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Biomedical subjects

M Satoh

Publications and source records attributed to M Satoh.

At least 937 records · Page 52Linked to original sources
PubMed1988

Antinociception induced in rats by intrathecal administration of antiserum against calcitonin gene-related peptide.

To determine whether or not endogenous calcitonin gene-related peptide (CGRP) participates in pain transmission in the spinal dorsal horn, effects of an intrathecal injection of anti-CGRP antiserum on nociceptive threshold in the paw-pressure test was examined in non-arthritic and adjuvant arthritic rats. An intrathecal injection of the antiserum increased the nociceptive threshold in non-arthritic animals, while 0.9% saline, pre-immune serum and antiserum, previously absorbed by synthetic CGRP, were without effect. Adjuvant arthritic rats showed a hyperalgesia, and improvement occurred with intrathecal injection of the antiserum. Saline and absorbed antiserum were without effect on the hyperalgesia. These results suggest that the endogenous CGRP present in primary afferents probably has a facilitating function in nociceptive transmission in the spinal dorsal horn.

Animals↗
PubMed1988

The lateral vestibular nucleus is a site for the depressant action of benzodiazepines on the crossed extensor reflex.

The effects of diazepam microinjected into the subcerebellar nuclei, the lateral vestibular nucleus (LVN), the red nucleus and the substantia nigra were investigated using the crossed extensor reflex (CER) model in chloralose-anesthetized rats. Microinjections of diazepam at doses of 1 and 25 ng/animal into the left LVN, ipsilateral to the testing muscle, produced a dose-related CER depression, while injections of diazepam at a dose of up to 100 ng/animal into the right LVN and into other regions tested produced little effect. The CER depression produced by diazepam could be clearly reversed by a subsequent intravenous administration of Ro 15-1788, a benzodiazepine antagonist. Electrical lesions of the left LVN decreased the amplitude of CER in otherwise untreated rats. Intravenously administered diazepam at a dose of 0.01 or 0.05 mg/kg decreased spontaneous firing of LVN neurons. Iontophoretically applied GABA or flurazepam, a water-soluble benzodiazepine, decreased the spontaneous firing of LVN neurons. Depressant actions on neuronal activity in the LVN produced by both diazepam and flurazepam were clearly antagonized by intravenously administered Ro 15-1788, while it failed to reverse the depression produced by GABA. These findings indicate that the LVN is a major site of the CER depressant action of benzodiazepines and a possible mechanism of action is discussed.

Action Potentials↗
PubMed1988

Endogenous GABA released into the fourth ventricle of the rat brain in vivo is enhanced by noxious stimuli.

In vivo release of endogenous gamma-aminobutyric acid (GABA) and glutamic acid into the 4th ventricle of the rat brain in response to noxious stimuli was examined. Both these compounds were dansylated and the concentrations determined, using high-performance liquid chromatography (HPLC) combined with an UV detector. Following noxious stimuli (subcutaneous injection of diluted formalin into the hind-paw or noxious pinch of the hind-paws), there was a remarkable release of GABA, but not of glutamic acid. Basal on our heretofore obtained data that bicuculline methiodide, a GABAA antagonist, produces a potent analgesia in mice, the present results suggest that the GABAergic system in the brain stem may promote nociceptive transmission in rats.

Animals↗
PubMed1988

Calcium-activated neutral protease (CANP), a putative processing enzyme of the neuropeptide, kyotorphin, in the brain.

Kyotorphin (Tyr-Arg) accumulation in the dialysed synaptosol from the rat brain in the presence of an inhibitor of kyotorphin-degrading enzyme, was maximal at neutral pH. This accumulation was activated by calcium ions, but was inhibited by leupeptin and SH-blocking agents, a finding which suggests the involvement of calcium-activated neutral protease (CANP or calpain). In addition, the kyotorphin-precursor protein, being processed by purified mu- or m-CANP, was detected at about 160 kDa on Sephacryl S-300 chromatography of the synaptosol. The present findings seem to be the first evidence for the role of CANP as a processing enzyme of neuropeptide-precursor in nerve terminals.

Animals↗
PubMed1988

Glucocorticoid-induced growth inhibition with enhanced expression of ductal epithelium of human salivary gland adenocarcinoma cells transplanted into athymic nude mice.

The effect of glucocorticoid on growth and the histologic features of adenocarcinoma induced in nude mouse by the inoculation of neoplastic epithelial cells of salivary duct origin (HSG) were studied. Subcutaneous injection of dexamethasone (low-dose group: 0.05 micrograms/g, high-dose group: 0.25 micrograms/g) four times a week for 8 weeks significantly (P less than 0.05) inhibited tumor growth, and in one mouse the tumor had almost completely disappeared by the middle of the sixth week of treatment. In addition, dexamethasone induced an apparent luminal structure in the tissue section of the tumor and enhanced the immunoperoxidase reaction to epithelial membrane antigen. The results indicate that dexamethasone inhibited the proliferation of HSG cells in the nude mouse transplantation system probably by inducing the cellular differentiation of the HSG cells toward the more differentiated ductal epithelia via glucocorticoid receptors.

Adenocarcinoma↗
PubMed1988

Cytoplasmic pH change induced by leukotriene B4 in human neutrophils.

Leukotriene B4 induced a biphasic change in the cytoplasmic pH of human neutrophils: an initial rapid acidification followed by an alkalinization. The acidification was slightly reduced by the removal of extracellular Ca2+, but the subsequent alkalinization was not. The leukotriene B4-induced alkalinization was dependent on extracellular Na+ and pH, and was inhibited by amiloride and its more potent analogue, 5-(N,N-hexamethylene)amiloride. These characteristics indicate that the cytoplasmic alkalinization is mediated by the Na+-H+ exchange. Oxidation products of leukotriene B4, 20-hydroxyleukotriene B4, 20-carboxyleukotriene B4, and (5S)-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) also stimulated the Na+-H+ exchange, but higher concentrations were required. Treatment of the cells with pertussis toxin inhibited both phases of the leukotriene B4-induced pHi change, while cholera toxin did not affect the pHi change. The alkalinization induced by leukotriene B4 was inhibited by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C, but was not inhibited by N-(2-guanidinoethyl)-5-isoquinolinesulfonamide which has a less inhibitory effect on protein kinase C. Acidification was not affected by the drugs. These findings suggest that a GTP-binding protein sensitive to pertussis toxin and protein kinase C are involved in the activation of the Na+-H+ exchange stimulated by leukotriene B4.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1988

Binding of heparin onto ethylene-vinyl alcohol copolymer membrane.

Heparin was ionically bound onto the surface of an ethylene-vinyl alcohol copolymer (EVAL) membrane which was derivatized by aminoacetalization to produce cationic surface charges. The amount of bound heparin was proportional to the ion exchange capacity of the aminoacetalized membrane and the maximal amount obtained in this experiment was 96 Unit/cm2 (0.59 mg/cm2). Plasma recalcification times were measured for the heparinized membrane thus obtained. Recalcification times increased proportionally with the amount of heparin bound on the membrane, while original EVAL membranes and the non-heparinized aminoacetalized membrane did not show increases in recalcification times. This means that the heparinized EVAL membrane has a more nonthrombogenic property due to the release of heparin. The apparent amount of heparin released from the membrane into plasma was estimated from plasma recalcification times. The release rate was 0.30-0.33 Unit/cm2/h (1.8 X 10(-3)-2.0 X 10(-3) mg/cm2/h) for the membranes whose surface was considered to be saturated with heparin. The release amount was about 0.6% compared to the adsorbed heparin in the case of the 96 Unit/cm2-heparinized membrane incubated in plasma for 60 min.

Binding Sites↗
PubMed1988

Metallothionein induction prevents toxic side effects of cisplatin and adriamycin used in combination.

The protective effects of metallothionein (MT) preinduction by bismuth subnitrate (BSN) against the renal toxicity of cis-diamminedichloroplatinum (cis-DDP), the cardiotoxicity of adriamycin (ADR), and the lethal and bone marrow toxicities of these drugs were observed in mice receiving cis-DDP and ADR simultaneously. Preinduction of MT biosynthesis by BSN, which is currently used as an antidiarrheal drug, did not affect the antitumor activities of the two drugs, suggesting that the beneficial effects of the preinduction of MT biosynthesis by BSN may be applicable for therapy involving cis-DDP and ADR, either alone or in combination.

Adenocarcinoma↗
PubMed1988

Age-related changes of the granular intercalated duct cells of male rat submandibular gland.

The granular intercalated duct (GID) cells showed a progressive increase in number from two to four months of age (p less than 0.01). Their secretory granules also increased in number. Among all the age groups (2-22 months), the number of the GID cells in submandibular gland was highest of six months; they were then also most conspicuous with many electron-dense secretory granules in the cytoplasm. From 12 to 22 months, they showed regressive changes such as a decrease in cell number and in the number of secretory granules. The significance of these age-related changes of the GID cells is unknown.

Aging↗
PubMed1988

A new model of counterion condensation in polyelectrolyte solutions. III. Theoretical predictions of competitive condensation between counterions of different valences.

Our model has been extended for theoretical estimation of competitive condensation of counterions of different valences onto polyelectrolytes in solution. The estimations are compared with those obtained from Manning theory and with experimental data on counterion activity coefficients. The agreement with the data for sodium polystyrenesulfonate/MgCl2, CaCl2 is satisfactory.

Journal Article↗
PubMed1988

Reconstitution of rat brain mu opioid receptors with purified guanine nucleotide-binding regulatory proteins, Gi and Go.

Reconstitution of purified mu opioid receptors with purified guanine nucleotide-binding regulatory proteins (G proteins) was investigated. mu opioid receptors were purified by 6-succinylmorphine AF-AminoTOYOPEARL 650M affinity chromatography and by PBE isoelectric chromatography. The purified mu opioid receptor (pI 5.6) migrated as a single Mr 58,000 polypeptide by NaDodSO4/PAGE, a value identical to that obtained by affinity cross-linking purified mu receptors. When purified mu receptors were reconstituted with purified Gi, the G protein that mediates the inhibition of adenylate cyclase, the displacement of [3H]naloxone (a mu opioid antagonist) binding by [D-Ala2,MePhe4,Gly-ol5]enkephalin (a mu opioid agonist) was increased 215-fold; this increase was abolished by adding 100 microM (guanosine 5'-[gamma-thio]triphosphate. Similar increases in agonist displacement of [3H]naloxone binding (33-fold) and its abolition by guanosine 5'-[gamma-thio]triphosphate were observed with Go, the G protein of unknown function, but not with the v-Ki-ras protein p21. In reconstituted preparations with Gi or Go, neither [D-Pen2,D-Pen5]enkephalin (a delta opioid agonist; where Pen is penicillamine) nor U-69,593 (a kappa opioid agonist) showed displacement of the [3H]naloxone binding. In addition, the mu agonist stimulated both [3H]guanosine 5'-[beta,gamma-imido]triphosphate binding (in exchange for GDP) and the low-Km GTPase in such reconstituted preparations, with Gi and Go but not with the v-Ki-ras protein p21, in a naloxone-reversible manner. The stoichiometry was such that the stimulation of 1 mol of mu receptor led to the binding of [3H]guanosine 5'-[beta,gamma-imido]triphosphate to 2.5 mol of Gi or to 1.37 mol of Go. These results suggest that the purified mu opioid receptor is functionally coupled to Gi and Go in the reconstituted phospholipid vesicles.

Animals↗
PubMed1988

Membrane-bound trypsin-like enzyme functioning in degradation of dynorphin in neuroblastoma cells. Purification and characterization.

A trypsin-like enzyme has been purified to apparent homogeneity from neuroblastoma cell membranes by a procedure including extraction with Triton X-100, soybean trypsin inhibitor-immobilized Sepharose 4B affinity chromatography, and gel filtration. SDS-polyacrylamide gel electrophoresis under reducing conditions of the purified enzyme gave a single band corresponding to a molecular weight of 28,000. The molecular weight of the enzyme was also estimated to be 32,000 by gel filtration. The pH optimum of the activity was 8.5-9.0. The purified enzyme was inhibited by diisopropylphosphorofluoridate, p-aminobenzamidine, and leupeptin, and moderately by chymostatin, but not, or only scarcely, by bestatin, phosphoramidon, p-chloromercuribenzoate, and N-ethylmaleimide. The substrate subsite specificity of the purified enzyme was broad toward various peptidyl-arginine (or lysine) 4-methylcoumaryl-7-amides, but it cleaved dynorphin(1-17) only at two sites, i.e., between the Arg6-Arg7 and Lys11-Leu12 bonds, both of which correspond to the initial cleavage sites of dynorphin with a membrane preparation of neuroblastoma cells. A trypsin-like enzyme was also purified from a synaptic membrane preparation of rat brain, which shows almost the same properties as those of the enzyme from the neuroblastoma cell membrane. Thus, the trypsin-like enzyme present in the synaptic membrane would participate in the degradation of dynorphin.

Cell Membrane↗
PubMed1988

Specific reduction of toxic side effects of adriamycin by induction of metallothionein in mice.

The effect of preinduction of metallothionein (MT) by bismuth (Bi) compounds on the toxic side effects and antitumor activity of adriamycin (ADR) was investigated in mice. Preinduction of MT by oral administration of bismuth subnitrate (BSN) significantly decreased the lethal toxicity, cardiotoxicity and bone marrow toxicity observed with a single subcutaneous injection of ADR. A significant increase in the concentration of cardiac MT was observed in mice treated with BSN. The MT level in the heart was significantly correlated with the protective effect of BSN against the cardiotoxicity of ADR. In tumor-bearing mice, pretreatment with BSN did not affect the antitumor activity of ADR, although its cardiotoxicity was significantly depressed. The ability of BSN to reduce specifically the toxicity of ADR may be ascribed to the fact that Bi induces MT in the target tissue of ADR toxicity but not in a tumor. The protective effect of MT against the toxicity of ADR, which is believed to act as an anticancer agent by generating active oxygen, can be assumed to be due to its ability to scavenge free radicals or inhibit their formation.

Animals↗
PubMed1988

Syncope in aortic stenosis during continuous electrocardiographic monitoring--a case report.

A female patient with severe aortic stenosis had suffered from repeated syncope. Transaortic valve pressure gradient at cardiac catheterization was 117 mmHg. Continuous electrocardiographic monitoring was done after admission. During syncope, the electrocardiogram showed bradycardia with the lowest heart rate 44 beats per minute, while arterial pulses were not palpable. Rather than arrhythmia, other mechanisms, such as an inhibitory reflex from left ventricular receptors, should be postulated as the cause of syncope in patients with severe aortic stenosis.

Aged↗
PubMed1988

Endoscopic observation of peripheral airway lesions.

Peripheral airways of 2 mm or less in diameter were observed in 142 patients by means of an ultrathin bronchofiberscope measuring 1.8 mm in outside diameter. On the basis of the observed and photographed endoscopic findings, an endoscopic classification of peripheral airway lesions was proposed. The endoscopic findings showed changes in the bronchial wall consisting of reddening, pallor, absence of mucosal luster, edema, engorgement of blood vessels, irregular mucosal surface, and elevated mucosa. In the lumen, stenosis, obstruction, ectasis, and deformation due to pressure were recognized, in addition to excessive secretion and pigmentation as morphologic abnormalities or abnormal findings at bifurcation.

Adolescent↗