Gender's equality in evaluation of urine particles: Results of a multicenter study of the Italian Urinalysis Group.

OBJECTIVE: We performed a multicenter study to calculate the upper reference limits (URL) for urine particle quantification in mid-stream samples by using automated urine analyzers. DESIGN & METHODS: Two laboratories tested 283 subjects using a Sysmex UF-100, two other laboratories tested 313 subjects using Sysmex UF-1000i, whereas two other laboratories tested 267 subjects using Iris IQ®200. RESULTS: The URLs of UF-100 in females and males were 7.8/µL and 6.7/µL for epithelial cells (EC), 11.1/µL and 9.9/µL for red blood cells (RBC), 10.2/µL and 9.7/µL for white blood cells (WBC), and 0.85/µL and 0.87/µL for cylinders (CAST). The URLs of UF-1000i in females and males were 7.6/µL and 7.1/µL for EC, 12.2/µL and 11.1/µL for RBC, 11.9/µL and 11.7/µL for WBC, and 0.88/µL and 0.86/µL for CAST. The URLs of Iris IQ®200 in females and males were 7.8/µL and 6.6/µL for EC, 12.4/µL and 10.1/µL for RBC, 10.9/µL and 9.9/µL for WBC, and 1.1/µL and 1.0/µL for CAST. CONCLUSION: The URLs obtained in this study were comparable to the lowest values previously reported in the literature. Moreover, no gender-related difference was observed, and analyzer-specific upper reference limits were very similar.

Suppression of tumor growth and cell proliferation by p13II, a mitochondrial protein of human T cell leukemia virus type 1.

Human T cell leukemia virus type 1 encodes an "accessory" protein named p13(II) that is targeted to mitochondria and triggers a rapid flux of K(+) and Ca(2+) across the inner membrane. In this study, we investigated the effects of p13(II) on tumorigenicity in vivo and on cell growth in vitro. Results showed that p13(II) significantly reduced the incidence and growth rate of tumors arising from c-myc and Ha-ras-cotransfected rat embryo fibroblasts. Consistent with these findings, HeLa-derived cell lines stably expressing p13(II) exhibited markedly reduced tumorigenicity, as well as reduced proliferation at high density in vitro. Mixed culture assays revealed that the phenotype of the p13(II) cell lines was dominant over that of control lines and was mediated by a heat-labile soluble factor. The p13(II) cell lines exhibited an enhanced response to Ca(2+)-mediated stimuli, as measured by increased sensitivity to C2-ceramide-induced apoptosis and by cAMP-responsive element-binding protein (CREB) phosphorylation in response to histamine. p13(II)-expressing Jurkat T cells also exhibited reduced proliferation, suggesting that the protein might exert similar effects in T cells, the primary target of HTLV-1 infection. These findings provide clues into the function of p13(II) as a negative regulator of cell growth and underscore a link between mitochondria, Ca(2+) signaling, and tumorigenicity.