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Biomedical subjects

M Yamazaki

Publications and source records attributed to M Yamazaki.

At least 595 records · Page 33Linked to original sources
PubMed1991

Responses to dopamine of isolated human and monkey veins compared with those of the arteries.

Isolated human gastroepiploic vein tributaries responded to dopamine only with contractions, whereas the gastroepiploic artery branches in the same region of the omentum responded with relaxations. Treatment with phentolamine converted the vein contraction to a relaxation, which was not influenced by propranolol but was abolished by droperidol. The relaxation was converted to a contraction by SCH23390 but unaffected by domperidone. Endothelium denudation abolished the relaxation caused by substance P but did not significantly alter the dopamine-induced relaxation. Dopamine increased the cyclic AMP content in the human veins. Monkey mesenteric, renal and portal veins and vena cava contracted in response to dopamine. Treatment with phentolamine converted the contraction to a slight relaxation in the mesenteric and renal veins; however, even in the presence of high concentrations of the alpha adrenoceptor antagonist, no relaxation was induced in the portal vein and vena cava partially contracted with prostaglandin F2 alpha. It is concluded that gastroepiploic veins and arteries in the human omentum respond quite differently to dopamine; the alpha adrenoceptor-mediated contraction predominates over the relaxation mediated via dopamine D1 receptor subtype in the veins, and vice versa in the arteries. Dopamine relaxes the human vein, possibly as a result of increased production of intracellular cyclic AMP by stimulation of D1 receptors. The predominant action of dopamine on alpha adrenoceptors may contribute to increasing venous return and cardiac output.

Adult↗
PubMed1991

Prothrombin Himi; an abnormal prothrombin characterized by a defective thrombin activity.

An abnormal prothrombin has been detected in a 26-year-old female, who had no history of excessive bleeding. Prothrombin activity was approximately 10% when measured using either the classical one-stage assay or the assay with Echis carinatus venom, whereas prothrombin antigen level was normal. In keeping with current nomenclature practices, the abnormal prothrombin was designated "Prothrombin Himi". The electrophoretic behavior and calcium binding properties of Prothrombin Himi did not differ significantly from normal. Prothrombin Himi was isolated by chromatography on Q-Sepharose. Electrophoretic migration of the purified abnormal prothrombin on SDS-PAGE was normal. Upon prothrombin activation by Echis carinatus venom, the clotting activity produced from Prothrombin Himi was only 37% of the normal level after 90 minutes of the activation time, where as the amidolytic activity was almost the same as normal. The cleavage patterns of Prothrombin Himi by factor Xa or Echis carinatus venom investigated by SDS-PAGE, were found to be normal. These results indicate that Prothrombin Himi was characterized by a defective thrombin enzymatic activity.

Adult↗
PubMed1991

Chemical synthesis and biological activities of 6,6'-di-O-mycoloyl-beta,beta- and -alpha,beta-trehalose.

6,6'Di-O-mycoloyl-beta,beta-trehalose (beta,beta-TDM) and 6,6'-di-O-mycoloyl-alpha,beta-trehalose (alpha,beta-TDM) were synthesized and their toxicity and ability to activate peritoneal macrophages in situ were examined in mice, in comparison with 6,6'-di-O-mycoloyl-alpha,alpha-trehalose (TDM). Both beta,beta-TDM and alpha,beta-TDM caused a decrease in body weight two days after injection, however the weights reverted to a normal level. No deaths were caused by either analog. On the other hand, TDM showed potent toxicity, causing decrease in body weight and death of all animals injected. Beta,beta-TDM and alpha,beta-TDM were effective in the in situ activation of mouse peritoneal macrophages.

Animals↗
PubMed1991

Anti-bilirubin monoclonal antibody. III. Preparation and properties of monoclonal antibodies to unconjugated bilirubin-IX alpha.

Anti-bilirubin-IX alpha monoclonal antibodies exclusively specific for unconjugated bilirubin-IX alpha are prepared and characterized. Using modified MBS (metamaleimidobenzoyl-N-hydroxysuccinimide ester) method, bilirubin-IX alpha was covalently coupled to bovine serum albumin (BSA) retaining its intramolecular hydrogen bonds as well as three-dimensional structure. Somatic cell fusion was performed between murine spleen cells immunized with the bilirubin-IX alpha-BSA and murine myeloma P3-X63-Ag8-U1 cells. After screening assay, 58 clones were identified which were producing antibodies not to albumin nor MBS, but to haptenic bilirubin-IX alpha. In inhibition analysis, the antibodies in the culture supernatant reacted only with bilirubin-IX alpha to a varying degree, but did not react with conjugated bilirubin-IX alpha, including bilirubin-IX alpha monoglucuronide, bilirubin-IX alpha diglucuronide, and ditauronic bilirubin-IX alpha.

Animals↗
PubMed1991

Phase separation of Triton X-100 micelle solution induced by osmotic stress.

We have found out that the phase separation of Triton X-100 micelle solution was caused by the addition of poly(ethylene glycol) (PEG) above a critical concentration. The critical concentration of PEG depended on its molecular weight and temperature, larger molecular weight or higher temperature giving lower critical concentration. These results were analyzed on the basis of the osmoelastic coupling theory recently proposed by us (Biochemistry (1989) 28, 3710-3715; Biochemistry (1989) 28, 5626-5630).

Chemical Phenomena↗
PubMed1991

Changes in plasma levels of tissue-plasminogen activator/inhibitor complex and active plasminogen activator inhibitor in patients with disseminated intravascular coagulation.

Plasma levels of tissue-plasminogen activator.plasminogen activator inhibitor (t-PA.PAI) complex and active PAI were assayed in 58 cases of disseminated intravascular coagulation (DIC). A significant elevation of both parameters was observed in most cases of DIC, especially in patients with non-Hodgkin lymphoma, sepsis, or some patients with acute leukemia, but no such elevation was observed in patients with acute promyelocytic leukemia (APL). The levels of both parameters were higher in cases of DIC with multiple organ failure (MOF) than in those without MOF. Since no elevation of t-PA.PAI complex was observed in most cases of APL, t-PA did not seem to play an important role in the activation of fibrinolytic system in APL. Active PAI, which reflects the inhibitory regulation in fibrinolytic system, was considered to play a role in the progression of MOF. Plasma levels of active PAI were low in the cases of APL, which had no complication of MOF.

Disseminated Intravascular Coagulation↗
PubMed1991

Plasma levels of soluble thrombomodulin increase in cases of disseminated intravascular coagulation with organ failure.

We examined the changes in plasma levels of soluble thrombomodulin in 66 cases of disseminated intravascular coagulation (DIC), to investigate the damage to vascular endothelial cells and its relationship to multiple organ failure. A significant elevation of plasma levels of soluble thrombomodulin was observed in most cases of DIC, especially in patients with sepsis. However, no such significant elevation was observed in patients with acute promyelocytic leukemia. Plasma levels of both soluble thrombomodulin and active plasminogen activator inhibitor were higher in the cases of DIC with multiple organ failure than in those without multiple organ failure. The levels of soluble thrombomodulin were decreased with the clinical improvement in most cases of DIC but were further increased or remained at high levels in patients who showed no improvement of DIC. It was suggested that an increase in soluble thrombomodulin indicates the damage to the vascular endothelial cells in cases of DIC and that the damage to vascular endothelial cells plays some role in further progression of multiple organ failure.

Disseminated Intravascular Coagulation↗
PubMed1991

Galactosialidosis: neuropathological findings in a case of the late-infantile type.

The neuropathological findings in a 13-year-old Japanese male showing decrease of sialidase and beta-galactosidase activities are reported. The patient was the product of normal pregnancy to consanguineous parents. He started to sit at 8 months, stand at 20 months and walk at age of 2; mental retardation, visual disturbance, cerebellar ataxia, myoclonus and epilepsy developed by the age of 10, and he died at 13. Neuropathological investigation revealed neuronal loss and storage. Severe loss of neurons was observed in the thalamus, globus pallidus, lateral geniculate body, gracile nucleus, Purkinje and retinal ganglion cells. Marked ballooning was seen in the Betz cells and neurons in the basal forebrain, the motor neurons in the cranial nerve nuclei and spinal cord, and in the trigeminal and spinal ganglia. The storage material varied in staining from region to region and from neuron to neuron. Electron microscopic investigation revealed a variety of intracytoplasmic and intranuclear inclusions: membranous cytoplasmic bodies, parallel, wavy-lamellar or tortuous tubular structures, lipofuscin-like irregular-shaped pleomorphic bodies, and cytoplasmic vacuoles with fine granules and lamellar materials. The severity of the neuronal loss did not seem to correlate with the amount of the storage materials, but with the presence of tortuous tubular inclusion.

Brain↗
PubMed1991

Role of platelet-activating factor in aggregation of leukocytes and platelets in cerebral ischemia.

Leukocyte and platelet aggregation stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP) was measured in 32 patients with cerebral ischemia and in 15 controls, using a whole blood aggregometer. The increases in impedance and the reductions in leukocyte and platelet counts were significantly greater in stroke patients than in controls. Aggregation was inhibited by oral ticlopidine, but not by oral aspirin. The effects were clearly counteracted by platelet-activating factor (PAF) antagonists, and counteracted in part by a 5-lipoxygenase inhibitor. The results suggest that platelets tend to be activated by PAF and leukotrienes liberated from hyperaggregable leukocytes in patients with ischemic stroke.

Blood Platelets↗
PubMed1991

Lesion-induced establishment of the crossed corticorubral projections in kittens is associated with axonal proliferation and topographic refinement.

The aberrant crossed corticorubral projection of the cat, which is very weak compared to the uncrossed one at about 1 month postnatal, becomes pronounced following unilateral lesions of the sensorimotor cortex. In order to determine whether or not terminal proliferation of pre-existing axons underlie this enlargement, the morphological changes of the crossed axons were examined, using the anterograde tracer Phaseolus vulgar- is leukoagglutinin (PHA-L). The crossed corticorubral axons in normal kittens were mostly simple in morphology with infrequent branching and did not often exhibit growth-cone-like axonal endings at 1 month postnatal. Two to 5 days after unilateral lesions of the sensorimotor cortex placed at this age, the axons were as simple as those in normal animals but ended in growth cones more frequently. Seven to 10 days post-lesion, the axons often bore side-branches which ended in growth cones. Two to 3 weeks post-lesion axons with sprays of finger-like fine sprouts occurred throughout the projection zone. There was no clear topography for the crossed projection in normal animals, but at 1-2 weeks post-lesion the axons started to show a certain amount of localization in the regions of the red nucleus which corresponded to the densely innervated region on the ipsilateral side. The topography of the crossed projections roughly mirrors that of the ipsilateral projection at about 1 month post-lesion. Thus, the lesions of the sensorimotor cortex induce substantial growth and proliferation of the crossed corticorubral axons. The post-lesion changes in axonal morphology and topographic refinement are reminiscent of developmental events. It is likely that the lesions permit the crossed axons, which normally fail to develop, to develop like the uncrossed ones.

Aging↗
PubMed1991

The course of disseminated intravascular coagulation is predicted by changes in thrombin-antithrombin III complex levels--is there any difference between treatment with standard heparin or low-molecular-weight heparin?

Changes in thrombin-antithrombin III complex (TAT) over a one week period studied in 42 cases of disseminated intravascular coagulation (DIC); 19 treated with standard (or unfractionated) heparin (UFH) and 23 treated with low-molecular-weight heparin (LMWH). Closer examination of short term changes in TAT (determined 2, 6, 12, 24, 48, and 72 h after starting anticoagulant therapy) was performed in ten cases of DIC; six treated with UFH and four treated with LMWH. In twelve of the 19 cases of DIC treated with UFH and 19 of the 23 cases treated with LMWH, plasma levels of TAT decreased one day after starting anticoagulant therapy, and no exacerbation of DIC was observed for the following week. In the other cases, these levels further increased and most patients had persistently high levels of TAT for the next week. Plasma levels of TAT were significantly lower in patients treated with LMWH than in those treated with UFH, which may suggest that LMWH is more beneficial in DIC. A transient increase in plasma levels of TAT was observed 6 h after the start of anticoagulant therapy in two of the six cases treated with UFH and one of the four cases treated with LMWH. From these results we conclude that fluctuation of TAT was not influenced by the type of heparin (UFH or LMWH), and that the course of DIC for the following week can be predicted by the changes in plasma TAT levels one day after starting anticoagulant therapy.

Antithrombin III↗
PubMed1991

Transient lupus anticoagulant induced by Epstein-Barr virus infection.

A 25-year-old woman presented with an episode of left calf deep vein thrombosis and pulmonary thrombosis. She was found to have a lupus anticoagulant with anticardiolipin antibodies, some autoimmune antibodies and antibodies for primary Epstein-Barr (EB) virus infection. Six months later, lupus anticoagulant and other autoimmune antibodies were found to be negative and EB virus antibodies were shown to be seroconverted. We suggest that the transient presence of lupus anticoagulant was due to EB virus infection caused by activation of polyclonal B-lymphocytes.

Adult↗
PubMed1991

Inhibition spectra of solar urticaria: a case report and a review of the Japanese cases.

A 34-year-old Japanese female with solar urticaria is described, who had an episode of urticarial response when she was exposed to indoor fluorescent light first and sunlight later. The action spectrum was found to range from 480 to 520 nm with an inhibition spectrum above 650 nm in the visible light by both postirradiation and preirradiation. Injection of in vitro-irradiated serum did not produce an urticarial wheal on the patient. In the Japanese literature, 17 cases of solar urticaria with inhibition spectra have been reported. The wavelength of the inhibition spectrum was longer than that of the action spectrum in each case.

Adult↗
PubMed1991

Augmentation and suppression of release of tumor necrosis factor from macrophages by negatively charged phospholipids.

We recently reported that some lipid species of cell membranes and lipoproteins induced the growth of peripheral macrophages. In this study, the effects of phospholipids on tumor necrosis factor (TNF)-releasing activity of macrophages were examined. Ten to 20 micrograms/ml of cardiolipin, which is a suboptimal concentration for macrophage growth-stimulation, augmented macrophage TNF release triggered by lipopolysaccharide (LPS) in vitro. This priming effect appeared with 1 day of preincubation and was still potent on day 3, whereas the priming effect of interferon-gamma (IFN-gamma) peaked at 3 h and then gradually decreased. In contrast, a high concentration of cardiolipin (40 micrograms/ml) which is optimal for the induction of macrophage growth, completely suppressed LPS-triggered TNF release from not only untreated macrophages but also IFN-gamma-primed macrophages. The suppressive effect was potent even with 3 h preincubation, was still potent on day 3, and was not abolished by indomethacin. Cardiolipin had scarcely any effect on the triggering activity of LPS. Similar augmentative and suppressive activities were observed in peroxidized phosphatidylserine, which is also highly active in inducing macrophage growth, but was not found in native phosphatidylserine, which is less active in inducing macrophage growth, but was not found in native phosphatidylserine, which is less active, nor in phosphatidylcholine, which is an inactive species toward macrophage growth. These results suggest that lipids may be important endogenous factors in regulating both activation and growth states of peripheral macrophages.

Animals↗
PubMed1991

Multiple neurite formation in neuroblastoma cell lines by griseolic acid, a potent inhibitor of cyclic nucleotide phosphodiesterases.

The morphological change of several neuroblastoma cell lines induced by griseolic acid, a novel and potent inhibitor of cyclic nucleotide phosphodiesterase (PDE), was examined. In the cell lines tested, Neuro-2a (a murine neuroblastoma cell line) showed dose-dependent (1 microM-1 mM) neurite extension. Griseolic acid markedly increased the intracellular cyclic AMP level of Neuro-2a cells, suppressed DNA synthesis (82% at 1 mM), and induced multipolar (multiple-neurite-bearing)-type neuritogenesis. A similar type of neurite outgrowth was induced by 8-bromo-cyclic AMP, which also elevated the intracellular cyclic AMP concentration. In contrast, when Neuro-2a cells were treated with retinoic acid, neurite formation was of the monopolar (single-neurite-bearing) type. Papaverine and theophylline, which have been frequently used as PDE inhibitors, failed to induce these morphological changes up to 1 mM, probably owing to the lesser potency of these compounds as compared with griseolic acid on the inhibition of PDE. Retinoic acid, theophylline, and papaverine were ineffective at elevating the intracellular cyclic AMP level. These results suggest that multipolar-type cell shape change in Neuro-2a cells is correlated with the accumulation of intracellular cyclic AMP and that griseolic acid is a useful compound to induce neuroblastoma cells into terminal differentiation.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1991

Comparison of endothelium-dependent responses of monkey cerebral and temporal arteries.

1. Endothelium-dependency of vasodilator responses was compared in helical strips of monkey cerebral and superficial temporal arteries contracted with prostaglandin F2 alpha. Acetylcholine produced an endothelium-dependent relaxation in the temporal arteries, but did not consistently alter the tone of cerebral arteries. 2. Adenosine 5'-triphosphate (ATP) produced a transient contraction followed by a relaxation in the temporal and cerebral arteries; removal of the endothelium partially attenuated the relaxation of the cerebral arteries and markedly suppressed the relaxation in the temporal arteries. The dependency of adenosine 5'-diphosphate (ADP)-induced relaxations on the endothelium was also greater in temporal arteries than in cerebral arteries. 3. Histamine-induced relaxations in the temporal arteries were independent of the endothelium and were reversed to contractions by cimetidine. Cerebral arterial relaxations induced by histamine were partly dependent on the endothelium. Relaxations caused by substance P were reversed to contractions by removal of the endothelium in the temporal arteries, whereas the peptide did not consistently alter the tone of cerebral arteries. 4. The Ca2+ ionophore, A23187, relaxed the temporal and cerebral arteries to a similar extent; removal of the endothelium abolished these relaxations. Glyceryl trinitrate elicited similar relaxation of cerebral and temporal arteries, and these were independent of the endothelium. 5. These findings clearly indicate heterogeneity in the endothelium-dependency of several vasodilator responses in monkey intra- and extracranial arteries, although the ability of these arteries to respond to A23187 and glyceryl trinitrate does not appear to differ. The heterogeneous responses observed so far could therefore be due to different distributions of receptors or to variation in receptor-effector coupling in endothelial cells.

Acetylcholine↗
PubMed1991

Modulation of leukotriene B4 and platelet-activating factor binding to neutrophils.

Preincubation of human neutrophils with the human hormone granulocyte-macrophage colony-stimulating factor (GM-CSF) inhibits the specific binding of leukotriene B4 ([3H]LTB4) but not the nonmetabolizable bioactive platelet-activating factor ([3H]C-PAF) to intact cells. This inhibition requires that the GM-CSF interacts with intact cells. The action of GM-CSF is not prevented by pertussis toxin. Moreover, the rise in calcium produced by LTB4 but not by PAF is also inhibited in human neutrophils pretreated with GM-CSF. Interestingly, neither the inhibitory action of GM-CSF on [3H]LTB4 binding or LTB4-induced calcium rise nor the potentiation of superoxide production by GM-CSF is reduced by inhibitors of arachidonic acid metabolism by the lipoxygenase pathway. In contrast, preincubation of human neutrophils with either the chemotactic factor formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe) or the active phorbol ester, phorbol 12-myristate 13-acetate (PMA), inhibits the binding of both [3H]LTB4 and [3H]C-PAF to intact cells. The inhibitory actions of GM-CSF, PMA, and fMet-Leu-Phe require that they interact with the intact cells; their actions cannot be reproduced in plasma membrane preparations. The effects of both GM-CSF and fMet-Leu-Phe cannot be prevented by the protein kinase C inhibitor staurosporine. The mechanisms of fMet-Leu-Phe and GM-CSF actions are probably not mediated through the release of LTB4 by the cells. Interestingly, this new action, unlike other reported effects of GM-CSF, is not mediated through a pertussis toxin-sensitive G protein (Gi alpha 2). This indicates that not all GM-CSF receptors are coupled to Gi alpha 2.

Alkaloids↗