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The rare presence of proliferative nodules in cases of giant congenital naevus can, in some cases, be potentially misdiagnosed as neonatal melanoma. We report here a case of multiple, proliferative nodules found in a giant congenital naevus lesion in a female neonatal patient diagnosed with neurocutaneous melanosis. Our initial clinical observations of this case suggested the possibility of primary cutaneous neonatal melanoma or skin metastasis from a melanoma in the meninges or elsewhere in the central nervous system. However, histological examination revealed no sign of melanoma, abnormal mitosis, necrosis or any malignant change. Pagetoid arrays of naevus cells in the junctional zone and myxoid changes present in a significant portion of the dermis led to the diagnosis of proliferative nodules. Distinct histological patterns seen in the proliferative nodules in our neonatal patient were useful to differentiate between benign pigmented nodular lesions in a giant congenital naevus and malignant melanoma, and reduced the chance of misdiagnosis.

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Hailey-Hailey disease (HHD; familial benign chronic pemphigus) is a hereditary blistering disorder characterized by episodic maceration and erosions mainly in intertriginous areas, and generalized eruptions are rarely seen. We report here a 51-year-old woman with generalized HHD who was successfully treated with oral etretinate. The present case suggests that oral etretinate is effective against the generalized eruptions even in cases in which bacterial infection has triggered the generalization of HHD.

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Transforming growth factor-beta(TGF-beta) is known to play an important role in controlling embryonal development, cell proliferation and homeostasis. The purpose of this study is to elucidate the involvement of the TGF-beta pathway in colorectal carcinogenesis. DNA was extracted from 100 patients with colorectal cancer. Then, all coding regions of the TGF-beta type II receptor (TRII) and the genes for Smad2, Smad3, Smad4, Smad6, and Smad7 were analyzed by PCR-SSCP and direct sequencing. Also, a LOH analysis of 18q21, where the Smad2 and Smad4 genes are located, was performed. We detected 11 cases of frameshift mutation in the TRII gene (11%) and 5 cases of point mutations in the Smad4 gene (5.0%); LOH at 18q21 was detected with 33% frequency. No abnormalities were found in the genes for Smad2, Smad3, Smad6, and Smad7. These results suggest that the abnormalities of TRII and Smad4 play an important role inhibiting TGF-beta signaling in colorectal carcinogenesis.

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The clinical usefulness of catheter fragmentation and aspiration therapy was studied in 8 patients with acute pulmonary embolism who received thrombolytic therapy using urokinase or tissue-type plasminogen activator (t-PA) (thrombolysis group) and 8 patients who underwent catheter fragmentation and aspiration therapy using a percutaneous transluminal coronary angioplasty (PTCA) guide catheter (catheter group). The patients were selected from 20 patients with a definite diagnosis of acute pulmonary embolism based on pulmonary arteriography and nuclear imaging. Urokinase (48 x 10(4) to 96 x 10(4) unit/day) or t-PA (12 x 10(6) unit/day) was administered intravenously for mean 4 days in the thrombolysis group. Pulmonary artery pressure was first measured using a Swan-Ganz catheter via the jugular vein or the femoral vein in the catheter group. Then, a PTCA guide catheter was advanced into the pulmonary artery, and the thrombus was disrupted repeatedly using a Radifocus wire, followed by manual aspiration. Subsequent treatment consisted of intravenous infusion of heparin (10,000 to 15,000 unit/day) and urokinase (24 x 10(4) to 48 x 10(4) unit/day) for mean 6 days. Partial revascularization was achieved in all patients in both groups. Five patients in the thrombolysis group died within 1 month due to respiratory failure, re-embolization, and/or hemorrhagic complications. One patient in the catheter group died of hemorrhagic shock. Pulmonary artery systolic pressure in the catheter group was significantly reduced from 47.4 to 26.5 mmHg (p < 0.01). Catheter treatment of acute pulmonary embolism associated with acute circulatory failure such as shock can lead to rapid hemodynamic improvement. In contrast, thrombolysis is an effective treatment, but bleeding problems are common and caution is required. Catheter fragmentation and aspiration therapy is effective for acute pulmonary embolism, is minimally invasive, and should be considered the treatment of first choice.

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We studied the role of S-adenosylmethionine (SAM) as a methyl group donor in the methylation of inorganic arsenic in mammalians. The SAM and S-adenosylhomocysteine (SAH) levels in the livers of untreated hamsters were 74.3 +/- 8.2 and 40.0 +/- 6.4 nmol/g, respectively. The SAM level was 63.9 +/- 6.5 nmol/g following oral administration of 1.5 mg/kg of arsenic trioxide, which was 14% lower than the control level (t-test, p less than 0.05). This fall of the SAM level in the liver presumably derived from the SAM having acted as a methyl group donor. Oral administration of 1.5 mg/kg of arsenic trioxide once only to hamsters pretreated intraperitoneally with 2.0 mg/kg of SAM once only gave the following arsenic levels in the liver and urine. The dimethylated arsenic (DMA) levels in the livers of hamsters treated with SAM plus arsenic trioxide were significantly high, that is, 2 times as high as the control value at 6 hours, and 1.5 times as high as the control value at 24 hours after the administration of arsenic trioxide. The urinary DMA excretion rate was significantly higher, that is, higher by 36%, than the control value. The urinary DMA excretion rate following pretreatment with SAM was not dose-dependent. Pretreatment with methionine failed to exert any significant acceleratory effect on the methylation of arsenic trioxide. The decreasing pattern of the SAM level in the liver following administration of arsenic trioxide and the DMA behavior in the liver and urine following administration of SAM and arsenic trioxide revealed that SAM accelerated the methylation of inorganic arsenic. In other words, it appeared that SAM could be a very potent methyl group donor to inorganic arsenic.

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In an attempt to establish a method for biological monitoring of inorganic arsenic exposure, the chemical species of arsenic were measured in the urine and hair of gallium arsenide (GaAs) plant and copper smelter workers. Determination of urinary inorganic arsenic concentration proved sensitive enough to monitor the low-level inorganic arsenic exposure of the GaAs plant workers. The urinary inorganic arsenic concentration in the copper smelter workers was far higher than that of a control group and was associated with high urinary concentrations of the inorganic arsenic metabolites, methylarsonic acid (MAA) and dimethylarsinic acid (DMAA). The results established a method for exposure level-dependent biological monitoring of inorganic arsenic exposure. Low-level exposures could be monitored only by determining urinary inorganic arsenic concentration. High-level exposures clearly produced an increased urinary inorganic arsenic concentration, with an increased sum of urinary concentrations of inorganic arsenic and its metabolites (inorganic arsenic + MAA + DMAA). The determination of urinary arsenobetaine proved to determine specifically the seafood-derived arsenic, allowing this arsenic to be distinguished clearly from the arsenic from occupational exposure. Monitoring arsenic exposure by determining the arsenic in the hair appeared to be of value only when used for environmental monitoring of arsenic contamination rather than for biological monitoring.

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The purification of the osteoblast-like cells (2-3%) among the bone marrow cells (BMC) of C57BL/6 mice using a specific anti-osteoblast serum and a fluorescence-activated cell sorter is described. The antiserum was raised against osteoblast cells isolated from calvaria from neonatal mice. The majority of the cells of the osteoblast-enriched fraction from bone marrow showed a parathormone-induced increase in cyclic adenine monophosphate but no response to calcitonin. This is similar to the response of osteoblast cells obtained from the calvaria. Electron microscopic studies of the extracellular matrix of cultured osteoblast-like cells purified from bone marrow showed the deposition of apatite crystals within and in close apposition to the vesicles. These findings suggest that the isolated cell population was enriched in osteoblasts. Such a cell system from bone marrow might provide an experimental system for investigating the mechanism of bone formation.

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The enzyme of Aspergillus fumigatus which produces di-D-fructose 1,2'; 2,1' dianhydride (difructose anhydride I) (Tanaka et al., 1979) was investigated for its mode of action. Fractionation and purification of the enzyme showed that it produced difructose anhydride I not from inulin but from inulobiose by the reverse reaction of the partial hydrolysis of difructose anhydride I.

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Immunization with MMC-treated EL-4 tumor cells could raise cytotoxic activity of non-adherent PE cells and resistance against rechallenge with small or medium doses of viable tumor cells. Administration of PSK augmented the generation of cytotoxic lymphocytes and the induction of resistance against rechallenge in mice immunized with such MMC-treated tumor cells. Augmented generation of cytotoxic lymphocytes may be ascribed to systemic effects of PSK but not to local effects in the peritoneal cavity, since augmenting effects of PSK were observed not only after intraperitoneal administration but also after oral administration. Either after intraperitoneal administration or after oral administration cytotoxic activity was detected in PE cells but not in spleen cells. Cytotoxic activity was detected in PE cells but not in spleen cells after intraperitoneal injections of MMC-treated tumor cells. Cytotoxic lymphocytes appear to differentiate to their mature form capable of being detected by 51Cr-release test principally at the site of direct graft rejection. Intraperitoneal administration of PSK was more effective in the augmentation of cytotoxicity of PE cells than oral administration. PSK may be able to have contact with precursors of cytotoxic lymphocytes more efficiently after intraperitoneal administration. Immunity against syngeneic tumor cells appears to be effective in elimination of small doses of tumor cells but to be overcome by medium or large doses of tumor cells at the rechallenge. Administration of PSK increased the threshold number to be eliminated by immune hosts. This finding seems to be important in relation to augmentation of resistance against metastasis or local implantation with a limited number of tumor cells.

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