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M Isobe

Publications and source records attributed to M Isobe.

At least 289 records · Page 16Linked to original sources
PubMed1989

[A very rare autopsy case of metastatic brain tumor originating from ureteral cancer].

We report here a very rare case of metastatic brain tumor originating from ureteral cancer which was verified at autopsy. An 88-year-old elderly woman was admitted to our department because of recurrent convulsions which started in March, 1987. Following this episode, right hemiparesis and speech disturbance appeared on June 6, 1987. Neurological examinations at admission on August 12, 1987 showed slightly disturbed consciousness, motor dominant aphasia, and dysphasia. Enhanced CT scan demonstrated a large tumor in the left frontal lobe with perifocal edema, and a small mass in the right frontal lobe (Fig. 1). Left carotid angiogram showed downward displacement of the middle cerebral artery complex at the Sylvian portion. After admission, she developed marked distention of the abdomen, with occurrence of hematuria followed by aggravation of respiration and consciousness. She died on September 2, 1987. Removal of metastatic brain tumor had not been performed due to the poor general condition of the patient. An autopsy was permitted. A coronal section of the cerebrum clearly demonstrated a large tumor in the left frontal lobe with small mass in the right frontal lobe (Fig. 2). Kidney and the ureter at the right side showed hydronephrosis and hydroureter because of the presence of ipsilateral ureteral tumor at the distal end (Fig. 3). Microscopical findings verified that the metastatic brain tumor was a transitional cell carcinoma, which was, histologically, completely the same as the ureteral tumor (Fig. 4, 5). No case of metastatic brain tumor originating from ureteral cancer has yet been reported, as far as the authors know.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Molecular cloning and characterization of an antigen associated with early stages of melanoma tumor progression.

The melanoma-associated antigen ME491 is expressed strongly during the early stages of tumor progression. The ME491 gene was molecularly cloned by means of DNA-mediated gene transfer followed by screening a lambda genomic library with human repetitive Alu sequences as a probe. The cloned DNA, after transfection into mouse L-cells, generated a protein with characteristics that were indistinguishable in Western blot analysis from the ME491 antigen expressed by human melanoma cells. Repeat-free subfragments of the cloned DNA were used for further studies. By Northern blot analysis, the subfragments detected a single 1.2-kilobase mRNA in the transformants and various human melanoma cell lines. ME491 complementary DNA clones were then obtained by probing a melanoma complementary DNA library with the genomic subfragments. Nucleotide sequence analysis of the cloned complementary DNA indicated that the ME491 antigen consists of 237 amino acids (Mr 25,475) with four transmembrane regions and three putative N-glycosylation sites. No significant structural homology was observed with other proteins thus far reported. We observed that the amounts of mRNA varied greatly with different melanoma cell lines. Southern blot analysis revealed no amplification or rearrangement of the ME491 gene in the human melanoma cell lines tested, including both high and low expressors of this antigen. The ME491 gene has been mapped to chromosome region 12p12----12q13 by somatic cell hybrid analysis and more narrowly localized to 12q12----12q14 by in situ hybridization.

Amino Acid Sequence↗
PubMed1988

Molecular analysis of a t(7;14)(q35;q32) chromosome translocation in a T cell leukemia of a patient with ataxia telangiectasia.

Molecular analysis of somatic cell hybrids derived from T cells carrying a t(7;14)(q35;q32) chromosomal translocation from a patient with ataxia telangiectasia and T cell leukemia indicates that the breakpoint on chromosome 14 is proximal to the IgH locus and to the D14S1 locus, while the breakpoint on chromosome 7 involves the T cell receptor beta chain locus immediately 5' to J beta 1.5 on chromosome 7. The separation of V beta and C beta observed in somatic cell hybrids defined the orientation of the T cell receptor beta chain locus on chromosome 7 where the V beta genes are centromeric and the C beta genes are telomeric. A novel chromosomal alteration, undetected cytogenetically, was revealed as being an inversion with duplication of the distal band of chromosome 14q32. The importance of the 14q32 region in the leukemogenic process is discussed.

Ataxia Telangiectasia↗
PubMed1988

Coordinates transformation and learning control for visually-guided voluntary movement with iteration: a Newton-like method in a function space.

In order to control visually-guided voluntary movements, the central nervous system (CNS) must solve the following three computational problems at different levels: (1) determination of a desired trajectory in the visual coordinates, (2) transformation of the coordinates of the desired trajectory to the body coordinates and (3) generation of motor command. In this paper, the second and the third problems are treated at computational, representational and hardware levels of Marr. We first study the problems at the computational level, and then propose an iterative learning scheme as a possible algorithm. This is a trial and error type learning such as repetitive training of golf swing. The amount of motor command needed to coordinate activities of many muscles is not determined at once, but in a step-wise, trial and error fashion in the course of a set of repetitions. Actually, the motor command in the (n + 1)-th iteration is a sum of the motor command in the n-th iteration plus two modification terms which are, respectively, proportional to acceleration and speed errors between the desired trajectory and the realized trajectory in the n-th iteration. We mathematically formulate this iterative learning control as a Newton-like method in functional spaces and prove its convergence under appropriate mathematical conditions with use of dynamical system theory and functional analysis. Computer simulations of this iterative learning control of a robotic manipulator in the body or visual coordinates are shown. Finally, we propose that areas 2, 5, and 7 of the sensory association cortex are possible sites of this learning control. Further we propose neural network model which acquires transformation matrices from acceleration or velocity to motor command, which are used in these schemes.

Central Nervous System↗
PubMed1988

Synergistic actions of disulfide-reducing agents on 1-methyladenine-induced oocyte maturation in starfish.

Several disulfide-reducing agents, such as dithiothreitol, 2,3-dimercapto-1-propanol, cysteine ethyl ester, and cysteine methyl ester enhanced the effectiveness of 1-methyladenine (1-MeAde) to induce oocyte maturation in the starfish Asterina pectinifera. This enhancement occurred at relatively low concentrations at which these agents by themselves were ineffective in inducing oocyte maturation. The agents caused a marked (about twofold) increase in specific [1-3H]MeAde binding. The binding increased directly in relation to the potency of the agents in enhancing 1-MeAde action. Scatchard analysis indicated that dithiothreitol increased the Bmax without affecting the affinity of 1-MeAde binding. These results strongly suggest that disulfide-reducing agents enhance the maturational action of 1-MeAde by increasing the number of 1-MeAde binding sites in oocyte cortices.

Adenine↗
PubMed1988

Cloning of the gene encoding the delta subunit of the human T-cell receptor reveals its physical organization within the alpha-subunit locus and its involvement in chromosome translocations in T-cell malignancy.

By taking advantage of "chromosomal walking" techniques, we have obtained clones that encompass the T-cell receptor (TCR) delta-chain gene. We analyzed clones spanning the entire J alpha region extending 115 kilobases 5' of the TCR alpha-chain constant region and have shown that the TCR delta-chain gene is located over 80 kilobases 5' of C alpha. TCR delta-chain gene is rearranged in the gamma/delta-expressing T-cell line Peer and is deleted in alpha/beta-expressing T-cell lines. Sequence analysis of portions of this genomic region demonstrates its identity with previously described cDNA clones corresponding to the C delta and J delta segments. Furthermore, we have analyzed a t(8;14)-(q24;q11) chromosome translocation from a T-cell leukemia and have shown that the J delta segment is rearranged in cells deriving from this tumor and probably directly involved in the translocation. Thus, the newly cloned TCR delta chain is implicated in the genesis of chromosome translocations in T-cell malignancies carrying cytogenetic abnormalities of band 14q11.

Base Sequence↗
PubMed1988

Characterization of 1-methyladenine binding in starfish oocyte cortices.

1-Methyladenine (1MeAde) is the naturally occurring maturation-inducing hormone of starfish oocytes. We have prepared a biologically active [3H]1MeAde of high purity and relatively high specific radioactivity. This ligand binds to cortices isolated from full-grown prophase-arrested oocytes of the starfish Asterina pectinifera. The binding of [3H]1MeAde to cortices was rapid and reached equilibrium in approximately 15 min. This is in excellent agreement with the hormone-dependent period required for the induction of oocyte maturation. Binding was maximal between pH 6.4 and 8.0 and diminished sharply above and below this range. Analysis of Scatchard plots of the equilibrium binding of [3H]1MeAde to cortices indicates the existence of a single class of binding site with a dissociation constant of 0.3 microM and a binding capacity of 0.02 fmol per cortex. Whereas biologically active analogs (1-benzyladenine, 1-ethyladenine) inhibited the specific binding of [3H]1MeAde by cortices, biologically inactive analogs (2-methyladenine, 3-methyladenine, 1,9-dimethyladenine, and 1-methylhypoxanthine) did not. These results suggest that the 1MeAde binding characterized herein is necessary for the maturational action of 1MeAde on starfish oocytes.

Adenine↗
PubMed1988

Localization of the human JUN protooncogene to chromosome region 1p31-32.

The oncogene jun is the putative transforming gene of avian sarcoma virus 17; jun appears to be derived from a gene of the chicken genome and has homologues in several other vertebrate species. Recent genetic and immunological data indicate that jun codes for a protein that is closely related and probably identical to the transcription factor AP-1. We have isolated a genomic DNA clone encompassing the human cellular counterpart of the gene, JUN, and used this DNA to determine the chromosomal location of the gene. A panel of DNA preparations derived from rodent-human somatic cell hybrids with defined chromosome complements was first screened with the JUN probe. This Southern blot analysis indicated that JUN is situated on the short arm of chromosome 1. In situ hybridization then assigned JUN to chromosome region 1p31-32, a chromosomal region involved in both translocations and deletions of chromosomes seen in human malignancies.

Animals↗
PubMed1988

Chromosomal mapping of human keratin genes: evidence of non-linkage.

We have determined the chromosomal location of the genes for the human keratin intermediate filament proteins K1 (type II; 67 kDa) and K10 (type I; 57 kDa) by the use of specific cDNA clones in conjunction with somatic cell hybrid analysis and in situ hybridization. The K1 keratin gene maps to chromosome region 12q11----q13; the K10 keratin gene maps to chromosome region 17q12----q21. Each gene has been mapped relative to other genes known to be localized on chromosomes 12 and 17, respectively. In somatic cell hybrid analysis, the K1 gene segregates concordantly with the Hox-3 homeo box gene cluster at chromosome region 12p12----q13. The K10 gene localizes to a region proximal to a breakpoint at 17q21 which is involved in a t(17;21)(q21;q22) translocation associated with an acute leukemia. K10 appears to be distal (telomeric) to the gene loci for G-CSF, erb-A, and Her-2, which map to chromosome region 17q12----q21. The NGFR gene and Hox-2 homeo box locus are localized distal to the 17q21 break point and thus distal to the K10 gene. These data demonstrate that keratin genes K1 and K10, which are coexpressed in terminally differentiated epidermis, are not linked in the human genome, implying the existence of trans-acting factors involved in the regulation of expression of these genes.

Chromosome Mapping↗
PubMed1988

[Effects of antipyretics and anticancer drug on human cells at high temperature condition].

The effects of antifebriles and anticancer drug on human vascular endothelial cells (HVE) and several cultured human cells were investigated. The HVE were isolated from umbilical cord veins by enzyme treatment and cultured successively in aerated synthetic medium, RPMI-1640, with 20% preclostrum new born calf serum. The presence of factor VIII antigen in the HVE was determined by enzyme-labeled antibody method. Cell count and protein amount were examined at regular intervals. At 3 hour-expose, sulpyrine was more toxic to the cultured cells than aspirin at 37 degrees C. The cytotoxicity of sulpyrine was markedly enhanced at 40 degrees C than at 37 degrees C. However, there was no enhancement in the cytotoxicity of aspirin at 40 degrees C. Cultured HVE and normal human fetal lung (HAIN-55) cells at 37 degrees C were sensitive to sulpyrine, and their sensitivity of the cells to the drug were markedly enhanced when they were incubated at 41 degrees C. In contrast, sensitivity of malignant human cells (HeLa cells) to sulpyrine was not found at 37 degrees C, however sensitivity of the cells to the drug was manifested at 41 degrees C of incubation. There was no effect of 5-fluorouracil (FU) on the growth of HVE and HAIN-55 cells at 41 degrees C, while HeLa cells showed high susceptibility to FU at the same temperature. The results showed the possibility that normal human cells may be sensitive to antifebrile drugs but not to anticancer drug at ordinary and high temperature, whereas malignant human cell may be susceptible to both antifebrile drugs and anticancer drug at high temperature.

Aspirin↗
PubMed1988

[A case of squamous cell carcinoma of the breast].

A case of squamous cell breast carcinoma is presented. The patient was 31-year old woman with a complaint of a right breast mass. The tumor was found to measure 7.0 x 8.0 cm without any inflammatory signs, and was associated with a bloody nipple discharge. Lymph-node metastases of the ipsilateral axillary and supraclavicular nodes were noted, and metastasis to the fifth lumbar vertebrae also was seen. Because of a diagnosis graded T4bN3M1, stage IV, an extended radical mastectomy was performed. Histologically, the major portion of this tumor consisted of a squamous cell carcinoma with a minimal component of adenocarcinoma and accompanying keratinization. The patient died of this cancer 5 months after the operation.

Adult↗
PubMed1987

Right ventricular filling detected by pulsed Doppler echocardiography during the convalescent stage of inferior wall acute myocardial infarction.

To evaluate right ventricular (RV) diastolic function in patients with inferior wall acute myocardial infarction (AMI), flow velocity patterns of the RV inflow tract were studied in patients with anterior AMI (n = 32), inferior AMI (n = 32) and angina pectoris without left ventricular asynergy (n = 10) using pulsed Doppler echocardiography. Doppler examinations were performed at least 4 weeks after the attack. Twenty-seven healthy persons served as control subjects. Three Doppler variables were measured at the RV inflow tract: the ratio of the late diastolic peak flow velocity due to atrial contraction to the rapid filling peak flow velocity in early diastole (A/E) and the acceleration time and deceleration time of the RV rapid filling wave. A/E in patients with inferior AMI (1.01 +/- 0.24, mean +/- standard deviation) was significantly greater than in those with anterior AMI (0.80 +/- 0.16, p less than 0.001) and angina pectoris (0.79 +/- 0.17, p less than 0.01) and in normal subjects (0.70 +/- 0.17, p less than 0.001). A/E in patients with inferior AMI correlated with the ratio of left ventricular to RV end-diastolic pressure (r = -0.60, p less than 0.05). A/E in inferior AMI with relatively high RV end-diastolic pressure (more than 8 mm Hg, n = 8) was significantly greater than that in those with normal pressure (8 mm Hg or less, n = 9). A/E in patients with proximal right coronary artery occlusion was significantly greater than that in those with distal occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Lampteromyces bioluminescence--1. Identification of riboflavin as the light emitter in the mushroom L. japonicus.

The bioluminescence of the luminous mushroom, Lampteromyces japonicus, was studied by using the mushroom gills and also the luminous mycelia, the latter being cultured from the isolated spores and grown in a potato sucrose medium. The luminescence intensity of the mushroom gills and the cultured mycelia was measured in an aqueous suspension under various conditions. The original intensity was enhanced by exposing the luminous cells to oxygen for several hours or to acids or bases for a short period. This enhancement enabled measurement of their bioluminescence spectra which were identical to the fluorescence spectrum of riboflavin, having a maximum at 524 nm. The green fluorescent substance was extracted with cold water from the mushroom and it was identified as riboflavin by spectroscopic and chromatographic analyses. Riboflavin was concluded to be the light emitter of this mushroom.

Basidiomycota↗
PubMed1987

Mapping of four distinct BCR-related loci to chromosome region 22q11: order of BCR loci relative to chronic myelogenous leukemia and acute lymphoblastic leukemia breakpoints.

A probe derived from the 3' region of the BCR gene (breakpoint cluster region gene) detects four distinct loci in the human genome. One of the loci corresponds to the complete BCR gene, whereas the others contain a 3' segment of the gene. After HindIII cleavage of human DNA, these four loci are detected as 23-, 19-, 13-, and 9-kilobase-pair fragments, designated BCR4, BCR3, BCR2, and BCR1, respectively, with BCR1 deriving from the original complete BCR gene. All four BCR loci segregate 100% concordantly with human chromosome 22 in a rodent-human somatic cell hybrid panel and are located at chromosome region 22q11.2 by chromosomal in situ hybridization. The BCR2 and BCR4 loci are amplified in leukemia cell line K562 cells, indicating that they fall within the amplification unit that includes immunoglobulin lambda light chain locus (IGL) and ABL locus on the K562 Philadelphia chromosome (Ph1); additionally, in chronic myelogenous leukemia-derived mouse-human hybrids retaining a Ph1 chromosome in the absence of the 9q+ and normal chromosome 22, BCR2 and BCR4 loci are retained, whereas the 3' region of BCR1 and the BCR3 locus are lost, indicating that BCR3 is distal to BCR1 on chromosome 22. Similarly, in mouse-human hybrids retaining a Ph1 chromosome derived from an acute lymphoblastic leukemia-in the absence of the 9q+ and 22, only BCR2 and BCR4 loci are retained, indicating that the breakpoint in this acute lymphoblastic leukemia, as in chronic myelogenous leukemia, is proximal to the BCR1 3' region, but distal to the IGLC locus and the BCR2 and BCR4 3' loci. Thus, the order of loci on chromosome 22 is centromere----BCR2, BCR4, and IGL----BCR1----BCR3----SIS, possibly eliminating BCR2 and BCR4 loci as candidate targets for juxtaposition to the ABL gene in the acute lymphoblastic leukemia Ph1 chromosome.

Chromosome Aberrations↗
PubMed1987

Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

To estimate the extent of myocardial infarction after coronary artery reperfusion, serum levels of cardiac myosin light chain (LC) I and creatine kinase (CK) were determined serially in 49 patients with acute myocardial infarction. Intracoronary thrombolysis was successful in 25 patients (reperfusion group), and 24 patients were treated in a conventional manner (control group). The peak level of CK appeared significantly earlier in the reperfusion group (11.3 +/- 3.1 hr, mean +/- SD) than in the control group (21.6 +/- 7.2 hr). Cumulative release of CK was significantly related to angiographically determined left ventricular ejection fraction 1 month after the attack in both groups (r = -.50; -.45, respectively). However, the amount of cumulative release of CK in the reperfusion group was greater compared with that in those with the same left ventricular ejection fraction in the control group. Peak appearance time of LCI was almost equal in the two groups (3.8 +/- 1.4 vs 3.9 +/- 1.2 days). Peak levels of LCI were related to the left ventricular ejection fraction in the reperfusion group (r = -.63) and in the control group (r = -.74), and the slopes of their regression lines were similar. The cardiac index obtained on the day of onset in the two groups was related to peak levels of LCI but not to total release of CK. These results suggest that serum levels of LCI reflect the changes in left ventricular function after acute myocardial infarction, regardless of the presence of coronary reperfusion. Thus, serial determinations of LCI in serum facilitate noninvasive assessment of the effects of intracoronary thrombolysis on infarct size.

Adult↗