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Biomedical subjects

M Isobe

Publications and source records attributed to M Isobe.

At least 271 records · Page 15Linked to original sources
PubMed1990

Leiomyosarcoma of the rectum with sarcoid-like reaction--a case report.

A 57 year-old man was admitted to the hospital because of bloody stools. A barium enema and coloscopy disclosed a tumor of the rectum. The resected tumor was diagnosed as a leiomyosarcoma, histologically. Many epithelioid granulomas with Langhans type giant cells were found in the tumor, and there was no evidence suggestive of generalized sarcoidosis, tuberculosis or mycosis. Thus, the epithelioid granulomas seen in the leiomyosarcoma were interpreted as a sarcoid-like reaction. As far as could be determined, there has been no reported case of a sarcoid-like reaction associated with a leiomyosarcoma. The occurrence of the sarcoid-like reaction in the present case could be due to the reaction to the metabolites or a degenerative substance of the leiomyosarcoma, or to host resistance to the tumor itself.

Humans↗
PubMed1990

FAB-MS/MS spectrometry in determining the primary structure of gamma-glutamyl-containing peptides.

Positive fast atom bombardment tandem mass spectrometry (FAB-MS/MS) was applied for peptide sequencing, particularly for determining the gamma glutamyl linkage involved in metal-binding peptides such as Cadystin (gamma EC)3G = Cadystin A and Cadystin (gamma EC)2G = Cadystin B (MW 771 and 539, respectively). The fragmentation patterns between the natural gamma glutamyl peptide and the synthetic alpha glutamyl one were clearly distinguishable. FAB-MS/MS was proved to be a good method for determining these peptides, since it needed no chemical degradation and only a small amount of the peptide was needed for determination.

Amino Acid Sequence↗
PubMed1990

[Radiotherapy on the basis of quality of life].

Considering the relationship between tumor lethal dose and normal tissue tolerance: the therapeutic ratio, radiation oncologists have been performed the radiotherapy for cancer patient. The basic principle of radiotherapy is to have a good result (curability), to be tolerable in side effects and to have a comfortable life after radiation. Radiotherapy is the important strategy for an early stage of cancer with conserving the function and structure, and for an advanced or a recurrent stage of cancer with contributing to improve the quality of life. Recently, advantage of radiation tools and supportive care of cancer treatment, have been able to decrease the incidence of late injuries and complications. Radiotherapy must be planned on basis of considering therapeutic ratio and should be performed with optimum radiation in the multimodal treatment for cancer.

Humans↗
PubMed1990

[Reduction of myocardial infarct size by early intracoronary thrombolysis as assessed by serum cardiac myosin light chains and left ventricular function].

Cardiac myosin light chains are released from the infarcted myocardium soon after the onset of infarction, and the level of myosin light chains in the serum reflects infarct size, regardless of the presence of early coronary reperfusion. In this study, we used serum myosin light chains and assessed changes in left ventricular function to evaluate the effects of intracoronary thrombolysis on infarct size, with special reference to the interval between the onset of infarction and the time of reperfusion. Forty patients with acute myocardial infarction who underwent coronary angiography and intracoronary thrombolysis for the left anterior descending artery (LAD) early after the onset of infarction were categorized in four groups: in group A (n = 9) the LAD was already patent at the start of intracoronary thrombolysis, in group B (n = 12) antegrade flow in the LAD was achieved within three hours of the onset of symptoms, in group C (n = 10) antegrade flow was achieved later than three hours after the onset of symptoms, and in group D (n = 9) antegrade flow in the LAD was not achieved. The peak appearance time of creatine phosphokinase (CPK) in group D was significantly later than in the other groups. The total release of CPK in group C (3,119 +/- 414 IU/l) was greater than that in group A (1,332 +/- 346 IU/l) (p less than 0.01), but the total CPK release in group D (2,525 +/- 525 IU/l) was not statistically different from those of any other group. In all four groups myosin light chain I appeared in the serum from the first day on and reached their peak values between the third and fifth days. The peak values of myosin light chain I were 14.7 +/- 2.1 ng/ml for group A, 16.3 +/- 2.3 ng/ml for group B, 24.6 +/- 2.4 ng/ml for group C, and 25.1 +/- 1.8 ng/ml for group D. The peak myosin light chain levels in groups A and B were less than those in groups C and D. Twenty-nine of the 40 patients had no previous episodes of infarction, and these 29 patients were classified in two groups according to the Forrester's subset class on the first day: four of seven patients in group D were in subsets II, III or IV; whereas, the majority of patients in groups A, B and C were in subset I.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Vessels↗
PubMed1990

[Suspected primary tumor in the diaphragm revealing large cell carcinoma in the lung with sarcomatous change].

A 59-year-old female was admitted to our institute with coughing. A primary tumor of the diaphragm was suspected by chest X-ray, CT and angiograms preoperatively. Intraoperative findings also suggested a large primary tumor in the diaphragm with invasion to the lung, pericardium and liver. Therefore, we performed partial resection of the diaphragm, lung, pericardium and liver all together through a right thoraco-abdominal approach and the diaphragm was reconstructed using polyglycolic acid mesh. Histologically, the large tumor located mainly in the diaphragm was sarcomatous, with transposition from the carcinomatous cells to the sarcomatous cells. A large cell tumor of the lung was also confirmed. Immunohistologically, the diaphragm tumor was positively stained by keratin and by epithelial membrane antigen. In addition, desmosomes were demonstrated under electron microscopy studies. The tumor of this case was sarcoma in the diaphragm developed from a minor large cell tumor in the lung. Though commonly thought difficult to prove sarcomatous change development from large cell tumor in the lung, we were able to determine this clearly with immunohistology and electron microscopy.

Carcinoma, Small Cell↗
PubMed1989

Human TCR-gamma+/delta+, CD8+ T lymphocytes recognize tetanus toxoid in an MHC-restricted fashion.

We have analyzed the ability of human gamma+/delta+ T cells to recognize a nominal antigen in association with MHC molecules. A TT-specific T cell line with approximately 40% gamma+/delta+ T cells was established from a hyperimmunized donor, D.F., by stimulation with antigen and autologous APC. Three DF-derived gamma+/delta+ clones were CD8+ as determined by immunofluorescence staining, and by Southern and Northern blotting with probes detecting delta chain rearrangement and delta and gamma chain transcripts, respectively. The gamma+/delta+ clones responded to stimulation with TT, but not TNP-BSA, and autologous APC by proliferation and IFN-gamma production. No proliferation or IFN-gamma production was detected when TT-specific T cell clones were stimulated with either TT or autologous APC only. The response to TT was enhanced by addition of exogenous IL-2. The use of allogeneic APC from 19 donors sharing one HLA-determinant with the autologous donor D.F., showed that the gamma+/delta+ T cells responded to TT with HLA-DR4-related restriction as measured by proliferation and IFN-gamma production. These results demonstrate that gamma/delta receptors can recognize non-MHC-encoded foreign antigen in a self-MHC-restricted fashion.

Antigen-Presenting Cells↗
PubMed1989

elk, tissue-specific ets-related genes on chromosomes X and 14 near translocation breakpoints.

The myb-ets-containing acute leukemia virus, E26, transforms myeloblasts and erythroblasts in culture and causes a mixed erythroid and myeloid leukemia in chicks. Genes (ets-1, ets-2, and erg) with variable relatedness to the v-ets oncogene of the E26 virus have been identified, cloned, and characterized in several species. Two new members (elk-1 and elk-2) of the ets oncogene superfamily have now been identified. Nucleotide sequence analysis of the elk-1 cDNA clone revealed that this gene encodes a 428-residue protein whose predicted amino acid sequence showed 82% similarity to the 3' region of v-ets. The elk or related sequences appear to be transcriptionally active in testis and lung. The elk cDNA probe detects two loci in the human genome, elk-1 and elk-2, which map to chromosome regions Xp11.2 and 14q32.3, respectively. These loci are near the translocation breakpoint seen in the t(X;18) (p11.2;q11.2), which is characteristic of synovial sarcoma, and the chromosome 14q32 breakpoints seen in ataxia telangiectasia and other T cell malignancies. This suggests the possibility that rearrangements of elk loci may be involved in pathogenesis of certain tumors.

Amino Acid Sequence↗
PubMed1989

Molecular genetics of lymphoid tumorigenesis.

The body of this work illustrates the utility of the combined cytogenetic and molecular approach to lymphoid tumorigenesis. A number of tumor-specific translocations have proven amenable to dissection by molecular techniques. We have a firm grasp of the general principles that underlie lymphoid neoplasia; in particular, the activation of cellular oncogenes by translocation into genes of the immunoglobulin superfamily is a widespread phenomenon. However, numerous lymphopoietic malignancies are only poorly understood. These remain a challenge for the continued application of these methodologies.

Base Sequence↗
PubMed1989

Molecular analysis of a t(14;14) translocation in leukemic T-cells of an ataxia telangiectasia patient.

We have detected and cloned two rearrangements in the T-cell receptor alpha locus from a clone of somatic cell hybrids carrying a t(14;14)(q11;q32) chromosomal translocation derived from an ataxia telangiectasia patient with T-cell chronic lymphocytic leukemia. The T-cell clone carrying the t(14;14) chromosomal translocation was known to be present for greater than 10 years before the onset of overt leukemia. One molecular rearrangement of the T-cell receptor alpha locus corresponded to a functional variable-joining region (V-J) joining, whereas the other derived from the breakpoint of the t(14;14)(q11;q32) translocation. Chromosomal in situ hybridization of the probe derived from the t(14;14) breakpoint localized the breakpoint region to 14q32.1, apparently the same region that is involved in another ataxia telangiectasia characteristic chromosome translocation, t(7;14)(q35;q32). The 14q32.1 breakpoint is at least 10,000 kilobase pairs (kbp) centromeric to the immunoglobulin heavy chain locus. Sequence analysis of the breakpoint indicates the involvement of a J alpha sequence during the translocation. Comigration of high-molecular weight DNA fragments involved with t(7;14) and t(14;14) translocations suggests the presence of a cluster of breakpoints in the 14q32.1 region, the site of a putative oncogene, TCL1.

Alleles↗
PubMed1989

Activation of MYC in a masked t(8;17) translocation results in an aggressive B-cell leukemia.

We have analyzed the oncogene rearrangements involving BCL2 and MYC in the leukemia cells of a patient with an aggressive prolymphocytic leukemia that had an abnormal karyotype including a t(14;18) translocation and a chromosome 17q+. Molecular analysis showed that BCL2 was rearranged in the major breakpoint cluster region and had joined into the immunoglobulin heavy chain gene as in follicular lymphoma. Cloning and sequence analysis of the rearranged MYC gene revealed that MYC was truncated at the Pvu II site at the end of the first exon of MYC and had joined into the regulatory elements of a gene that we called BCL3 (B-cell leukemia/lymphoma 3). The BCL3 locus was mapped to chromosome 17 band q22. We found BCL3 transcribed as a message of 1.7 kilobases in many hematopoietic cell lines representing all hematopoietic lineages. In the patient's leukemia cells, the truncated MYC gene was highly expressed under the influence of BCL3 regulatory elements, leading to an aggressive B-cell leukemia that presumably had been derived from an indolent lymphoma carrying a rearranged BCL2 gene.

Base Sequence↗
PubMed1989

Quantification of myocardial infarct size after coronary reperfusion by serum cardiac myosin light chain II in conscious dogs.

The effects of early coronary artery reperfusion on the relation between the extent of myocardial infarction and serum levels of cardiac myosin light chain II or plasma creatine kinase levels were evaluated in the conscious dog. Hydraulic occluders were placed on the left anterior descending arteries of 38 dogs. Seven to 10 days later, myocardial infarction was produced. Coronary reperfusion was performed 3 hours (group A1, n = 13) and 6 hours (group A2, n = 12) after the occlusion. In the other 13 dogs, coronary occlusion was sustained throughout the course of the experiment (group B). Seven days after the occlusion, the heart was cut from the apex to the base into 4-mm slices, and infarct size was determined macroscopically. Rapid appearance and early peaking of creatine kinase were observed in group A. Cumulative release of creatine kinase significantly correlated with infarct size in group A (infarct size ranged from 0.1 to 20.1 g, r = 0.90) and group B (from 0.6 to 26.8 g, r = 0.91). However, since creatine kinase release in group A was greater in comparison with that from infarcts of the same size in group B, the slope of the regression line for group A was significantly steeper (p less than 0.05). Cardiac myosin light chain II appeared as early as creatine kinase did and continued to be elevated for 7 days. A very close relation was observed between infarct size and total cardiac myosin light chain II release (r = 0.87 for group A, and r = 0.88 for group B) or peak level of light chain II (r = 0.85 for group A, and r = 0.81 for group B). In addition, the slopes of the regression lines for infarct size and both peak and total release of light chain II did not differ between group A and group B. On histological examination, viable myocardium was frequently observed in the epicardium of the ischemic area in group A1; therefore, infarct size was greater in group B than in group A1 (p less than 0.05). Also, myocardial creatine kinase content in the epicardium of the center of the ischemic area in group A1 was greater than that in group B. Cardiac myosin light chain II release in group A1 was less than that in group B, whereas no difference was found in plasma creatine kinase release among groups A1, A2, and B.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

7-ethenyloxycoumarin as a new substrate for fluorophotometric assay of hepatic microsomal epoxidizing activities.

7-Ethenyloxycoumarin (7-vinyloxycoumarin, VOC) was metabolized by rat liver microsomes in the presence of a reduced nicotinamide adenine dinucleotide phosphate-generating system to 7-hydroxycoumarin (HOC) and glycolaldehyde via the unstable epoxide, 7-(epoxyethoxy)coumarin, as an obligatory intermediate which had a half life of 5.4 min in 0.1 M phosphate buffer, pH 7.4, at 37 degrees C. The epoxide of VOC accumulated in the microsomal incubation mixture in the presence of the epoxide hydrolase inhibitor, 3,3,3-trichloropropene 1,2-oxide, was isolated and identified. HOC and glycolaldehyde were auto-decomposition products of the putative highly unstable intermediate, 7-(1',2'-dihydroxyethoxy)coumarin, mostly formed by microsomal epoxide hydrolase from the epoxide. Direct fluorophotometry of HOC made it possible to determine epoxidizing activities of very small quantities of the microsomes from untreated rat liver (greater than or equal to 5 micrograms protein). VOC was epoxidizied by rat liver microsomal cytochrome P-450, inducible by 3-methylcholanthrene (3-MC) and phenobarbital (PB), and the microsomal epoxidation reactions were inhibited by IgG preparations raised against the major cytochrome P-450 components isolated from 3-MC- and PB-pretreated rat liver microsomes. In the untreated, 3-MC- and PB-pretreated rat liver microsomes, at least two monooxygenase components with different affinity were strongly suggested by a kinetic study, carried out using the antibodies, to be involved in the epoxidation of VOC.

Animals↗
PubMed1989

Comparative studies on the metabolism and mutagenicity of vinyl ethers.

4-Nitrophenyl vinyl ether (1), umbelliferyl vinyl ether (2), 4-cyanophenyl vinyl ether (3), and 4-acetylphenyl vinyl ether (4) were mutagenic toward Salmonella typhimurium TA100 and TA100NR in the presence of the hepatic 9000 x g supernatant fraction fortified with a reduced nicotinamide adenine dinucleotide phosphate generating system (S9mix), but no significant mutagenicity of 4-chlorophenyl vinyl ether (5), phenyl vinyl ether (6), n-butyl vinyl ether (7), and ethyl vinyl ether (8) was found. The epoxides of 1-4 were highly mutagenic toward the bacteria without the S9mix. Also, epoxides of 5 and 6 showed relatively weak mutagenicity. Studies on the metabolism of 1 showed that the epoxide (1a) formed from 1 by microsomes behaved as a labile intermediate in the incubation mixture. Untreated rat hepatic microsomes accumulated 1a and induced mutagenicity of 1 most effectively among the activation systems used. Mutagenic activities of vinyl ethers in the presence of the S9mix were correlated with stabilities of their epoxides. From these results, it is suggested that the critical factor for the mutagenicity of vinyl ethers is the formation and stability of epoxide intermediate in the biological system.

Animals↗
PubMed1989

[Pharmacokinetics of sodium 4-[alpha-hydroxy-5-(1-imidazolyl)-2-methylbenzyl]-3,5-dimethylbenzoate (Y-20811), a new thromboxane synthetase inhibitor. II. Pharmacokinetics of intact drug and main metabolite in dog].

The pharmacokinetics of sodium 4-[alpha-hydroxy-5-(1-imidazolyl)-2-methylbenzyl]-3,5-dimethylbenzoat e (I-Na) in the beagle dog was investigated after p.o. and i.v. administration. After the administration of I-Na at 3 mg/kg (p.o.), 70.9% of the dose was absorbed, and the maximum plasma concentration of free acid (I) was observed at 0.33 h. After p.o. administration, the area under the plasma concentration-time curve of I increased almost linearly in proportion to the dose. The metabolite, 4-[alpha-hydroxy-2-hydroxymethyl-5-(1-imidazolyl)benzyl]-3,5-dimethyl benzoic acid (II) was also detected in the plasma, but the concentration of II was lower than that of I. After the administration at 3 mg/kg (p.o.), 27.7% and 3.8% of the dose were recovered as I and II, respectively, in the urine, and 32.2% and 30.1% recovered as I and II in the feces. Therefore, 93.8% of the dose was totally recovered within five days. The inhibitory effect of II on the aggregation of rabbit platelets was studied in vitro. This metabolite showed only one sixth activity of I-Na. Thus, the inhibitory effect on the platelet aggregation of II is considered to be almost negligible in the beagle dog administered with I-Na.

Animals↗
PubMed1989

[Pharmacokinetics of sodium 4-[alpha-hydroxy-5-(1-imidazolyl)-2-methylbenzyl]-3,5-dimethylbenzoate (Y-20811), a new thromboxane synthetase inhibitor. I. Isolation and structure elucidation of urinary metabolite in dog].

The urinary metabolites of sodium 4-[alpha-hydroxy-5-(1-imidazolyl)-2-methylbenzyl]-3,5-dimethylbenzoat e (Y-20811) in dog were investigated. The main metabolite was isolated by high performance liquid chromatography and subsequent preparative thin layer chromatography. The structure of this metabolite was established as 4-[alpha-hydroxy-2-hydroxymethyl-5-(1-imidazolyl)benzyl]-3,5- dimethylbenzoic acid on the basis of spectral analyses and confirmed by its total synthesis.

Animals↗
PubMed1989

Infarct sizing after reperfusion by two-dimensional echocardiography and serum cardiac myosin light chain II in conscious dogs: dissociation between early left ventricular wall motion and ultimate infarct size.

The time course of recovery of left ventricular wall motion after coronary reperfusion and how that relates to anatomical infarct size, wall motion abnormality, and the amount of cardiac myosin light chain II release were evaluated in conscious dogs. One week after the implantation of hydraulic occluders on the left circumflex arteries, myocardial infarction was induced. Coronary reperfusion was performed 3 h after the occlusion in 9 dogs (R) and occlusion was sustained in 9 dogs (C). All dogs underwent serial 2-dimensional echocardiograms and determination of serum cardiac myosin light chain II. The infarct size was identified at 14 days. Systolic wall thickening at the center of the ischemic area (SWT) at 3 h was -7.7 +/- 2.8% (C), -9.9 +/- 3.0% (R). Systolic thinning was observed even at 14 days in C. Significant recovery of contraction was observed in R, but the improvement continued for as long as 2 days. SWT at 14 days was -1.5 +/- 2.8% (C) and 7.0 +/- 4.6% (R) (p less than 0.05). All of SWT or the extent of systolic thinning (EST) 3-hour and 14-day were correlated well with infarct size in C. In group R, 14-day SWT and 14-day EST correlated with infarct size but 3-hour SWT and 3-hour EST did not. Total release of serum cardiac myosin light chain II levels correlated well with infarct size (r = 0.88), 14-day SWT (r = -0.90) and 14-day EST (r = 0.89) in all dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Clinical application of immunoassays for cardiac myosin light chains].

We developed four types of immunoassays for cardiac myosin light chains (LC), which are two radioimmunoassays (RIA) for canine and human LC, and an immunoradiometric assay (IRMA) and an enzyme-linked immunosorbent assay (ELISA) for human LC. The first two assays make use of polyclonal antibodies and the last two use monoclonal antibodies. By using these immunoassays, we studied the release of cardiac LC into the serum following acute myocardial infarction (AMI). In experimental AMI in dogs, cardiac LC appeared in the serum within 4-12 hours, reached the maximum at 2-5 days and returned to normal at 7-10 days. This long time-course was suggested due to the continuous liberation of LC from the infarcted myocardium on the basis of a quick disappearance rate of LC from the circulation. The peak LC values were found to correlate well with the histological infarct size. Similar results were also obtained regarding the time-course of circulating LC in clinical patients with AMI. Thus LC measurement seems useful for diagnosis of AMI as well as for estimating the extent of myocardial damage. We also developed an IRMA and an ELISA for human LC by using anti-human LC monoclonal antibodies for a more rapid LC assay and for a consistent supply of antibodies. These assays showed sufficiently high sensitivities to measure 1-100 ng/ml of serum LC. Especially, serum LC can be assayed within 2.5 hours by our ELISA. Such progress in immunoassays for cardiac LC has made the measurement of LC an important laboratory test for the diagnosis of AMI.

Animals↗