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Biomedical subjects

K Ohata

Publications and source records attributed to K Ohata.

At least 55 records · Page 3Linked to original sources
PubMed1996

[Invasive amebiasis at an institution for the mentally retarded in Shizuoka Prefecture].

Amebiasis caused by Entamoeba histolytica at an institution for mentally retarded in Shizuoka Prefecture is reported. Five of the 50 patients showed E. histolytica cysts in their stools and 4 were positive serologically. The polymerase chain reaction and restriction fragment length polymorphism revealed that the isolates were pathogenic-type E. histolytica. Epidemiological analysis revealed that the amebic infection was caused by the abnormal behavior of mentally retarded patients. Administration of diloxanide furoate and metronidazole for cyst-carriers eliminated cysts from the stool and lowered the antibody titer.

Adult↗
PubMed1996

[A case of middle cerebral artery occlusion caused by dissecting aneurysm].

We reported a case of middle cerebral artery occlusion caused by a dissecting aneurysm that was successfully treated by intra-arterial fibrinolysis. A 38-year-old man suddenly developed left hemiparesis and became confused. He was transferred to our hospital one hour and 27 minutes after the ictus. Right carotid angiogram (CAG) revealed aneurysmal dilatation of the horizontal portion of the middle cerebral artery and occlusion of the anterior trunk. Twelve million IU of tissue plasminogen activator was injected to fibrinolyze the thrombus of the occlusion site through a microcatheter. After this, the patient became alert and hemiparesis disappeared. It took three hours and 30 minutes to gain recanalization after the ictus. Right CAG obtained the next day demonstrated the patency of the anterior trunk and the characteristic finding of the dissecting aneurysm viz "double lumen" as a result of fibrinolysis of the thrombus in the false lumen. Right CAG obtained two weeks later demonstrated "string and pearl sign" instead of the "double lumen" as a result of partial thrombosis in the false lumen. Follow-up CAG obtained nine months after the ictus demonstrated marked reduction of the aneurysmal size as the result of progressing thrombosis of the false lumen. The characteristic angiographic findings of the dissecting aneurysm such as "double lumen" and "string and pearl sign" seemed to be mostly influenced by the status of the thrombus in the false lumen. In case of major cerebral arterial occlusion caused by the embolus or thrombus from the dissecting aneurysm, intra-arterial fibrinolysis seems to be a possible treatment modality, even though it is accompanied by the risk of giving rise to subarachnoid hemorrhage.

Adult↗
PubMed1995

Mechanism of histamine release by endothelin-1 distinct from that by antigen in mouse bone marrow-derived mast cells.

The mechanisms of endothelin-1-induced histamine release were examined and compared with those responsible for antigen-induced release by using passively sensitized mouse bone marrow-derived mast cells and various drugs that may influence histamine release. The following results were obtained: (1) Although islet-activating protein potently inhibited endothelin-1-induced histamine release, it did not affect the antigen-induced release. (2) Histamine release induced by endothelin-1 was relatively more sensitive to ethylenediaminetetraacetic acid than that induced by antigen, although extracellular Ca2+ is a requisite for both types of the release. (3) (8R*, 9S*, 11S*)-(-)-9- hydroxy-9-methoxycarbonyl-8-methyl-2,3,9,10-tetrahydro-8,11-epoxy-1H,8H, 11H-2, 7b,11a-triazadibenzo[a,g]cycloocta[c,d,e]trinden-1-one and (8R*, 9S*, 11S*)-(-)-9-hydroxy-9-methoxycarbonyl-8-methyl-14-n-propoxy-2,3,9,10-tet rahydro - 8,11-epoxy-1H,8H,11H-2,7b,11a-triazadibenzo[a,g]cycloocta-[c ,d,e] trinden-1-one, which possibly inhibit protein kinases, strongly inhibited antigen-induced histamine release, while these drugs alone did not inhibit endothelin-1-induced release. (4) Staurosporine, a non-selective protein kinase inhibitor, prevented the elevation of cytosolic Ca2+ concentrations induced by antigen, whereas that induced by endothelin-1 was not influenced; histamine release induced by either stimulus was greatly inhibited by the drug. These results indicate and/or suggest that some biological events induced by endothelin-1 leading to histamine release are different from those involved in the histamine release induced by antigen.

Alkaloids↗
PubMed1995

The microsurgical anatomy of the jugular foramen.

The microsurgical anatomy of the jugular foramen was studied in 10 fixed cadavers, each cadaver consisting of the whole head and neck. Five of the cadavers were injected with latex. The jugular foraminal region was exposed using the infratemporal fossa type A approach of Fisch and Pillsbury in five cadavers (10 sides) and the combined cervical dissection-mastoidectomy-suboccipital craniectomy approach in five cadavers (10 sides). The right foramen was larger than the left in seven cases (70%), equal in two cases (20%), and smaller in one case (10%). The dura covering the intracranial portal of the foramen had two perforations, a smaller anteromedial perforation through which passed the ninth cranial nerve (CN IX), and a larger posterolateral perforation, through which passed the 10th and 11th cranial nerves (CNs X and XI) and the distal sigmoid sinus. The perforations were separated by a fibrous septum in 16 specimens (80%). After exiting the posterior fossa, CNs IX, X, and XI all lay anteromedial to the superior jugular bulb (SJB) within the jugular foramen. The inferior petrosal sinus (IPS) entered the foramen between CNs IX and X in most cases; however, in 10% of our cases it entered the foramen between CNs X and XI, and in 10% it entered the foramen caudal to CN XI. The IPS terminated in the SJB in 90% of our cases; in 40%, the IPS termination consisted of multiple channels draining into both the SJB and internal jugular vein. This study shows that the arrangement of the neurovascular structures within the jugular foramen does not conform to the hitherto widely accepted notion of discrete compartmentalization into an anteromedial pars nervosa containing CN IX and the IPS and a posterolateral pars venosa containing the SJB, CNs X and XI, and the posterior meningeal artery.

Accessory Nerve↗
PubMed1995

[Effect of mao-bushi-saishin-to (MBST), a formula of Chinese medicines, on 48 hr homologous passive cutaneous anaphylaxis in rats].

We studied the effect of oral administration of the extracts from MBST and its component chinese plants, and 1-ephedrine on 48 hr homologous passive cutaneous anaphylaxis (PCA), and histamine- or serotonin-induced skin reaction in rats. Administration (100-1,000 mg/kg) of MBST 1 hr before antigen challenge dose-dependently inhibited PCA. Skin reaction induced by histamine was also inhibited by this formula at 1,000 mg/kg 1 hr prior to the provocation in some degree. The inhibitory component of MBST of PCA was found to be Mao. Further examinations revealed that 1-ephedrine, which is contained in Mao in a large amount, did not substantially inhibit histamine- or serotonin-induced skin reaction. These results indicate that MBST has a significantly inhibitory activity on PCA, to which 1-ephedrine from Mao in the formula almost totally contributes, through the inhibition of chemical mediator release. Since MBST showed some inhibition of histamine-induced skin reaction, on which 1-ephedrine did not affect, it is suggested that some ingredient of MBST responsible for inhibition of PCA may be involved in addition to 1-ephedrine.

Animals↗
PubMed1995

[Effects of mao-bushi-saishin-to (MBST) on experimental allergic models in rats].

Effects of oral administration of MBST on 48 hr homologous passive cutaneous anaphylaxis (PCA) and allergic rhinitis in rats were examined. Administration of MBST (1,000 mg/kg/day) for 5 consecutive days with the final dosing at 1 day before antigen challenge did not effect on PCA. However, the reaction was significantly inhibited when the drug (1,000 mg/kg) was singly given 1 hr before antigen challenge. The drug (1,000 mg/kg, 1 hr prior to antigen challenge) tended to reduce the dye leakage into nasal cavities by antigen, while it did not affect on the anaphylactic histamine release into the cavities. The component of the chinese plants in the formula inhibiting the dye leakage was found to be Mao. However, l-ephedrine and d-pseudoephedrine, which are contained in Mao in a large amount, did not contribute to the inhibiting effect on dye leakage. These results suggest that MBST may be therapeutically effective for atopic disease including rhinitis, through the mechanism other than the inhibition of histamine release.

Animals↗
PubMed1994

Endothelin-1, one of the most potent histamine releasers in mouse peritoneal mast cells.

Whether endothelin-1 or -3 is capable of inducing histamine release from the peritoneal mast cells of BALB/c mice was investigated in vitro and compared to the release induced by compound 48/80. In contrast to the mouse bone marrow-derived mast cells, which originated from the same strain and have been reported upon previously, the (both crude and purified) peritoneal mast cells potently secreted histamine in response to either endothelin-1 or endothelin-3 in a concentration-dependent fashion. Even at a concentration as low as 10 nM, endothelin-1 induced a histamine release of more than 50% from the peritoneal mast cells. Cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123), an endothelin ETA receptor antagonist, markedly suppressed not only the histamine released induced by endothelin-1 but also that due to endothelin-3 at a similarly low concentration range. Treatment with islet-activating protein (IAP) for 3 h, an inactivator of guanosine triphosphate (GTP) (Gi)-protein, markedly reduced the histamine release induced by endothelin-1. Neomycin at 0.1 and 1 mM or ethylenediaminetetraacetic acid (EDTA) at 0.1 mM in the absence of Ca2+, neither of which affected the histamine release induced by endothelin-1, substantially reduced histamine release caused by compound 48/80. On the other hand, treatment with O-O'-bis(2-aminophenyl)ethyleneglycol-N,N,N',N'-tetraacetic acid, tetraacetoxymethyl ester (BAPTA-AM), an intracellular calcium chelating agent, completely inhibited the release induced by both endothelin-1 and compound 48/80. These results indicate that endothelin-1 is one of the most potent histamine releasers in mouse peritoneal mast cells discovered so far.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Endothelin-1 induces release of histamine and leukotriene C4 from mouse bone marrow-derived mast cells.

Whether specific binding sites for endothelin-1 and endothelin-3 exist in mouse bone marrow-derived mast cells (BMMC) and if these endothelins are capable of stimulating chemical mediator release from the cells was investigated. A single component of binding sites for endothelin-1 was found in the cells, but no binding sites for endothelin-3 were observed. Endothelin-1 at 1-100 nM concentration dependently induced release of histamine and immunoreactive leukotriene C4 from BMMC, while endothelin-3 at up to 100 nM did not stimulate the release of either mediator. Time course experiments revealed that the release of histamine and immunoreactive leukotriene C4 induced by endothelin-1 occurred rapidly, reaching near maximal levels within 20 s and 2 min, respectively, after the stimulation, while histamine release induced by antigen, at the concentration which induced an extent of release similar to that induced by 100 nM endothelin-1, required comparatively prolonged incubation (approximately 10 min for submaximal levels). Cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123), a selective antagonist of endothelin ETA receptors, not only dissociated [125I]endothelin-1 specifically bound to BMMC but also inhibited the release of both mediators from endothelin-1-induced cells. These results suggested strongly that BMMC have endothelin ETA receptors on their cell membrane, stimulation of which leads to chemical mediator release, probably via a mechanism different from that involved in the antigen-induced release.

Animals↗
PubMed1994

Inhibitory effect of ONO-1078 on specific binding of peptide leukotrienes to human lung crude membrane.

We investigated the effects of ONO-1078, a newly synthesized peptide leukotriene (p-LT antagonist, on the specific binding of radiolabelled [3H]-LTC4, [3H]-LTD4 and [3H]-LTE4 to a human lung crude membrane fraction (HLMF). The binding assay was performed under conditions in which [3H]-LTC4 and [3H]-LTD4 were not metabolized by HLMF; that is, the metabolism of LTC4 to LTD4 or LTE4 was almost completely prevented by pretreating HLMF with 5 mM acivicin at 37 degrees C for 180 min, and metabolism of LTD4 to LTE4 was inhibited by including 5 mM L-cysteine and 5 mM glycine in the assay. [3H]-LTD4 specific binding was potently and concentration-dependently dissociated by ONO-1078. Its potency was 180-fold stronger than that of FPL 55712, a standardized p-LT antagonist, whereas high concentrations of ONO-1078 similar to those of FPL 55712 were required to inhibit [3H]-LTC4 specific binding. The rank order of the inhibitory potencies of p-LT agonists and antagonists for [3H]-LTD4 specific binding was LTD4 > ONO-1078 > LTE4 > LTC4 > FPI 55712. On the other hand, not only high concentrations of ONO-1078 and FPL 55712 but also more than a 100-fold excess of unlabelled LTE4 was required to inhibit [3H]-LTE4 specific binding, indicating that the binding sites do not appear to be receptors of LTE4. From these results, it is suggested that ONO-1078 is a highly potent LTD4 antagonist which is expected to be very effective on bronchial asthma.

Cell Membrane↗
PubMed1994

Possible participation of histamine H3-receptors in the regulation of anaphylactic histamine release from isolated rat peritoneal mast cells.

Anaphylactic histamine release from isolated rat peritoneal mast cells was concentration-dependently blocked by a 5-min treatment with exogenous histamine at 0.9 and 9 microM and enhanced by a 20- to 30-min treatment with thioperamide (H3-antagonist) at 3 microM with significance, but little affected by mepyramine (H1-antagonist) and cimetidine (H2-antagonist) at the cell concentration of 10(6) mast cells/ml. At a low concentration of mast cells (10(4) mast cells/ml), (R)-alpha-methylhistamine (alpha-MH), an H3-agonist, at 0.9-90 microM also inhibited the release in a concentration-dependent fashion. Thioperamide, but neither mepyramine nor cimetidine, significantly restored the decreased release by alpha-MH. However, the complete restoration by thioperamide could not be achieved because the drug itself slightly but concentration-dependently inhibited anaphylactic histamine release. On the other hand, not only betahistine and dimaprit but also alpha-MH did not suppress histamine release from the mast cells induced by compound 48/80. In rat plasma, considerable levels of histamine were detected. From these results, it is strongly suggested that histamine H3-like receptors are largely responsible for the negative feedback regulation of the anaphylactic histamine release from rat peritoneal mast cells.

Anaphylaxis↗
PubMed1994

Two-phase increment of Ca2+ uptake, intracellular Ca2+ concentration, and histamine release following antigen stimulation in mouse bone marrow-derived mast cells (BMMC).

The relationship between the influx of Ca2+ into cells or cytosolic Ca2+ concentration ([Ca2+]i) and the histamine release following antigen stimulation in mouse bone marrow-derived mast cells (BMMC) was examined, and the results were compared with those from human lung mast cells (HLMC) and rat peritoneal mast cells (RPMC) in some experiments. Anaphylactic histamine release from BMMC as well as HLMC, but not that from RPMC, was dependent on the extracellular Ca2+. When BMMC were challenged by antigen following radioactive 45Ca2+ addition, two phases of 45Ca2+ influx into the cells were observed. The first phase, which was initiated and completed within 30 sec and 2 min, respectively, after antigen treatment, appeared to be related to anaphylactic histamine release. The second influx began 30 sec subsequent to the first one and lasted for at least 2 min, and this occurred after the completion of the histamine release; So far, it is not known how this second influx participates in the intracellular event(s). On the other hand, only one sustained elevation of [Ca2+]i occurred that reached its maximum within 2 min after antigen stimulation. Following stimulation of BMMC with antigen in the absence of Ca2+, Ca2+ addition 1 to 5 min later time-dependently enhanced the histamine release, although the release was deteriorated by further extension of Ca2+ addition. In contrast, the releasability of HLMC was rapidly decreased. These results indicate that extracellular Ca2+ not only is prerequisite for anaphylactic histamine release from BMMC, but also may modulate the release and participate in some intracellular event(s) which has yet to be focused upon.

Anaphylaxis↗
PubMed1993

[Resting tonus of isolated airway smooth muscles].

The regulation of airway caliber is important for supporting the physiological respiratory function and is considered to be mainly controlled by the central and peripheral nervous systems. In the present review, we discussed the resting tonus of the isolated airway smooth muscle of the guinea pig and compared it with that of the human; the former is similar to the latter because both are well-developed in the airway and well-responsive to a variety of mediators. The resting tonus of the isolated guinea pig trachea is largely decreased by indomethacin, a cyclooxygenase inhibitor, while that of the isolated human bronchus is increased following transient decrease by indomethacin. Furthermore, the human bronchus is markedly decreased by not only a selective peptide leukotriene antagonist, MCI-826, but also 5-lipoxygenase inhibitors, AA 861 and cirsiliol. These results indicate that contractile prostanoid(s) and peptide leukotrienes are possible mediators for the maintaining the resting tonus of the respective preparations. Both preparations still have a small but substantial part of the resting tonus resistant to these drugs, the mediator(s) responsible for which is not clarified yet. In short, arachidonate metabolites are major candidates for the resting tonus of either isolated guinea pig or human airway smooth muscle and may contribute to at least a part of the regulation of the airway caliber as autacoids in vivo.

Animals↗
PubMed1993

Important role of peptide leukotrienes (p-LTs) in the resting tonus of isolated human bronchi.

The quality of the resting tonus in isolated human bronchi was investigated using a peptide leukotriene (p-LT) antagonist, a 5-lipoxygenase inhibitor and others. (E)-2,2-Diethyl-3'-[2-[2-(4-isopropyl)-thiazoyl]ethenyl]succina nilic acid sodium salt (MCI-826), a newly synthesized compound that is a highly selective antagonist to LTD4 and LTE4, markedly relaxed the isolated human bronchi at low concentrations. A selective and competitive arachidonate 5-lipoxygenase inhibitor, 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA-861), also potently lowered the tonus. In addition, a large amount of spontaneously formed p-LTs was detected in the isolated human bronchial tissue as well as the lung parenchymal tissue. The isolated human bronchi responded to indomethacin treatment with contractions and the acceleration of p-LT formation. Atropine, an anticholinergic; mepyramine, an antihistaminic; and OKY-046, a thromboxane synthetase inhibitor, all showed no effect on the resting tonus. Taking into consideration the high responsiveness of the human airway smooth muscle to p-LTs and the present results, which were different from those on isolated guinea pig tracheas, it is strongly suggested that the spontaneously formed p-LTs largely participate in the resting tonus of the majority of isolated human bronchi.

Animals↗
PubMed1993

Dimaprit, a histamine H2-agonist, inhibits anaphylactic histamine release from mast cells and the decreased release is restored by thioperamide (H3-antagonist), but not by cimetidine (H2-antagonist).

Whether anaphylactic histamine release from rat peritoneal mast cells is influenced by betahistine, a histamine H1-receptor agonist/H3-antagonist, and dimaprit, an H2-agonist, was examined. Treatment with dimaprit at 6 and 60 microM for 20 min significantly inhibited the anaphylactic histamine release, whereas betahistine at up to 80 microM under the same conditions did not affect it. Treatment with dimaprit at 6 and 60 microM for 1 to 20 min and for 5 to 20 min, respectively, caused a time-dependent inhibition of the release, but up to 30 min treatment with 8 and 80 microM betahistine had no effect. The decreased histamine release induced by dimaprit was recovered by neither mepyramine nor cimetidine. However, thioperamide, an H3-selective antagonist, dose-dependently restored the diminished release. From these results, the inhibition of anaphylactic histamine release by dimaprit is not produced by the stimulation of H2-receptors, but involves the stimulation of H3-like receptors or H3-subtype receptors, which are distinct from the H3-receptors located in brain, and suggests that the receptor plays an important role in the negative feedback regulation of histamine release.

Anaphylaxis↗
PubMed1993

[Inhibitory effects of AA-2414, a thromboxane (Tx) A2 receptor antagonist, on U-46619-, prostaglandin (PG) D2- and 9 alpha, 11 beta PGF2-induced contractions of guinea pig tracheas and isolated human bronchi].

The effects of a novel TXA2 receptor antagonist, AA-2414 [(+-)-7-(3,5,6-trimethyl-1,4-benzoquinone-2-yl)-7-phenyl-heptanoic acid], on U-46619-, PGD2- and 9 alpha, 11 beta-PGF2 alpha-induced contractions of isolated guinea pig tracheas and human bronchi were investigated. AA-2414 competitively inhibited the contractile responses of both human and guinea pig preparations induced by U-46619 with similar pA2 values (7.7 and 7.6, respectively). In addition, the compound also inhibited the contractions of both preparations caused by PGD2 and 9 alpha, 11 beta-PGF2 alpha, the IC50 values of which were 1.2 x 10(-7) and 1.8 x 10(-7) M in guinea pig tracheas and 2.8 x 10(-8) and 8.5 x 10(-8) M in human bronchi. These results suggest that AA-2414 may be a therapeutically useful drug for bronchial asthma.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

A tiaramide derivative, 5-chloro-3-(4-hydroxypiperadinocarbonylmethyl)benzothiazoline-2-one (HPR-611), a potent inhibitor of anaphylactic chemical mediator release--a distinctive feature from disodium cromoglycate.

Effects of a tiaramide derivative, 5-chloro-3-(4-hydroxypiperadinocarbonylmethyl)benzothiazoline++ +-2-one (HPR-611), on anaphylactic chemical mediator release from rat peritoneal exudate cells (RPEC), guinea pig lung fragments (GPLF) and human lung fragments (HLF) were investigated in comparison with those of tiaramide and disodium cromoglycate (DSCG). HPR-611 at 10(-6) - 10(-4) g/ml showed a concentration-dependent inhibition of the histamine release from RPEC regardless of its pretreatment time. Tiaramide also inhibited the release with slightly less potency than HPR-611. The treatment of DSCG 1 min before antigen challenge markedly prevented the release but the inhibitory potency was clearly deteriorated by prolongation of the pretreatment time. Tiaramide tended to influence the anaphylactic release of histamine from GPLF with only 20% inhibition of the release at either 10(-5) or 10(-4) g/ml, whereas HPR-611 at 10(-5) and 10(-4) g/ml significantly suppressed the release in a concentration-dependent fashion. DSCG was not effective on that even at higher concentrations. Anaphylactic release of not only histamine but also immunoreactive leukotriene B4 (i-LTB4) and i-LTC4 from HLF was markedly inhibited by 10(-8) - 10(-4) g/ml of HPR-611. Tiaramide inhibited the release to a somewhat less extent than HPR-611, while nominal or no inhibitions by DSCG were found. From these results, it is clearly apparent that anti-allergic actions of HPR-611 are quite different from those of DSCG.

Animals↗
PubMed1992

Effect of AS-35 on agonist-induced contractions and the resting tonus of airway smooth muscles and the in vitro release of chemical mediators from passively sensitized lung fragments from humans and guinea pigs.

Effects of 9-[(4-acetyl-3-hydroxy-2-n-propylphenoxy)methyl]-3-(1H-tetrazol -5-yl)-4H-pyrido[1,2-alpha]pyrimidin-4-one (AS-35) on the resting tonus or contractions induced by agonists, such as leukotriene (LT) D4 and specific antigen of isolated guinea pig tracheas or human bronchi, and the in vitro anaphylactic release of histamine and LTs from human lung fragments were investigated and compared with the effects of FPL 55712 and disodium cromoglycate. AS-35 as well as FPL 55712 did not affect the contractions induced by acetylcholine and histamine of the isolated guinea pig trachea. However, the compound at relatively low concentrations obviously inhibited contractions induced by LTD4, and the antagonistic activity was stronger than that of FPL 55712. Treatment of the isolated human bronchus with AS-35 tended to induce the inhibition of both LTD4- and antigen-induced contractions and the relaxation of the resting tonus in a concentration-dependent manner. The inhibitory potency at 10(-6) g/ml was slightly stronger than that of FPL 55712, but this was not statistically significant. The anaphylactic release of histamine and LTs from the lung fragments appeared to be inhibited by the treatment with AS-35 5 min prior to the antigen challenge. From these results, it is suggested that AS-35 is effective against allergic asthma through antagonism towards peptide-LTs released anaphylactically in addition to inhibition of the chemical mediator release.

Animals↗