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Y Amano

Publications and source records attributed to Y Amano.

226 records · Page 13Linked to original sources
PubMedDate not supplied

Gd-DTPA enhanced MRI of reactive hematopoietic regions in marrow.

OBJECTIVE: The purpose of this report was to study the contrast enhancement of reactive hematopoietic regions in bone marrow on Gd-diethylenetriamine pentaacetic acid (DTPA) enhanced MRI. MATERIALS AND METHODS: We compared the contrast enhancement of reactive hematopoietic regions in the marrow of patients with aplastic anemia and drug-induced pancytopenia and that of normal bone marrow on Gd-DTPA enhanced MRI. RESULTS: The reactive hematopoietic marrow observed in aplastic anemia of moderate grade and drug-induced pancytopenia markedly enhanced after Gd-DTPA administration; normoplastic marrow showed no enhancement. CONCLUSION: Gd-DTPA enhanced MRI was useful in detecting the reactive hematopoietic regions in bone marrow.

Adult↗
PubMedDate not supplied

MR signal changes in bone marrow of mandible in hematologic disorders.

OBJECTIVE: Signal intensity changes in bone marrow of the mandible were observed in cases with hematologic disorders. MATERIALS AND METHODS: Using MRI, bone marrow intensity of the mandible was observed in six patients with polycythemia vera, acute leukemia, myelofibrosis, and malignant lymphoma. A control group was also evaluated for comparison. RESULTS: The bone marrow of the condyloid process of the mandible converts to yellow marrow in early childhood. Therefore, T1-weighted imaging showed the marrow of the mandible to have a high signal intensity similar to that of fat in the control cases. In contrast, the bone marrow of the mandible in the patients exhibited lower intensity than that of fat and was enhanced after Gd-DTPA injection. CONCLUSION: In hematologic diseases MRI detected the signal changes of the mandible. More attention should be focused on the marrow intensity of the mandible in the routine cranial MR examinations in patients with hematologic disorders.

Adolescent↗
PubMedDate not supplied

Proton MR imaging and spectroscopy evaluation of aplastic anemia: three bone marrow patterns.

PURPOSE: The purpose of this study was to classify bone marrow intensity patterns in aplastic anemia with proton MRI and to compare them with MR spectroscopic findings quantitatively and qualitatively. METHOD: Twelve patients with aplastic anemia and six normal volunteers were examined with a 1.5 T MR unit. T1-weighted SE, fast STIR, and opposed-phase T1-weighted RF-spoiled GE images (op-SPGR) were acquired with MR images, while MR spectroscopy was performed with a stimulated echo acquisition mode without water suppression. RESULTS: Three bone marrow patterns were determined in aplastic anemia with MR images: marrow a with low intensity on fast STIR and high intensity on T1-weighted imaging and op-SPGR, marrow b with low intensity on T1-weighted imaging and op-SPGR and high intensity on fast STIR, and marrow c with low intensity on T1-weighted imaging and high intensity on fast STIR and op-SPGR. MR spectroscopy quantitatively showed that the ratio of water to fat of marrow a significantly decreased (mean 0.41) and that of marrow c increased (mean 3.40) compared with those of marrow b (mean 1.09) and normal bone marrow (mean 1.04). There were no differences of the types of fat signals between aplastic anemia and normal bone marrow with MR spectroscopy. CONCLUSION: MR imaging and spectroscopy were noninvasive methods of classifying bone marrow patterns and quantifying bone marrow content in aplastic anemia, which may improve the results currently obtained with biopsy.

Adolescent↗
PubMedDate not supplied

Classification of hematopoietic regions in out-of-phase T1-weighted images: a quantitative comparison study with T1-weighted and STIR images.

The hematopoietic regions were classified into two groups on the basis of out-of-phase T1-weighted images (op-T1WI): regions with lower intensity than that of muscle (LH) and regions with intensity equal to or higher than that of muscle (HH). We quantitatively evaluated the differences in signal intensity between LH and HH in order to examine this classification. Forty-two hematopoietic areas in aplastic anemia were classified into two groups of 23 LH and 19 HH. The signal ratios of hematopoietic areas to muscle on T1WI and STIR were calculated, and the differences between LH and HH were statistically evaluated. The signal ratios of LH were significantly higher on T1WI and lower on STIR than those of HH (unpaired t-test, p < 0.05). This result indicated that LH consisted of more hypocellular marrow than HH. Op-T1WI were useful in differentiating between LH and HH and defining the degree of hematopoiesis in aplastic anemia.

Adipose Tissue↗
PubMedDate not supplied

Gastric carcinoma metastasis to calf muscles: MR findings.

We report the MR findings of a rare case of gastric carcinoma metastasis to muscles in the calf. T2-weighted images showed the diffuse enlargement of skeletal muscles in the calf with remarkable hyperintensity.

Adenocarcinoma↗
PubMedDate not supplied

Calcium mobilization during nicotine-induced cell death in human glioma and glioblastoma cell lines.

Nicotine dose-dependently induced cytotoxicity in human glioma (KG-1-C) and glioblastoma (GBS-1, T98G) cell lines, but could not induce internucleosomal DNA cleavage, in contrast to apoptosing human myelogenous leukemic cell lines. Human glioma/glioblastoma cell lines thus might have a chromatin structure resistant to endonuclease digestion. Nicotine induced a rapid increase in the intracellular calcium concentration. Confocal experiments with Fluo-3 fluorescence revealed that nicotine elevated the free Ca2+ concentration in both nuclear and cytoplasmic regions of the cells, and the elevation of Ca2+ in the nuclear region was more pronounced than that of the cytoplasmic region. The present study suggests that nuclear accumulation of Ca2+ is an important initial step for cell death induction by nicotine.

Apoptosis↗
PubMedDate not supplied

Uncoupling of incorporation of ascorbic acid and apoptosis induction.

Exposure of human promyelocytic leukemic HL-60 cells to millimolar concentration of sodium ascorbate induced apoptotic cell death. The extent of apoptosis induction was a positive function of temperature at the time of exposure. The incorporation of [1-14C] ascorbic acid into the cytosolic fraction of HL-60 cells was also temperature-dependent, and competitively inhibited by active analogs (L-ascorbic acid, sodium L-ascorbate, D-isoascorbic acid, sodium 6-beta-O-galactosyl-L-ascorbate, sodium 5,6-benzylidene-L-ascorbate), but not by inactive analogs (L-ascorbic acid-2-phosphate magnesium, L-ascorbic acid 2-sulfate). Calcium depletion, which had considerably reduced the apoptosis-inducing activity of sodium ascorbate, did not affect the intracellular incorporation of [14C] ascorbic acid. These data suggests that cell death might not be simply induced by the intracellular incorporation of ascorbate, but rather initiated by the rapid elevation of intracellular Ca2+ concentration, possibly mediated by an as yet unidentified temperature-sensitive mechanism.

Apoptosis↗
PubMedDate not supplied

Induction of DNA fragmentation by nicotine in human myelogenous leukemic cell lines.

The effect of nicotine, a component of tobacco, on the cytokine production and cell growth of various cultured cells was investigated. Nicotine did not stimulate, but rather inhibited the tumor necrosis factor production by human peripheral blood mononuclear cells at higher doses. Cytotoxic concentrations of nicotine did not induce the monocytic and granulocytic differentiation of human myelogenous leukemic cell lines (HL-60, ML-1). Nicotine induced internucleosomal DNA cleavage in these leukemic cell lines but not in human peripheral blood lymphocytes and polymorphonuclear cells. The fragmentation-inducing activity of nicotine was not prevented by simultaneous addition of ascorbic acid. Flow cytometry showed a slight increase in the number of G2 + M phase cells, before the appearance of the apoptosis peak. Nicotine transiently increased the intracellular calcium concentration to higher levels in leukemic cells than in normal leukocytes. These data suggest that the induction of DNA fragmentation requires elevation of intracellular calcium concentration above a certain threshold level.

Ascorbic Acid↗