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Infected urachal cysts present with protean clinical manifestations. Diagnosis is frequently difficult in spite of the use of modern genitourinary radiologic imaging techniques. Patients with intra-abdominal or pelvic symptoms are frequently misdiagnosed. Surgical excision is the treatment of choice for infected urachal cysts.

The antibiotic tunicamycin blocks the transfer of GlcNAc-1-P from UDP-GlcNAc to dolichol phosphate, thereby blocking the synthesis of N-linked oligosaccharide chains on glycoproteins. Its effect on the biosynthesis of gangliosides has not been reported. We report that tunicamycin caused a 70-80% reduction in incorporation of [(3)H]GlcN into gangliosides and neutral glycosphingolipids of the neuroblastoma-glioma hybrid cell line NG 108-15 at antibiotic concentrations that caused a 90% reduction of the radiolabel incorporation into glycoproteins. The effect of tunicamycin on ganglioside biosynthesis was apparent after only 4 hr of incubation, and maximum inhibition was seen within 6 hr. When control or tunicamycin-treated (5 mug/ml) cells were collected and fractionated to separate glycoproteins, neutral glycosphingolipids, gangliosides, and nucleotide sugar-precursor pools, the following results were obtained: (i) UDP-GlcNAc and UDP-GalNAc pool sizes increased >3-fold, and specific activities decreased 50% upon treatment with tunicamycin; (ii) when corrected for this value, the percentage inhibition of GlcN incorporation into various glycoconjugates by tunicamycin in these cells was 82% for glycoproteins, 54% for neutral glycosphingolipids, and 50% for gangliosides; and (iii) the different gangliosides were affected differentially, with the most striking inhibition apparent in GM(3) biosynthesis, which was decreased 78% in the presence of tunicamycin. These data suggest that the effects of tunicamycin on glycosphingolipids as well as on glycoproteins must be considered when interpreting its effects on intact cells and organisms.

Cell-cell recognition and adhesion are thought to be complex, multistep phenomena, and may involve cell surface carbohydrates and their receptors on apposing cell surfaces. We have modeled such interactions using hepatocytes and polymer (gel) surfaces derivatized with carbohydrate ligands, and have demonstrated carbohydrate-specific cell adhesion (Schnaar, R. L., Weigel, P. H., Kuhlenschmidt, M. S., Lee, Y. C., and Roseman, S. (1978) J. Biol. Chem. 253, 7940-7951). In the present studies, we have developed a method to quantitate the forces involved in cell-gel adhesion. Our method is based on that of McClay et al. (McClay, D. R., Wessel, G. M., and Marchase, R. B. (1981) Proc. Natl. Acad. Sci. U. S. A. 78, 4975-4979) which was designed to measure the forces involved in intercellular adhesion. The following results were obtained. 1) Chicken and rat hepatocytes adhere specifically to gels derivatized with N-acetylglucosamine and galactose, respectively, at either 4 degrees C or 37 degrees C. 2) At 37 degrees C, after a lag of 10-20 min, stabilization of the adhesion occurs, resulting in a 15-fold (or greater) increase in the force of adhesion. 3) This marked strengthening of adhesion does not occur at 4 degrees C and is blocked by inhibitors of oxidative phosphorylation. These data demonstrate that cells can recognize and adhere to specific carbohydrates on apposing surfaces, and can then respond by mobilizing cellular energy to strengthen that adhesion. This series of events is strikingly similar to that shown for cell-cell adhesion between hepatocytes or between neural retina cells (Umbreit, J., and Roseman, S. (1975) J. Biol. Chem. 250, 9360-9368; McClay, D. R., Wessel, G. M., and Marchase, R. B. (1981) Proc. Natl. Acad. Sci. U. S. A. 78, 4975-4979). The present results suggest that the cell surface analogs described may provide a well controlled experimental system to probe the molecular events involved in cell-cell adhesion.