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Biomedical subjects

J Morita

Publications and source records attributed to J Morita.

At least 37 records · Page 2Linked to original sources
PubMed1992

Wilson's disease treatment by triethylene tetramine dihydrochloride (trientine, 2HCl): long-term observations.

Wilson's disease is an autosomal recessive disorder characterized by an accumulation of a toxic amount of copper in the body. Triethylene tetramine dihydrochloride (trientine, 2HCl) is a new chelating agent that may be effective in the removal of excess copper but long-term efficacy has not yet been investigated. Here we report the use of trientine over more than 8 years in 2 patients with Wilson's disease who could not tolerate D-penicillamine. We found no significant side effect, except a decreased serum iron concentration without clinical symptoms of anemia. In annual examinations at a steady state, the serum copper levels remained below 20 micrograms/100 ml. The 24-hour urinary copper excretion was less than that found using D-penicillamine, while the basal copper excretion, after 5 days abstinence from trientine, was maintained below 100 micrograms/day. Both hepatic and neurological manifestations except bulbar symptoms were recovered without any initial deterioration.

Adolescent↗
PubMed1991

Identification of the sequence of the regulatory light chain required for the phosphorylation-dependent regulation of actomyosin.

The amino acid structure of regulatory light chain which is essential to express the phosphorylation-mediated regulation of smooth muscle actomyosin ATPase was studied. Regulatory light chain of smooth muscle heavy meromyosin (HMM) was truncated by either lysylendopeptidase or trypsin. Lysylendopeptidase cleaved the regulatory light chain initially at the C-terminal side of lysine 6 (Lys C(1)-HMM) and subsequently at the C-terminal side of lysine 12 (Lys C(2)-HMM). On the other hand, trypsin cleaved at the C-terminal side of arginine 16 (tryp-HMM). While the actin activated ATPase activity of Lys C(1)-HMM and Lys C(2)-HMM was markedly activated by phosphorylation, that of tryp-HMM was not activated by phosphorylation. The exchange of cleaved regulatory light chain of tryp-HMM with undigested regulatory light chain restored the phosphorylation-mediated regulation on the actin activated ATPase activity. The regulatory light chain of the undigested HMM was also exchanged with the trypsin-digested regulatory light chain and this abolished the phosphorylation dependence of acto-HMM ATPase activity. These results show that the amino acid sequence arginine 13-arginine 16 is essential to express the regulation of actin activated ATPase of smooth muscle myosin which is mediated by the phosphorylation at serine 19 of the regulatory light chain.

Actomyosin↗
PubMed1991

Exchange of the fluorescence-labeled 20,000-dalton light chain of smooth muscle myosin.

The 20,000-dalton light chain of smooth muscle myosin was exchanged with exogenous light chain in a solution containing 0.5 M NaCl and 10 mM EDTA at 40 degrees C. The light chain was almost completely exchanged within 30 min under the above conditions. The exchange was markedly inhibited either below 37 degrees C or in the presence of Mg2+ concentrations higher than 10 microM. The 20,000-dalton light chain was selectively labeled of a single thiol (Cys-108) with 5-[[2-[(iodoacetyl)amino]ethyl]amino-naphthalene-1-sulfonic acid (1,5-IAEDANS). The labeled light chain was exchanged stoichiometrically into myosin and was used as a probe to investigate the conformation of smooth muscle myosin. The resulting myosin hybrids showed enzymatic properties virtually identical with those of the control, untreated myosin; i.e., actin-activated ATPase activity was dependent on the 20,000-dalton light-chain phosphorylation catalyzed by myosin light chain kinase, and the 10S-6S conformational transition of myosin correlating with the changes in ATPase was also affected either by the light-chain phosphorylation or by the change in the ionic strength. Steady-state fluorescence antisotropy measurements were performed by varying the temperature. The Perrin-Weber plots were constructed in order to obtain information about the average rotational mobility of the probe and to estimate the rotational correlation time for the AEDANS-myosin head. The fluorescence probe on the 20,000-dalton light chain was found to be quite immobile as indicated by its limiting anisotropy (A0 = 0.33).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Postpneumonectomy space control with SF6.

Four cases of patients whose postpneumonectomy spaces had been controlled with SF6 were examined at autopsy, which showed that the spaces were entirely covered with thickening parietal pleura and that the mediastinum had moderate elasticity. Histologically, fibrotic changes with minimum inflammation patterns were seen in the pleura. We consider that mediastinal elasticity becomes a factor in improving pulmonary function and the above observations confirmed that SF6 prevents the proliferative reaction of postpneumonectomy spaces without any toxicity.

Aged↗
PubMed1991

[Mediastinal ganglioneuroma with the secretive activity of catecholamines, visualized by 131-I-MIBG scintigraphy].

A 6-year-old girl with mediastinal ganglioneuroma was reported. Preoperative examinations revealed that the tumor had both secretive activity of catecholamine and uptake of 131-I-MIBG. Clinical symptom was only supraventricular premature beat on ECG. The tumor, which was located at the left upper mediastinum, was well encapsulated. Total surgical removal was accomplished. Subsequently serum and urine levels of catecholamine were normalized. Detailed histological examination of the tumor revealed benign ganglioneuroma. No blastic change was recognized. We postulate that secretive activity of catecholamine and uptake of 131-I-MIBG cannot suggest malignancy necessarily.

3-Iodobenzylguanidine↗
PubMed1990

Cystic pulmonary hamartoma.

A case of cystic pulmonary hamartoma is reported and the literature is reviewed. According to the literature, only 6 well-documented cases have been previously reported, and all the patients including our patient fared well after operation.

Hamartoma↗
PubMed1990

Instability of pleomorphic tubulin paracrystals artificially induced by Vinca alkaloids in tissue-cultured cells.

The processes of tubulin paracrystal induction in Chinese hamster ovary cells treated with a Vinca alkaloid, ie, vinblastine or vincristine, and treated simultaneously with one of the Vinca alkaloids and colcemid or colchicine were followed by four different microscopic techniques, in particular by tubulin-immunofluorescence. Vinca alkaloid alone, in lower concentrations, induced basically tactoid or needle-shaped (N-shaped) paracrystals. However, the formation of crystalloid was greatly enhanced by increasing the concentration of Vinca alkaloid. Square or barrel-shaped (S-shaped) and hexagonal paracrystals were also commonly induced by simultaneous treatment with a Vinca alkaloid and colcemid or colchicine. Large rectangular paracrystals often displayed fibrillar or lamellar fine structures which ran perpendicular to the long axis but tended to cleave into fragments by spontaneous splitting. Electron micrographs revealed the fine structure of crystalloids to be aggregates of numerous filaments. The growth of paracrystals, particularly N-shaped crystals, was markedly inhibited when cells were exposed to drug(s) at a low temperature (4 degrees C). We confirmed that both N- and S-shaped paracrystals dissociated rapidly after the culture medium was replaced with fresh, drug-free medium. Glutaraldehyde-fixed paracrystals treated with RNase solution were stained with acridine orange, showing a weak orange color. Possible factors involved in the assembly and disassembly of tubulin paracrystals are discussed.

Animals↗
PubMed1990

[A surgical case report of acute pyogenic pericarditis in a 9-month infant].

A surgical case of acute pyogenic pericarditis in a 9-month old infant who developed pericardial tamponade rapidly is reported. An anterior pericardiectomy through a left lateral thoracotomy was performed. The baby subsequently made an uncomplicated recovery and was discharged on the 16th postoperative day.

Acute Disease↗
PubMed1989

Persistent hyperkalaemia in vitamin B12 unresponsive methylmalonic acidaemia.

Persistent hyperkalaemia was found in a patient with vitamin B12 unresponsive methylmalonic acidaemia associated with hyperuricaemia. At 3 years and 8 months of age, a serum potassium level of 6.8 mmol L-1 was found when blood gas measurement was normal. One year later azotaemia was noted. At the age of 5 years, renal function studies disclosed hyperaldosteronism, decreased creatinine clearance, reduction of the reabsorption of sodium at distal diluting segments and inadequate concentration of urine at the collecting ducts. The reduction of the reabsorption of sodium, which may have resulted in decreased potassium excretion, and the decrease in glomerular filtration rate, together with the superimposed excess intake of potassium, appeared to be responsible for the hyperkalaemia. Dietary potassium restriction was effective in suppressing the hyperkalaemia.

Child↗
PubMed1989

Interleukin 2 promotes expression of an interleukin 2 receptor and proliferation of T cells stimulated with non-mitogenic dose of concanavalin A.

Interleukin 2 (IL-2) initiated proliferation of the cells of T-enriched population stimulated with non-mitogenic dose of concanavalin A (Con A), whereas it could not induce proliferation of the cells treated with non-mitogenic lectin wheat germ agglutinin (WGA). Use of monoclonal antibody (MAb) directed against interleukin 2 receptor (IL-2R) showed that IL-2 significantly increased expression of IL-2R on the cells of T-enriched population stimulated with Con A, whereas it could not cause any significant enhancement of expression of IL-2R on the cells treated with WGA. We concluded that IL-2 activated T cells in combination with non-mitogenic does of Con A, and induced both expression of IL-2R and proliferation.

Concanavalin A↗
PubMed1989

[Study on cefotaxime in respiratory surgery: transfer to lung tissue and kinetics in serum].

Cefotaxime (CTX) was intravenously administered in a dose of 1 g to patients just prior to lung surgery. Lung tissue specimens were collected at 1, 2 and 3 hours after the CTX administration, and the concentration of CTX in each specimen was determined. At the same time, the concentration of CTX in the serum was also measured. The results are summarized below. 1. Determination of the CTX concentration in the lung tissue using bioassay showed values of 3.78 +/- 1.93 micrograms/g at 1 hour after CTX administration, 1.91 +/- 0.92 microgram/g at 2 hours, and 1.19 +/- 1.04 micrograms/g at 3 hours. 2. Determination of the CTX concentration in the serum using bioassay showed values of 36.9 +/- 14.4 micrograms/ml at 30 minutes after CTX administration, 22.5 +/- 10.5 micrograms/ml at 1 hour, 12.8 +/- 6.32 micrograms/ml at 2 hours, 8.52 +/- 5.54 micrograms/ml at 3 hours, and 3.98 +/- 3.19 micrograms/ml at 6 hours. The serum half-life was calculated to be 1.82 hours. 3. The CTX concentration of 3.78 +/- 1.93 micrograms/g in the lung tissue at 1 hour after CTX administration was more than 10 times higher than the MIC80 values for Streptococcus pneumoniae (MIC80 less than or equal to 0.025 microgram/ml) and Klebsiella pneumoniae (0.05 micrograms/ml), 2 of the principal causative organisms of respiratory tract infections. The pattern of change in concentrations of CTX in the serum of these surgical patients was concluded to be similar to the pattern in healthy adult subjects. On the basis of the results summarized above, it appears that CTX is a useful antimicrobial agent for application in the field of respiratory surgery.

Adult↗
PubMed1988

DNA damage induced by ascorbate in the presence of Cu2+.

DNA damage induced by ascorbate in the presence of Cu2+ was investigated by use of bacteriophage phi X174 double-stranded supercoiled DNA and linear restriction fragments as substrates. Single-strand cleavage was induced when supercoiled DNA was incubated with 5 microM-10 mM ascorbate and 50 microM Cu2+ at 37 degrees C for 10 min. The induced DNA damage was analyzed by sequencing of fragments singly labeled at their 5'- or 3'-end. DNA was cleaved directly and almost uniformly at every nucleotide by ascorbate and Cu2+. Piperidine treatment after the reaction showed that ascorbate and Cu2+ induced another kind of DNA damage different from the direct cleavage. The damage proceeded to DNA cleavage by piperidine treatment and was sequence-specific rather than random. These results indicate that ascorbate induces two classes of DNA damage in the presence of Cu2+, one being direct strand cleavage, probably via damage to the DNA backbone, and the other being a base modification labile to alkali treatment. These two classes of DNA damage were inhibited by potassium iodide, catalase and metal chelaters, suggesting the involvement of radicals generated from ascorbate hydroperoxide.

Ascorbic Acid↗
PubMed1986

Sequence-specific modification of DNA by 6-hydroxybenzo[a]pyrene.

6-Hydroxybenzo[a]pyrene cleaved phi X174 supercoiled DNA to open circular DNA in the presence of heavy metal ions. It induced an alkali-labile modification in DNA via an oxygen-radical-mediated reaction; the most frequent alkali-labile sites were on the 3' side of the pyrimidine residues of the pyrimidine cluster.

Bacteriophage phi X 174↗
PubMed1986

Sequence-specific alkali-labile lesions in DNA caused by D-isoglucosamine.

The site-specific induction of DNA damage by 1-amino-1-deoxy-D-fructose (D-isoglucosamine) was investigated. When 32P-end-labeled DNA restriction fragments of known sequence were reacted with D-isoglucosamine in the presence of Cu2+, and the DNA products were analyzed on high-resolution denaturing polyacrylamide gels after treatment with aqueous piperidine (1 M) at 90 degrees C for 30 min, the DNA strands were cleaved at pyrimidine residues at a statistically significant frequency, and 80.5% of the extensively damaged sites were induced at pyrimidine residues in dinucleotide sequences of pyrimidine-purine (5'----3'). These cleavages were scarcely observed without piperidine/heat treatment. The damaged DNA sites increased in proportion to the reaction time and concentration of D-isoglucosamine. Metal-chelating agents (EDTA, diethylenetriaminepentaacetic acid) and some oxygen radical scavengers inhibited the induction of alkali-labile lesions. These results indicate that some oxygen radicals are involved in the induction of alkali-labile lesions.

Base Sequence↗
PubMed1986

Effect of kallikrein-kinin system on calcium-vitamin D3 metabolism.

Kallikrein has been reported to stimulate callus formation and cell proliferation. It is well-known that vitamin D3 play an role on the metabolism of calcium. However, the relation between vitamin D3 and kallikrein are still poorly understood. We have studied the effect of kallikrein on calcium and vitamin D3 with canine kidney. Mongrel dogs were anesthetized with sodium pentobarbital and prepared by the method of Nakanishi et al. Drugs were infused into renal artery for 60 minutes under three different serum calcium concentrations (Exp. I, Exp. II, Exp. III). Blood samples were collected at the midpoint of the 60 minutes urine collection period. Plasma vitamin D3 concentrations were measured by the metabolites of 25-hydroxyvitamin D3 and 1 alpha,25-dihydroxyvitamin D3. 25-hydroxyvitamin D3 was estimated by competitive protein binding assay and 1 alpha,25-dihydroxyvitamin D3 was determined by radioreceptor assay after separated using HPLC. Electrolytes of sodium, potassium, chloride, calcium and phosphorus in serum and urine, plasma cyclic AMP, glomerular filtration rate, renal blood flow and blood pressure were also measured respectively. Plasma 1 alpha,25-dihydroxyvitamin D3 concentration was found to be decreased by the infusion of kallikrein (0.02 KU/kg/min) in three experimental conditions, especially in Exp. II. Bradykinin (0.02 microgram/kg/min) also caused to kallikrein-like changes of vitamin D3. It is suggested that kallikrein-kinin system is related to inhibit the mechanism of vitamin D3 activation system on kidney.

Animals↗
PubMed1986

Hypocarnitinemia in the handicapped individuals who receive a polypharmacy of antiepileptic drugs.

Decrease in the serum concentrations of total and free carnitine were found in patients who had received multiple doses of antiepileptic drugs, either including or excluding sodium valproate. These concentrations were more depressed in a former patient group. In all patients there were no abnormal losses of carnitine in urine. Several factors which may be relevant to the hypocarnitinemia were surveyed statistically. The univariate correlation analyses revealed that in all the patients the total and the free carnitine levels were each correlated with the values of arm muscle circumference, and they were inversely correlated with the dosages of sodium valproate. Double regression analyses again revealed that the value of arm muscle circumference is the most critical positive factor, and dosage of sodium valproate is the most critical negative contributor, to both the total and the free serum carnitine concentrations. There was, however, some additional negative contribution by the dosage of phenytoin to the total carnitine concentration. These results indicate that although sodium valproate itself reduces the carnitine concentrations in serum, a poor muscle volume and co-administration of phenytoin with sodium valproate enhance hypocarnitinemia.

Adolescent↗
PubMed1985

Site-specific DNA damage caused by lipid peroxidation products.

DNA damage induced by autoxidized lipids was investigated using covalently closed circular (supercoiled) DNA and DNA fragments of defined sequence. DNA-strand-breaking substances accumulated during autoxidation of methyl linolenate, and strand breakage was measured with samples taken at different times. The DNA-strand-breaking activity reached its maximum a little after the peak value of peroxide and decreased upon further autoxidation. The peak of the DNA-strand-breaking activity did not always coincide with the peak of thiobarbituric acid reactants or of conjugated diene, either. The DNA-strand-breaking reaction was dependent on metal ions and was inhibited by potassium iodide and tiron and partially by catalase, suggesting the involvement of radical species and/or oxygen radicals. No direct cleavage of singly end-labeled 100-200 basepair DNA fragments by autoxidized methyl linolenate and cupric ion was detected under the conditions used. Cleavage occurred during subsequent heating in piperidine after the reaction. The alkali-labile damage was preferentially induced at pyrimidine residues, especially in dinucleotide sequences of pyrimidine-guanine (5'----3'), which was determined by sequencing.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗