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A 76-year-old man was treated with bilateral orchiectomy, estramustine phosphate and pelvic irradiation for prostate cancer. Osteogenic sarcoma of the prostate developed 18 months after the treatment. Postmortem examination revealed that the tumor was 8 cm in diameter and had infiltrated into the bladder and rectal walls and had resulted in peritoneal dissemination. There was no distant metastasis. Macroscopically, the tumor was ashen, firm and relatively homogenous and diffusely spread. Histologically, it was composed of spindle and pleomorphic cells, which were making osteoid with calcification. There was no ordinary tubular formation as shown in adenocarcinoma of the prostate. No positive immunostaining for prostate-specific antigen, epithelial membrane antigen and cytokeratin (AE-1, AE-3) were confirmed. Positive immunostaining for nonepithelial marker vimentin was confirmed. The ultimate diagnosis was osteogenic sarcoma of the prostate.

The possibility of one-week application of terbinafine cream for tinea pedis was studied in a double-blind test at four institutes, comparing four-week application as a control. Of a total of forty-three patients studied, nineteen were randomized into a four-week application group, Group I, and twenty into a one-week application group, Group II. Group I was evaluated as moderate to extremely useful in twelve (63.2%) of the nineteen patients and Group II in twelve (60.0%) of the twenty patients. No statistical differences were observed between two groups. These findings appeared to indicate that the short term, one-week application of terbinafine cream had results equivalent to the four-week application. This short-term treatment which aids in improving patient compliance and reducing the total amount of drug applied, thus lowering drug cost, is viewed as a useful way of treating tinea pedis.

We report cases of two 4-year-old boys with tinea capitis who attend the same daynursery. Clinically, on the first visit both lesions were a superficial type, however we initiated treatment with a dose of 50 mg/day of oral itraconazole. Althougth the lesion of case 2 improved after 11 weeks of treatment, case 1 developed to kerion celsi and required continued treatment for 22 weeks for cure. Microsporum canis was isolated from the hairs of both cases and MIC of itraconazole against both isolates was 1 micro g/ml. We specurate that secondary bacterial infection was responsible for the development to kelion celsi in case 2.

Background: Kindler syndrome is a rare, inherited skin disease characterized by acral bullae formation, fusion of fingers and toes, and generalized progressive poikiloderma. The purpose of this study was to clarify the nature of the bullous component of Kindler syndrome and to determine whether this inherited skin disorder represents a variant of dystrophic epidermolysis bullosa or a unique independent clinical entity., Observations: Two unrelated patients with Kindler syndrome were studied. Electron microscopy demonstrated marked duplication of the lamina densa, and clefts were observed in areas where the lamina densa was destroyed or obscured. Hemidesmosomes and anchoring fibrils showed normal features. Indirect immunofluorescence revealed normal linear labeling with antibodies against hemidesmosomal components (alpha 6 and beta 4 integrins, BPAG1, and BPAG2) and against anchoring filament components such as uncein, as detected by the 19-DEJ-1 monoclonal antibody. However, antibodies against the 3 respective laminin 5 chains, type IV collagen, and various type VII collagen epitopes (the aminoterminal NC1 domain, the central triple helical collagenous domain, and the carboxyterminal end of the triple helical collagenous domain) revealed a broad reticular staining pattern. Molecular screening of the type VII collagen gene (COL7A1) in the patients and their parents by heteroduplex analysis failed to detect any band shifts indicative of pathologic mutations., Conclusions: These results suggest that the bullous component of Kindler syndrome is distinct from dystrophic epidermolysis bullosa caused by mutations in the type VII collagen gene. Additionally, the differential distribution patterns of uncein and laminin 5 in the patients' skin samples support the hypothesis that uncein and laminin 5 are different molecules.

In order to investigate the correlation between uterine contraction and Interleukin-6 (IL-6), we studied the effects of the prenatal course and uterine contraction on IL-6 and the soluble Interleukin-6 receptor (sIL-6R) concentration in human amniotic fluid. We also determined the effects of IL-6 on the permeability of the human amnion cell monolayer. The results were as follows: 1) The level of IL-6 at full term delivery was significantly higher than that at premature delivery. 2) The level of IL-6 without uterine contraction was significantly (p < 0.05) higher than that with uterine contraction. 3) The mean sIL-6R value at full term delivery was 1.28 +/- 0.21 ng/ml. There was no correlation between sIL-6R and the prenatal course. 4) IL-6 enhanced permeability in the human amniotic cell monolayer. This effect of Il-6 was concentration dependent and time dependent. These results show that uterine contractions increased the IL-6 concentration in human amniotic fluid, and suggest that uterine contraction enhanced the permeability of the human amniotic cell in vivo.

We report a case of 6 year old girl with Fanconi syndrome the origin of which was suspected to be cystinosis. Pathological findings of a renal biopsy showed needle-like materials in the epithelial cells but the cystine content of the white blood cells was normal. Although excessive urinary loss of growth hormone was detected, the height and weight of the patient was normal. Urinary loss of growth hormone did not cause growth retardation in this case.

Rat erythrocytes contained ganglio-series gangliosides, GM1, fucosyl GM1, and GD1a, in a high concentration. The concentrations of GM1, fucosyl GM1, and GD1a in rat erythrocyte ghosts were 889.0 nmol, 470.6 nmol, and 462.0 nmol per g dry weight, respectively, and the molar ratio of lipid-bound sialic acid, cholesterol and lipid-bound phosphorus was 3.1:73.9:100.0. The reactions of fucosyl GM1 and GM1 on rat erythrocytes with rabbit anti-fucosyl GM1 and anti-GM1 antisera were measured by means of haemolysis in the presence of complement and a binding assay of antibodies with a FACS after staining erythrocytes by the indirect membrane immunofluorescence technique. When measured by ELISA, anti-fucosyl GM1 antiserum was found to react almost exclusively with fucosyl GM1 with a slight cross-reaction with GM1, but anti-GM1 antiserum cross-reacted to a significant extent with asialo GM1. Rat erythrocytes were haemolyzed specifically with anti-fucosyl GM1 antiserum, but not with antisera to GM1, asialo GM1, asialo GM2, Forssman and globoside, and the haemolysis was proved to be definitely caused by the specific recognition of fucosyl GM1 on rat erythrocytes by anti-fucosyl GM1 antibody according to the haemolysis inhibition reaction using various glycosphingolipid-containing liposomes as inhibitors. In addition, although the binding of anti-fucosyl GM1 antibody on rat erythrocytes was clearly demonstrated with a FACS, anti-GM1 antibody did not bind. The observations that the haemolysis of rat erythrocytes and the binding of antibody to rat erythrocytes were found only with anti-fucosyl GM1 antiserum, and not with anti-GM1 antiserum, but that nevertheless the titer of anti-GM1 antiserum was higher than that of anti-fucosyl GM1 antiserum and GM1 on rat erythrocytes was more abundant in concentration than fucosyl GM1, seem to be a matter of great importance in assessing the specificity of anti-ganglioside antibody and the surface distribution of gangliosides on the cell.