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Biomedical subjects

T Masuda

Publications and source records attributed to T Masuda.

At least 325 records · Page 18Linked to original sources
PubMed1994

Establishment of a human T-cell line with deficient surface expression of glycosylphosphatidylinositol (GPI)-anchored proteins from a patient with paroxysmal nocturnal haemoglobinuria.

A novel interleukin-2 dependent T-cell line, PMT-2Y, was established from the peripheral blood of a patient with paroxysmal nocturnal haemoglobinuria (PNH) by human T lymphotropic virus type I (HTLV-I)-mediated transformation. PMT-2Y cells are positive for CD2, CD3, CD4, CD25, T cell receptor alpha beta and HLA-DR, but negative for CD1, CD7, CD8, CD19 and CD20, indicating that the clone belongs to a helper/inducer subset of T cells. PMT-2Y cells have the monoclonal integration of HTLV-I proviral DNA, suggesting that they derived from a single clone. Moreover, they lack surface expression of complement regulatory proteins such as DAF (CD55) and CD59, that are the most important glycosylphosphatidylinositol (GPI)-anchored membrane proteins defective in haemopoietic cells of patients with PNH. Northern blot analysis, however, revealed the production of normal levels of DAF mRNAs. Thus, PMT-2Y is derived from a PNH T cell clone and may be a useful model to study PNH.

Antigens, CD↗
PubMed1994

Changes in neuropeptide-containing nerves in human colonic mucosa with inflammatory bowel disease.

The distribution abnormality of vasoactive intestinal polypeptide-containing nerves (VIP-nerves) and substance P-containing nerves (SP-nerves) was immunohistochemically investigated in the colonic mucosa with inflammatory bowel disease (IBD) in relation to colonic glands and blood vessels in the lamina propria. In active ulcerative colitis (UC), VIP- and SP-nerves decreased in severe inflammatory lesions. VIP-nerves were almost absent particularly around crypt abscesses. Even in resolving and quiescent UC, VIP-nerves still decreased, depending on the decrease of glands and blood vessels. On the other hand, both nerves increased in some hypervascular lesions. In the uninvolved mucosa of UC, they did not change their distribution. In Crohn's disease, the distribution abnormality of both nerves resembled that of UC. These results suggest that the changes in VIP- and SP-nerve distributions in the mucosa with IBD are subsequent to mucosal inflammation and damage. However, these peptides are known to be immunoregulators, and their distribution abnormalities may induce the disorder of immunoregulation in the IBD mucosa and cause the mucosal damage and/or chronicity.

Adolescent↗
PubMed1994

Bone marrow transplantation for erythroleukemia: a case report.

A 2 year old girl was diagnosed as having erythroleukemia (EL; M6 according to the French-American-British classification). After one course of low-dose cytosine arabinoside (Ara-C), complete remission was obtained. After three courses of low-dose Ara-C for consolidation, allogeneic bone marrow transplantation was performed from HLA-identical sibling. The course of post-transplantation was uneventful. Two years after transplantation, she continues to have durable engraftment and remission. In children with EL, conventional chemotherapy appears to be inadequate for producing durable long-term disease-free survival. Bone marrow transplantation should be considered in children with EL, in cases where suitable donors are available.

Bone Marrow Transplantation↗
PubMed1994

Generation and characterization of a human immunodeficiency virus type 1 (HIV-1) mutant resistant to an HIV-1 protease inhibitor.

A synthetic peptide, RPI 312, that specifically inhibits the protease of the human immunodeficiency virus type 1 (HIV-1) showed a potent inhibition on virus production, maturation, and infectivity. Treatment with this agent prevented the cleavage of Gag protein at the site between p17 and p24 in HIV-1 chronically infected MOLT-4 cells as well as in the released virus. Passage of HIV-1 in the presence of gradually increasing concentrations of this protease inhibitor resulted in emergence of a variant that could evade the drug effects. In the resistant variant the maturation of Gag proteins appeared normal, but its infectivity was reduced compared with that of the parent virus. The nucleotides coding the amino acids at and around the cleavage site between Gag proteins p17 and p24 were not changed. One point mutation (A-->G) at site 2082 of the pol gene that resulted in one amino acid change at site 84 of the protease from isoleucine to valine (I-84-->V) could be detected in the resistant variant. An HIV-1 infectious DNA clone with the I-84-->V mutation also showed reduced sensitivity to this protease inhibitor. The findings that the resistant variant had lower infectivity and was still affected by higher doses of the drug support the speculation that resistance to protease inhibitors may not be as problematic as other drug resistance.

Amino Acid Sequence↗
PubMed1994

Inhibition of murine AIDS (MAIDS), development by the transplantation of bone marrow cells carrying the Fv-4 resistance gene to MAIDS virus-infected mice.

To examine whether the resistance allele of the Fv-4 gene (the Fv-4r gene) is a dominant inhibitory-product-encoding gene which an be used to prevent the development of murine AIDS (MAIDS), bone marrow cells from BALB/c-Fv-4wr mice were transplanted into BALB/c mice and C57BL/6 mice infected with MAIDS virus. Almost all of the virus-infected BALB/c and C57BL/6 mice developed MAIDS within 4 months and died 2 or 3 months later. However, when the virus-infected mice were subjected to cobalt irradiation and then given an intravenous injection of 10(7) BALB/c-Fv-4wr mouse bone marrow cells, the recipient mice survived much longer than the untreated mice, which suggests that the Fv-4 gene is a dominant inhibitory gene that is potentially useful in gene therapy of MAIDS.

Animals↗
PubMed1994

The p15gag and p12gag regions are both necessary for the pathogenicity of the murine AIDS virus.

The defective murine AIDS (MAIDS) virus has unique sequences in its p15gag and p12gag regions. To clarify whether these sequences are responsible for the development of MAIDS, we constructed recombinant viruses by replacing various regions of the gag gene of the nonpathogenic replication-competent LP-BM5 ecotropic virus with those of the MAIDS virus. Recombinants containing both unique sequences of the MAIDS virus were replication defective and induced MAIDS. However, a recombinant containing either the p15gag or p12gag region of the MAIDS virus was also replication defective but nonpathogenic in mice. A recombinant virus containing only the p30gag region of the MAIDS virus was replication competent and nonpathogenic. These results indicate that the p15gag and p12gag regions of the MAIDS virus do not function like those of replication-competent viruses and that both of the unique sequences in the p15gag and p12gag regions are required to develop MAIDS.

Animals↗
PubMed1994

Circadian variation in fibrinolytic activity in patients with variant angina.

BACKGROUND: Coronary artery spasm induces activation of the coagulation system. Turnover and maintenance of thrombus depend not only on formation but also on lysis. The relation between coronary spasm and fibrinolytic system has not been elucidated. OBJECTIVE: To examine whether there is impairment of or a circadian variation in fibrinolytic activity in patients with variant angina. METHODS: Plasminogen activator inhibitor (PAI) activity and concentrations of tissue plasminogen activator (t-PA) antigen were measured in venous plasma samples taken at 2200, 0600, and 1400 and 24 h Holter tapes were recorded in 15 patients with variant angina, 12 patients with stable exertional angina, and 12 controls. RESULTS: There were significant circadian variations in PAI activity and t-PA antigen with peak values at 0600 in all three groups. Mean (SEM) PAI activity (IU/ml) at 2200, 0600, and 1400 was 6.1 (1.1), 11.0 (1.3), and 4.4 (0.6) in the variant angina group; 1.8 (0.7), 5.6 (1.1), and 1.2 (0.3) in the stable exertional angina group; and 1.1 (0.5), 4.5 (0.8), and 0.7 (0.3) in the control group. Furthermore, both plasma PAI activity and t-PA antigen concentrations were significantly higher in the variant angina group than in the stable exertional angina group and the control group at each sampling time. CONCLUSIONS: In patients with variant angina there was a circadian variation in fibrinolytic activity, which was lowest in the early morning, and impaired fibrinolytic activity particularly in the early morning, when attacks of angina occur most frequently.

Aged↗
PubMed1994

Two-phase increment of Ca2+ uptake, intracellular Ca2+ concentration, and histamine release following antigen stimulation in mouse bone marrow-derived mast cells (BMMC).

The relationship between the influx of Ca2+ into cells or cytosolic Ca2+ concentration ([Ca2+]i) and the histamine release following antigen stimulation in mouse bone marrow-derived mast cells (BMMC) was examined, and the results were compared with those from human lung mast cells (HLMC) and rat peritoneal mast cells (RPMC) in some experiments. Anaphylactic histamine release from BMMC as well as HLMC, but not that from RPMC, was dependent on the extracellular Ca2+. When BMMC were challenged by antigen following radioactive 45Ca2+ addition, two phases of 45Ca2+ influx into the cells were observed. The first phase, which was initiated and completed within 30 sec and 2 min, respectively, after antigen treatment, appeared to be related to anaphylactic histamine release. The second influx began 30 sec subsequent to the first one and lasted for at least 2 min, and this occurred after the completion of the histamine release; So far, it is not known how this second influx participates in the intracellular event(s). On the other hand, only one sustained elevation of [Ca2+]i occurred that reached its maximum within 2 min after antigen stimulation. Following stimulation of BMMC with antigen in the absence of Ca2+, Ca2+ addition 1 to 5 min later time-dependently enhanced the histamine release, although the release was deteriorated by further extension of Ca2+ addition. In contrast, the releasability of HLMC was rapidly decreased. These results indicate that extracellular Ca2+ not only is prerequisite for anaphylactic histamine release from BMMC, but also may modulate the release and participate in some intracellular event(s) which has yet to be focused upon.

Anaphylaxis↗
PubMed1994

Radiation-chemical discussion on inverse dose-rate effect observed in radiation-induced strand breaks of plasmid DNA.

Experimental results of inverse dose-rate effect, so-called Kada Effects, which was published by Takakura and her coworkers on radiation-induced strand breaks of plasmid DNA in aerated aqueous solution, have been kinetically analyzed and discussed on the basis of radiation chemistry, the kinetic analysis indicates that there are two possible mechanisms; 1) equilibrium mixture of O2- and HO2 is responsible for strand breaks of DNA, and 2) peroxyl radical produced from citrate is effective for the strand breaks. However, the detailed kinetic analysis revealed that the latter is improbable because unimolecular decay of the peroxyl radical must be assumed to be negligible for its participation despite fast decay of analogous organic peroxyl radicals. The analysis has also given 9.93 +/- 0.10 dm3 mol-1 s-1 per nucleotide unit, which corresponds to 7.62 x 10(4) dm3 mol-1 s-1 per DNA molecule, as the rate constant for the reaction of the equilibrium mixture with plasmid pBR 322 DNA. Furthermore the probability that the reaction of the mixture with a nucleotide unit of DNA leads to strand breaks was obtained to be 3.36 x 10(-3) for gamma-irradiated system and 1.98 x 10(-3) for beta-irradiated system, respectively.

DNA↗
PubMed1994

Inhibitory effect of a selective thromboxane synthetase inhibitor, OKY-046, on acetaldehyde-induced bronchoconstriction in asthmatic patients.

We recently reported that inhaled acetaldehyde causes bronchoconstriction indirectly via histamine release in patients with asthma. The purpose of this study was to investigate a role of thromboxane A2 in acetaldehyde-induced bronchoconstriction in asthmatic airways. We investigated the bronchial response to inhalation of ascending doses (5, 10, 20, and 40 mg/ml) of acetaldehyde in nine asthmatic subjects who were treated with placebo or OKY-046, a selective thromboxane A2 synthetase inhibitor, of 200 mg twice a day for 3 days, and 200 mg on the fourth day (test day) in a double-blind, randomized, placebo-controlled, crossover fashion. Percentage decreases in FEV1 caused by 20 and 40 mg/ml of acetaldehyde inhalation were significantly (p < 0.05 and p < 0.01, respectively) prevented by the pretreatment with OKY-046. Geometric mean value (geometric standard error of the mean) of acetaldehyde concentration producing a 20 percent fall in FEV1 (PC20-Ac-CHO) was significantly (p < 0.01) greater with the OKY-046 pretreatment (72.2 [1.1] mg/ml) than with the placebo pretreatment (19.8 [1.2] mg/ml). We conclude that thromboxane A2 is one of contributors to acetaldehyde-induced bronchoconstriction in asthmatic subjects. It suggests that thromboxane A2 may play an important role in endogenous histamine-induced bronchoconstriction caused by acetaldehyde in asthmatic airways. We believe that this is a first report on the interaction between endogenous histamine and thromboxane A2 in asthmatic subjects.

Acetaldehyde↗
PubMed1994

Failure to detect brown adipose tissue uncoupling protein mRNA in benign symmetric lipomatosis (Madelung's disease).

We report a case of benign symmetric lipomatosis with hypothyroidism. Functional abnormalities and distribution of lipomas in benign symmetric lipomatosis suggest that the lipomas in this disorder may represent brown adipose tissue. In conditions where mRNAs of uncoupling protein, which is believed to be unique for brown adipose tissue mitochondria, were detected in one microgram of poly (A+) rat brown fat RNA, no signal at all was found in the lipomatous tissue, suggesting that the masses of benign symmetric lipomatosis are not functional brown adipose tissue.

Adipose Tissue, Brown↗
PubMed1994

Concurrent development of hemiplegia and angina pectoris in a 46-year-old man with familial hypercholesterolemia and elevated serum Lp(a) concentrations.

We report a 46-year-old man with familial hypercholesterolemia who simultaneously developed angina pectoris and left hemiplegia. Angiography revealed complete tapering occlusion of the right internal carotid artery and a 75% stenosis of the right coronary artery. In addition to hypercholesterolemia, his serum Lp(a) levels were very high, with a mean (+/- SE) of 62 +/- 2 mg/dl.

Angina Pectoris↗
PubMed1994

Cytostatin, a novel inhibitor of cell adhesion to components of extracellular matrix produced by Streptomyces sp. MJ654-NF4. I. Taxonomy, fermentation, isolation and biological activities.

Cytostatin has been identified as a novel inhibitor of cell adhesion to components of extracellular matrix (ECM) in cultured broth of Streptomyces sp. MJ654-NF4. Though cytostatin did not inhibit EL-4 cell adhesion to ECM components such as laminin and fibronectin; it inhibited the adhesion of B16 melanoma cells to laminin and collagen type IV but not to fibronectin. It exhibited antimetastatic activity on B16 melanoma cells in mice. The cytotoxicity of cytostatin are also reported.

Animals↗
PubMed1994

[Adhesion molecular and markers on endothelial cells].

Leukocyte endothelial cell interactions are mediated by adhesion molecules expressed on leukocytes and endothelial cells, resulting in extravasation of leukocytes and activation of the immune system. On the basis of the experiment using a murine endothelial cell line, F-2, the authors will review two issues; 1) the adhesion systems applied for endothelial cells, neutrophils and lymphocytes, and 2) production of cytokines in endothelial cells.

Animals↗
PubMed1994

[A case of systemic lupus erythematosus presenting with myelofibrosis as a cause of pancytopenia].

A 54 year-old woman who had a 6 month history of polyarthralgias, oral ulcers, weight loss and fatigue was admitted to the Urawa Municipal Hospital. She developed high fever, dyspnea and thrombocytopenia. Chest radiograph revealed massive right pleural effusion. At this time, laboratory investigations gave the following results: hemoglobin 12.7 g/dl, WBC 7700/microliters and platelet count 9.2 x 10(4)/microliters. Antibody to DNA was negative. Antinuclear antibody was positive at a titer of 320x in a centromere pattern; Anti-RNP and anti-Sm antibodies were negative. CH50 was 18.6 u/ml. C3 was 42.9 mg/dl. C4 was 11.5 mg/dl. Circulating immune complex (Clq) was 30.5 micrograms/ml. Circulating lupus anti-coagulant and anticardiolipine antibodies were positive. Thoracocentesis was performed; the material was a straw-colored exudate with over two thousands white cell per ul and showed marked reduction of complement titiers and elevated immune complex levels. She was then diagnosis as having SLE. Two weeks after admission, progressive leukopenia and anemia succeedingly occurred and resulted in severe pancytopenia. Bone marrow biopsy demonstrated marked marrow fibrosis and increased reticulin content with no evidence of malignancy. Steroid pulse therapy for 3 days started, and subsequently she was treated with 60 mg/day of prednisolone. Three weeks after starting on steroids, the massive pleural effusion was completely disappeared and complement titiers were normalized. Circulating immune complex has not been detected any more. After 8 weeks, the peripheral blood count was normalized. The dose of prednisolone was reduced progressively. On this occasion, the biopsy showed normocullular marrow with a marked reduction in the amount of reticulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Antinuclear↗
PubMed1994

[Aspiration cytology of salivary gland lesions--analysis of 55 cases].

Aspiration cytology of 55 salivary gland lesions (10 cases of non-neoplastic lesions, 36 cases of benign tumors and 9 cases of malignant tumors) were reviewed with histologic examination. Accuracy of benign and malignancy was 91.8% (benign lesion 97.6%, malignant tumor 57.1%), accuracy rates was almost of satisfactory for benign lesions, but not for malignant tumors. Agreement rate with histological type was 73.5%. One case (1.8%) was false positive, basal cell adenoma with adenoid cystic like pattern was falsely taken for adenoid cystic carcinoma. Three false negative cases (5.5%) consist of 1 acinic cell carcinoma, 1 adenoid cystic carcinoma with minimum cellular atypia and 1 partial malignant change (minor area) in pleomorphic adenoma. Six cases (10.9%) belong to group of insufficient material. Technical improvement of cell sampling is expected.

Biopsy, Needle↗