[A study on myocardial protection in valve replacement surgery].
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Heart Arrest, Induced↗
Biomedical subjects
H Maeda
Publications and source records attributed to H Maeda.
[Long term results of the treatment of oropharyngeal carcinoma].
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Adult↗
A new simple fluorometric assay for phagocytosis.
A highly sensitive, but simple and quantitative, fluorometric assay method for phagocytosis by cells such as macrophages and polymorphonuclear leukocytes was developed by utilizing fluorescent particles. Escherichia coli, Serratia marcescens, yeast, and latex particles were conjugated with fluorescein isothiocyanate and used as fluorescent particles. The assay procedure requires phagocytic cells, appropriate medium, fluorescent particles, sodium dodecyl sulfate, microtiter culture plate (24 wells), clinical centrifuge, and fluorescence spectrophotometer. One hundred assays can be done within 30 min after the incubation period. A time course analysis with this method showed that the phagocytosis of all these particles was dependent on temperature, and that the number of particles ingested by cells increased rapidly during the initial 30 min of incubation at 37 degrees C. Free fluorescent particles can be removed effectively by aspiration from the well. At 0 degree C, very few particles were ingested by cells or adsorbed onto the phagocytic cell surface as confirmed by fluorescence microscopy. An inhibitory effect of cepharanthin and sodium azide on phagocytosis was also confirmed by this method. The differential susceptibility of E. coli B and S. marcescens to phagocytosis also could be determined by this method.
Alkaloids↗
Trans-acting nuclear protein responsible for induction of rearranged human immunoglobulin heavy chain gene.
A complete human gamma 1 heavy chain gene (HIG1) was transferred into mouse cells by protoplast fusion. The HIG1 gene was strongly expressed in mouse myeloma cells but not in mouse fibroblasts (L cells). Nuclear extracts from myeloma cells were injected into L cell transformants containing one copy of the HIG1 gene; this triggered accurate transcription of the HIG1 gene in the transformants. The induction of HIG1 gene expression by a myeloma nuclear factor (or factors) appeared to depend on the enhancers in the heavy chain gene. Nuclear proteins prepared from cells of the B lineage could induce the transcription of HIG1 gene in the L cell transformants, while those from the cells of non-B-lineage could not. The present study shows that positive regulatory trans-acting factors are involved in the activation of the immunoglobulin heavy chain gene through its enhancers and are contained only in cells of the B lineage.
B-Lymphocytes↗
Dopaminergic facilitation of recovery from amygdaloid lesions which affect hypothalamic defensive attack in cats.
Influence of dopamine agonists, methamphetamine (MAT, 1 mg/kg, i.p.) and apomorphine (APO, 1 mg/kg, i.p.), on the effects of amygdaloid lesions on thresholds for the defensive attack behavior elicited by electrical stimulation of the ventromedial hypothalamic nucleus was studied in cats. The thresholds were measured in two situations, one with provocation by a human and the other without provocation. Electrolytic lesions of the basolateral part of the amygdala attenuated markedly facilitatory influences of the visual provocation on the thresholds, but subsequent administration of MAT or APO rapidly abolished the effects of the lesions. The effects of MAT lasted for at least 3.5 h while the effects of APO were of shorter duration. The results were discussed from the viewpoint of possible rapid compensation by the remaining intact tissue of the amygdala which was produced by excessive dopaminergic inputs to it.
Aggression↗
Suppression of interferon gamma production in mice treated with carrageenan.
Effects of carrageenan (CAR) treatment on the response of interferon (IFN) production in vivo and in vitro after stimulation with an IFN-gamma inducer, staphylococcal enterotoxin A (SEA), was investigated. The IFN-gamma production in mice stimulated with SEA was impaired after i.v. administration of a 20 mg/kg dose of CAR. Spleen cells (SC) from CAR-treated mice had decreased ability to produce IFN in vitro after stimulation with the same inducer. SC obtained from mice during the suppressive state inhibited IFN-gamma production when they were co-cultured with mononuclear cells prepared from spleens of untreated control mice. This suppressor cell activity could be removed from SC by an adherence technique to plastic surface. The SC with suppressor activity were not inactivated by treatments with monoclonal anti-Thy-1.2 antibody, anti-asialo GM1 antisera and anti-mouse immunoglobulin antisera followed by complement. The suppressive activity was detected in cell-free culture fluids of macrophage fractions containing suppressor cell activity. These results suggest that the decrease in IFN-gamma production in mice pretreated with CAR may associate with the presence of suppressor cells characterized to the monocyte/macrophage lineage.
Animals↗
Enhancement of vascular permeability upon serratial infection: activation of Hageman factor--kallikrein--kinin cascade.
A zinc dependent serratial 56K protease caused enhancement of vascular permeability followed by edema formation when injected into the guinea pig peripheral cornea, the subconjunctival space, or the skin. Because this enhancement was not affected by antihistamine, involvement of the kinin-generating system in this permeability enhancement was investigated. The 56K protease induced permeability much greater extent than that by bradykinin on weight basis, and more so on molar basis. The phenomenon was inhibited by soybean trypsin inhibitor, a well known inhibitor of plasma kallikrein, and also by corn trypsin inhibitor, which is the best inhibitor of the activated Hageman factor. In vitro experiments using numbers of synthetic peptide substrates, the 56K protease exhibited a similar substrate specificity to that of plasma kallikrein. Kallikrein is a known endogenous activator of Hageman factor. The enhancement by 56K protease was greatly augmented by inhibition of kininase II with Glu-Trp-Arg-Pro-Gln-Ile-Pro-Pro-OH (SQ 20,881), suggesting generation of bradykinin. Thus, these results indicate that the enhancement of vascular permeability induced by the 56K protease is caused by an activation of Hageman factor by 56K protease followed by subsequent activation of cascade amplification, and resulted in kinin generation in vivo.
Animals↗
Reexamination of the primary structure of an antitumor protein, neocarzinostatin.
The primary structure of an antitumor protein, neocarzinostatin, has been reinvestigated by conventional and gas-phase Edman degradation procedures. Sequence analyses of tryptic peptides of both S-carboxymethylated and S-aminoethylated derivatives as well as peptic peptides of the native protein revealed a revised primary structure of neocarzinostatin. The present sequence of 113 amino acid residues thus established agrees with results obtained by fast atom bombardment and gas chromatographic mass spectrometry which were published recently [B.N. Gibson, W.C. Herlihy, T.S.A. Samy, K.S. Hahm, H. Maeda, J. Meienhofer, and K. Biemann (1984) J. Biol. Chem. 259, 10801-10806]. The assignment of four intriguing asparagine/aspartic acid residues has been also achieved.
Amino Acid Sequence↗
An ultrastructural study of acute and long-term lung response to commercial diatomaceous earth.
The acute pulmonary effects of intratracheally instilled particles of calcined diatomaceous earth were found to include a pronounced neutrophil invasion of the bronchioles by 4 h after exposure which remained well developed through 1 day post-exposure. The number of macrophages and neutrophils in the alveoli continued to increase through 1 day post-exposure and remained above control values through 7 days post-exposure. The number of macrophages, many of which contained diatomaceous earth, remained elevated for the duration of the experiment. Most phagocytosis of the particles was carried out by macrophages, with minor participation by neutrophils. Many of the reactive macrophages in the groups with post-exposure periods longer than 2 h showed various types of pathological alterations. A few particles were found in type I epithelial cells. Oedematous changes were observed in some type I epithelial cells and proliferation of type II epithelial cells was evident in some alveoli, particularly those near the respiratory bronchioles. Mild diffuse fibrosis was first observed at 6 months and was still present at 15 months but remained confined to the areas containing the diatomaceous earth.
Animals↗
Delayed reinforcement of switch-off behavior and amygdaloid lesions in cats.
Effects of amygdaloid lesions on the switch-off behavior (SOB) and behavioral changes induced by a delayed reinforcement (DR) for SOB were investigated in 12 cats. The DR consisted of putting a delay time of 1.6 or 2.4 sec between a plate-pushing response and the actual termination of hypothalamic stimulation, and it produced a marked prolongation of response time for SOB (delay phenomenon). Bilateral electrolytic lesions of the amygdala had only limited effects on the SOB and the delay phenomenon; they tended to enhance the prolongation of response time induced by DR in 6 cats and it was accompanied by mild prolongation of response time of subsequent immediate reinforcement trials. These effects were interpreted to be due to apparent attenuation of emotion-producing potency of the hypothalamic stimulation, induced by reduction of facilitatory environmental influences on it.
Amygdala↗
TA10 and 2B3, two new alleles in the HLA-DQ region recognized by monoclonal antibodies.
The monoclonal antibodies (MoAbs) A10/13 and IIB3 were studied in parallel with routine HLA-DR typings. The specificities TA10 and 2B3, recognized by A10/13 and IIB3 MoAb, respectively, showed clear segregation in families and never occurred together on the same haplotype. TA10 and 2B3 appeared to be in perfect Hardy-Weinberg equilibrium. The TA10 specificity is DQw3 related and is in linkage disequilibrium with DR5 (DRw11 and DRw12) and it is also weakly associated with DR4. The 2B3 specificity is DQw1 related and it is in linkage disequilibrium with DR2, DR4, DRw9, and DRw13. The 2B3 and TA10 specificities appear to be alleles of a polymorphic system, closely related, but different from HLA-DQ.
Alleles↗
Molecular characterization of three HLA class II molecules on DR4 and DRw9 haplotypes: serologic and structural relationships at the polypeptides level.
By using alloantisera, three distinct HLA-D/DR region-encoded class II molecules were identified from cells carrying the HLA-DR4 and DRw9 haplotypes. Both DRw-53 and DQw3 molecules that bear the "supertypic" specificity were isolated independently from the DR antigen. The light chains of the DR4 antigens from different HLA-D types were distinct from one another, whereas the DRw53 molecules had identical charge and molecular weight in both heavy and light chains. On the other hand, the DQw3 molecules from the DR4 cell lines (Dw4 and Dw 10) were apparently identical but were polymorphic at least in the light chains among the DR4, DR5, and DRw9 haplotypes. In addition, monoclonal antibodies which specifically precipitate DR4 and DQw3 molecules have been isolated. The variable extent of homogeneity and diversity of three class II molecules may aid in our understanding of the role of class II antigens in the human immune regulation.
Antibodies, Monoclonal↗
Experimental pulmonary cavity formation by mycobacterial components and synthetic adjuvants.
An investigation was undertaken to determine the components of mycobacteria responsible for pulmonary cavity formation in tuberculosis. Rabbits received an intrapulmonary injection through the chest wall, of mycobacterial protein, II-p, mixed with either mycobacterial lipids, synthetic adjuvants or Nocardia cell wall skeleton as adjuvant. Six weeks later, they were killed and the lung lesions were examined. Cavities and necrosis were produced by the injection of II-p mixed with cord factor, Nocardia cell wall skeleton or N-acetylmuramyl dipeptide conjugated with long-chain branched fatty acids. Cavities were not produced by either the injection of II-p together with phospholipid, N-acetylmuramyl dipeptide (MDP), MDP-derivatives having no long-chain branched fatty acid, or by the injection of individual components of the mixtures. The results suggest that in tuberculosis a mycobacterial component with a long-chain branched fatty acid such as mycolic acid plays an important role in pulmonary cavity formation by enhancing the antigenicity of mycobacterial protein and helping it induce cell-mediated immunity at the site of the lesion. Passive transfer with sera from rabbits highly sensitized with tubercle bacilli failed to enhance cavity formation in the recipient animals.
Adjuvants, Immunologic↗
Multiple epitopes on a single DQ molecule from the DQw3-carrying haplotypes.
Multiple polymorphisms on the DQ molecule(s) have been detected by monoclonal antibodies (MoAbs). Among these, TA10 and IIB3 have been described as two new alleles in the DQ region other than the conventional DQw1-w3 allelism. The TA10 specificity is DQw3-related and is in linkage disequilibrium with DR5 and weakly associated with DR4. The IIB3 specificity is DQw1-related and is in linkage disequilibrium with DR2, DR4, DRw9 and DRw13. Thus, the DQw3-carrying haplotypes are either positive with TA10 or IIB3. The molecular and topological analysis has revealed that both TA10 and IIB3 determinants were expressed on a single DQ molecule that also carried the DQw3 determinants on DR5 and DR4 cell lines, respectively. Thus, a single DQ molecule generated multiple epitopes detected by alloantisera and/or MoAbs at least on the DQw3-carrying haplotypes. These would be useful for unraveling the largely unknown functions of the DQ class II molecules.
Antibodies, Monoclonal↗
Cytology of fetal ascites and antenatal diagnosis of meconium peritonitis.
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Adult↗
Immunocytochemical detection of normal and abnormal megakaryocytes using monoclonal antibody to glycoprotein IIb-IIIa (TP80): the quantitative assay in normal and in leukaemic patients.
We identified bone marrow megakaryocytes by an immunocytochemical technique using a monoclonal antibody (TP80) against platelet glycoprotein IIb-IIIa (GPIIb-IIIa). The immunocytochemical technique using TP80, specific to megakaryocytes, enabled us to observe cellular morphology and immunological reaction under light microscopy, and permitted quantitative assessment of megakaryocytes. In normal marrow, TP80 labelled 22 +/- 5 megakaryocytes/10(4) mononuclear cells (mean +/- 1 SD, n = 14). In addition to typical large megakaryocytes, small immature megakaryocytes (less than or equal to 20 micron) were recognized in 10-15% of total megakaryocytes. 4 out of 18 patients with acute myeloblastic leukaemia and 9 of 10 patients with myelodysplastic syndrome showed increased numbers of megakaryocytes. In these patients, cell size distribution was abnormal, i.e., most of the megakaryocytes consisted of small, atypical megakaryocytes. None of the patients with acute lymphoblastic leukaemia showed increased megakaryocytes. Immunocytochemical identification of megakaryocytes using a specific antibody is useful to quantitate the megakaryocytes and to detect the proliferation of atypical megakaryocytes in several leukaemic conditions.
Acute Disease↗
Effect of excisional wounding on DMBA-induced hamster tongue carcinogenesis.
The purpose of this study was to investigate histologically the effect of wounding on the hamster tongue after pretreatment with DMBA. The animals in which the tips of the tongues were pretreated with DMBA for 8 weeks, subsequently excised, and had no treatment or received applications of acetone, showed epithelial dysplasias. The animals which had the same pretreatment, excision, and received additional post-excision applications of DMBA for 9-13 days, developed squamous cell carcinomas. However, the animals which were pretreated with DMBA for 8 weeks but had no excision, did not show any pathologic changes, even though they received additional applications of DMBA for 9-13 days. The animals which received no pretreatment with DMBA for 8 weeks but had an excision, showed normal wound healing, even though they had a post-treatment with DMBA for 9-13 days. The results of the present study indicated that excisional wounding acted as a promotional stimulus in inducing the appearance of epithelial dysplasias or carcinomas of tongues initiated with the carcinogen DMBA.
9,10-Dimethyl-1,2-benzanthracene↗
Degradation of protease inhibitors, immunoglobulins, and other serum proteins by Serratia protease and its toxicity to fibroblast in culture.
We investigated the effect of the extracellular protease of Serratia marcescens on human serum constituents such as immunoglobulins, fibronectin, alpha 1-protease inhibitor, alpha 2-macroglobulin, lysozyme, and transferrin. At a very low concentration of Serratia 56-kilodalton protease (56K protease), purified human plasma fibronectin was degraded rapidly into three structural domains or small fragments. Immunoglobulin G3 (IgG3) and IgA1 were also degraded within 30 min with 1 microgram of this protease per ml, more rapidly than their other subclass of IgG or IgA. alpha 1-Protease inhibitor, which did not inhibit the 56K protease, was degraded similarly by the protease. These events were demonstrated by fluorescence polarization and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The protease was considerably inhibited by human alpha 2-macroglobulin and chicken ovomacroglobulin. However, when there was a 2 M excess of ovomacroglobulin or a 4 M excess of alpha 2-macroglobulin over the 56K protease, about 25 or 40% proteolytic activity remained, respectively. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that the protease degraded the alpha 2-macroglobulin extensively during prolonged incubation, which paralleled with regeneration of the protease activity. The protease also cleaved human lysozyme, although moderately. Human serum transferrin was degraded slightly, and human serum albumin was almost resistant to the 56K protease. The enzyme seemed to have no effect on reconstituted collagen, but it degraded rat tropocollagen and yielded fragments of beta and gamma chains by cleaving the intramolecular cross-links. Most of the above proteolysis by the 56K protease appears to result in a limited type of substrate specificity. Thus, the present study demonstrates that the protease is capable of degrading defense-oriented humoral proteins and tissue constituents. Furthermore, it is toxic to fibroblasts. These findings also clarified the possible role of Serratia protease as a virulence factor in the pathogenesis of serratial infections. We recently demonstrated this notion in vivo with rabbit cornea (R. Kamata et al., Ophthalmology 92:1452-1459, 1985).
Blood Proteins↗