[A case of synovial sarcoma with bone metastasis identified by bone marrow scintigraphy].
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Biomedical subjects
Publications and source records attributed to M Fukunaga.
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Airborne particulate samples were collected on a glass fiber filter or quartz filter using Hi-volume air sampler from November, 1980 through February, 1983 at a west part of Yahata district, Japan. The concentrations of airborne particulates, polynuclear aromatic hydrocarbons (PAH), heavy metals and dustfall were determined, and mutagenic activities of tarry materials obtained from suspended particulates were also measured. The following results were obtained. (1) The airborne particulate contents were 22.1 - 188 mg/1000 m3 (mean : 74.6 mg/1000 m3), and the values were high in spring and low in summer. (2) PAH contents in airborne particulates were in the following order: benzo(ghi)perylene greater than benzo(a)pyrene greater than benz(a)anthracene greater than chrysene greater than benzo(k)fluoranthene greater than pyrene greater than perylene. PAH contents were higher in winter that in summer. The benzo(a)pyrene contents were 1.97 micrograms/1000 m3 in 1981 and 1.92 micrograms/1000 m3 in 1982. (3) Heavy metals content was about 2.1 - 3.6 higher in winter in comparison with that in summer time. (4) Mutagenic activity showed 90 - 11900 revertants/1000 m3 for TA 98 strain with S-9 mix and 50 - 7190 revertants/1000 m3 for TA 98 strain without S-9 mix. Mutagenic activities for TA 98 with S-9 mix were higher than those for TA 98 without S-9 mix. (5) As a result of the analysis of airborne particulate samples, a significant correlation was observed between mutagenic activities and the concentrations of PAH and heavy metals. These results indicated that the mutagenic survey may be useful as an index for air pollution study.
Human erythrocytes were examined for acetaldehyde-oxidizing capacity of intact cells, in comparison with its uptake under various conditions. The oxidation was found to be predominant over other possible acetaldehyde-metabolizing pathways, particularly with low concentrations of acetaldehyde. Further investigation using three media which differed in the initial pyruvate level showed an independence of acetaldehyde oxidation rate up to the high cellular lactate/pyruvate concentration ratio. The apparent non-oxidative acetaldehyde uptake obtained by subtraction of oxidation from the total uptake, was reduced when pretreating the erythrocytes with pyridoxal but not with pyridoxal 5'-phosphate. Though N-ethylmaleimide also inhibited the non-oxidative uptake, another sulfhydryl blocking reagent, p-chloromercuribenzoate was without effect. Thus, in addition to the oxidation, acetaldehyde may be involved in a reaction such as binding to the red cell components, as the minor metabolizing pathway in the erythrocytes.
The relation between the mutagenic activities and chemical structure of phenanthridinium derivatives were tested by using Salmonella typhimurium strain TA 98 and yeast Saccharomyces cerevisiae. The 3,8-diamino analog and amino-azido isomers caused frameshift type mutation in Salmonella. However, mutagenicity was severely reduced for the diazido analog, and mutagenic activities of monoamino and monoazido analogs were minimal. The deaminated analog was not mutagenic. Diamino analog and two amino-azido isomers induced mitochondrial mutation of yeast in both resting and growing conditions. Two monoamino and deaminated analogs were mutagenic only in growing yeast but not in resting cells. Two monoazido and diazido analogs were less mutagenic even in the growing conditions.
The mutagenic activity of some phenanthridinium compounds was examined by using Salmonella typhimurium strain TA98. Microsomal enzyme activation of the compounds was necessary for the detection of frameshift mutagenesis. Amino and/or azido functions at both R3 and R8 were structural requisites for significant mutagenic activity, although mutagenicity was severely reduced for the diazido analog. When an azido or amino group was substituted by hydrogen at either R3 or R8, mutagenic activities were minimal, and the deaminated compound (3,8-dihydro derivative) was not mutagenic. Propidium was only slightly more mutagenic than the monoamino and monoazido analogs. Relationships between mutagenic activity and chemical structure of phenanthridinium compounds are discussed.
In a case study of medullary thyroid carcinoma (MTC) associated with Cushing's syndrome, elevated levels of urinary 17-hydroxycorticosteroids, plasma ACTH, cortisol, calcitonin (CT) and somatostatin (GHRIH) were documented. Lysine vasopressin administration further increased the levels of plasma ACTH, cortisol and CT, whereas the administration of calcium and pentagastrin increased only the level of plasma CT. Immunoreactive ACTH, CT and GHRIH were highly concentrated in the tumour tissues. Basal plasma ACTH levels were more progressively increased than plasma CT during the postoperative course when the patient was treated with o,p'-DDD, since the tumour was not completely resected. These findings suggest that the secretion of ACTH and CT from MTC were regulated in a different manner.
A 43-year-old male suffering from liver cirrhosis was admitted with complaints of general malaise and anorexia. Admission laboratory data evidenced high levels of serum alpha-fetoprotein (AFP) and human chorionic gonadotropin (HCG). Histopathologically, the resected left testis and supraclavicular enlarged lymph nodes revealed mixed germ cell tumor. After castration, the serum HCG level normalized, but AFP continued to increase. Autopsy findings did not unequivocally show mixed germ cell tumor, however, massive type hepatocellular carcinoma was present. These findings suggest that the hepatocellular carcinoma produced AFP, while the mixed germ cell tumor produced HCG.
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A papillary adenocarcinoma of the rete testis in a 67-year-old man is presented. The tumor was localized in the rete testis, showing no involvement of the adjacent testicular parenchyma or the epididymis. The tumor cells manifested a transition to the normal epithelial cells of the rete testis. The electron microscopic features of this tumor are compared with those of the normal epithelial cells of the rete testis.
Plasma concentrations of vitamin D3, 25-OH-D3, 24, 25(OH)2D3 and 1, 25(OH)2D3 were measured in patients with various diseases using the multiple assay system previously reported. In patients with hyperparathyroidism, the plasma levels of 1, 25(OH)2D3 tended to increase, while the levels of 24, 25(OH)2D3 tended to decrease in many cases. On the other hand, plasma 1, 25(OH)2D3 levels were low, while 24, 25(OH)2D3 levels were high in patients with hypoparathyroidism. No significant differences in the levels of plasma D3 derivatives among idiopathic-, postoperative- and pseudo- hypoparathyroidism were observed. In a majority of hemodialyzed patients with advanced renal failure who showed no overt bone changes on X-ray films, both the plasma 1, 25(OH)2D3 and 24, 25(OPH)2D3 levels were distributed from normal to very low. In a majority of patients with osteoporosis and hypoparathyroidism, plasma 1, 25(OH)2D3 levels rose quickly after the administration of 1 alpha-OH-D3. In hypophosphatemic vitamin D resistant rickets, however, the response to the relatively large amounts of 1 alpha-OH-D2 was poor, although the concentrations of plasma 24, 25(OH)2D3 were elevated by the 1 alpha-OH-D3 administration in most of these cases. The plasma 1, 25(OH)2D3 and 24, 25(OH)2D3 concentrations in patients with senile osteoporosis were distributed from lower to higher range than those of normal adults. There was a relatively good correlation between plasma levels of 25-OH-D3 and D3 only in cases with plasma D3 levels higher than 5 ng/ml. In addition, a hyperbolic regression curve was obtained between the plasma D3 and 25-OH-D3 ratio. These results may indicate that a possible negative feedback homeostatic mechanism exists between plasma levels of D3 and 25-OH-D3, but only with low plasma levels of D3.
Inhibition of human erythrocyte aldehyde dehydrogenase (ALDH) activity was studied using disulfiram and its reduced metabolite, diethyldithiocarbamate (DDC). The enzyme was rapidly inactivated by disulfiram and the inhibition was protected by reduced glutathione (GSH), in a concentration dependent manner when the enzyme premixed with GSH was reacted with disulfiram. Higher reactivity of the thiol group of the enzyme than that of GSH to disulfiram was suggested from the observation that half of the enzyme activity was inhibited when the ratio of disulfiram to GSH was 1:10. Although DDC alone showed no inhibitory effect on the enzyme, inactivation was mediated by a low concentration of heme-containing peroxidases, but not by methemoglobin. Under this condition, the inhibition potential was not protected, even with a high concentration of GSH. The constant reoxidation system of DDC is probably directly related to the enzyme inactivation.
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A histologically proven case of pulmonary alveolar microlithiasis that demonstrated intense lung uptake of Tc-99m-MDP on a bone scan is presented. The spatial distribution within the lungs of the radioactivity and density was assessed either by single photon emission computed tomography (SPECT), or x-ray computed tomography (CT) respectively, and the regional magnitude of the two parameters were compared. The quantitative study of regional radioactivity and density revealed that both the parameters distributed symmetrically, showing gradual increase in magnitude from the upper to the lower lung regions. The radioactivity-density association observed in our patient may indicate on-going formation of microcalculi throughout the lungs, the degree of which is greater at the sites of more severe involvement.
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