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Biomedical subjects

N Okamura

Publications and source records attributed to N Okamura.

At least 217 records · Page 12Linked to original sources
PubMed1982

The eosinophilic and amyloid-like materials in adenomatoid odontogenic tumor.

This paper is concerned with the relationship between eosinophilic material (EM) and amyloid-like material and adenomatoid odontogenic tumors. In duct-like structures between opposing rows of tall columnar cells, EM did not stain for amyloid. Under electron microscopy, EM was composed of fibrillar and granular materials, and the fibrillar material was not amyloid. Two different kinds of EM were found in solid cell masses. Lesions from cases 2, 3, 4 and part of case 1 contained small droplet-shaped EM and these EM did not stain for amyloid. Case 1 also contained EM that stained positively for amyloid. The structure of amyloid positive EM resembled developing enamel of human tooth germs. This material was tubular and finely granular. The tubular material resembled enamel matrix fibers rather then amyloid and the fine granular material was stippled. The cells surrounding EM appeared similar to ameloblasts between secretory and maturation stages.

Adolescent↗
PubMed1982

Outer membrane mutants of Salmonella typhimurium LT2 have lipopolysaccharide-dependent resistance to the bactericidal activity of anaerobic human neutrophils.

The capacity of neutrophil polymorphonuclear granulocytes (PMNs) to phagocytize bacteria under anaerobic as well as aerobic conditions afforded the opportunity to compare the bactericidal activities of oxygen-independent and oxygen-dependent antimicrobial mechanisms in human PMNs challenged with Salmonella typhimurium LT2 and its lipopolysaccharide mutants (outer membrane mutants). Anaerobic human PMNs challenged with either opsonized LT2 or serum-treated zymosan failed to produce detectable superoxide anion (O2-) or to reduce nitroblue tetrazolium, although aerobic PMNs readily produced O2- in response to such challenge. Anaerobic PMNs killed these bacteria in an ordered fashion that appeared to be dependent on their lipopolysaccharide chemotype. As the carbohydrate content of the mutant lipopolysaccharide decreased, the bacteria became less resistant to the oxygen-independent bactericidal activity. The results resembled the ordered resistance to oxygen-independent killing observed with LT2 and its mutants in PMN-free systems with PMN granule proteins. Studies on the kinetics of killing showed these to be less rapid in anaerobic as compared with aerobic conditions. Opsonization increased the rate of phagocytosis, but such factors as opsonization and the rate of phagocytosis did not appear to affect intraleukocytic bactericidal capacity in that the resultant proportion of bacteria remaining viable after ingestion was similar regardless of which serum was used (normal serum, C6-deficient serum, C8-deficient serum, or no serum at all). The results are consistent with an active and substantial participation by oxygen-independent systems in the antimicrobial effects of neutrophils.

Anaerobiosis↗
PubMed1980

Cooperation of cytochalasin D and anti-microtubular agents in stimulating superoxide anion production in polymorphonuclear leukocytes.

Superoxide anion production in polymorphonuclear leukocytes obtained from guinea pig peritoneal cavities was stimulated by treatment with 5 microgram/ml of cytochalasin D in vitro. The stimulation was further enhanced by the addition of either 10(-5)-10(-7) M vinblastine or 10(-3)-10(-8) M colchicine to cytochalasin D. Higher concentrations of these anti-microtubular agents were inhibitory to the stimulating effect of cytochalasin D on the superoxide anion production, while lower concentrations had almost no effect. In the resting leukocytes, i.e. without cytochalasin D, the anti-microtubular agents by themselves had no effect on the superoxide anion production. The cooperation of cytochalasin D and the anti-microtubular agents was also observed in the stimulation of NADPH oxidase activity and bactericidal function of the leukocytes.

Animals↗
PubMed1979

Evidence for bactericidal activity of polymorphonuclear leukocytes without phagocytosis.

The relationship between phagocytosis and bactericidal action of polymorphonuclear leukocytes was examined by comparing the functions of cytochalasin D-treated leukocytes with those of the control. Measurement of phagocytotic and bacterial DNA-degrading activities using Escherichia coli prelabeled with [3H]thymidine revealed that phagocytosis and bacterial DNA degradation were inhibited by treatment with cytochalasin D to about 50 and 10% of the control, respectively. Nevertheless, the bactericidal activity of the cytochalasin D-treated leukocytes was almost the same as that of the control leukocytes; almost all the bacteria were phagocytized by the latter leukocytes. Under the same experimental conditions, the production and release of superoxide anions and hydrogen peroxide, which are both known to be involved in the bactericidal action of the leukocytes, were markedly increased by cytochalasin D. Release of several lysosomal hydrolases was also increased markedly by cytochalasin D treatment, except for myeloperoxidase. However, lactate dehydrogenase, a typical cytosolic marker, was not released by the same treatment. Thus, it is unlikely that the increase in the release of the above-mentioned bactericidal factors was due to decomposition of the leukocytes. These results indicate that the site of bactericidal action of cytochalasin D-treated leukocytes is not necessarily intracellular but may be around the external surface of the cells.

Animals↗
PubMed1978

Change of coupling system of receptor-adenylate cyclase induced by epinephrine and GTP in plasma membranes of rat liver.

1. The binding of [3H]epinephrine to plasma membranes was affected (temporary release of bound epinephrine and characteristic retardation of epinephrine binding) not only by GTP but also by dGTP and guanylylimidodiphosphate, whereas the binding of [3H]dihydroalprenolol was not affected by GTP. GTP affected the binding of [3H]epinephrine in the presence of alpha-antagonists, but not in the presence of beta-antagonists, suggesting that the GTP effects are specific to beta-agonists and beta-receptors. 2. The half-maximal release of bound [3H]epinephrine was found at 8.8 . 10(-6) M GTP in the absence of ATP, whereas it was found at 1.6 . 10(-6) M GTP in the presence of 0.3 mM ATP in coincidence with the half-maximal activation of adenylate cyclase by GTP in the presence of 0.3 mM ATP (as measured at 30 s of incubation). 3. In the presence of 4 . 10(-5) M GTP, adenylate cyclase activity as measured at 30 s of incubation (State I) tended to increase with epinephrine concentration, showing no saturation tendency even at 1 . 10(-4) M epinephrine. The activity of State II, which is established at 4 min of incubation, was much lower than that of State I but was found to reach a plateau as the epinephrine concentration increased, showing half-maximal activation at an epinephrine concentration between 2 . 10(-6) and 2 . 10(-7) M. 4. Apparent kinetic parameters (Km and V) for State I as assayed at 30 s of incubation suggested that GTP alone may increase V slightly, whereas epinephrine plus GTP may increase the V to a further extent and simultaneously decrease the Km. 5. Adenylate cyclase of plasma membranes pretreated with epinephrine plus GTP was stimulated by GTP alone similarly to untreated membranes, but it was no longer responsive to the synergistic activation by epinephrine plus GTP. Accordingly, the binding of [3H]epinephrine to the pretreated plasma membranes was no longer affected by GTP. 6. The results of the present study seem to support the idea that the most active and coherently coupling state (State I) of the beta-receptor-adenylate cyclase system generated in the presence of epinephrine plus GTP is very labile and degenerates before reaching equilibrium. In turn, State II, in which the coherently coupling mechanism is largely impaired, seems to be established in due time. The characteristic biphasic kinetics of [3H]epinephrine binding in the presence of GTP seem to be related to the above change occurring in the beta-receptor-adenylate cyclase system.

Adenylyl Cyclases↗
PubMed1977

Prostaglandin receptor-adenylate cyclase system in plasma membranes of rat liver and ascites hepatomas, and the effect of GTP upon it.

1. Adenylate cyclase in plasma membranes from rat liver was stimulated by prostaglandin E1, and to a lesser extent by prostaglandin E2. Prostaglandin F1alpha and A1 did not stimulate the cyclase. The prostaglandin E1-mediated activation was found to require GTP when the substrate ATP concentration was reduced from 3 mM to 0.3 mM in the reaction mixture. Adenylate cyclase of the plasma membranes from rat ascites hepatomas AH-130 and AH-7974 was not stimulated by prostaglandin E1 in the presence or the absence of GTP, although the basal activity of adenylate cyclase as well as its stimulation by GTP alone were similar to normal liver plasma membranes. 2. Liver plasma membranes were found to have two specific binders for [3H] prostaglandin E1 with dissociation constants of 17.6-10(-9) M and 13.6-10(8) M (37 degrees C) and one specific binder for [3H]prostaglandin F2alpha with a dissociation constant of 2.31-10(8) M (37 degrees C). The specific binders for prostaglandin E1 could not be detected in the hepatoma plasma membranes. 3. Binding of [3H] prostaglandin E1 to the liver plasma membranes was exchange by, GTP dGPT, GDP, ATP and GMP-P(N)P, but not by GMP, CGMP, DTTP, UTP or CTP. The increase in the binding of [3H] prostaglandin E1 was found to be due to the increased affinity of the specific binders to prostaglandin F2alpha was not affected by GTP. 4. GTP alone was found to increase V of adenylate cyclase of liver plasma membranes, while GTP plus prostaglandin E1 was found to decrease Km of adenylate cyclase in addition to the increase of V to a further extent.

Adenosine Triphosphate↗
PubMed1977

Rough mutant of Shigella flexneri 2a that penetrates tissue culture cells but does not evoke keratoconjunctivitis in guinea pigs.

A rough mutant, designated 5503-01, has been isolated from a virulent strain of Shigella flexneri 2a 5503. Strain 5503-01 produced smooth opaque colonies, whereas its parent strain produced characteristic green-gold translucent ones. Characterization of 5503-01 by agglutination tests, rhamnose content, and sensitivity spectra to "rough-specific" phages revealed that it had lost the specific somatic antigens. When 5503-01 was used to infect HeLa or L cells, it penetrated the cells and multiplied within the cytoplasm. On the other hand, it could not evoke keratoconjunctivitis in guinea pigs. The properties of this strain were remarkably stable against serial passages and preservation for a long period. The presence of a rough mutant with the ability to penetrate tissue culture cells suggest that specific O antigen is not of significance in the early step of the invasive process of shigellosis.

Animals↗
PubMed1976

Comparison of the epinephrine-mediated activation of adenylate cyclase in plasma membranes from liver and ascites hepatomas of rats.

(1) The apparent [3H]epinephrine binding parameters of plasma membranes from rat liver and ascites hepatomas such as AH-7974, AH-371A and AH-130, as measured by equilibrium dialysis and/or Millipore filtration, were almost similar to each other. The epinephrine binding sites in the plasma membranes were heterogenous (alpha, beta-receptors and non specific sites), but the pattern of these binding sites in the liver membranes appeared almost similar to that in the hepatoma membranes. 2. The beta-receptor seemed to be specifically involved in the epinephrine-mediated activation of adenylate cyclase of the liver membranes. In spite of the presence of almost similar beta-receptors and adenylate cyclase, the adenylate cyclase of hepatoma membranes was found to be less sensitive to the epinephrine-mediated activation. 3. GTP alone was found to activate adenylate cyclase of liver and hepatoma membranes to some extents when the concentration of ATP was lower (0.3 mM). When GTP was added with epinephrine, a marked, synergistic activation of adenylate cyclase was observed in liver plasma membranes, but not in hepatoma ones. 4. The synergistic activation of adenylate cyclase by epinephrine plus GTP showed a characteristic kinetic feature, reaching a maximal peak within 1 min or so after mixing. 5. Binding of [3H]epinephrine to liver membranes proceeded monophasically in the absence of GTP, while it proceeded biphasically in the presence of GTP, showing the retardation of binding at some earlier stages. GTP added at the time of binding equilibrium induced the temporary release of bound epinephrine from the beta-receptors. The GTP-induced temporary release of bound epinephrine, occurring within 4-5 min after the addition of GTP, was less marked in the hepatoma membranes as compared with the liver membranes. 6. Possible impairment of the GTP-dependent coupling mechanism in the receptor-adenylate cyclase system of hepatoma plasma membranes was suggested.

Adenylyl Cyclases↗
PubMed1976

Method for determining pilot stress through analysis of voice communication.

Factors inherent in aircraft communication systems hinder customary approaches to voice analysis in the determination of the degree of stress experienced by a pilot during an inflight emergency. By means of a sound spectrogram, the mean vibration space of a voice can be analyzed if the space between the vertical deflections of the vowel sounds is calculated in micrometers. The vibration space shift rate (VSSR) is calculated by comparing the widest vibration space of the voice during the normal phase of the same flight (standard vibration space: SVS) with that encountered during the emergency situation (EVS) by the following formula: VSSR = ((SUS-EVS)/SUS) X 100%. The number of measuring points in each case differs in regard to the length of communication during the emergency. The VSSR can be divided into three phases - normal, urgent, and emergency - each with three grades of 0.5 S.D. apiece.

Adult↗