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Biomedical subjects

T Morisaki

Publications and source records attributed to T Morisaki.

At least 127 records · Page 7Linked to original sources
PubMed1991

Evidence that induction and regulation of lymphokine-activated killer (LAK) activity are mediated by changes in tumour-binding potential of lymphocytes after activation by interleukin-2 (IL-2).

The changes in the tumour-binding potential of human peripheral blood lymphocytes (PBL) after activation by interleukin-2 (IL-2) was investigated by directly counting the number of lymphocytes bound to lined hepatoma cell monolayers. A significant increase in the tumour-binding potential of PBL was found after activation by more than 100 U/ml of IL-2. Maximal tumour-binding potential was achieved at 1000 U/ml of activation, and an overdose of IL-2 activation slightly decreased this potential. These changes were almost exactly the same as the changes in anti-tumour cytotoxicity as measured by a 4-hr 51Cr-release assay. In addition, the kinetics of tumour binding by lymphokine-activated killer (LAK) cells was shown to be almost identical to that of tumour cell lysis. These results thus provide evidence that induction and regulation of LAK activity are mediated by changes in tumour-binding potential of lymphocytes after activation by IL-2.

Animals↗
PubMed1991

[Immunological assessment of the pathogenesis of septic-MOF: relationship between complement activation and changes in neutrophil functions].

We investigated the pathogenesis of septic-MOF through the relationship between changes in neutrophil functions and degree of complement activation. The patients' neutrophils exhibited enhanced adherence to HUVEC, suppressed chemotaxis toward C5a, enhanced production of oxygen radicals and lysosomal enzymes. These changes in neutrophil functions related to complement activation elicited via classical pathway. Moreover, the activated complement participated in tissue injuries due to the cytolytic action of the terminal complement complexes such as membrane attack complex (MAC). In conclusion, the combination of neutrophil and complement was strongly associated with the pathogenesis of the septic-MOF.

Bacterial Infections↗
PubMed1990

Adenylate deaminase. A multigene family in humans and rats.

Multiple AMP deaminase (AMP-D) isoforms have been found in vertebrates, and tissue-specific inherited deficiencies of AMP-D have been described in two unrelated clinical syndromes suggesting there may be more than one AMP-D gene in higher eukaryotes. Using a newly isolated cDNA cloned from an adult rat brain library and a previously reported cDNA cloned from adult rat skeletal muscle, two linked AMP-D genes have been identified in rat and man. ampd1 is expressed at high levels in skeletal muscle of the adult rat. ampd2 is the predominant gene expressed in non-muscle tissues and smooth muscle of the adult rat, and it is also the predominant gene expressed in embryonic muscle and undifferentiated myoblasts. Both genes are expressed in cardiac muscle of the adult rat. The peptides encoded by these two genes have distinct immunological properties. The conservation of nucleotide sequence and exon/intron boundaries in these two genes suggests they arose by duplication of a common primordial gene around 150 million years ago.

AMP Deaminase↗
PubMed1990

Characterization of the human and rat myoadenylate deaminase genes.

AMP deaminase is an ubiquitous enzyme in eukaryotic cells, and tissue-specific isoforms are produced in mammals by differential expression of the two genes which encode this enzyme activity as well as by alternative splicing of the primary transcript of one of these genes. Deficiency of this enzyme activity is one of the most common causes of metabolic myopathy in man. To provide a framework for understanding the molecular basis of this inherited disorder and the mechanisms responsible for regulating the expression of this enzyme activity, both the human and rat muscle-specific genes for AMP deaminase have been cloned and partially sequenced. Comparison of the two genes shows a high degree of conservation of sequence and structural organization. The two genes share the following characteristics: 1) both are approximately 20 kilobases in size, have identical exon/intron boundaries, and exhibit similar intron/exon structural organization; 2) the transcription start site is located at the same position in both genes, and comparison of 5'-flanking sequences reveals four highly conserved domains that together contain the information necessary for muscle-specific expression of a receptor cDNA; 3) coding sequences are 88% identical and the 5'-untranslated regions are 67% identical; 4) both genes have extremely short 3'-untranslated regions (13-17 nucleotides); 5) highly conserved intervening sequences of several hundred nucleotides surround most exon/intron boundaries. In situ hybridization and analysis of human-mouse somatic cell hybrids have localized the human gene (designated AMPD1) to chromosome 1 in the region p13-p21. The implications of these structural properties for identifying functional domains in the AMP deaminase peptide, regulation of expression of this gene, and inheritance of AMP deaminase deficiency are discussed.

AMP Deaminase↗
PubMed1989

A case of a postoperative aneurysm of the common hepatic artery which ruptured into the remnant stomach after a radical gastrectomy.

A rare case of an iatrogenic aneurysm of the common hepatic artery which ruptured into the remnant stomach is described herein. The patient had undergone a radical gastrectomy with regional lymphadenectomy one month previously. The iatrogenic surgical trauma to the common hepatic artery incurred during the regional lymphadenectomy with the resection of the perivascular lymphatics and neural plexuses, was considered as the main cause responsible for the postoperative aneurysmal development.

Adenocarcinoma↗
PubMed1989

Endobronchial non-Hodgkin's lymphoma.

A 64-year-old man with non-Hodgkin's lymphoma suffered a complete collapse of the left upper lobe of the lung. Fibreoptic bronchoscopy demonstrated a large number of distinct polypoid tumours of the lymphoma in the trachea and bilateral sub-segmental bronchi. The left upper lobe bronchus was completely occluded by the tumours, which responded to the combination chemotherapy against the lymphoma. This report presents the seventh case of non-Hodgkin's lymphoma with multiple endobronchial tumours.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

Genotypic analysis using a Y-chromosome-specific probe following bone marrow transplantation.

To monitor successful engraftment after bone marrow transplantation, we performed Southern hybridization analysis or dot blot analysis of DNA in a set of sex-mismatched cases using a Y-chromosome-specific DNA probe (pHY10). This method was extremely sensitive and rapid for checking which cells contain the Y-chromosome. Using this probe, analysis of cells from peripheral blood and bone marrow after transplantation demonstrated the usefulness of confirming engraftment of donor cells and of detecting mixed lymphohematopoietic chimerism.

Adult↗
PubMed1988

Elevated erythrocyte adenosine deaminase activity in a patient with primary acquired sideroblastic anemia.

We report a case of primary acquired sideroblastic anemia (PASA) associated with elevated erythrocyte adenosine deaminase (ADA) activity. The patient was an 85-year-old Japanese male. Analysis of the peripheral blood revealed pancytopenia, and the bone marrow findings showed marked ringed sideroblasts and chromosomal deletion (46XY, 11q-). The erythrocyte ADA activity was 17 times higher than that of normal control, the leukocyte ADA activity was within the normal range, and the plasma ADA activity was 2 times higher than the normal mean. The adenine nucleotides in the patient's erythrocytes were within normal range. According to starch gel electrophoresis, ADA isozyme of the patient was ADA 1. Western blotting showed an increased amount of ADA protein in the patient's erythrocytes. Southern blotting revealed no gene amplification or large structural change. Dot blot analysis of the reticulocyte mRNA showed no increase in the amount of ADA mRNA in the patient's reticulocytes compared with those of reticulocyte-rich controls. We considered that the mechanism of elevated ADA activity in this acquired defect was similar to that found in hereditary hemolytic anemia associated with ADA overproduction.

Adenine Nucleotides↗
PubMed1988

Genetic analysis of adenosine deaminase expression in adult T-cell leukemia.

We investigated the genetic basis for the increased adenosine deaminase (ADA) expression in adult T-cell leukemia (ATL). We found a correlation between the levels of ADA-specific mRNA and ADA immunoreactive protein in ATL. Southern blot analysis revealed no gene amplification or rearrangement of the ADA gene. These findings indicate that increased ADA expression in ATL cells reflects increased transcriptional activity for the ADA gene or increased stability of ADA mRNA.

Acute Disease↗
PubMed1988

Two homozygous cases of erythrocyte pyruvate kinase (PK) deficiency in Japan: PK Sendai and PK Shinshu.

Two new erythrocyte pyruvate kinase (PK) variants with severe nonspherocytic hemolytic anemia are presented. These cases are both considered to be homozygous because of the consanguineous marriages in their parents. Their erythrocyte PK's were characterized by the recommended methods of the International Committee for Standardization in Haematology (ICSH). These two variants have been named PK Sendai and PK Shinshu. PK Sendai showed a high K0.5S (phosphoenolpyruvate), was remarkably inhibited by ATP, and was thermolabile, while PK Shinshu demonstrated remarkably low enzyme activity and required a high level of fructose 1,6-diphosphate for activation.

Adolescent↗
PubMed1988

A new glucose-6-phosphate dehydrogenase variant (G6PD Tsukui) associated with congenital hemolytic anemia.

A new glucose-6-phosphate dehydrogenase (G6PD) variant associated with chronic nonspherocytic hemolytic anemia was found in a 20-year-old Japanese male who showed mild hemolysis after an upper respiratory tract infection. The patient had been noted to have jaundice and reticulocytosis several times before this episode. The enzyme activity of the variant was 1.5% of normal. The enzymatic characteristics were slow anodal electrophoretic mobility, high Km G6P, normal Km NADP, decreased heat stability, and a normal pH optimum. From these results, the enzyme was considered to be a new class 1 variant and was designated G6PD Tsukui.

Adult↗
PubMed1988

Molecular analysis of Lesch-Nyhan syndrome found in Japan.

Molecular analysis of four unrelated patients with Lesch-Nyhan (L-N) syndrome was performed. All four cases had typical clinical features of L-N syndrome, and the activities of hypoxanthine-guanine phosphoribosyltransferase (HPRT) were absent. No structural gene abnormalities were found by Southern blot analysis in all cases, and a decrease of HPRT mRNA was not detected by dot blot analysis in two of the four cases. However, HPRT enzyme proteins were detected by Western blot analysis in all cases. Our results showed that the production of immunologically reactive but enzymatically inactive mutant HPRT protein was pathogenic for all four patients.

Adult↗