Search PubMed⌕ Search

Biomedical subjects

N Kono

Publications and source records attributed to N Kono.

At least 163 records · Page 9Linked to original sources
PubMed1989

Demonstration of interleukin-1 beta on perifollicular endothelial cells in the thyroid glands of patients with Graves' disease.

We examined the presence of interleukin-1 (IL-1) in the thyroid glands of 20 patients with Graves' disease and 10 control subjects, using anti-IL-1 monoclonal antibodies in conjunction with immunohistochemical techniques. In 13 (65%) Graves' disease patients, IL-1 beta, but not IL-1 alpha, was demonstrated on the capillary endothelial cells (EC) around follicles (perifollicular EC). However, the EC of arteries and veins were negative for both IL-1 beta and IL-1 alpha. In the control group, none of the thyroid glands showed positive staining for IL-1 beta or IL-1 alpha. There was a significant correlation (P less than 0.025) between the presence of IL-1 beta on perifollicular EC and the presence of serum antimicrosomal antibodies. These results provide an important insight into the involvement of IL-1 beta in the development of Graves' disease.

Adolescent↗
PubMed1989

Localization of actin and cytokeratin in hepatocytes and biliary epithelial cells in normal human livers using a low temperature resin and post-embedding immunohistochemistry.

Using a low temperature resin Lowicryl K4M and post-embedding immunogold labeling, localization of actin and cytokeratin was examined in hepatocytes and biliary epithelial cells in normal human livers. Preservation of the liver tissues was satisfactory at the electron microscopic level. In immunolabeling of actin, gold particles were mainly found on microvilli and around the junctional complexes and at cell borders in the hepatocytes as well as biliary epithelial cells. In immunolabeling of cytokeratin, the gold particles were rather preferentially found in the perinuclear cytoplasm and around the junctional complexes in the biliary epithelial cells and hepatocytes. These particles were mainly found to be located on the intermediate filaments at higher magnification, although a considerable number of intermediate filaments were not labeled in the hepatocytes and biliary epithelial cells. Double straining method using the gold particles of different sizes clearly confirmed the abovementioned distribution of actin and cytokeratin in the same cells. From these observations, it was suggested that post-embedding immunoelectron microscopy using Lowicryl K4M is a useful tool for analysis of cytoskeletal organization in the liver tissue.

Actins↗
PubMed1989

Glucagonostatic and insulinotropic action of glucagonlike peptide I-(7-36)-amide.

We examined the effect of glucagonlike peptides (GLPs), which are cleaved from preproglucagon in the enteroglucagon cells, on rat endocrine pancreas with the isolated perfused system. GLP-I-(7-36)-amide, a truncated form of full-sequence GLP-I-(1-37), showed a potent inhibitory effect on glucagon secretion. This inhibitory effect of GLP-I-(7-36)-amide was demonstrated at concentrations of 0.25, 2.5, and 25 nM in 11.2 and 2.8 mM glucose. In contrast, insulin release was significantly stimulated by GLP-I-(7-36)-amide at its concentration from 0.025 to 25 nM in a high glucose concentration, whereas in a low glucose concentration, the stimulation was seen only at the highest concentration (25 nM). Neither GLP-I-(1-37) nor GLP-II showed any effect on glucagon and insulin release. Although several gastrointestinal hormones have been nominated as incretins, none of them may suppress the glucagon secretion. A truncated form of GLP-I, GLP-I-(7-36)-amide thus seems to be a unique incretin that exerts glucagonostatic action.

Animals↗
PubMed1989

Occurrence of Yersinia enterocolitica in the Tokyo Tama Zoo.

Yersinia enterocolitica serogroups O5A and O8 were isolated from fecal samples of one colony of Japanese macaques (Macaca fuscata) from the Tokyo Tama Zoo (Japan). Serogroup O5A was detected in brown bear (Ursus arctos) prior to the isolation from the macaques. Serogroup O5A organisms also were isolated from the Japanese macaques' breeding area. Serogroup O5A and O8 isolates were not pathogenic. Serogroup O8 isolates did not possess the O7 or O19 antigens.

Animals↗
PubMed1989

Hepatic calcification in proliferated bile ductules in a uremic patient.

Hepatic calcification in uremia is rare and, to our knowledge, only two cases have been reported in the English literature. In both previous reports, calcification was found in the damaged hepatocytes in the centrilobular to midzonal area of the hepatic lobules. The patient, a 61-year-old man, was uremic due to diabetic nephropathy. He had suffered posttransfusion hepatitis just before his death. Antemortem radiographic examination of the abdomen failed to visualize the calcification in the liver. At autopsy, microscopic examination of the liver revealed bile ductular proliferation and calcification mainly in the ductular epithelial cells. We suggest that calcification could occur preferentially in abnormally proliferated ductules when the serum calcium and serum phosphorus products are elevated.

Bile Ducts, Intrahepatic↗
PubMed1989

Hepatic granulomata in long-term hemodialysis patients with hyperaluminumemia.

We describe two long-term hemodialysis patients with hyperaluminumemia, in whom multiple granulomata were found in the livers at autopsy. The granulomata were mainly composed of modified macrophages, and aluminum was constantly detected in the cytoplasm of these macrophages by histochemical analysis, as well as by X-ray microanalysis. These granulomata were also found in the spleen and lymph nodes. The constant presence of aluminum in the mononuclear phagocytic system might have been followed by the development of granulomata. Functional disturbances of the liver were not evident.

Adult↗
PubMed1988

Trophic effect of glucagon-(1-21)-peptide on the isolated rat ileal mucosal cells.

The trophic effect of glucagon-(1-21)-peptide on rat ileal epithelial cells was studied in vitro. Glucagon-(1-21)-peptide stimulated [3H]thymidine incorporation of mucosal cells significantly in a dose-dependent manner. Then glucagon-related peptides which have common sequences with glucagon-(1-21)-peptide were also tested. The biological potencies to augment [3H]-thymidine uptake were closely related with their amino-acid residues of N-terminal region. The result suggests that the N-terminal amino-acid sequence of glucagon molecule plays an important role in intestinal cell growth.

Amino Acid Sequence↗
PubMed1988

Molecular analysis of peroxisomal beta-oxidation enzymes in infants with Zellweger syndrome and Zellweger-like syndrome: further heterogeneity of the peroxisomal disorder.

The biosynthesis of enzymes of peroxisomal beta-oxidation was investigated in an attempt to elucidate the mechanism of deficiencies of proteins of these enzymes in 3 infants with Zellweger syndrome and in a baby with Zellweger-like syndrome with clinical and biochemical findings consistent with Zellweger syndrome except that the peroxisomes were detected electronmicroscopically. Enzyme proteins of peroxisomal beta-oxidation, acyl-CoA oxidase, bifunctional protein and 3-ketoacyl-CoA thiolase were hardly detectable, in both syndromes. Total hepatic RNA extracted from the liver of one patient with each syndrome and three controls was translated in a rabbit reticulocyte lysate protein-synthesizing system in the presence of [35S]methionine. Translatable mRNAs for all of the peroxisomal beta-oxidation enzymes were detected in both patients at much the same levels seen in the controls. Pulse labelling and chase experiments of fibroblasts from the control revealed that the 72 kDa subunit of acyl-CoA oxidase was first synthesized, after which the 52 kDa and 21 kDa subunits were processed from the 72 kDa subunit. In the patient with Zellweger syndrome, little of the 52 kDa and 21 kDa subunits of acyl-CoA oxidase were synthesized. The mature form of peroxisomal 3-ketoacyl-CoA thiolase was also not processed from its precursor form, in this patient. We consider that Zellweger-like syndrome is a new variant form of a peroxisomal disorder in which biogenesis of peroxisomes is intact, while in contrast, the biogenesis of peroxisome is considered to be defective in those with Zellweger syndrome. Multiple defects of enzymes of beta-oxidation in Zellweger-like syndrome are assumed to be caused by a defect of transport or localization of these enzymes. Our molecular analyses indicate that the enzymes of peroxisomal beta-oxidation are synthesized in patients with Zellweger and Zellweger-like syndrome but that these enzymes are not processed normally and are degraded rapidly.

Abnormalities, Multiple↗
PubMed1988

Resistance of the peripheral nerve to ischemia in diabetic patients--an electrophysiological study.

We studied the effect of ischemia on the excitability of the sensory fibers of the median nerve in 43 patients with non-insulin-dependent diabetes mellitus (NIDDM) by a double stimulation method. Ischemia caused significantly less reduction of nerve excitability in patients with poor glycemic control and in patients diseased for 5 years or longer than in the normal control group. Hyperexcitability after ischemia was markedly greater than normal among short-term, poorly controlled diabetics, and markedly less pronounced among long-term, poorly controlled diabetics. In many diabetic patients with normal conduction velocity or without sensory disturbance, post-ischemic hyperexcitability was remarkable. A study of nerve excitability may be useful as one means of detecting early-stage disturbance of the diabetic peripheral nerve.

Adult↗
PubMed1988

Survey of copper granules in liver biopsy specimens from various liver abnormalities other than Wilson's disease and biliary diseases.

Copper granules in hepatocytes were examined by the p-dimethylaminobenzylidene rhodanine method in 965 liver biopsy specimens obtained from patients with various liver abnormalities other than Wilson's disease and biliary diseases. The granules were found in chronic active hepatitis (incidence of positive cases: 17.2%) and alcoholic fibrosis (22%) with lobular disarray and fibrosis, nonbiliary liver cirrhosis (28%), and drug-induced cholestasis (15%). Copper granules were present in the periportal or periseptal hepatocytes where the granules were mainly found in the perinuclear cytoplasm. These intracellular and intralobular distribution patterns of copper granules resembled those of primary biliary cirrhosis. These data suggest that hepatic fibrosis and lobular disarray with fibrosis in these chronic liver disease may lead to distortion or interruption of small biliary branches followed by disturbance of bile flow and deposition of copper granules. Copper stain seems to provide a valuable information for assessment of progression of these chronic liver diseases. Impaired biliary excretion seems important in deposition of copper granules in drug-induced cholestasis.

Biliary Tract Diseases↗
PubMed1988

Transcatheter arterial chemo-embolization for humoral hypercalcemia of hepatocellular carcinoma.

A 50-year-old male with unresectable hepatocellular carcinoma (HCC) had a hypercalcemic crisis with a serum calcium concentration of 7.8 mEq/zeta, without any evidence for bone metastases or parathyroid lesions. The hypercalcemia was thought to be due to increased renal reabsorption of calcium and increased bone resorption, which was probably caused by humoral factors derived from the HCC, some being parathyroid hormone-like factors. Since conservative therapy for hypercalcemia was not sufficiently effective and was accompanied by progressive exacerbation of ascites and leg edema, transcatheter arterial chemo-embolization (TACE) was performed. On the following day, serum calcium concentration decreased from 6.3 mEq/zeta to the normal range, although serum alpha-fetoprotein levels decreased only slightly. Thereafter hypercalcemia did not develop for about 4 weeks. The results demonstrated that TACE can be effective for humoral hypercalcemia of HCC.

Carcinoma, Hepatocellular↗
PubMed1988

Zellweger-like syndrome with detectable hepatic peroxisomes: a variant form of peroxisomal disorder.

A male infant with typical clinical and biochemical findings of Zellweger syndrome, but in whom hepatic peroxisomes were detected by electron microscopy, had profound hypotonia, hepatomegaly, typical facial appearance including large fontanelle and frontal bossing, convulsions, panaminoaciduria, and hyperammonemia. He died of liver failure at age 5 months. There were increased levels of very long chain fatty acids and trihydroxycoprostanic acid in serum, and increased excretion of dicarboxylic acids and tyrosine metabolites in the urine. Levels of peroxisomal enzymes, acyl coenzyme A oxidase, bifunctional protein, 3-ketoacyl coenzyme A thiolase, and dihydroxyacetone phosphate acyltransferase in the liver tissue from the patient were all deficient, findings consistent with Zellweger syndrome. However, immunocytochemical study and electron microscopic examination of the liver at autopsy revealed that hepatic peroxisomes were present at a level similar to that in a control subject. These observations suggest further heterogeneity in Zellweger syndrome and a different pathogenesis in this variant case.

Bile Acids and Salts↗
PubMed1988

Increases in hepatic fructose-2,6-bisphosphate level and fructose-6-phosphate,2-kinase activity in rats with ventromedial lesions of the hypothalamus.

To investigate altered fructose-2,6-bisphosphate (fructose-2,6-P2) metabolism, we measured fructose-2,6-P2 levels and fructose-6-phosphate,2-kinase (fructose-6-P,2-kinase) activities in various tissues, including liver, kidney, heart, and skeletal muscle, of ventromedial hypothalamus (VMH)-lesioned rats during feeding and starvation. The plasma insulin level was 6 times or more higher in these rats than in the controls. The fructose-2,6-P2 level in liver was much greater in VMH-lesioned rats than in the controls: 15.1 +/- 2.2 nmol/g tissue versus 7.7 +/- 0.7 in the fed state, 5.3 +/- 1.1 versus 1.6 +/- 0.4 in the starved state. In kidney, heart, and skeletal muscle, fructose-2,6-P2 levels were not different between the two animal groups. The activity of hepatic fructose-6-P,2-kinase remained high after 20 h of starvation in VMH-lesioned rats, whereas it was decreased markedly in the controls. The hepatic concentration of fructose-6-phosphate was also high in VMH-lesioned rats. Both fructose-6-P,2-kinase activity and fructose-6-phosphate concentration in the liver of starved VMH-lesioned rats were comparable to those of control rats in fed conditions. These results indicate that the alteration of fructose-2,6-P2 metabolism is characteristic of liver in VMH-lesioned rats, and that the increase in hepatic fructose-2,6-P2 may activate hepatic glycolysis not only during feeding but also during starvation, leading to the enhanced lipogenesis in these obese rats.

Animals↗