Use of magnetic resonance urography.

OBJECTIVES: Magnetic resonance urography (MRU) is a new technique that uses heavily weighted T2 coronal images with fat suppression pulse. Urine appears white on MRU, resembling an intravenous urogram (IVU). Contrast agents are not necessary. This study describes the use of MRU in the diagnosis and treatment of patients with hematuria. METHODS: One hundred six patients with microscopic or gross hematuria and 6 normal volunteers underwent MRU between 1992 and 1995. A modified, heavily weighted T2 technique with intravenous administration of furosemide and ureteral compression was used. Thirty-two patients had other imaging techniques as well for comparison. RESULTS: MRU provided high-resolution images in almost all cases; 73 (69%) had a normal MRU. Significant findings in the 33 patients with abnormalities included renal cysts in 17 (51%), renal cell carcinoma in 6 (18%), transitional cell carcinoma in 5 (15%), ureteropelvic junction obstruction in 3 (9%), and stones causing obstruction in 6 (18%). Five patients with renal failure also had good visualization of the entire urinary tract. MRU was comparable to other imaging modalities except in identifying nonobstructing calculi. CONCLUSIONS: MRU provides an alternative to conventional imaging of the urinary tract, especially in those patients who have contraindications to ionizing radiation and contrast agents. Improvements in resolution, technique, and cost have to be addressed before it can be used regularly in urologic practice.

Human T-cell lymphotropic virus type 1 (HTLV-1)-induced syncytium formation mediated by vascular cell adhesion molecule-1: evidence for involvement of cell adhesion molecules in HTLV-1 biology.

While studying the potential role of vascular cell adhesion molecule-1 (VCAM-1) in infection of endothelial cells by human immunodeficiency virus (HIV), we found that VCAM-1 can mediate human T-cell lymphotropic virus type 1 (HTLV-1)-induced syncytium formation. Both expression-vector-encoded and endogenously expressed VCAM-1 supported fusion of uninfected cells with HTLV-1-infected cells. Fusion was obtained with cell lines carrying the HTLV-1 genome and expressing viral proteins but not with an HTLV-1-transformed cell line that does not express viral proteins. In clones of VCAM-1-transfected cells, the degree of syncytium formation observed directly reflected the level of VCAM-1 expression. Syncytium formation between HTLV-1-expressing cells and VCAM-1+ cells could be blocked with antiserum against HTLV-1 gp46 and with a monoclonal antibody (MAb) against VCAM-1. Fusion was not blocked by antiserum against HIV or a MAb against VLA-4, the physiological counter-receptor for VCAM-1. The results indicate that VCAM-1 can serve as an accessory molecule or potential coreceptor for HTLV-1-induced cell fusion and provide direct evidence of a role for cell adhesion molecules in the biology of HTLV-1.