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Biomedical subjects

Y Honda

Publications and source records attributed to Y Honda.

At least 325 records · Page 18Linked to original sources
PubMed1997

Alacepril, an angiotensin-converting enzyme inhibitor, prevents cerebral vasospasm in subarachnoid hemorrhage model in rats.

The effects of angiotensin-converting enzyme (ACE) inhibitors was investigated on the development of cerebral vasospasm and on the endothelium-dependent relaxation in the rat subarachnoid hemorrhage (SAH) model. Alacepril or enalapril was used as an ACE inhibitor with or without a thiol moiety in the structure. SAH rats or sham-operated rats were produced by the injection of homologous blood or artificial cerebrospinal fluid into the cisternal magna, respectively. In the SAH rat, cerebral vasospasm was observed at 24 h after blood injection. Acetylcholine (Ach)-induced relaxation in basilar arteries from SAH rats significantly decreased compared to that from sham-operated rats, although the relaxation induced by 3-morpholinosydnonimine, sodium nitroprusside or papaverine did not decrease. These results suggest that the endothelium cell function of basilar arteries in SAH rats is damaged. Alacepril prevented both the development of cerebral vasospasm and the suppression in the Ach-induced relaxation of basilar artery in SAH rats. However, enalapril did not prevent the suppression of Ach-induced relaxation in SAH rats, despite the tendency to prevent cerebral vasospasm. Therefore, it is suggested that the preventive effect of alacepril on cerebral vasospasm could be based on its protective effect on endothelium-dependent relaxation system.

Acetylcholine↗
PubMed1996

Prevention by the new Ca2+ channel antagonist, AJ-3941, of loss of endothelium-dependent relaxation after subarachnoid hemorrhage in rats.

AJ-3941 ((+/-)-(E)-1-(3-fluoro-6,11-dihydrodibenz[b,e]-oxepine-11-yl ) -4-(3-phenyl-2-propenyl)-piperazine dimaleate; CAS No. 143110-70-7), a cerebrovascular-selective Ca2+ channel antagonist having anti-lipid peroxidative action, was reported to prevent cerebral vasospasm following subarachnoid hemorrhage in rats. The present study was undertaken to determine whether AJ-3941 protects the impairment of cerebroarterial endothelium-dependent relaxation which is concomitantly induced with cerebral vasospasm. Subarachnoid hemorrhage biphasically suppressed the response to acetylcholine in rat basilar artery, at 0.5 h (n = 4; P < 0.06) and 1 day (n = 5; P < 0.05) after subarachnoid hemorrhage. The reduction of the responses was correlated significantly to the degree of vasospasm determined angiographically. This reduction was accompanied by a 49% increase of arterial lipid peroxide contents. Endothelium-independent relaxation in subarachnoid hemorrhage rats was preserved in response to 3-morpholinosydnonimine, sodium nitroprusside and papaverine. AJ-3941 prevented (n = 6-8, P < 0.05) the suppression of the acetylcholine-induced response and the increase in lipid peroxide content in subarachnoid hemorrhage rats. These results suggest that AJ-3941 could exert its vasospasmolytic effect by preserving endothelial function through its anti-lipid peroxidative action, in addition to its inhibition of vasospasmogen-induced vasoconstriction related to intracellular Ca2+ mobilization.

Acetylcholine↗
PubMed1996

Monoclonal antibody, KK1, recognizes human retinal astrocytes and distinguishes a subtype of astrocytes in mouse brain.

Astrocytes exhibit a diverse morphology and numerous functions in the central nervous system as well as in the retina. In order to obtain markers for the analysis of astrocytes, we prepared monoclonal antibodies that recognized antigens specific to astrocytes. Monoclonal antibody (mAb), designated KK1, reacted with the processes of astrocytes in the nerve fiber layer and the ganglion cell layer in the human retina as detected by indirect immunofluorescence. Normal Müller cells, whose processes are localized vertically in retina, were not labeled by KK1 mAb. In mouse brain, KK1 mAb reacted specifically with astrocytes in the white matter, but not with those in the gray matter. Studies employing a high-resolution confocal laser scanning microscope and double-labeling with KK1 mAb and commercially available anti-glial fibrillary acidic protein (GFAP) mAb (GA5) revealed that KK1 mAb visualized the processes that were not recognized by anti-GFAP mAb (GA5) in both human retina and mouse brain. In cultured mouse astrocytes, KK1 mAb reacted only with anti-GFAP mAb (GA5)-positive cells, but a small percentage of anti-GFAP mAb (GA5)-positive cells were labeled with KK1 mAb. In addition, the subcellular distribution of the KK1 antigen in cultured astrocytes apparently differed from that of GFAP labeled by anti-GFAP mAb (GA5). The antigen that was purified from the normal mouse brain by KK1 mAb-conjugated beads reacted with anti-GFAP mAb(GA5) in immunoblotting. No reactivity of KK1 mAb was observed in immunohistochemical analysis in GFAP -/- mutant mouse brain. These results demonstrate that KK1 mAb specifically recognized an epitope of GFAP that did not react with other anti-GFAP mAb (GA5). Retinal astrocytes and a subtype of astrocytes in the white matter of mouse brain shared the epitope that was recognized by KK1 mAb. KK1 mAb might be a powerful tool to investigate a subtype of astrocytes.

Animals↗
PubMed1996

Involvement of Fas ligand and Fas-mediated pathway in the cytotoxicity of human natural killer cells.

The cytotoxicity of NK cells has been thought to be mediated mainly by the perforin-dependent pathway. We investigated the involvement of Fas-mediated pathway in the killing activity of purified human CD3-, CD16+ NK cells. Fas ligand mRNA was expressed in freshly isolated NK cells. Apoptosis, which was identified by the fragmented chromatin in individual cells, was induced in the cells that expressed high levels of Fas via direct NK-to-target cell interaction or Ab-dependent cell-mediated cytotoxicity, even in Ca(2+)-free medium, in which perforin pores are known not to be formed. Apoptosis in both the presence and absence of external Ca2+ was inhibited by Fab of an anti-Fas mAb. Transfection of the Fas gene in target cells facilitated the induction of apoptosis, compared with the parental cell line. The function of the Fas-mediated pathway in the coexistence of the perforin-dependent pathway was examined in 10 cell lines expressing different levels of Fas by Ca2+ imaging and morphologic observation of single cells. With a certain boundary level, low or high levels of Fas expression in target cells were correlated to a great degree with either acute necrosis due to severe membrane damage after NK-target cell contact or apoptosis at a later period, respectively. We concluded that Fas ligand/Fas interaction is present and plays a significant role in the human NK cell-induced apoptosis.

Antibodies, Monoclonal↗
PubMed1996

A dnaA box can functionally substitute for the priming signals in the oriV of the broad host-range plasmid RSF1010.

The initiation of replication from oriV RSF1010, the replication origin of the broad host-range plasmid RSF1010, depends on RepA (helicase), RepB' (primase), and RepC (initiator protein), encoded by RSF1010 itself, while this initiation event in E. coli is independent of dnaA, dnaB, dnaC, and dnaG [Scherzinger et al. (1984) Proc. Natl. Acad. Sci. USA 81, 654-658; Scholz et al. (1985) in: Plasmids in Bacteria, pp. 243-259, Plenum, New York; Haring and Scherzinger (1989) in: Promiscuous Plasmids of Gram-negative Bacteria, pp. 95-124, Academic Press, London; Scherzinger et al. (1991) Nucl. Acids Res. 19, 1203-1211]. We showed in this work that a newly constructed origin consisting of an oriV RSF1010 and a DnaA protein binding site, the dnaA box, inserted near oriV RSF1010 (oriV RSF1010-dnaA box) could function without RepB' primase, but required RepA and RepC. This oriV RsF1010-dnaA box could not replicate in a dnaA46 strain in which only RepA and RepC were supplied, even at a permissive temperature. These results indicate that an inserted dnaA box can functionally substitute for the RSF1010-specific ssi signals, the RepB' dependent priming signals in oriV RSF1010, and can direct a priming pathway different from the RSF1010-specific one, but related to DnaA protein.

Bacterial Proteins↗
PubMed1996

Dual actions of nitric oxide in N-methyl-D-aspartate receptor-mediated neurotoxicity in cultured retinal neurons.

This study was performed to elucidate the role of nitric oxide (NO) in N-methyl-D-aspartate (NMDA) receptor-mediated glutamate neurotoxicity in the retina. The experiments were done with primary retinal cultures obtained from 17- to 19-day-old rat fetuses. The NOS activity measured by monitoring the conversion of [3H]arginine to [3H]citrulline was approximately 5 pmol/min/mg protein. A 10-min exposure of the cultured cells to glutamate (1 mM) or NMDA (1 mM) followed by a 1-h incubation in a normal medium consistently resulted in 60% cell death. The concomitant addition of an inhibitor of NOS, Nomega-nitro-L-arginine (300 microM), with glutamate or NMDA reduced cell death by 70%. A brief exposure of the cells to sodium nitroprusside (SNP, 500 microM) or S-nitrosocysteine (SNOC, 500 microM), NO-generating agents, caused 60% cell death. Depletion of NO by reduced hemoglobin prevented the cell death induced by either glutamate, NMDA, or NO generating agents. Fifty microM SNOC alone had no effect on the cell viability. However, pretreatment with 50 microM SNOC as well as simultaneous application of 50 microM SNOC with NMDA inhibited cell death induced by NMDA. These findings indicate that a low concentration of NO plays a protective role in glutamate neurotoxicity via closing the NMDA receptor gated ion channel. However, elevated concentrations of NO, interacting with oxygen radicals, become toxic and mediate glutamate-induced neurotoxicity in the cultured retinal neurons.

Animals↗
PubMed1996

Interferon alfa induces leukocyte capillary trapping in rat retinal microcirculation.

BACKGROUND: Interferon alfa has been suggested as a possible treatment for choroidal neovascularization. However, retinal complications following interferon therapy have been reported. OBJECTIVE: To evaluate the effects of interferon alfa on leukocyte dynamics in the rat retinal microcirculation. METHODS: Interferon alfa of different doses was intravenously administered in rats. Leukocyte dynamics were observed with acridine orange digital fluorography, which uses a nuclear fluorescent dye of acridine orange and scanning laser ophthalmoscopy. This technique allows visualization of leukocyte movements in the retinal microcirculation in vivo. RESULTS: After interferon alfa was administered, leukocytes adhered to vascular walls and became trapped in the retinal microcirculation. Leukocyte trapping was dose-dependent. CONCLUSIONS: Interferon alfa increased leukocyte adherence to vascular endothelium and subsequent leukocyte trapping in the retinal capillaries. Interferon alfa may activate leukocytes, and activated leukocytes may be involved in the pathogenesis of microinfarction associated with interferon-induced retinopathy.

Acridine Orange↗
PubMed1996

Evaluation of left ventricular relaxation using the continuous-wave Doppler velocity profile of aortic regurgitation: noninvasive measurement of left ventricular negative dP/dt and time constant.

BACKGROUND: The maximal negative dP/dt [max (-)dP/dt] and time constant (T) are useful indices for evaluating left ventricular (LV) relaxation, but they require invasive procedures. HYPOTHESIS: The purpose of this study was to obtain max (-)dP/dt and T using the continuous-wave Doppler aortic regurgitation velocity curve (AR-CW) noninvasively. Using the Bernoulli equation, the AR-CW allows accurate determination of the pressure gradients (PG) between the aorta and the left ventricle. METHODS: In 10 patients with trivial to mild AR, the rising segment of the AR-CW reflecting LV pressure decrease was digitized with the cardiac image analysis system. Transpulmonary contrast-enhanced Doppler echocardiography was used in three patients to obtain intense velocity envelope. The PG curve and the firs derivative curve were reconstructed and the maximal point of the first derivative curve, which is consistent with max(-)dP/dt, was termed as maximal rate of pressure fall (maxRPF). As T (calculated according to the method of Weiss) can be obtained from T=Pm/max(-)dP/dt [Pm: LV pressure at the phase of max(-)dP/dt], we calculated T from Pm/maxRPF (Pm=dicrotic notch pressure-4Vm2) (Vm: AR velocity at the phase of maxRPF). RESULTS: The Doppler-derived maxRPF and T (TD) approximated the catheter-derived max(-)dP/dt and T (y = 0.85x + 245, r = 0.97, p < 0.001, y = 0.79x + 4, r = 0.87, p < 0.001). In addition, dobutamine echocardiography was performed in nine patients showing increased maxRPF and decreased TD, indicating improvement of LV relaxation. CONCLUSION: These Doppler-derived new indices are sufficiently useful to evaluate LV relaxation noninvasively.

Adult↗
PubMed1996

Inducible nitric oxide synthase in retinal ischemia-reperfusion injury.

The purpose of this study was to determine whether inducible nitric oxide synthase (iNOS) was implicated in the pathogenesis of retinal ischemia-reperfusion injury. Semi-quantitative reverse transcription-polymerase chain reaction showed that the level of iNOS mRNA expression was markedly increased in rat retina following transient ischemia, with peak expression at 12 hr after reperfusion (15.7-fold increase over pre-ischemic levels). In situ hybridization showed that iNOS mRNA was expressed by resident retinal cells, most likely glial cells in the innermost retina, and also by the neutrophils that had infiltrated the retina. Intraperitoneal administration of NG-(1-iminoethyl)-L-ornithine (L-NIO), an inhibitor of iNOS, significantly increased the rate of b-wave recovery compared to that of control animals. The values (mean +/- S.E.M.) were 55.0 +/- 4.4% versus 40.1 +/- 5.1% (P < 0.05) at 1 day and 68.6 +/- 6.6% versus 45.8 +/- 3.5% (P < 0.05) at 3 days. This study shows that iNOS mRNA is highly expressed by non-neuronal cells of the inner retina during reperfusion following transient retinal ischemia. It also shows that L-NIO treatment provides some protection against ischemia-reperfusion injury. We suggest that nitric oxide produced by iNOS may mediate retinal ischemia-reperfusion injury.

Animals↗
PubMed1996

Long-term follow-up of the residual intracanalicular tumours after subtotal removal of acoustic neurinomas.

We examined growth potential of residual intracanalicular tumours left from subtotal removal of large acoustic neurinomas. Eleven patients were followed-up by magnetic resonance (MR) imaging. The interval between surgery and MR study ranged from 12 to 29 years (median, 16 years). MR images of two patients showed no evidence of tumour remnant, and in six a small tumour was localized in the internal auditory canal. The other three showed an intracanalicular tumour protruding slightly towards the intracranial portion. This result suggests that the intracanalicular residual tumours have less risk of regrowth after subtotal removal of acoustic neurinomas. It is advisable to choose intracapsular, subtotal removal without opening the internal auditory canal in the treatment of acoustic neurinoma, if it is large in size and there is a high risk of nerve injury.

Adult↗
PubMed1996

Extracellular polysaccharides produced by tuberose callus.

A high yield of extracellular polysaccharide (ECP) was obtained from callus cultures of tuberose (Polianthes tuberosa), which could be separated into an unadsorbed and two acidic fractions (TPS-1, -2) by ion-exchange column chromatography. The yields of each fraction were markedly increased by the addition of 10(-5) M 2,4-dichlorophenoxyacetic acid to the medium. Of the three fractions, the amount of TPS-1 accounted for over 60% of total yield of ECP, which was a predominant polysaccharide consisting of arabinose (Ara), mannose (Man) and galactose (Gal) as major neutral monosaccharides. Judging from the patterns of electrophoresis and ultra-centrifugation, TPS-1 was identified to be homogeneous. Methylation and GC-mass spectrometry analyses of this fraction revealed the presence of 1,2,3-linked Man, 1-linked Ara, 1,3-linked Ara, 1-linked Gal and 1,3,4-linked glucuronosyl (GlcUA) residues in a molar ratio of 1.0:1.08:0.85:0.75:1.08. Based on additional analyses of the mild acid hydrolysate and the absolute configuration of the constituent monosaccharides, a possible structure for TPS-1 was a glucuronomannan possessing the unit of -->4)-beta-D-GlcUAp-(1-->2)-alpha-D-Manp-(1--> with branching at the C-3 position, where -->1)-alpha-L-Araf, -->1)-beta-D-galp, -->1)-alpha-L-Araf-(3-->1)-alpha-L-Araf or -->1)-alpha-L-Araf-(3-->1)-beta-D-Galp were attached randomly. About 35% of the GlcUA moieties were present as methyl esters. Further confirmation was made by 1H and 13C NMR spectroscopy.

Carbohydrate Conformation↗
PubMed1996

Distinct Ca2+ response patterns in human natural killer cells during induction of necrosis or apoptosis of target cells.

Human CD3-, CD16+ natural killer cells (NKs) induced necrosis in the cell line K562 and the minor population of MOLT-4, while induced apoptosis in the majority of MOLT-4, in one-to-one cell interaction. Simultaneous Ca2+ imaging of NK and target cells revealed remarkable differences in changes of cytosolic Ca2+ concentration ([Ca2+]i) during the process of distinct target cell killing. A rapid [Ca2+]i rise in NK was generated within 2 min after contact with any target. For induction of necrosis, the [Ca2+]i rise in NK reached a peak of 580 +/- 195 nM (mean +/- SD, n = 41) and was followed by an abrupt large [Ca2+]i rise in target cells probably due to Ca2+ entry through pores formed by perforin which was released from NK. The interval between onsets of NK and target Ca2+ responses (Tnk-t) was shorter than 3 min in most cases. Target cells were soon permeabilized, and NK Ca2+ responses ceased in 14 +/- 7 min. For induction of apoptosis, NK Ca2+ responses were relatively smaller (405 +/- 125 nM, n = 16), and Tnk-t was widely scattered up to 30 min. NK Ca2+ responses lasted much longer in a form of Ca2+ oscillations (total duration, 66 +/- 33 min) in parallel with target Ca2+ responses, and ceased as apoptotic changes such as cellular and nuclear fragmentation advanced. The difference in Tnk-t suggests that rapid synchronous release of perforin tends to cause necrosis rather than apoptosis. The duration of NK Ca2+ responses suggests that some 'off signals' may be transmitted to NK following recognition of target cell damage.

Apoptosis↗
PubMed1996

Acetylcholine releases of mesopontine PGO-on cells in the lateral geniculate nucleus in sleep-waking cycle and serotonergic regulation.

1. Five adult cats were prepared with standard sleep-recording electrodes, microinjection cannulae in the bilateral mesopontine tegmentum X area and cannulae for microdialysis probes in the LGN. 2. Dialysates were collected at 5 min intervals during SWS, REM sleep and wakefulness, and during pre- and post-stimulation periods of 5MeODMT microinjection in the bilateral mesopontine tegmentum of freely moving cats. 3. A REM sleep-specific increase of ACh release was observed in the LGN, but not out of the LGN. 4. ACh release was depressed up to 33% by bilateral 5MeODMT microinjection in the mesopontine tegmentum where the microinjection of carbachol also depressed ACh in the LGN probably by stimulating the auto receptor. 5. Our observations indicate that PGO-on neurons of mesopontine tegmentum release more ACh in the LGN during REM sleep by burst discharge than during wakefulness and SWS, and that presumptive cholinergic PGO-on cells are regulated by serotonergic inputs.

Acetylcholine↗
PubMed1996

Trabeculotomy ab externo, cataract extraction, and intraocular lens implantation: preliminary report.

PURPOSE: To compare the results of a triple procedure using either extracapsular cataract extraction (ECCE) or one of two phacoemulsification techniques combined with trabeculotomy ab externo and intraocular lens (IOL) implantation. SETTING: Kyoto University Hospital, Kyoto, Japan, and Nagata Eye Hospital, Nara, Japan. METHODS: In this comparative study, 25 eyes with primary open-angle glaucoma had ECCE combined with trabeculotomy ab externo and IOL implantation and 22 had the same procedure using phacoemulsification instead of ECCE. Of the eyes that had phacoemulsification, 10 had a single-flap and 12 had a double-flap procedure. RESULTS: All 22 eyes that had phacoemulsification had a postoperative IOP of 21 mm Hg or less, as did all ECCE eyes except 2. Although the self-sealing incision might have caused the higher incidence of IOP spikes in the immediate postoperative period, IOPs in the phacoemulsification groups were lower after 3 months. Results were similar in the single-flap and double-flap phacoemulsification groups. There were no significant complications. CONCLUSION: Cataract extraction by phacoemulsification or ECCE combined with IOL implantation and trabeculotomy ab externo is a safe, effective treatment for patients with coexisting glaucoma and cataract.

Aged↗
PubMed1996

Mutations and oxidative DNA damage in phage M13mp2 exposed to N-nitrosomorpholine plus near-ultraviolet light.

Previously we reported that a direct-acting mutagen can be formed from N-nitrosomorpholine (NMOR) on exposure to near-ultraviolet light (UVA, 320-400 nm). We have now studied the spectrum of mutations caused by NMOR plus UVA. M13mp2 phages suspended in a sodium phosphate buffer were treated with NMOR under UVA irradiation and Escherichia coli NR9099 was then infected with the phage. Mutations induced in the phage DNA lacZ alpha region were analyzed. The majority (approximately 50%) of the induced sequence changes were G to T transversions. This suggested that modifications in guanine residues were responsible for these transversions. We explored the formation of 7,8-dihydro-8-oxodeoxyguanosine (8-oxodG) in the DNA. When the phage were treated with NMOR plus UVA, 8-oxodG/dG in DNA increased up to 12-fold over the value in untreated control. When a mutM-deficient mutant of E. coli CSH50 was used as the host, the mutation level was higher than that observed with CSH50. We conclude that 8-oxodG may be involved in mutations induced by NMOR plus UVA.

8-Hydroxy-2'-Deoxyguanosine↗