Research) could be better operationalized in veterinary hospitals.

Vps54 regulates Drosophila neuromuscular junction development and interacts genetically with Rab7 to control composition of the postsynaptic density.

Vps54 is a subunit of the Golgi-associated retrograde protein (GARP) complex, which is involved in tethering endosome-derived vesicles to the trans-Golgi network (TGN). In the wobbler mouse, a model for human motor neuron (MN) disease, reduction in the levels of Vps54 causes neurodegeneration. However, it is unclear how disruption of the GARP complex leads to MN dysfunction. To better understand the role of Vps54 in MNs, we have disrupted expression of the Vps54 ortholog in Drosophila and examined the impact on the larval neuromuscular junction (NMJ). Surprisingly, we show that both null mutants and MN-specific knockdown of Vps54 leads to NMJ overgrowth. Reduction of Vps54 partially disrupts localization of the t-SNARE, Syntaxin-16, to the TGN but has no visible impact on endosomal pools. MN-specific knockdown of Vps54 in MNs combined with overexpression of the small GTPases Rab5, Rab7, or Rab11 suppresses the Vps54 NMJ phenotype. Conversely, knockdown of Vps54 combined with overexpression of dominant negative Rab7 causes NMJ and behavioral abnormalities including a decrease in postsynaptic Dlg and GluRIIB levels without any effect on GluRIIA. Taken together, these data suggest that Vps54 controls larval MN axon development and postsynaptic density composition through a mechanism that requires Rab7.