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Biomedical subjects

M Maeda

Publications and source records attributed to M Maeda.

At least 1,297 records · Page 72Linked to original sources
PubMed1985

Chemiluminescence enzyme immunoassay for thyroxin with use of glucose oxidase and a bis(2,4,6-trichlorophenyl)oxalate-fluorescent dye system.

In this chemiluminescence enzyme immunoassay for thyroxin, glucose oxidase (EC 1.1.3.4) is the enzyme label and the bound and free fractions are separated by the double-antibody solid-phase technique. In the assay of enzyme activity, hydrogen peroxide generated from glucose substrate is measured by its chemiluminescence reaction with bis(2,4,6-trichlorophenyl)oxalate and 8-anilino-1-naphthalene-sulfonic acid. The measurable range of thyroxin is 2.5 to 200 micrograms/L. The coefficients of variation for thyroxin concentrations of 43.2 and 12.8 micrograms/L were 7.0% and 8.6% (intra-assay), and 6.4% and 12.3% (interassay), respectively. The proposed method is applicable to large-scale preliminary screening of neonates for congenital hypothyroidism, with samples consisting of dried blood spotted on filter paper.

Congenital Hypothyroidism↗
PubMed1985

Nicolas Andry Award, 1984. Deleterious interactions of immune complexes in cartilage of experimental immune arthritis. I. The erosion of pannus-free hyaline cartilage.

Immune complexes were detected by plain and immunoelectron microscopy amongst electron-dense material that rapidly formed and extended over and into the cartilaginous surfaces of immune arthritic rabbits' knees. The sinuous extension of electron-dense material into the surface matrix was associated with fragmentation and detachment, resulting in erosions. The findings implicate the formation of immune complexes in the destructive process of the matrix. Since the eroded pannus-free matrix of rheumatoid cartilage surfaces contains extensive concentrations of immune complexes, the data of this immune arthritis model suggest a causative relation between immune complexes and matrix loss in rheumatoid arthritis.

Animals↗
PubMed1985

The metabolic response of intrasplenic islet autografts.

Islet tissue was prepared by collagenase ductal perfusion in mongrel dogs and transplanted to the spleen as autografts following total pancreatectomy. The graft was introduced into the spleen by reflux through tributaries of the splenic vein. Total insulin output by the in situ islet cell mass and by the heterotopically transplanted islet cell mass was studied by measuring insulin in the portal vein prior to pancreatectomy and two weeks after grafting. Basal insulin as well as the insulin output in response to 0.5 gram per kilogram of intravenous glucose were measured. Normoglycemia was achieved immediately in all grafted dogs. The results of intravenous glucose tolerance testing suggested only a mild degree of carbohydrate intolerance in the grafted dogs. Insulin output in 60 minutes after glucose stimilation was similar for in situ and grafted islet cells. The results of glucose clamp studies did not reveal any significant change in the insulin sensitivity of grafted as opposed to normal dogs. Islets of Langerhans may be harvested by the ductal perfusion method to yield a completely adequate islet cell mass for grafting purposes in the canine model following total pancreatectomy.

Animals↗
PubMed1985

Failure of canine islet allografts and autografts with cyclosporine.

Intrasplenic autotransplantation of islet fragments prepared by ductal perfusion constitutes a reproducible system for islet delivery to apancreatic dogs. The animals are normoglycemic from the time of grafting, and graft failure is rare. In this study, apancreatic dogs received islet autografts (controls), autografts plus oral cyclosporine, and allografts plus oral cyclosporine. Therapeutic blood levels of cyclosporine were documented by radioimmunoassay. However, allografts and autografts ceased to function after initial normoglycemia in all animals that received cyclosporine, and four out of six autografts failed. Normoglycemia persisted in the control-autografted animals for the duration of the study. Microscopic sections of the failed grafts demonstrated meager tissue survival but no evidence of rejection by cellular infiltration.

Animals↗
PubMed1985

[A case of pycnodysostosis].

Pycnodysostosis is a term introduced by Maroteaux and Lamy in 1962 to describe characteristic features such as dwarfism, separated cranial sutures, open fontanelles, hypoplasia and absence of mandibular angle, partial aplasia of the terminal phalanges of the fingers and toes, generalized condensation of bone shadow, bone fragility, and autosomal recessive inheritance. We reported a such case in a 13-years old boy associated with an epidural hematoma. Four weeks after removal of the hematoma, lumbar puncture was performed with the initial pressure of 200mm H2O in an awake state and the plateau waves were observed several times during sleep. Such increased intracranial pressure may have caused the open fontanelle and cranial sutures in addition to dysostosis. Thus such patients require careful attention in order to prevent major bleeding from the superior sagittal sinus directly beneath the separated sagittal suture.

Adolescent↗
PubMed1985

[Focal nodular hyperplasia-like lesion of the liver associated with thorotrast liver disease--report of a case].

A 66-year-old man with Thorotrast liver disease underwent a partial hepatectomy for a small tumor of the liver, which was demonstrated by digital subtraction angiography. The resected specimen was grossly a sharply circumscribed, gray-yellow nodule, 7.5 mm in diameter. Microscopically, the nodule was an ill-defined hepatic cell mass, which was divided by fine fibrous septa irregularly and incompletely. Central veins and Glisson's capsules were not observed inside the nodule. Bile duct proliferation and infiltration of lymphocytes were found in the fibrous septa. There were Thorotrast depositions within the fibrous tissues around the nodule. Because a typical fibrous boundary and central scar were not found, we have termed this condition a focal nodular hyperplasia-like lesion. A relationship between focal nodular, hyperplasia as a precancerous state and Thorotrast liver disease was suggested.

Aged↗
PubMed1985

Synthesis of 1-beta-D-ribofuranosyl-1,2-dihydropyrimidin-2-one derivatives and their biological activities.

Several alkyl substituted 1-beta-D-ribofuranosyl-1,2-dihydropyrimidin-2-one derivatives were synthesized by the method of stannic chloride-catalyzed glycosidation method to elucidate their inhibitory activity of cytidine deaminase and also their antitumor activities in vitro and in vivo. Alkyl substitution at position 4 or 6 of the derivatives decreased their inhibitory activity for cytidine deaminase and also decreased antitumor activity against L1210 cells in vitro.

Animals↗
PubMed1984

pH-dependent Ca2+ interaction with phospholipids related to phosphatidylethanolamine N-methylation.

The interactions of PE and its N-methylated derivatives (PME, PDE AND PC) WITH Ca2+ were examined. PE and the intermediate phospholipids of PE N-methylation (PME and PDE) interacted with Ca2+ in a pH-dependent and reversible manner. When these phospholipids were present in the heptane phase, Ca2+ in the aqueous phase was translocated into the heptane phase at alkaline pH but not at acidic pH. PDE was also effective for the translocation even at around neutral pH, while PC hardly translocated Ca2+ at pH 6.0-9.2. The amounts of Ca2+ interacting with these phospholipids were in the following order: PDE is greater than PME is greater than PE is much greater than PC. P1, phosphatidic acid and PS interacted with Ca2+ in the whole pH range examined. The Ca2+ interactions with P1 and phosphatidic acid were independent of pH, while PS interacted with more Ca2+ at alkaline pH. These phospholipids interacted with Ca2+ most strongly among the cations studied. Liposomes containing PDE also bound the highest amounts Ca2+ among PE and its N-methylated derivatives. Furthermore, mammalian cultured cell membranes, which contain increased amounts of PDE by in vivo modification with N,N'-dimethylethanolamine, bound more Ca2+ than those prepared from choline-treated control cells.

Animals↗
PubMed1984

Regulation of phosphatidylcholine metabolism in mammalian cells. Isolation and characterization of a Chinese hamster ovary cell pleiotropic mutant defective in both choline kinase and choline-exchange reaction activities.

By means of an in situ autoradiographic assay for the base-exchange reaction of phospholipids with L-serine in Chinese hamster ovary cell colonies immobilized on filter paper ( Esko , J.D. and Raetz , C.R.H. (1978) Proc. Natl. Acad. Sci. U.S.A. 75, 1190-1193), a mutant (designated 89.1) was isolated in which the specific activity of the serine-exchange enzyme was about 2-fold less than in the parent. Unexpectedly, it was demonstrated that in extracts of the mutant the specific activities of both ATP:choline phosphotransferase (choline kinase) (EC 2.7.1.32) and the enzyme that catalyzes the base-exchange of phospholipids with choline (choline-exchange enzyme) were strikingly reduced (3- to 4-fold and 10- to 15-fold, respectively), while the specific activities of other enzymes of phosphatidylcholine synthesis were normal. Several lines of evidence presented here suggested that the partial defect of serine-exchange activity in this mutant was due to a decrease of acceptor phospholipid(s) for the reaction. The growth rates and phospholipid compositions of the mutant and parent were quite similar. However, mutant 89.1 exhibited a significant defect in its ability in vivo to synthesize phosphatidylcholine. The fact that the mutant was also defective in phosphorylcholine biosynthesis in vivo, together with the finding of an enzymatic lesion of the mutant in choline kinse in vitro as described above, clearly demonstrated that with respect to the reduced phosphatidylcholine biosynthesis the primary defect was at the level of choline kinase. In addition to the decreased synthetic rate of phosphatidylcholine, the turnover rate of phosphatidylcholine was also reduced approximately 2-fold in this mutant. These decreased rates of both synthesis and degradation of phosphatidylcholine probably account for the identical phosphatidylcholine contents between the mutant and parent. As a conclusion, it may be given that strain 89.1 is a pleiotropic mutant which possesses several alterations in phosphatidylcholine metabolism, and such mammalian mutants have not been isolated previously.

Animals↗
PubMed1984

Neurological control of fetal heart rate in 20 cases of anencephalic fetuses.

Fetal heart rate (FHR) is influenced by the central nervous system, cardiac automatism, biochemical factors, etc. Changes in FHR were correlated with the anatomic defect in autopsy material from 20 anencephalic infants, and, on this basis, the following hypotheses were formed, subject to later experimental proof. (1) The FHR baseline level is controlled by the medulla oblongata and vagus nerve. (2) The biphasic sleep-awake pattern is controlled by the cerebral cortex. (3) The midbrain is involved in the occurrence of acceleration. (4) A relative high level of short-term variability is shown when small lesions of the lesser central nervous system are present, but we cannot conclude that the cortex is critical for short-term variability. On the other hand, long-term variability seems to be correlated to the presence of the medulla oblongata and midbrain, and might be amplified by the cerebral cortex. (5) U-shaped decelerations are connected with the medulla oblongata, but V-shaped decelerations depend on intracardiac reflexes and myocardial stretch.

Anencephaly↗