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Biomedical subjects

H Hirata

Publications and source records attributed to H Hirata.

At least 91 records · Page 5Linked to original sources
PubMed1997

Solution Behavior of Anionic Surfactant Molecular Complexes

We have already reported the solution behavior as examined by electrical conductivity for cationic surfactant molecular complexes composed of quaternary ammonium salts such as CTAB and various aromatic additive species such as phenols and amines. By the same electrical conductivity method, we have obtained many valuable results which establish the newly obtained anionic surfactant molecular complexes to be novel surfactant species displaying their own characteristic CMCs and Krafft points different from those of their mother surfactants. Through the solution behavior, furthermore, we could deduce that a solubilized solution system that was of molar composition equal to that of the complex in the surfactant and the solubilizate (additive) was perfectly identical to the dissolution system of the complex. The facts satisfactorily confirmed that a solubilized solution system was only the dissolution system of the complex which spontaneously resulted in the process of solubilization.

Journal Article↗
PubMed1997

Affinity labeling displays the stepwise activation of ICE-related proteases by Fas, staurosporine, and CrmA-sensitive caspase-8.

The activation of multiple interleukin-1beta converting enzyme-related proteases (caspases) in apoptotic mammalian cells raises questions as to whether the multiple active caspases have distinct roles in apoptotic execution as well as how these proteases are organized in apoptotic signaling pathways. Here we used an affinity-labeling agent, YV(bio)KD-aomk, to investigate the caspases activated during apoptotic cell death. YV(bio)KD-aomk identified six distinct polypeptides corresponding to active caspases in Fas-stimulated Jurkat T cells. On staurosporine treatment, four polypeptides were detected. Competition experiments showed that the labeled caspases have distinct substrate preferences. Stepwise appearance of the labeled caspases in each cell death event was consistent with the view that the activated caspases are organized into protease cascades. Moreover, we found that stepwise activation of caspases similar to that induced by Fas ligation is triggered by exposing non-apoptotic Jurkat cell extracts to caspase-8 (MACH/FLICE/Mch5). Conversely, CrmA protein, a viral suppressor of Fas-induced apoptosis, inhibited the protease activity of caspase-8. Overall, these findings provide evidence that caspase-8, a CrmA-sensitive protease, is responsible for initiating the stepwise activation of multiple caspases in Fas-stimulated cells.

Affinity Labels↗
PubMed1997

Fibroblasts spread on immobilized fibrin monomer by mobilizing a beta1-class integrin, together with a vitronectin receptor alphavbeta3 on their surface.

Human and murine fibroblasts were found to spread far more avidly on fibrin monomer monolayers than on immobilized fibrinogen, indicating that removal of fibrinopeptides by thrombin is a prerequisite for the fibrin-mediated augmentation of cell spreading. In fact, cell spreading was not efficiently augmented on monolayers of a thrombin-treated dysfibrinogen lacking the release of fibrinopeptide A due to an Aalpha Arg-16 --> Cys substitution. Since a synthetic Arg-Gly-Asp (RGD)-containing peptide inhibited the fibrin-mediated cell spreading, subsequent dissociation of the carboxyl-terminal globular domain of the Aalpha-chains appears to render the RGD segments accessible to the cell-surface integrins. In support of this, fibrin-augmented cell spreading was inhibited by an antibody recognizing a 12-kDa peptide segment with gamma Met-89 at its amino terminus, which is located in close association with the RGD segment at Aalpha 95-97 in the helical coiled-coil interdomainal connector. The fibrin-mediated augmentation of cell spreading was inhibited not only by an antibody against human vitronectin receptor (LM 609) but also by an antibody against the beta1 subunit of integrin (mAb13), suggesting that the beta1-class integrin together with a vitronectin receptor, alphavbeta3, is mobilized onto the surface of fibroblasts upon contact with the fibrin monomer monolayer.

Animals↗
PubMed1997

Redox regulation of lipopolysaccharide (LPS)-induced interleukin-8 (IL-8) gene expression mediated by NF kappa B and AP-1 in human astrocytoma U373 cells.

LPS-induced expression of the IL-8 gene was markedly enhanced by H2O2 or by deprivation of the cellular antioxidant glutathione by L-buthionine-(S,R)-sulfoximine (BSO) in human astrocytoma U373 cells. In contrast, it was markedly suppressed by the reductant N-acetyl-L-cysteine (NAC) and other antioxidants. Transient expression analysis using the chloramphenicol acetyltransferase assay revealed that activation of the IL-8 promoter by LPS was stimulated by BSO and was suppressed by NAC; likewise LPS-induced activation of both NF kappa B and AP-1 was enhanced by BSO and inhibited by NAC. These results suggest that LPS-induced IL-8 gene expression is regulated by cellular redox via modulation of these transcription factors.

Acetylcysteine↗
PubMed1997

omega-Conotoxins block neurotransmission in the rat vas deferens by binding to different presynaptic sites on the N-type Ca2+ channel.

Electrically-induced twitch responses of the prostatic segment of vas deferens (0.1 Hz, 65 V, 1 ms) are mainly due to the transient presynaptic release of ATP, which acts postsynaptically on non-adrenergic receptors to contract smooth muscle cells. These responses were fully blocked by nanomolar concentrations of the omega-conotoxins GVIA, MVIIA, and MVIIC, most likely by inhibiting Ca2+ entry through presynaptic N-type Ca2+ channels controlling the release of ATP. Repeated washout of the toxins allowed the recovery of contractions, except for omega-conotoxin GVIA, whose inhibitory effects remained unchanged for at least 60 min. In addition, micromolar concentrations of omega-conotoxin MVIIC were unable to protect against the irreversible inhibition of twitch contractions induced by nanomolar concentrations of omega-conotoxin GVIA. At low extracellular Ca2+ concentrations (1.5 mM), 20 nM of omega-conotoxin GVIA or MVIIA inhibited completely the twitch contractions in about 10 min. In 5 mM Ca2+ the blockade of twitch contractions after 10 min was 70% for both toxins. In 1.5 mM Ca2+ omega-conotoxin MVIIC (1 microM) inhibited completely the twitch contraction after 10 min. In 5 mM Ca2+ blockade developed very slowly and was very poor after 30 min, omega-conotoxin MVIIC depressed the response by only 20%. These results are compatible with the idea that the three omega-conotoxins block the purinergic neurotransmission of the vas deferens by acting on presynaptic N-type voltage-dependent Ca2+ channels. However, omega-conotoxin MVIIC seems to bind to sites different from those recognised by omega-conotoxin GVIA and MVIIA, which are markedly differentiated by their Ca2+ requirements for binding to their receptors.

Animals↗
PubMed1997

Nerve expansion in nerve regeneration: effect of time on induction of ornithine decarboxylase and Schwann cell proliferation.

We studied the effect of initiation time of nerve expansion after nerve transection on the induction of ODC activity and Schwann cell proliferation in nerve tissue under Wallerian degeneration. The levels of ODC activity and Schwann cell proliferation decreased as the initiation time of nerve expansion was delayed after nerve transection, and peak levels of ODC activity following nerve expansion preceded peak levels of Schwann cell proliferation.

Animals↗
PubMed1997

Transient damage to the axonal transport system without Wallerian degeneration by acute nerve compression.

The aim of this study was to examine whether acute nerve compression damages an axonal transport system based on microtubules and how the fibers recover after the compression. A 5-mm segment of the tibial nerve of male wistar rat was compressed with a specially designed clip. Functional recovery was assessed using Tibial Nerve Functional Index (TFI). Rats were sacrificed each day from Day 0 to Day 2 and every 2 days between Day 4 and Day 10. For immunohistochemical analysis of the tibial nerve, the proximal uncompressed, the middle compressed, and the distal uncompressed segments of each section were assessed under immunofluoroscent microscopy for anti-dynein, anti-tubulin, and anti-neurofilament antibodies staining. In rats whose tibial nerve was compressed by 25 g/mm2 of pressure for 5 min, staining of dynein and mirotubules in the compressed portion were obscure on Days 4-8, suggesting that the microtubules based axonal transport system was temporarily damaged, while neurofilaments were retained. In contrast, in the distal portion, anti-neurofilament staining showed no abnormality throughout the experimental period, indicating that Wallerian degeneration did not occur. We conclude that acute nerve compression can cause transient damage to the axonal transport system in nerve fibers without Wallerian degeneration.

Acute Disease↗
PubMed1997

Kainate-induced hippocampal DNA damage is attenuated in superoxide dismutase transgenic mice.

Peripheral administration of kainic acid (KA) can cause cell death in the hippocampus of rodents. This is thought to involve oxidative stress. In the present study, we tested the possibility that KA-induced neuronal cell death might be attenuated in CuZn superoxide dismutase transgenic (SOD-Tg) mice. Acute administration of KA causes animal death in a dose-dependent fashion; this was attenuated in SOD-Tg mice. Similarly, KA caused dose-dependent neuronal cell death in the hippocampus of wild-type mice; this cell death was attenuated in the SOD-Tg mice, in a gene-dosage-dependent fashion, with homozygous mice showing complete protection even at the highest dose (45 mg/kg) of KA used in this study. These results provide further support for the involvement of oxygen-based radicals in the toxic effects of KA.

Animals↗
PubMed1997

Non-mutagenic repair of (6-4)photoproducts by (6-4)photolyase purified from Drosophila melanogaster.

The (6-4)photoproduct DNA photolyase ((6-4)photolyase) repairs UV-induced pyrimidine (6-4) pyrimidone photoproduct ((6-4)photoproduct, pyr[6,4]pyr) in a light dependent manner. Drosophila (6-4)photolyase was purified to near homogeneity from Drosophila embryonic cells and is shown to be a 62 kDa protein as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The purified (6-4)photolyase repairs (6-4)photoproducts induced at 5'-CC-3' site (C[6,4]C) as well as T[6,4]T and T[6,4]C. Photoreactivation of (6-4)photoproduct constructed in M13 phage eliminates the replication block and abolishes induced mutagenesis in E. coli cells, suggesting that the (6-4)photolyase repairs the photoproduct to the unmodified form.

Animals↗
PubMed1997

p53-knockout mice are protected against the long-term effects of methamphetamine on dopaminergic terminals and cell bodies.

p53-knockout mice provide a useful model to test the role of p53 in the neurotoxic effects of drugs in vivo. To test the involvement of p53 in methamphetamine (METH)-induced toxicity, wild-type mice, as well as heterozygous and homozygous p53-knockout male mice, were administered four injections of three different doses (2.5, 5.0, and 10.0 mg/kg) of the drug given at 2-h intervals within the space of 1 day. METH caused a marked dose-dependent loss of dopamine transporters in both the striatum and the nucleus accumbens of wild-type mice killed 2 weeks after drug administration. However, this METH-induced decrease in dopamine transporters was attenuated in both homozygous and heterozygous p53-knockout mice, with homozygous animals showing significantly greater protection. The possibility for p53 involvement in METH-induced toxicity was also supported by the observation that METH caused marked increases in p53-like immunoreactivity in the striata of wild-type mice and very little change in heterozygous p53-knockout mice, whereas no p53-like immunostaining was detected in the homozygous p53-knockout mice. Further support for p53 involvement was provided by the fact that METH treatment caused significant decreases in dopamine transporter mRNA and the number of tyrosine hydroxylase-positive cells in the substantia nigra pars compacta and the ventral tegmental area of wild-type but not homozygous p53-knockout mice killed 2 weeks after cessation of METH administration. These results provide concordant evidence for a role of the tumor suppressor, p53, in the long-term deleterious effects of a drug acting on brain dopamine systems.

Animals↗
PubMed1997

Ventilatory support during exercise in patients with pulmonary tuberculosis sequelae.

STUDY OBJECTIVE: The aim of this study was to determine whether intermittent positive pressure ventilation through a nasal mask (NIPPV) applied during exercise in patients with pulmonary tuberculosis sequelae (PTS) could improve arterial blood gas measurements, ameliorate breathlessness, and increase exercise endurance. PATIENTS: Seven PTS patients with a severe restrictive ventilatory defect (mean [SD] vital capacity, 1.02 [0.25] I) enrolled in this study had experienced NIPPV previously, and were familiar with the procedure. DESIGN: The patients underwent four constant-load cycle ergometer tests in the supine position to tolerance. The tests were performed with and without NIPPV, while breathing normoxic air (Air) or supplemental oxygen (O2; 35%). NIPPV was delivered during exercise in a controlled, volume-cycled mechanical ventilation mode, and the ventilator settings were modulated manually to meet patients' respiratory demands as estimated from the airway pressure waveform and the patient's breathlessness. RESULTS: All patients matched their breathing to the ventilator cycle during most of the exercise while receiving NIPPV. NIPPV significantly prolonged their exercise endurance time, from a mean (SD) of 180 (58) s to 310 (96) s in Air, and from 227 (64) s to 465 (201) s in O2. During exercise, NIPPV effectively decreased their breathlessness and significantly improved arterial blood gas measurements. CONCLUSIONS: NIPPV applied during exercise can effectively support ventilation, significantly ameliorate breathlessness, and consequently improve exercise endurance in patients with PTS.

Aged↗
PubMed1997

Histamine poisoning after ingestion of spoiled raw tuna in a patient taking isoniazid.

An 83-year-old woman taking isoniazid (INH) suddenly developed a headache, palpitations, and skin eruptions with itching while eating raw tuna. The symptoms were compatible with those of histamine intoxication. When given fresh raw tuna to eat, no such reactions were evoked in this patient. The episode was speculated to be due to two conditions; eating spoiled raw tuna and at the same time being on a course of INH, a potent histaminase inhibitor. We should therefore be aware of the possible adverse effects due to the interactions between drugs and foods.

Aged↗
PubMed1996

Suppression of nerve growth factor-induced neuronal differentiation of PC12 cells. N-acetylcysteine uncouples the signal transduction from ras to the mitogen-activated protein kinase cascade.

The cellular redox state is thought to play an important role in a wide variety cellular signaling pathways. Here, we investigated the involvement of redox regulation in the nerve growth factor (NGF) signaling pathway and neuronal differentiation in PC12 cells. N-acetyl-L-cysteine (NAC), which acts as a reductant in cells both by its direct reducing activity and by increasing the synthesis of the cellular antioxidant glutathione, inhibited neuronal differentiation induced by NGF or by the expression of oncogenic ras in PC12 cells. NAC suppressed NGF-induced c-fos gene expression and AP-1 activation. These results suggest that neuronal differentiation and NGF signaling are subject to regulation by the cellular redox state. NAC also suppressed the NGF-induced activation of mitogen-activated protein kinases (MAPKs) and decreased the amount of tyrosine phosphorylation of MAPKs. The suppression of MAPK by NAC was independent of glutathione synthesis. In parallel with the suppression of MAPK, the activation of MAPK kinase kinase activity was also suppressed in the presence of NAC. In contrast, NGF-induced activation of Ras was not inhibited by NAC. The inhibitory effect of NAC on the MAPK cascade was independent of transcription and translation. Thus, NAC suppresses NGF-induced neuronal differentiation by uncoupling the signal transduction from Ras to the MAP kinase cascade in PC12 cells.

Acetylcysteine↗
PubMed1996

Nerve growth factor and forskolin prevent H2O2-induced apoptosis in PC12 cells by glutathione independent mechanism.

PC12 cells died by apoptosis at relatively low concentrations of H2O2, of which cytotoxicity was effectively suppressed by nerve growth factor (NGF), forskolin, and dbt-cAMP. Treatment with NGF or forskolin for 24 h increased the level of cellular antioxidant glutathione (GSH) by 1.6-2.0-fold. However, both NGF and forskolin protected cells against H2O2-stress even when cellular GSH was depleted by treatment with L-buthionine-(S,R)-sulfoximine (BSO). The GSH-independent protection effects of NGF and forskolin did not require new protein or RNA synthesis. Exogenous expression of an oncogenic ras suppressed apoptosis caused by H2O2 indicating that Ras protein also plays a role in suppressing apoptosis caused by oxidative radical stress.

Animals↗
PubMed1996

Functional properties of agmatine in rat vas deferens.

Experiments were performed with rat vas deferens to verify whether agmatine, an endogenous ligand for adrenoceptors and imidazoline receptors, can influence sympathetic neurotransmission, with respect to contractions induced by transmural nerve stimulation, contractions induced by exogenous noradrenaline, and overflow of endogenous noradrenaline. It was shown that agmatine (a) caused a dose-dependent potentiation of electrically induced twitches, up to about 70% in relation to controls, (b) shifted to the right the inhibitory concentration-response curves for clonidine on electrically induced twitches, indicating competitive antagonism at presynaptic alpha-adrenoceptors, with a pA2 value of 4.12 +/- 0.10, (c) shifted to the right the concentration-response curves for noradrenaline-induced contractions, indicating competitive antagonism at postsynaptic alpha-adrenoceptors as well, with a pA2 value of 4.03 +/- 0.10, and (d) caused a dose-dependent increase of KCI-induced overflow of noradrenaline, up to about 90% in relation to controls. It is concluded that agmatine has multiple effects on sympathetic neurotransmission in rat vas deferens.

Agmatine↗
PubMed1996

Long-latency responses of brain noradrenergic neurons to noxious stimuli are preferentially attenuated by intravenous morphine.

The nucleus locus coeruleus (LC) has been strongly implicated in the processing of noxious stimuli. Consistent with this, previous studies have shown that spontaneous LC discharge is depressed by morphine. However, effects of morphine on evoked responses of LC neurons to noxious stimuli have not been systematically examined. We reported recently that responses to footshock stimuli in rat locus coeruleus neurons consist of an early (A-fiber mediated) component and a previously undescribed late (C-fiber mediated) component. In the present study, we administered analgesic doses of morphine (0.1, 0.5, or 1.0 mg/kg, i.v.) to determine the effect on A- and C-fiber components of footshock responses in LC neurons. Doses of 0.5 and 1.0 mg/kg significantly attenuated the C-fiber mediated response of LC neurons without affecting the A-fiber response component. Spontaneous LC discharge was reduced by administration of all doses of morphine. Both depressive effects of morphine were abolished by intravenous administration of naloxone. In contrast, local microinfusion of naloxone into the LC abolished the morphine-induced decrease of spontaneous discharge but did not prevent the depression of the C-fiber mediated footshock response by morphine. This indicates that the site of action for morphine's attenuation of the late LC response to footshock stimulation is outside of the LC. The results are consistent with the hypothesis that the late (C-fiber-mediated) footshock responses in locus coeruleus are involved in the processing of noxious stimuli and may contribute to anti-nociceptive mechanisms.

Adrenergic Fibers↗