Retained surgical textile foreign bodies are a problem despite precautions taken by surgeons. Computed tomography (CT) is a method of choice in diagnosing the cases of retained textilomas. Over 12 years, we diagnosed 11 acute textilomas in 10 patients in the early postoperative period within 3 months after abdominal surgery. The presence of considerable amount of air bubbles within textile fibers was the most representative sign. A 3-10 mm wide peripheral rim was present in all textilomas. In additional 3 cases, chronic, encapsulated foreign body granulomas were found, two were mimicking renal neoplasms. All granulomas contained discrete or coarse calcifications. The period between surgery and CT diagnosis was from 6 months to 14 years in chronic lesions. It is important to emphasize that 9 textilloma in 8 patients were associated with the years of war in Croatia (1991 and 1992), in hospitals on battle fronts, where surgeons worked under extremely strenuous conditions and with great inflow of wounded soldiers and civilians.

Ligand binding causes the EGF receptor (EGFR) to become ubiquitinated by Cbl upon association with the adaptor protein Grb2. We have investigated the role of ubiquitin and Grb2 in ligand-induced endocytosis of the EGFR. Incubation of cells with EGF on ice caused translocation of Grb2 and Cbl from the cytosol to the rim of coated pits. Grb2 with point mutations in both SH3 domains inhibited recruitment of the EGFR to clathrin-coated pits, in a Ras-independent manner. On overexpression of the Cbl-binding protein Sprouty, ubiquitination of the EGFR was inhibited, the EGFR was recruited only to the rim of coated pits, and endocytosis of the EGFR was inhibited. Conjugation-defective ubiquitin similarly inhibited recruitment of EGF-EGFR to clathrin-coated pits. Even though this does not prove that cargo must be ubiquitinated, this indicates the importance of interaction of ubiquitinated protein(s) with proteins harboring ubiquitin-interacting domains. We propose that Grb2 mediates transient anchoring of the EGFR to an Eps15-containing molecular complex at the rim of coated pits and that Cbl-induced ubiquitination of the EGFR allows relocation of EGFR from the rim to the center of clathrin-coated pits.