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Biomedical subjects

T Masuda

Publications and source records attributed to T Masuda.

At least 415 records · Page 23Linked to original sources
PubMed1992

Synergistic effects of interleukin 3 and interleukin 11 on murine megakaryopoiesis in serum-free culture.

We investigated the effects of interleukin 11 (IL-11) on murine megakaryopoiesis in serum-free cultures, using nonadherent, nonphagocytic, and T-cell-depleted bone marrow cells. IL-11 alone had no influence on megakaryocyte (Meg) colony formation in serum-free methylcellulose cultures, but it significantly enhanced the growth of Meg and granulocyte-macrophage-Meg colonies supported by optimal and suboptimal concentrations of interleukin 3 (IL-3). IL-11 also increased the size of IL-3-dependent Meg colonies as well as increasing the size and DNA content of constituent Meg. In liquid cultures, IL-11 alone did not increase the number of Meg, but it enhanced their size and acetylcholinesterase (AchE) levels. The addition of IL-11 to cultures containing suboptimal concentrations of IL-3 resulted in a synergistic increase of Meg AchE. These results suggest that IL-11, similarly to interleukin 6, has an effect on Meg and acts synergistically with IL-3 to augment murine megakaryopoiesis in vitro.

Acetylcholinesterase↗
PubMed1992

[Left ventricular approach for muscular ventricular septal defects in infant].

Two infants less than 4 months of age underwent repair of apical muscular VSD with left ventriculotomy. First case was 3 months old boy who had already undergone enlargement of the hypoplastic aortic arch with subclavian flap aortoplasty and pulmonary artery banding because of the associated aortic coarctation. Second case was 4 months old Down syndrome girl who associated with ASD and PDA. Both infants were diagnosed the apical muscular VSD with echocardiography and left ventriculography. We performed short longitudinal left ventriculotomy which was parallel to the left anterior descending coronary artery between the diagonal branch and left circumflex artery. VSD was closed with Gore-Tex patch using 6-0 prolene buttress stitches. Post operative echocardiography showed good LV contractile function (Ejection Fraction = 71%, 80%), and no residual interventricular shunt. Left ventriculotomy for the apical VSD closure allowed good exposure and did not reduce the LV function even in infants. Therefore, we concluded that left ventriculotomy was an useful procedure for the apical muscular VSD in infants.

Cardiac Surgical Procedures↗
PubMed1992

Lymphotoxin activates hepatic T cells and simultaneously induces profound thymic atrophy.

We have recently demonstrated that the liver may be a major site of extrathymic T-cell differentiation. This hepatic pathway was shown to be activated in mice injected with heat-killed bacteria. It is conceivable that the resulting activation of macrophages or lymphocytes, and the production of cytokines may be responsible for a subsequent activation of hepatic T cells. In this context, we investigated the possibility of whether certain cytokines may activate hepatic T cells. It was demonstrated that the administration of lymphotoxin [tumour necrosis factor-beta (TNF-beta)] more than doubled the number of hepatic mononuclear cells (MNC) yielded 3-5 days after the treatment. More strikingly, such treatment induced profound thymic atrophy and resulted in a decrease of more than 95% in the number of thymocytes. Spontaneous proliferation in an in vitro culture of hepatic MNC from treated mice increased, and inversely such activity of thymocytes decreased. The increased number of hepatic MNC was mainly due to an increase in intermediate alpha beta T-cell receptor (TcR) cells, which are extrathymic T cells uniquely seen in the liver. On the other hand, the thymic atrophy was caused by the prompt apoptotic death of dull alpha beta TcR cells with double-positive (DP) CD4+ CD8+ phenotype. These results indicate that lymphotoxin may be one of the factors that activates extrathymic T cells in the liver and at the same time inhibits intrathymic T-cell differentiation.

Animals↗
PubMed1992

[Frequency of Helicobacter pylori in chronic gastritis with endoscopically defined erosion].

The frequency of Helicobacter pylori was histopathologically evaluated in biopsy specimens of the gastric mucosa from 112 patients which endoscopically diagnosed as erosion. The specimens, histopathologically diagnosed as chronic gastritis, were divided into eight groups according to age, sex and location. The Helicobacter pylori infection was revealed in 65% of all specimens observed, and the frequency in patients of their sixties was lower than that of the forties. The frequency in the elder was the lowest in the transitional zone of the gastric mucosa. These findings indicate that the decrease in the frequency of Helicobacter pylori begins in the transitional zone and subsequently in the antrum.

Adult↗
PubMed1991

Acetyl-CoA carboxylase from Escherichia coli: gene organization and nucleotide sequence of the biotin carboxylase subunit.

Biotin carboxylase [biotin-carboxyl-carrier-protein:carbon-dioxide ligase (ADP-forming), EC 6.3.4.14] is the enzyme mediating the first step of the acetyl-CoA carboxylase [acetyl-CoA:carbon-dioxide ligase (ADP-forming), EC 6.4.1.2] reaction. We screened an Escherichia coli DNA library and a DNA fragment carrying the biotin carboxylase gene fabG, and its flanking regions were cloned. The gene for biotin carboxyl carrier protein was found 13 base pairs upstream of the fabG gene. Nucleotide sequencing of the recombinant plasmids revealed that the fabG codes for a 449-amino acid residue protein with a calculated molecular weight of 49,320, a value in good agreement with that of 51,000 determined by SDS/polyacrylamide gel electrophoresis of the purified enzyme. The deduced amino acid sequence of biotin carboxylase is also consistent with the partial amino acid sequence determined by Edman degradation. The primary structure of this enzyme exhibits a high homology with those of other biotin-dependent enzymes and carbamoyl-phosphate synthetase [carbon-dioxide:L-glutamine amino-ligase (ADP-forming, carbamate-phosphorylating), EC 6.3.5.5]; therefore, all these enzymes probably function through the same mechanism of reaction.

Acetyl-CoA Carboxylase↗
PubMed1991

Expansion of the population of double negative CD4-8- T alpha beta-cells in the liver is a common feature of autoimmune mice.

There have been several reports that double negative (DN) CD4-8- T alpha beta-cells might be responsible for the onset of autoimmune diseases in humans and mice. We previously revealed that such DN T alpha beta-cells are generated in the liver of autoimmune MRL-lpr/lpr mice. In the present study, we further characterize the histology of the liver in these mice by light and electron microscopic studies. An intensive accumulation of mononuclear cells in the liver was demonstrated and a significant proportion of these mononuclear lymphocytes was found to intimately interact with Kupffer cells or endothelial cells of the hepatic sinusoids. The majority of such lymphocytes were TcR+CD4-8-Pgp-1+ alpha beta-cells. Identification of DN T alpha beta-cells was then performed in various autoimmune model mice. Interestingly, all autoimmune mice tested (i.e., MRL-lpr/lpr, C3H/HeJ-gld/gld, BXSB, NOD, MRL(-)+/+ and NZB/W F1 mice), showed an increased proportion of DN T alpha beta-cells (greater than 11% among all MNC) in the liver when they became old and diseased. On the other hand, young and old normal mice and young autoimmune mice before the onset of disease did not have such a high proportion of DN T alpha beta-cells (less than 10%) in the liver. Among autoimmune mice, MRL-lpr/lpr and C3H/HeJ-gld/gld mice had lymphadenopathy, which consisted of DN T alpha beta-cells (greater than 25%), after the onset of disease. Autoimmune mice of the other strains had neither lymphadenopathy nor DN T alpha beta-cells in the periphery, even when they were diseased. These results suggest that the expansion of the DN T alpha beta-cell population in the liver is a common feature of autoimmune mice, irrespective of the information of lymphadenopathy.

Animals↗
PubMed1991

Reciprocal T cell responses in the liver and thymus of mice injected with syngeneic tumor cells.

We investigated the T cell responses in various tissues, especially in the liver and thymus, of mice injected with syngeneic tumors. This study was undertaken since recent evidence indicated that the liver is one of the important immune organs for T cell proliferation. When C3H/He mice were intraperitoneally injected with mitomycin-treated syngeneic MH134 tumors (1 x 10(7)/mouse), a transient increase of liver mononuclear cells (MNC) was induced, showing a peak at Day 4 after injection. Histological study of such liver showed a sinusoidal dilatation and an accumulation of MNC in the sinusoids. The most predominant MNC induced were double negative (CD4-8-) alpha beta T cells and gamma delta T cells. These gamma delta T cells varied, showing unique time-kinetics. Despite a continuous increase of whole liver MNC and alpha beta T cells, the proportion of gamma delta T cells in the liver decreased beginning 4 days after injection. In contrast with the response in the liver, a striking decrease in the cell number of thymocytes was induced after tumor injection, showing a basal level at Day 6. This hypocellularity in the thymus appears to be an inverted response of the lymphocytosis in the liver. At this time, a corresponding decrease in the proportion of double positive (CD4+8+) T cells was always seen in the thymus. Analysis of cell proliferative response showed that the increase of liver MNC after tumor injection was accompanied by augmented proliferation, whereas the decrease of thymocytes was accompanied by depressed proliferation. The present results indicate that there exists a unique, reciprocal response of T lymphocytes between the liver and thymus, and that the presence of tumor appears to stimulate T cell response in the liver but alternatively inactivates such response in the thymus.

Animals↗
PubMed1991

The appearance of T cells bearing self-reactive T cell receptor in the livers of mice injected with bacteria.

We demonstrated in the present study that with bacterial stimulation, an increased number of alpha/beta T cells proliferated in the liver of mice and that even T cells bearing self-reactive T cell receptor (TCR) (or forbidden T cell clones), as estimated by anti-V beta monoclonal antibodies in conjunction with immunofluorescence tests, appeared in the liver and, to some extent, in the periphery. The majority (greater than 80%) of forbidden clones induced had double-negative CD4-8-phenotype. In a syngeneic mixed lymphocyte reaction, these T cells appear to be self-reactive. Such forbidden clones and normal T cells in the liver showed a two-peak pattern of TCR expression, which consisted of alpha/beta TCR dull and bright positive cells, as seen in the thymus. A systematic analysis of TCR staining patterns in the various organs was then carried out. T cells from not only the thymus but also the liver had the two-peak pattern of alpha/beta TCR, whereas all of the other peripheral lymphoid organs had a single-peak pattern of TCR. However, T cells in the liver were not comprised of double-positive CD4+8+ cells, which predominantly reside in the thymus. The present results therefore suggest that T cell proliferation in the liver might reflect a major extrathymic pathway for T cell differentiation and that this hepatic pathway has the ability to produce T cells bearing self-reactive TCR under bacterial stimulation, probably due to the lack of a double-positive stage for negative selection.

Animals↗
PubMed1991

An appropriate in vitro culture condition for the induction of human TCR gamma delta + cells by heat-killed bacteria.

TCR gamma delta + cells proliferated when MNC were stimulated with various heat-killed bacteria. We investigated here the culture conditions for their maximum proliferation. MNC were cultured for 6 days with Streptococcus pyogenes, and for 3 days with T cell mitogens, PHA and anti-CD3 mAb, in medium supplemented with various concentrations (0.05-50%) of human sera. TCR gamma delta + and TCR gamma delta- CD2+3- double negative cells induced by Str. pyogenes required high concentrations of sera (greater than 6%) for their proliferation. Moreover, increased sera (up to 50%) greatly augmented their proliferation. On the other hand, TCR alpha beta + cell proliferation induced by T cell mitogens was supported by a small concentration (even 0.1%) of the sera, and the addition of high concentrations of sera (greater than 6%) somewhat suppressed responses. Similar serum requirement patterns were evident for the induction of cytotoxic cells. These results clearly demonstrated the existence of an appropriate culture condition for the proliferation of TCR gamma delta + cells induced in vitro.

Adult↗
PubMed1991

Surfactant apoprotein-A concentration in sputum for diagnosis of pulmonary alveolar proteinosis.

Pulmonary alveolar proteinosis (PAP), a disease characterised by accumulation of surfactant in alveoli, is diagnosed on the basis of invasive biopsy procedures. We have measured apoprotein A (SP-A) concentrations in sputum to see if this is useful for the diagnosis of PAP. Sputum samples from three patients with PAP and twenty patients with other pulmonary disease were assayed using monoclonal antibodies to SP-A. SP-A concentrations were 400 times higher in patients with PAP than in the controls, suggestions that this measurement is useful for the diagnosis of PAP especially where lung biopsy is contraindicated.

Anti-Infective Agents↗
PubMed1991

Distinct mechanisms of neonatal tolerance induced by dendritic cells and thymic B cells.

To assess the role of different types of antigen-presenting cells (APC) in the induction of tolerance, we isolated B cells, macrophages, and dendritic cells from thymus and spleen, and injected these into neonatal BALB/c mice across an Mls-1 antigenic barrier. One week after injection of APC from Mls-1-incompatible mice or from control syngeneic mice, we measured the number of thymic, Mls-1a-reactive, V beta 6+ T cells and the capacity of thymocytes to induce a graft-vs.-host (GVH) reaction in popliteal lymph nodes of Mls-1a mice. Injection of thymic but not spleen B cells deleted thymic, Mls-1a-reactive V beta 6+ T cells and induced tolerance in the GVH assay. The thymic B cells were primarily of the CD5+ type, and fluorescence-activated cell sorter-purified CD5+ thymic B cells were active. Injection of dendritic cells from spleen or thymus also induced tolerance, but the V beta 6 cells were anergized rather than deleted. Macrophages from thymus did not induce tolerance. Dendritic cells and thymic B cells were also effective in inducing tolerance even when injected into Mls-, major histocompatibility complex-incompatible, I-E- mice, but only thymic B cells depleted V beta 6-expressing T cells. Therefore, different types of bone marrow-derived APC have different capacities for inducing tolerance, and the active cell types (dendritic cells and CD5+ thymic B cells) can act by distinct mechanisms.

Animals↗
PubMed1991

Purification of megakaryocyte differentiation activity from a human fibrous histiocytoma cell line: N-terminal sequence homology with activin A.

We purified a protein possessing a potent ability to induce the differentiation of a murine megakaryoblastic cell line, L8057, from the supernatant of a human fibrous histiocytoma cell line, KHM-5M. The protein, a homodimer of a molecular weight of 25-kDa, has an N-terminal sequence identical with that of the beta A-chain of inhibin, indicating that it is identical to or highly homologous with activin A. Thus, it is speculated that activin A or its homologue is involved in megakaryocytic differentiation.

Activins↗
PubMed1991

Conserved V(D)J junctional sequence of cross-reactive cytotoxic T cell receptor idiotype and the effect of a single amino acid substitution.

A dominant T cell population bearing the cross-reactive idiotype of T cell antigen receptor (TcR) has been obtained using an anti-TcR monoclonal antibody (mAb) developed in syngeneic mice. Forty-four cytotoxic T cell (CTL) clones with reactivity to a mAb (N9-127) were selected out of 396 H-2Db-restricted CTL clones specific for FBL-3 tumor antigen from C57BL/6 mice. These CTL clones were divided into two groups according to the blocking pattern of cytotoxic activities with mAb N9-127. All eight CTL clones chosen from both groups expressed TcR with a specific combination of alpha and beta chains (V alpha 1J alpha 112-2/V beta 10D beta 2.1J beta 2.7), and the difference in the blocking susceptibility resided in a single amino acid substitution (Gly to Asp) in the D-J joint of beta chain. This provides direct evidence for the molecular basis of cross-reactive idiotypes of TcR recognized by mAb.

Amino Acid Sequence↗
PubMed1991

Peroxisomes in guinea pig liver: their peculiar morphological features may reflect certain aspects of lipoprotein metabolism in this species.

We have studied the ultrastructural characteristics and the distribution of peroxisomes in guinea pig liver using electron-microscopic cytochemistry for catalase and morphometry. By light microscopy, peroxisomes appear as dark 0.2-0.5 microns granules in the cytoplasm of liver parenchymal cells, often forming large clusters that measure up to 5 microns across. Rows of single peroxisomes or their aggregates line the sinusoidal surface of hepatocytes. Electron microscopy reveals that clusters of up to 25 individual peroxisomes are usually located in the subsinusoidal region of parenchymal cells. The mean diameter and the volume density of peroxisomes are larger in pericentral than in periportal regions of the liver lobule. Whereas large amounts of lipoprotein particles with a mean diameter of 160 nm (chylomicrons) are present in the Disse space, the cytoplasm of parenchymal cells contains multivesicular bodies and abundant lipid droplets. In addition, the Golgi complexes show distended lipoprotein-filled vesicles suggesting active biosynthesis of lipoproteins. We propose that the unique features of peroxisomes in guinea pig liver, such as cluster formation and alignment along the sinusoidal surface, may be related to the high levels of lipoproteins in the portal circulation and their hepatic catabolism in this species.

Animals↗
PubMed1991

A case of acute intermittent porphyria with acute pancreatitis.

A case of acute pancreatitis in a 29-year-old female associated with an attack of acute intermittent porphyria (AIP) is reported. Following the attack of AIP, serum pancreatic amylase originating from the pancreas increased transiently, and mild swelling of the pancreas was detected by ultrasonography. On this basis acute pancreatitis was diagnosed. Additionally, this patient had mild hepatic dysfunction. Laparoscopy disclosed diffuse slightly dark bluish pigmentation on the irregular surface of the liver. Mild fibrous dilatation of the portal area with lymphocytic infiltration was seen histologically. Acute pancreatitis and hepatic damage with AIP is extremely rare, however it is possible that these findings are etiologically connected in this patient.

Acute Disease↗