Assessing the Burden of Packaging and Recyclability of Single-Use Products in Interventional Radiology.

PURPOSE: With a shift to single-use products in interventional radiology (IR) centres for sterility and cost reasons, it is prudent to consider the burden of packaging and employ efforts to assess and reduce waste, as well as promote recycling wherever possible. This study aimed to quantify the amount of waste in IR packaging and what proportion is recyclable. MATERIALS AND METHODS: A range of IR products were weighed using mass scales. Products were assessed for total weight, overall waste, and potentially recyclable waste. Waste was defined as any packaging which was not considered vital to the product to perform its duty and thus was for packaging or shipping purposes. Products were pooled into one of the following categories: catheters and sheaths, wires, needles, devices, coils, and packs/ancillary. RESULTS: Seventy-two different products were collected from 26 manufacturers to represent a range of items. The weight of all products was 12,466 g (median 51, range 2-1600), and weight of waste was 6830.7 g (median 34, range 1.1-732). The weight of recyclable waste was 5202.2 g (median 11.5, range 0-701). There were median 2 waste packages per item (range 1-5). The proportion of waste of the overall weight was 54.8% and of this, 76% of all waste was potentially recyclable. CONCLUSION: There is a significant burden of waste in manufactured IR products, and while a high proportion is recyclable, we encourage manufacturers of IR products and devices to consider alternative means of transport and packaging of products which will reduce the overall waste burden. LEVEL OF EVIDENCE: Level 3.

Gab1 but not Grb2 mediates tumor progression in Met overexpressing colorectal cancer cells.

Hepatocyte growth factor receptor (Met) plays an important role in the progression of multiple cancer types. The overexpression of Met in DLD-1 colon carcinoma cells with kirsten rat sarcoma oncogene homolog (KRAS) oncogene activation resulted in enhanced subcutaneous and orthotopic tumor growth rate and increased metastatic potential. To elucidate the mechanism of this effect, we stably expressed kinase-inactive Met(K1110A), Src homology 2 (SH2)-binding domain-inactive Met(Y1349/1356F), growth factor receptor-bound protein 2 (Grb2) non-binding Met(N1358H) and mutant receptors with ability to selectively recruit signaling proteins Grb2, src homology domain c-terminal adaptor homolog (Shc), phospholipase c-gamma (PLCgamma) and p85 phosphatidyl inositol 3 kinase. As subcutaneous implants, DLD-1 cells that expressed the majority of these receptor constructs failed to recapitulate the tumor growth-enhancing effect of the wild-type Met receptor. The Grb2- and Shc-recruiting Met mutants demonstrated slight but consistent tumor-suppressive activity, whereas the expression of N1358H mutant stimulated tumor growth rate comparable with the wild-type receptor. This suggests that direct Grb2/Shc binding does not contribute to the tumor progression activity of Met receptor. The tumors expressing Grb2- and Shc-recruiting Met receptors demonstrated a marked loss in Grb2-associated adaptor protein 1 (Gab1) protein levels, which was not observed in the cell lines, consistent with a post-translationally regulated process. Moreover, a moderate level of Gab1 overexpression stimulated tumor growth. The findings suggest a delicate balance for intact Y1349/1356 SH2-binding domain to mediate the tumor progression activity of the coactivated Met-rat sarcoma oncogene homolog (RAS) pathways. Selectivity for specific adaptor protein involvement may be the key that determines the tissue- and cell-type specificity of Met-mediated tumorigenicity in human cancers.