Coagulation and fibrinolysis abnormalities in the acute stage of hypertensive intracerebral hemorrhage, with special reference to fibrinopeptides A and B beta 15-42.
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Aged↗
Biomedical subjects
Y Ohno
Publications and source records attributed to Y Ohno.
[Statistical study on tumors of the urinary bladder--multivariate analyses of prognostic determinants for bladder cancer].
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Analysis of Variance↗
[Comparative studies of human natural IFN-alpha, IFN-beta and IFN-gamma with regard to their effects on in vitro immune responses].
Interferon (IFN) is known to affect a variety of immune responses apart from its well-established antiviral and antineoplastic effects. Three human IFN species: IFN-alpha, IFN-beta and IFN-gamma are now clinically available as a result of recent rapid improvements in IFN technology. In view of only the scanty data presently available concerning comparative studies among IFNs with regard to their effects on immune regulation, this report deals comparatively with natural IFN-alpha, IFN-beta and IFN-gamma (all products of Green Cross) with respect to their effects on natural killer cell (NK) activity, chemiluminescence (CL) of fractionated NK cells, lymphoproliferative response induced by PHA, PWM and Staphylococcus aureus COWAN-1 (SAC), and IL-2 production under stimulation with PHA (1:1000). Comparison among IFNs for these immune responses was performed with the same level of antiviral activity (IU). NK activity in the peripheral blood was enhanced in the presence of IFN of all species: to the same extent with IFN-alpha and IFN-beta, but significantly less for IFN-gamma as compared with the former. CL of NK cells to IFN was again similar in extent for IFN-alpha and -beta, but less for IFN-gamma. Inhibition of PHA and PWM blastogenesis was similar for IFN-alpha and -beta but less for IFN-gamma as shown previously. SAC blastogenesis of both peripheral lymphocytes and tonsillar B cells was enhanced in the presence of IFN-gamma but not in the presence of IFN-alpha or -beta. IL-2 production of peripheral lymphocytes by PHA (1:1000) was dose-relatedly enhanced in the presence of IFN-gamma but not in the presence of IFN-gamma or -beta.
Cells, Cultured↗
Establishment of a novel acute monoblastic leukemia cell line (YK-M2) having a near-triploid karyotype.
The YK-M2 cell line was established from the peripheral blood of a patient with acute monoblastic leukemia in whom an anterior mediastinal tumor preceded the peripheral blood manifestation. The established cells grew in a single cell suspension with a doubling time of 60 h and consisted of primitive monoblastic cells. The cells were 52% positive for peroxidase staining and manifested strongly positive activity of alpha-naphthyl acetate esterase, which was completely inhibited by sodium fluoride. The cells showed strong expression of Fc gamma receptors and phagocytosed sensitized ox erythrocytes. When the cells were incubated with 1 alpha,25-dihydroxy-vitamin D3, they were induced to differentiate into mature monocyte-macrophage-like cells, which reduced the nitroblue tetrazolium dye and released a small amount of the superoxide anion. Cytogenetic studies revealed that the cells had a near-triploid karyotype with a modal chromosome number of 68, and the short arm of one No. 17 chromosome was deleted [del(17)(p11)]. The YK-M2 cell line is particularly unique in that the cells retained the polyploid karyotype that may be an initial cytogenetic change in the malignant transformation of the parent leukemia cells.
Adult↗
[Relations between neonatal heart rate variability and the behavioral state].
In sixty healthy newborn infants the relations between the neonatal heart rate variability (NHRV) and the behavioral state were investigated. The infants were divided to subsequent two subgroups according to the mode of delivery. One was normal vaginal delivery (N = 47), and the other was elective cesarean section (N = 13). R-R intervals less than 280 msec and more than 700 msec were excluded. The maximum difference in successive R-R intervals accepted was 60 msec. The standard deviation of R-R intervals as LTV index and the mean of absolute beat to beat difference as STV index were calculated with a minicomputer. The behavioral states were classified according to Prechtl's criteria. The LTV in state 2 and state 4 increased progressively and reached its maximum level on the third day after birth. The change of STV was neither consistent nor significant. In state 5, both the STV and the LTV were very low. The discriminant function gave percentages of correct classification of 85-100% for the active quiet states. The NHRV was similar in state 1 and state 3, and in state 2 and state 4 respectively. There was an increase in the LTV during the 24 hours after birth in the CS group. Thus, neonatal adaptation of CS differs from that of normal labor.
Adaptation, Biological↗
[A case-control study of prostatic cancer--with reference to dietary history].
The incidence rate of prostatic cancer in Japan is gradually increasing and the factor of its increase can be due to the environmental change "europeanization", especially of the dietary life. A Japanese-dutch case-control study for prostate cancer has been carried out in order to elucidate the environmental risk factors of prostatic cancer. Of Japan side, as far as dietary part of the result is concerned, vitamin A might be risk reducing factor for prostatic cancer when prostatic cancer is compared to benign prostatic hyperplasia or general control.
Aged↗
Pathologic fracture of the femur secondary to amyloid deposition.
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Adult↗
Studies of fibrinopeptide A, fibrinopeptide B beta 15-42, HMW-kininogen and kinin in cases of caesarean section.
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Cesarean Section↗
[An autopsy case of adult neuroblastoma].
The patient was a 31-year-old man with neuroblastoma of the right adrenal gland, which presented at first as metastatic spinal epidural tumor. Catecholamine and its products in the blood and urine and neuron-specific enolase in the blood were increased. Six months after right adrenectomy followed by chemotherapy, the patient died due to cachexia. Autopsy revealed widespread metastasis. By electron microscopy, the centers of the Homer-Wright rosettes were occupied by neuropil-like structures consisting of a number of cytoplasmic processes of tumor cells, but no cored vesicles were found either in the processes or perikaryons of the tumor cells.
Adrenal Gland Neoplasms↗
Reevaluation of cytochrome b and flavin adenine dinucleotide in neutrophils from patients with chronic granulomatous disease and description of a family with probable autosomal recessive inheritance of cytochrome b deficiency.
Chronic granulomatous disease (CGD) is a genetically heterogeneous syndrome characterized by a microbial killing defect of polymorphonuclear leukocytes (PMNs) due to lack of superoxide O2-. 2 generation. Recent studies indicate that the neutrophil O2-.-generating system consists of at least two components, flavoprotein--flavin adenine dinucleotide (FAD)--and cytochrome b. We evaluate the cytochrome b and FAD content in PMN from 30 CGD patients. The method for quantitating cytochrome b was modified by using PMN sonicates incubated with azide plus hydrogen peroxide. With this approach, several absorption peaks corresponding to myeloperoxidase and eosinophil peroxidase, which overlap with peaks of cytochrome b, were obliterated from reduced-minus-oxidized spectra, whereas the peaks of cytochrome b were not and could be readily quantitated. Cytochrome b was detected in PMNs from all 24 normal adults (47.4 +/- 2.9 pmol/7.5 X 10(6) cells), was absent in PMNs from 11 male CGD patients and one female CGD patient but was present in normal amounts in PMNs from nine male and nine female CGD patients. Stimulated nitroblue tetrazolium (NBT) tests performed on PMNs from mothers of CGD patients indicated that cytochrome b deficiency was associated with X-linked inheritance, except in one case in which probable autosomal recessive inheritance was demonstrated. The PMN NBT test of the mother of another male patient without cytochrome b deficiency suggested an X-linked form of inheritance. In related studies, the FAD content in PMN particulate fractions was reduced in 4 of 28 CGD patients studied. All four CGD patients with reduced FAD lacked cytochrome b. However, three patients with cytochrome b deficiency had normal FAD. Thus, the results indicate that PMN cytochrome b deficiency is observed in most X-linked and in some autosomal recessive CGD, that cytochrome b deficiency may be associated with FAD deficiency, and that cytochrome b and FAD are normal in most patients with non-X-linked CGD.
Adult↗
Dopamine D-2 receptor-mediated excitation of caudate nucleus neurons from the substantia nigra.
Microiontophoretic studies using cats anesthetized with alpha-chloralose were performed to elucidate whether the excitatory response of caudate nucleus (CN) neurons upon stimulation of the pars compacta of the substantia nigra (SN) is mediated by the dopamine D-1 or D-2 receptor. There were rare convergent inputs from the SN and motor cortex (MC) in the CN neurons. Iontophoretic application of haloperidol and domperidone (dopamine D-2 receptor antagonist) produced dose-dependent inhibition of spikes elicited by SN stimulation in 25 of 42 and 50 of 82 CN neurons, respectively, however, no alterations of spikes elicited by MC stimulation occurred in any 11 neurons tested. Iontophoretically applied SCH 23390 (D-1 antagonist) did not inhibit the SN-induced spikes in any CN neurons, of which spikes were inhibited by domperidone. These results suggest that the SN-induced spikes are mediated by dopamine, which acts on postsynaptic D-2 receptors.
Animals↗
Renin release from kidney cortical slices in response to isoproterenol and glucagon is decreased in vitamin E-deficient rats.
The effects of vitamin E (VE)-deficiency on renin release by various agents were examined using rat kidney cortical slices. Isoproterenol and glucagon in the presence or absence of theophylline increased renin release in the control group, while their stimulatory effects were attenuated by VE-deficiency. These decreased responses of renin release to isoproterenol and glucagon due to VE-deficiency were restored to the control level by dietary supplementation of dl-alpha-tocopheryl acetate or N,N'-diphenyl-p-phenylenediamine. The stimulatory effect of dibutyryl cyclic AMP or theophylline on renin release was not affected by VE-deficiency. These results suggest that in case of VE-deficiency, the response of renin release to stimuli is decreased via cyclic-AMP production.
Animals↗
Diffusion of extracellular hydrogen peroxide into intracellular compartments of human neutrophils. Studies utilizing the inactivation of myeloperoxidase by hydrogen peroxide and azide.
It is well known that catalase is transformed to nitric oxide-Fe2+-catalase by hydrogen peroxide (H2O2) plus azide. In this report, we show that myeloperoxidase is also inactivated by H2O2 plus azide. Utilizing this system, we studied the presence and source of intracellular H2O2 generated by activated neutrophils. Stimulation of neutrophils with phorbol myristate acetate (PMA, 100 ng/ml) plus azide (5 mM) for 30 min completely inactivated intragranular myeloperoxidase and reduced cytosolic catalase to 35% of resting cells. This intracellular inactivation of heme enzymes did not occur in normal neutrophils incubated with either PMA or azide alone or in neutrophils from patients with chronic granulomatous disease (CDG) which cannot produce H2O2 in response to PMA. Incubation of neutrophils with azide and a H2O2 generating system (glucose-glucose oxidase) inactivated 41% of neutrophil myeloperoxidase. Glutathione-glutathione peroxidase (GSH-GSH peroxidase), an extracellular H2O2 scavenger, totally protected neutrophil myeloperoxidase from inactivation by azide plus glucose-glucose oxidase. In addition, when a mixture of normal and CGD cells was stimulated with PMA in the presence of azide, 90% of the myeloperoxidase in CGD neutrophils was inactivated. Therefore, H2O2 released extracellularly from activated neutrophils can diffuse into cells. In contrast, myeloperoxidase in normal polymorphonuclear leukocytes stimulated with PMA in the presence of azide and GSH-GSH peroxidase was 75% inactivated. Thus, the results indicate that a GSH-GSH peroxidase-insensitive pool of H2O2 is also generated, presumably at the plasma membrane, and this pool of H2O2 can undergo direct internal diffusion to inactivate myeloperoxidase.
Animals↗
Relation between hepatic microsomal metabolism of N-nitrosamines and cytochrome P-450 species.
Effects of SKF 525A (0.1 mM), metyrapone (0.1 mM), alpha-naphthoflavone (ANF) (0.5 mM) and pyrazole (1.0 mM) on N-nitrosodimethylamine (NDMA), N-nitrosomethylbutylamine (NMBuA) and N-nitrosomethylbenzylamine (NMBeA) metabolism by hepatic microsomes from rats pretreated with inducers were investigated. NDMA demethylation was weakly increased by phenobarbital (PB) treatment. The demethylation was inhibited by SKF 525A and enhanced by metyrapone in non-treated and PB-treated microsomes, and weakly inhibited by ANF in 3-methylcholanthrene(MC)-treated microsomes. NMBuA demethylation was increased by PB treatment and inhibited by SKF 525A in all microsomes. Metyrapone inhibited the demethylation in PB-treated microsomes. NMBuA debutylation was increased by PB and MC treatments, and inhibited by metyrapone in all microsomes. The strongest inhibition by metyrapone was observed in PB-treated microsomes. The debutylation was inhibited by SKF 525A in non-treated and PB-treated microsomes and by ANF in MC-treated microsomes. NMBeA demethylation was decreased by MC treatment and weakly inhibited by SKF 525A in all microsomes. The effects of the inducers and inhibitors on NMBeA debenzylation were almost the same as those on NMBuA debutylation except that the increasing effect of MC was small. Pyrazole was a relatively selective inhibitor of NDMA demethylation. These results suggest the following: NDMA demethylation is catalyzed by PB-induced cytochrome P-450 species (P450-PB) and MC-induced cytochrome P-450 species (P448-MC). But their specific activity is low and the other cytochrome P-450 species demethylate NDMA. NMBuA demethylation is catalyzed by P450-PB. But the specific activity is not high and the other cytochrome P-450 species also demethylate NMBuA. NMBuA debutylation is catalyzed by P450-PB and P448-MC. Almost all of NMBeA demethylation is catalyzed by cytochrome P-450 species other than P450-PB and P448-MC. NMBeA debenzylation is catalyzed by P450-PB and P448-MC, but the specific activity of P448-MC is not high.
Animals↗
Cytochrome b translocation to human neutrophil plasma membranes and superoxide release. Differential effects of N-formylmethionylleucylphenylalanine, phorbol myristate acetate, and A23187.
The role of specific granules and cytochrome b in superoxide (O(2)) release was studied by comparing the effects of three different stimuli on normal human neutrophils, neutrophils congenitally deficient in specific granules, and granule-free normal neutrophil cytoplasts. Phorbol myristate acetate (PMA) stimulated normal neutrophils to release more O(2) than did N-formylmethionylleucylphenylalanine (fMet-Leu-Phe), which stimulated greater release than the calcium ionophore A23187. Neutrophils lacking specific granules produced variable amounts of O(2) in response to all stimuli. Stimulation with PMA, fMet-Leu-Phe, and A23187 produced maximal rates of O(2) release that were 32, 55, and 21% of that by normal cells. Likewise, granule-free neutrophil cytoplasts released 24, 20, and 0% of the O(2) released by intact cells. These data suggest that the stimuli require different mechanisms for activation. Three subcellular fractions (azurophil granule rich, specific granule rich, and plasma membrane rich) were separated by Percoll gradients from normal resting and stimulated neutrophils. In resting neutrophils, the cytochrome b content in the plasma membrane was 31% of the total, with the rest in the specific granule-rich fraction. Ten minutes after stimulation, PMA, fMet-Leu-Phe, and A23187 induced translocation of 27, 8, and 49%, respectively, of the cytochrome b from the specific granule-rich fraction to the plasma membrane. Although our data support a role for specific granule factors in A23187-induced O(2) release, there is no correlation between the amount of cytochrome b incorporated into the plasma membrane and the extent of O(2) production activated by the different stimuli.
Calcimycin↗
The fine structure of nerve endings on rat thyroid follicular cells.
Axon profiles in thyroid glands obtained from adult male Wistar rats were studied electron-microscopically, using common and serial thin sections. Bouton profiles of nerve fibers, resembling the terminal or en passant type, often appeared closely associated with vascular smooth muscle cells via basement membranes. These structures are probably adrenergic, since they contained mainly small-core vesicles (mean diameter: 41.2 nm), in addition to a few large-core (mean diameter: 88.4 nm) and flattened vesicles. Nerve fibers containing microtubules and sometimes mitochondria and vesicles were seen lying between basement membranes and follicular cells. The incidence of nerve fiber contacts on profiles of follicular cells was 0.0177 +/- 0.0092 (S.D.). Using serial sections, follicles were seen to have up to two nerve endings, separated from the plasma membranes of the follicular cells by a gap of 22 nm. They contained mainly flattened vesicles and several large-core vesicles (mean diameter: 95.1 nm). Small-core vesicles were rarely seen in these nerve endings. Furthermore, subsurface cistern-like rough endoplasmic reticulum was found immediately under the plasma membranes of follicular cells facing membranes of nerve endings. These results suggest that the nerve fibers in contact with follicular cells are different from the adrenergic type.
Animals↗
Formation, toxicity and inactivation of acrolein during biotransformation of cyclophosphamide as studied in freshly isolated cells from rat liver and kidney.
In the present study the formation and the effects of cyclophosphamide-derived acrolein were investigated using isolated cells from rat liver and kidney, with particular regard to the protective action of low molecular weight thiols against cellular toxicity. The results may be summarized as follows: Cyclophosphamide (CTX)-mediated toxicity to isolated cells is dependent on cytochrome P-450 activity; Loss of viability in cells incubated with cyclophosphamide is preceded by a depletion of cellular GSH; Stimulation of cellular GSH synthesis or the presence of low molecular weight thiols in the incubation medium protects against cyclophosphamide-induced toxicity; Acrolein is probably formed extracellularly as well as intracellularly and can be detoxified by thiol compounds, forming a thiochemiacetal or a thioether.
Acrolein↗
Allyl alcohol toxicity in isolated renal epithelial cells: protective effects of low molecular weight thiols.
The toxicity of allyl alcohol was studied in freshly isolated renal epithelial cells prepared from male and female rats. Cells from female rats demonstrated a greater susceptibility to allyl alcohol toxicity as assessed by glutathione depletion and loss of cell viability. The sensitivity of female rat renal cells appears to relate to the higher activity of alcohol dehydrogenase found in the female rat kidney, which metabolizes allyl alcohol to the highly reactive aldehyde, acrolein. Pyrazole, an inhibitor of alcohol dehydrogenase, abolished the cytotoxic effects of allyl alcohol whereas inhibition of aldehyde dehydrogenase by disulfiram treatment was found to increase the sensitivity of renal cells to the effects of allyl alcohol. The toxicity of allyl alcohol was decreased by a number of treatments which resulted in increased levels of glutathione or other low molecular weight thiols. These results indicate that acrolein is the toxic metabolite responsible for the renal cell injury following exposure to allyl alcohol, and unless immediately inactivated acrolein interacts with critical nucleophilic sites of the cell and initiates cell injury. These studies demonstrate that freshly isolated kidney cells represent a convenient model system for studies of thiol-mediated protective mechanisms against toxic renal cell injury.
1-Propanol↗