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Biomedical subjects

J Aoki

Publications and source records attributed to J Aoki.

At least 199 records · Page 11Linked to original sources
PubMed1986

Sclerotic bone metastasis: radiologic-pathologic correlation.

Radiographic appearances were correlated with histologic findings in sclerotic bone metastases. For this purpose, undecalcified ground sections were made from lumbar vertebrae obtained at 12 autopsies. The primary tumor sites were the prostate gland in five cases, the breast in three, the lung in two, the stomach in one, and the urinary bladder in one. After Villanueva bone staining and methyl methacrylate embedding, 1-mm-thick ground sections were made for low-kilovoltage contact radiography. In sclerotic bone metastases, new bone is deposited on preexisting trabeculae and in the intertrabecular spaces, forming lacy networks. The radiographic indications of these histologic changes are trabecular thickening, marginal obscurity (the "silhouette" sign), and homogeneous dense sclerotic change. The silhouette sign in bone is a new concept, one that is helpful when the changes in density are not reliable.

Adult↗
PubMed1985

Surgical treatment of skin depigmentation caused by burn injuries.

Thin split-skin autografts of normal color were performed on depigmented skin caused by second- and third-degree burns in 32 patients. Repigmentation appeared in almost all the recipient areas soon after grafting and no depigmentation occurred again in the treated area.

Adolescent↗
PubMed1985

Identification of 1,24(R)-dihydroxyvitamin D3-like bone-resorbing lipid in a patient with cancer-associated hypercalcemia.

A lipid indistinguishable from 1,24(R)-dihydroxyvitamin D3 [1,24(R)-(OH)2D3] was found in serum and tumor extracts from a hypercalcemic patient with a small cell carcinoma of the lung. The lipid comigrated with authentic 1,24(R)-(OH)2D3 on high performance liquid chromatography using both straight and reverse phase columns and competed with tritiated 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3)] for binding to intestinal 1,25-(OH)2D3 receptor. Increasing doses of the lipid factor from tumor and authentic 1,24(R)-(OH)2D3 gave parallel responses in a bone resorption assay, as assessed by 45Ca release from prelabeled mouse calvaria. The lipid factor from the patient's serum and authentic 1,24(R)-(OH)2D3 had identical biological activities in the receptor binding and bone resorption assays. In addition, the mechanisms of action of this lipid factor and 1,24(R)-(OH)2D3 were indistinguishable. Bone resorption by both was inhibited by calcitonin, and neither the lipid factor nor authentic 1,24(R)-(OH)2D3 affected cAMP content in osteoblast-like bone cells derived from mouse calvaria. The estimated concentrations of the 1,24(R)-(OH)2D3-like lipid, expressed as 1,24(R)-(OH)2D3 were 11 ng/g tumor wet wt by the receptor binding assay and 9.2 ng/g tumor wet wt by the bone resorption assay. The mean serum concentration was 1.4 +/- 0.3 (+/- SD) ng/ml (n = 3) by the receptor binding assay. No activity was detected in either bioassay when extracts of nontumor tissues from this patient or tumor extracts and sera from one hypercalcemic and four normocalcemic cancer patients were tested. The mean serum 1,25-(OH)2D level was low (6.4 +/- 0.5 pg/ml; n = 2), and serum 1,24(R),25-(OH)3D in this patient was high (103 pg/ml) compared to normocalcemic cancer patients, in whom the mean serum 1,25-(OH)2D level was 27 +/- 12 pg/ml (n = 4) and the 1,24(R),25(OH)3D level was 28 +/- 1.3 pg/ml (n = 4). Thus, the 1,24(R)-(OH)2D3-like lipid may be a substrate for metabolic conversion to 1,24(R),25-(OH)3D in vivo. These results provide evidence for the presence of a novel metabolite of vitamin D3, 1,24(R)-(OH)2D3. Detection of this bone-resorbing lipid in both tumor and serum suggests, but does not prove, that the tumor secreted this bioactive lipid into the circulation and that the high level of circulating bone-resorbing lipid was related to the hypercalcemia in this patient.

Animals↗
PubMed1984

ECG changes during cerebral angiography. An analysis of 334 patients--942 cerebral angiographies.

We have analyzed HR changes greater than 20% among 334 patients and 942 cerebral angiographies. A tachycardial effect was seen in 14.9% of patients, while a bradycardial effect was seen in 7.1% including two patients having cardiac standstill (0.5%). These two patients were examined without atropine premedication after subarachnoid hemorrhage. Patients under 19 years of age, unpremedicated with atropine sulfate and suffering from subarachnoid hemorrhage secondary to ruptured aneurysm or arteriovenous malformation showed a significantly high incidence of bradycardia. On the other hand, patients with the neoplastic disease and having an initial sinus bradycardia showed a significantly high incidence of a tachycardial effect.

Adolescent↗
PubMed1984

Basal cell epithelioma occurring in an epidermal nevus.

An unusual case is presented of a thirty-year-old woman in whom basal cell epithelioma developed from a preexisting localized epidermal nevus in the scalp. The epidermal nevus was not associated with any abnormal pilosebaceous complexes.

Adult↗
PubMed1983

Species variations in the metabolism of N-butyl-N-(4-hydroxybutyl) nitrosamine and related compounds in relation to urinary bladder carcinogenesis.

Species variations in response to urinary bladder carcinogens, N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), N-ethyl-N-(4-hydroxybutyl)nitrosamine (EHBN), and N,N-dibutylnitrosamine (DBN), were investigated in several animal species from the metabolic point of view. Since N-butyl-N-(3-carboxypropyl) nitrosamine (BCPN) and N-ethyl-N-(3-carboxypropyl) nitrosamine (ECPN) had been found to be the principal urinary metabolites which are responsible for the induction of bladder tumors by BBN or DBN and EHBN, respectively, in rats, acidic urinary metabolites with the N-nitroso moiety were isolated and determined by a colorimetric method after oral administration of these nitrosamines to rats, mice, hamsters, guinea pigs, and dogs. Qualitatively almost no species differences were observed among these animals in regard to the urinary metabolites except in the case of mice, in which the glycine conjugate of BCPN was isolated from the urine and identified as the principal metabolite of BBN and DBN. However, appreciable quantitative differences in the urinary excretion of BCPN or ECPN were found among these animal species, indicating that the differences in the susceptibilities of different animal species to urinary bladder carcinogenesis induced by BBN, DBN and EHBN may be closely related to the different extents of urinary excretion of the active metabolites of these nitrosamines.

Animals↗
PubMed1981

Metabolic fate of N-butyl-N-(4-hydroxybutyl) nitrosamine and N, N-dibutylnitrosamine in the guinea pig, with reference to their carcinogenic effects on the urinary bladder.

The metabolic fate of two urinary bladder carcinogens, N-butyl-N-(4-hydroxy-butyl) nitrosamine (BBN) and N-N-dibutylnitrosamine (DBN), was studied in the guinea pig, in order to elucidate species differences of response to these N-nitrosamines in this animal species and the rat. Based on the urinary metabolites characterized after oral administration of these compounds, the metabolic pathways of BBN and DBN in the guinea pig were shown to be essentially similar to those in the rat. The principal urinary metabolite of BBN and DBN in the guinea pig, however, was not N-butyl-N-(3-carboxypropyl) nitrosamine (BCPN), as was the case in the rat, but the glucuronic acid conjugate of BBN and that of N-butyl-N-(3-hydroxybutyl) nitrosamine, respectively. The species variation in response to BBN and DBN as bladder carcinogens in these animals is discussed on the basis of the urinary excretion of BCPN.

Animals↗