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Biomedical subjects

M Kudo

Publications and source records attributed to M Kudo.

At least 397 records · Page 22Linked to original sources
PubMed1986

Concept of the clinical stages of acute hepatic failure.

Serial medical diagnostic imagings were performed on 15 patients with acute hepatic failure to compare liver size and clinical picture. In patients showing hepatatrophy at the onset of coma, the interval between the onsets of disease and coma was long, ascites and edema supervened, high total bilirubin and low glutamic pyrubic transaminase levels tended to be found, and prothrombin time did not respond to treatment. All of these patients died. Based on liver size changes in patients who survived acute hepatic failure, acute hepatic failure was assumed to be classified into swelling, reduction, and recovery stages. The shorter the interval between the onsets of disease and coma, the earlier coma and prolonged prothrombin time occurred before hepatatrophy. In acute hepatic failure, signs of hepatic failure develop with various histological pictures and it is very important to institute the treatment before the liver is atrophied.

Acute Disease↗
PubMed1985

Morphology and laminar organization of electrophysiologically identified neurons in the primary auditory cortex in the cat.

The morphology of electrophysiologically identified neurons was examined in the primary auditory cortex (AI) of the cat. After stimulation of the medial geniculate nucleus (MG), second auditory cortex, posterior ectosylvian gyrus, contralateral AI, or corpus callosum, intracellular potentials were recorded from AI neurons, which were then injected intracellularly with horseradish peroxidase and recovered. Layer IV neurons, which receive MG fibers monosynaptically, are spiny and nonspiny stellate cells, small and medium-sized nonspiny tufted cells, and fusiform cells. They send their axons to layer III of the AI. Corticocortical AI neurons are medium-sized pyramidal cells in layer III. They receive axons from layer IV neurons of the AI and send their axons to layers I, II, IV, and V of the AI. Horizontal cells in layer I receive slow-conducting MG fibers monosynaptically, and send their axons to layer II of the AI. Stellate cells and small pyramidal cells in layer II receive afferent inputs polysynaptically from the MG. Layer II pyramidal cells receive afferent inputs from the MG via AI neurons in layers I and III, and send their axons to layers V and VI. The axons of layer II stellate cells were distributed within layer II. Pyramidal cells which send their axons to the MG are located in layers V and VI, distributing their axon collaterals to layers III-VI of the AI.

Animals↗
PubMed1985

Acidic glycosaminoglycans of SV40-transformed Werner's syndrome cells.

Acidic glycosaminoglycans (AGAGs) were isolated from the culture fluids of a SV40-transformed permanent line (PSV811) of the Werner syndrome skin cells and of a SV40-transformed permanent line (VA13) of WI-38 normal lung cells. The relative composition of component AGAGs was estimated by acetate membrane electrophoresis followed by Alcian blue staining and desitometry. Hyaluronic acid (HA) was the major AGAG component in all the preparations tested. The relative content of HA fluctuated considerably among the preparations obtained in independent experiments and among the results using three different buffer systems. However, the proportion of HA was persistently greater in PSV811 culture fluid than in VA13 culture fluid. VA13 cells released an appreciable amount of heparan sulfate as the second major AGAG component, but PSV811 released only a small amount. These results show a difference between the two cell lines, and suggest that PSV811 may possibly reflect the association of the Werner syndrome with abnormal HA metabolism.

Cell Transformation, Viral↗
PubMed1985

Cystic dysplastic kidneys associated with Dandy-Walker malformation and congenital hepatic fibrosis. Report of two cases.

The combined abnormalities of Dandy-Walker malformation, congenital hepatic fibrosis, and generalized cystic dysplastic kidneys were found in two sanguineously unrelated premature babies. This type of cerebrohepatorenal malformation is certainly unique and is generally diagnosed based on the characteristic renal lesion. Remarkably, similar renal lesions have been found in Meckel's syndrome, Goldston's syndrome, and Miranda's syndrome. The present cases can be distinguished from Meckel's syndrome on the basis of the presence of Dandy-Walker malformation and the absence of polydactyly and occipital meningoencephalocele. Although the authors' cases resemble the latter two syndromes in terms of the presence of Dandy-Walker malformation, it is tentatively considered that the distinct triads found in the present cases could represent a new variant of a multiple malformation syndrome with generalized cystic dysplastic kidneys. The etiology of these cases remains unclear, but a genetic factor, which has been suggested as for other syndromes, might be involved.

Abnormalities, Multiple↗
PubMed1985

Immunoreactive myelin basic protein in tumor cells associated with carcinomatous neuropathy.

Tumors from two patients with carcinomatous neuropathy were studied with an immunohistochemical method using anti-myelin basic protein (anti-MBP) sera. In both cases, immunoreactive MBP was clearly demonstrated in some of the tumor cells, which were widely distributed either singly or, more often, in clusters. The staining intensity varied from cell to cell. An autoimmune mechanism to nervous elements has been suggested in the pathogenesis of carcinomatous neuropathy. MBP is known to be a highly specific and potent antigen that can induce allergic neuritis in animals. In one patient the progressively worsening neurologic condition rapidly improved after gastrectomy removed the carcinoma. It is possible that immunoreactive MBP in tumor cells may function as an "antigen" in the development of carcinomatous neuropathy.

ACTH Syndrome, Ectopic↗
PubMed1985

Purification and some properties of a membrane-bound dipeptidyl peptidase IV of guinea pig casein-induced intraperitoneal leukocytes.

Dipeptidyl peptidase IV [EC 3.4.14.5] (DPP-IV) was demonstrated to exist in guinea pig casein-induced, peritoneal polymorphonuclear leukocytes (PMN) as well as contaminating macrophages and lymphocytes through the use of glycyl-L-prolyl-4-methylcoumaryl-7-amide (Gly-Pro-MCA) as a substrate. The DPP-IV of PMN was found to be located both on the plasma membrane and in the cytosol. For characterization, the plasma membrane-bound enzyme isolated from peritoneal cells mainly consisting of PMN was solubilized with 0.1% Triton N101 and purified by DEAE-cellulose chromatography, gel filtration, and affinity chromatographies on concanavalin A-Sepharose 4B and Gly-Pro-Sepharose 4B. The purification was more than 570-fold. The purified enzyme appears to be a noncovalent dimer of the 158K dalton DPP-IV. The pH optimum, isoelectric point and Km value for Gly-Pro-MCA were 7.2, 5.5, and 2.0 X 10(-4)M, respectively. The enzyme was inactivated by diisopropyl fluorophosphate and diprotin A. It was capable of cleaving dipeptidyl-MCA of an X-Pro-MCA type (X: free N-terminal amino acid). These properties are similar to those of DPP-IV purified from other tissues.

Animals↗
PubMed1985

Accumulation of Tc-99m methylene diphosphonate in calcified metastatic lesions of the liver from colonic carcinoma. Comparison with calcification on X-ray computed tomogram.

Abnormal accumulation of Tc-99m MDP in two metastatic lesions of the liver was observed in a patient with resected colon carcinoma. Single-photon emission computed tomography (SPECT) revealed characteristic marginal accumulation of Tc-99m MDP in both of those metastatic lesions. X-ray CT showed the corresponding marginal calcification in one of the metastases, but no apparent calcification was observed in the other lesion. Two months later, however, the latter also became calcified on x-ray CT. These findings suggest that the accumulation of Tc-99m MDP in the present case is strongly related to the calcium deposition and that Tc-99m MDP may accumulate in a calcified metastatic lesion before the calcification appears on x-ray CT.

Calcinosis↗
PubMed1985

Partial restoration of cerebral myelination of the congenitally hypothyroid mouse by parenteral or breast milk administration of thyroxine.

We attempted to define whether thyroid hormone can ameliorate the cerebral hypomyelination present in the congenitally hypothyroid (hyt) neonatal mouse, and to define the critical time period during early postnatal life when thyroxine (T4) is essential for myelin formation. We administered T4 to the hyt mouse by breast milk during the first 20 days of postnatal life, and through the diet during the second 20 days of postnatal life. Positive results were obtained only when hormone was given during the first 20 days of postnatal life. A distinct increase in cerebral 2',3'-cyclic nucleotide 3'-phosphohydrolase activity was noted, and brain sections stained for myelin basic protein correlated with the biochemical findings. The later administration of hormone through diet was ineffective.

Administration, Oral↗