T he podocyte is a highly differentiated cell that has characteristic interdigitating foot processes that cover the outer surface of the glomerular basement membrane (GBM) in the kidney (1). The turnover rate of podocytes is very low under normal and various pathologic conditions compared with that of other glomerular cells (2,3). Meanwhile, podocytes contribute to the hydraulic permeability of the glomerulus and play a crucial role as a filter for macromolecules (1). Because of these biologic and morphologic characteristics of podocytes, injuries to podocytes are accompanied by characteristic changes in morphology, as observed by electron microscopy (EM), including effacement of foot processes, microvillous transformation, and occasional detachment from the GBM (4 -7). In several immunologic and nonimmunologic forms of glomerulonephritis, the podocyte is the primary target of injury (8,9). Podocyte injury is also a key event leading to glomerular sclerosis. Recent studies have revealed that the denuded GBM left behind after a podocyte becomes detached and subsequently adheres to parietal epithelial cells, resulting in the formation of a synechia of the glomerular tuft to Bowman's capsule, which represents the earliest stage of segmental sclerosis (10,11).We recently demonstrated the presence of podocytes and their cell fragments in the urinary sediment of patients with glomerular diseases, in an immunofluorescence (IF) study using a specific monoclonal antibody against podocalyxin (PCX), a glycoprotein that is prominently expressed on podocytes (12). Quantification of urinary podocytes has clinical significance in its ability to predict acute glomerular lesions (13). In addition to urinary podocytes, urine sediments from nephritic patients contain PCX-positive granular structures (PPGS) in or around the urine casts. We hypothesized that these structures represent urinary podocytes and their cell debris. We subsequently found that PPGS are excreted in the urine in far greater numbers compared with urinary podocytes. However, because we also found PPGS in the urine of patients without any urinary podocytes, we questioned whether these structures truly represent cell debris from detached podocytes. Thus, the purpose of the present study was to trace PPGS to their origin immunohistochemically. Materials and Methods Patients, Urine Samples, and Kidney SpecimensUrine samples voided in the morning were obtained from 50 healthy children and adolescents (25 male and 25 female; mean age, 12.3 yr; range, 3 to 20 yr) and 53 patients with active glomerulonephritis or nephrotic syndrome (29 male and 24 female; mean age, 11.3 yr; range,

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We isolated two muskmelon (Cucumis melo) cDNA homologs of the Arabidopsis ethylene receptor genes ETR1 and ERS1 and designated them Cm-ETR1 (C. melo ETR1; accession no. AF054806) and Cm-ERS1 (C. melo ERS1; accession no. AF037368), respectively. Northern analysis revealed that the level of Cm-ERS1 mRNA in the pericarp increased in parallel with the increase in fruit size and then markedly decreased at the end of enlargement. In fully enlarged fruit the level of Cm-ERS1 mRNA was low in all tissues, whereas that of Cm-ETR1 mRNA was very high in the seeds and placenta. During ripening Cm-ERS1 mRNA increased slightly in the pericarp of fruit before the marked increase of Cm-ETR1 mRNA paralleled climacteric ethylene production. These results indicate that both Cm-ETR1 and Cm-ERS1 play specific roles not only in ripening but also in the early development of melon fruit and that they have distinct roles in particular fruit tissues at particular developmental stages.

Human herpesvirus 6 (HHV-6)-related virus was isolated from CD4+ CD8and CD3+ CD4+ mature T lymphocytes but could not be isolated from CD4-CD8+, CD4-CD8-, and CD3-T cells in the peripheral blood of exanthem subitum patients. HHV-6-related virus predominantly infected CD4+ CD8+, CD4+ CD8- ,

Studies of carrot embryogenesis have suggested that abscisic acid (ABA) is involved in somatic embryogenesis. A relationship between endogenous ABA and the induction of somatic embryogenesis was demonstrated using stress-induced system of somatic embryos. The embryonic-specific genes C-ABI3 and embryogenic cell proteins (ECPs) were expressed during stress treatment prior to the formation of somatic embryos. The stress-induction system for embryogenesis was clearly distinguished by two phases: the acquisition of embryogenic competence and the formation of a somatic embryo. Somatic embryo formation was inhibited by the application of fluridone (especially at 10(-4) M), a potent inhibitor of ABA biosynthesis, during stress treatment. The inhibitory effect of fluridone was nullified by the simultaneous application of fluridone and ABA. The level of endogenous ABA increased transiently during stress. However, somatic embryogenesis was not significantly induced by the application of only ABA to the endogenous level, in the absence of stress. These results suggest that the induction of somatic embryogenesis, in particular the acquisition of embryogenic competence, is caused not only by the presence of ABA but also by physiological responses that are directly controlled by stresses.