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Biomedical subjects

K Adachi

Publications and source records attributed to K Adachi.

At least 505 records · Page 28Linked to original sources
PubMed1987

[A case of primary extramedullary plasmacytoma in the posterior cervical portion].

This case involves a 16-year-old woman with a posterior cervical tumor. Histologically, it was found to be a extramedullary plasmacytoma (EMP). Immunohistochemically, IgG was present in the plasma cells that were shown to be atypia by the PAP method. Laboratory data revealed no other abnormalities. A surgical excision of the tumor was performed with a dissection of the relevant lymph nodes. Although irradiation and chemotherapy were administered postoperatively, multiple bone metastasis was found a month after the operation, and the patient died 8 months later.

Adolescent↗
PubMed1987

[An antiemetic effect of methylprednisolone plus droperidol against nausea and vomiting caused by administration of high-dose adriamycin to breast carcinoma patients].

An antiemetic combination of methylprednisolone and droperidol was administered to 10 patients with breast cancer showing postoperative recurrence, receiving high-dose adriamycin. Methylprednisolone was given twice intravenously at a dose of 500 mg, before and after administration of adriamycin, and droperidol was given just before administration of adriamycin. The 10 patients received a total of 20 chemotherapy courses. Complete relief of vomiting was achieved in 95% of these 20 courses, and mild nausea occurred in 40%. Side effects were drowsiness, acne and akathisia, which were minimal. It was concluded that an antiemetic combination of methylprednisolone and droperidol was very effective for prevention of high-dose adriamycin-induced nausea and vomiting.

Adult↗
PubMed1986

Serotonin metabolism in the CNS in cerebellar ataxic mice.

The metabolism of 5-hydroxytryptamine (5-HT) in the CNS was investigated in four kinds of morphologically different ataxic mice; reeler, staggerer, weaver and Purkinje cell degeneration mutants, and in hypocerebellar mice experimentally produced by injection of cytosine arabinoside. 5-HT and 5-hydroxyidoleacetic acid concentrations and tryptophan hydroxylase (TrpOH) activity were measured in the cerebrum, cerebellum and brain stem, respectively. TrpOH activity was significantly reduced only in the reeler mouse. The enhancements of the cerebellar 5-HT metabolism observed in the ataxic mice other than the reeler were supposed to be pseudo-enhancements subsequent to the cerebellar hypoplasia.

Animals↗
PubMed1986

Measurement of free and esterified carnitine in tissue extracts by high-performance liquid chromatography.

A high-performance liquid chromatographic (HPLC) method for the determination of L-carnitine in clamped and frozen rat livers is described. L-carnitine + acetyl-CoA in equilibrium with acetyl-L-carnitine + CoASH Using the above enzymatic reaction, release of CoASH is stoichiometric with the L-carnitine added. The present method has made possible the determination of carnitine in liver tissues, which is difficult by the conventional enzymatic spectrophotometric method using 5,5'-dithiobis(2-nitrobenzoic acid), owing to acetyl-CoA hydrolysis during prolonged incubations at pH 7.8.

Acetyl Coenzyme A↗
PubMed1986

[Pharmacokinetics of prednisolone (PSL) during PSL treatment. I. PSL pharmacokinetics during daily PSL treatment].

We studied the pharmacokinetics of prednisolone (PSL) in eight patients (two each with subacute thyroiditis, systemic lupus erythematosus, and nephrotic syndrome: and one each of Crohn's disease and aortitis syndrome) before and during the daily treatment with PSL(duration of 0.5-4.0 months with the mean of 1.9 months; total amount of 0.3-8.0 g with the mean of 2.8 g). PSL was measured by radioimmunoassay. Cmax, Tmax and AUCp.o. were calculated on the single oral administration of 40 mg PSL, and T1/2 beta, Vd and MCR were calculated when 25.6 mg of PSL sodium succinate (equivalent to 20 mg of PSL) was injected intravenously. Bioavailability was calculated by the ratio of AUCp.o. X PSL i.v. dose to AUCi.v. X PSL p.o. dose. With the oral administration, there was no difference in Cmax, Tmax and AUCp.o. between before and during the treatment, respectively. With the intravenous PSL administration, significant increase of AUCi.v. (p less than 0.01), significant decrease of MCR (p less than 0.01), significant elongation of T1/2 beta (p less than 0.05), and significant decrease of the bioavailability (p less than 0.001) were found in the PSL treatment period compared with before the treatment, but no significance was found in Vd between, before, and during the treatment. There was no difference in these changes in parameters among the diseases. Nor were any correlations found between the changes in these parameters of T1/2 beta, MCR or bioavailability and the duration or the total amount of PSL administered, respectively. These results indicate that the decreased MCR, elongated T1/2 beta and the decreased bioavailability of PSL were brought about by daily administration of PSL, regardless of the kind of diseases, or the total amount or the duration of PSL administration.

Acute Disease↗
PubMed1986

Impaired amylase activities caused by binding of abnormal immunoglobulin A in patients with macroamylasemia.

Eight of thirty analyzed samples of immunoglobulin A-linked macroamylases showed significantly higher enzyme activity with the low molecular (short-chain amylose) substrate than with the macromolecular (blue starch polymer) substrate. Immunoglobulin A, which had been separated from one macroamylase, was found to bind to normal amylases from different organs resulting in decreased affinity for the macromolecular substrate. These findings suggest that abnormal immunoglobulin A is stoichiometrically associated with a specific site adjacent to the active site of the amylase molecule. In addition, alpha-amylase inhibitor failed to inhibit the enzyme activity of some macroamylases with macromolecular substrate, suggesting that immunoglobulin A blocked the binding site for the inhibitor. We conclude that immunoglobulin A-linked macroamylases have heterogeneous binding sites for immunoglobulin A, resulting in functional abnormality of amylase activity.

Amylases↗
PubMed1986

Monoclonal antibodies to the beta-adrenergic receptor: modulation of catecholamine-sensitive adenylate cyclase by the antibody.

We have developed two types of hybridomas producing monoclonal antibodies to the turkey erythrocyte beta 1-adrenergic receptor in order to study the beta-adrenergic-cAMP system of epidermis. Splenic cells from BALB/c mice immunized with partially purified turkey erythrocyte beta 1-receptors were fused with mouse myeloma cell line SP2/0-Ag14. Five hybridomas of 17 positive cells producing antibodies which could precipitate soluble turkey erythrocyte beta 1-receptors were cloned by the limiting dilution method. The antibodies cross-reacted with beta 1- and beta 2-adrenergic receptors and stained epidermal basal cells with immunocytochemical techniques. Neither type of antibody interfered with the antagonist binding, i.e., all antibodies bound to sites other than the ligand binding site on the surface. One type of antibody inhibited epinephrine-stimulated adenylate cyclase activity in our "leaky" epidermal cell system. The data suggest that the antibody interferes with the coupling of the receptor to the regulatory protein.

Adenylyl Cyclases↗
PubMed1986

Concentrations of thyrotropin-releasing hormone in the brain of ataxic mice.

Concentrations of thyrotropin-releasing hormone (TRH) were studied in the brain of the Weaver ataxic mouse, the Purkinje cell degenerative ataxic mouse (pcd-ataxic mouse) and the cytosine arabinoside (ara-C)-induced ataxic mouse. The brain tissue was dissected into 4 parts, e.g., hypothalamus, cerebrum, cerebellum and brain stem. TRH concentrations in each part of the brain were measured by radioimmunoassay. TRH concentrations in the brain of Weaver ataxic mice were significantly higher in the cerebellum and brain stem than in the controls. In pcd-ataxic mice, the TRH concentrations in the brain were significantly higher in the cerebrum and brain stem. In ara-C-induced ataxic mice, the concentrations were significantly higher in the cerebrum, cerebellum and brain stem. TRH levels in the hypothalamus of ataxic mice did not differ from those of controls. The elution profile of methanol-extracted cerebellum of ataxic mice on Sephadex G-10 was identical to that of synthetic TRH. These findings suggest that changes in the TRH concentrations in the brain play a pathophysiological role in ataxic mice.

Animals↗
PubMed1986

Concentrations of thyrotropin-releasing hormone in the brain of patients with amyotrophic lateral sclerosis.

Concentrations of thyrotropin-releasing hormone (TRH) were measured by a specific radioimmunoassay in the brain of 11 patients with amyotrophic lateral sclerosis (ALS) and 6 controls (myocardial infarction, gastric cancer, multiple myeloma, cerebrovascular disease, amyloid neuropathy). TRH was found in all parts of the dissected brain tissues (pedunculus cerebri, corpus callosum, capsula interna, motor area) in patients with ALS and controls. The TRH concentrations in the brain of patients with ALS were significantly lower in the pedunculus cerebri, compared with controls, and tended to decrease in the motor area and corpus callosum, but not significantly. Changes in TRH concentrations did not always correlate with pathohistological changes. These findings suggest that TRH is widely distributed in the human brain and decreases in some part of the ALS brain.

Amyotrophic Lateral Sclerosis↗
PubMed1986

Thyrotropin releasing hormone levels in human cerebrospinal fluid in various neurologic diseases.

Thyrotropin releasing hormone (TRH) in the human cerebrospinal fluid (CSF) of 102 patients with non-neurologic and neurologic diseases was measured by a specific TRH radioimmunoassay. TRH levels in CSF were 17.6 +/- 3.4 pg/ml (mean +/- SE) in non-neurologic diseases. TRH levels in CSF were significantly elevated in cases of spinal cord tumor and multiple sclerosis (acute phase). Elevated TRH levels in CSF were decreased in these diseases by operation or prednisolone treatment, respectively. From these data, it is suggested that TRH is present in the human CSF and that measurement of TRH levels in CSF may be a useful indicator of the activity of certain neurologic diseases.

Adolescent↗
PubMed1986

A cell-spreading inhibitor exists in serum and in epidermal basal cells.

A unique monoclonal antibody was obtained by immunizing mice with complement-inactivated fetal bovine serum (FBS). This antibody, named SI-1, stained epidermal basal cells of humans, pig, guinea pig, and rat by an indirect immunofluorescence technique after pretreatment of cryostat sections with alkali buffer (pH 9.6). After dissociating pig epidermal cells by trypsin, the SI-1 antibody stained exclusively and strongly one type of uniquely shaped cells. They were small and hanging-bell or columnar in shape with one convoluted side on the base, consisting of less than 2.8% of the dissociated epidermal cell population. The antigen contained in FBS was partially purified by affinity chromatography using the SI-1 antibody. The affinity-purified antigen inhibited the spreading of PAM cells, a spontaneously transformed murine keratinocyte line, in serum-free medium in a dose-dependent manner at concentrations of 10(-5) to 10 ng/ml. The antigen also inhibited the spreading of trypsinized pig epidermal cells in the range of 10(-2) to 10(3) ng/ml in the presence of 0.05% FBS. Although there have been a few reports indicating that serum inhibited both spreading and attachment, a specific factor in serum has not been purified before. This is, to our knowledge, the first presentation of a cell-spreading inhibitor contained in serum.

Animals↗
PubMed1986

Monoclonal antibodies against epidermal cell surface and dermal-epidermal junction: antigens which may be epidermal cell spreading factors.

Two monoclonal antibodies which reacted with the epidermal cell surface (SF-1) and the dermal-epidermal-junction (SF-2), respectively, were obtained by immunizing mice with partially-purified human epibolin. The corresponding antigens were partially purified from fetal bovine serum by affinity chromatography using these antibodies. SDS-polyacrylamide gel electrophoresis showed that these antigens contained polypeptide components with molecular weights different from that of epibolin (mol. wt. 65,000 daltons); SF-1 antigen had a 68,000 dalton main component, and SF-2 antigen a broad 58,000-61,000 dalton main component. Both of these partially-purified antigens promoted the spreading of dissociated pig epidermal cells. SF-2 antigen also promoted the spreading of Pam cells (a murine keratinocyte line). The results suggest that proteins capable of promoting epidermal cell spreading may be present on the epidermal cell surface and at the dermal-epidermal junction. However, their physiological role in keratinization remains to be elucidated.

Animals↗