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Biomedical subjects

M Sawada

Publications and source records attributed to M Sawada.

At least 559 records · Page 31Linked to original sources
PubMed1976

Reverse plaque formation by hog cholera virus of the GPE-strain inducing heterologous interference.

A simple and rapid plaque procedure was developed for the assay of hog cholera virus (HCV) of a particular strain, GPE-, based on its intrinsic interference with vesicular stomatitis virus (VSV) on the primary swine testicle cells and on an established swine kidney cell line; the procedure is called the reverse plaque formation (RPF) method. The plaques were produced as colonies of HCV-infected cells which were VSV-sensitive, disintegrated cell sheet. These plaques became visible after 15 to 20 h of superinfection with VSV done 2 days after an initial inoculation of the GPE- strain. The plaque formation was inhibited by a specific antiserum against HCV. All cells within the plaque had HCV antigen detectable by fluorescent-antibody staining. The variations of reverse plaque count were low enough to permit virus titration. The relationship between virus concentration and the number of plaques was essentially linear. The titer measured by the RPF method was a little higher than that of the tube culture interference method.

Animals↗
PubMed1976

Effects of disulfide bond reduction on the excitatory and inhibitory postsynaptic responses of Aplysia ganglion cells.

Three kinds of the cholinoceptive neurons, nicotinic depolarizing (D)-, nicotinic hyperpolarizing (H)-, and muscarinic H-tyes, as well as two other kinds of neurons, GABA H- and dopamine H-types, were identified in Aplysia abdominal ganglion, and the effects of disulfide bond reduction and reoxidation on their postsynape acetylcholine-induced responses of both nicotinic types (D- and H-) were depressed by reducing the disulfide bonds with dithiothreitol (DTT) and restored by reoxidizing with 5, 5' -dithiobis-(2-nitrobenzoic acid): (DTNB), whereas the responses of the muscarinic H-, GABA H-, and dopamine H-cells were not affected at all by either DTT or DTNB. In contrast to the results obtained from the electroplax, the cholinergic receptors in our preparation showed neither the activation by hexamethonium nor the augmentation of decamethonium-induced responses after reduction of disulfide bonds. In addition, our preparation did not demonstrate the long-lasting responses to bromoaTT-induced depression of the nicotinic responses was studied on the dose-response curves; the mode of receptor inhibition was rather complexed, being neither type of competitive nor non-competitive. We concluded that the disulfide bond is a crucial element in both types of nicotinic receptors (D and H), and that this bond is related to the activation process of the receptors regardless of their ionic specificities.

Acetylcholine↗
PubMed1976

The late results of terminal esophagoproximal gastrectomy (TEPG) with intensive devascularization and splenectomy for bleeding esophageal varices in cirrhosis.

The operative procedure of terminal esophagoproximal gastrectomy (TEPG) with extensive esophagogastric devascularization and splenectomy is described in detail and its rationale is discussed. Late results of this operation performed therapeutically on 64 patients with posthepatitic cirrhosis revealed that (1) operative mortality rate (death within a month) was 11%, mostly being contributed by poor-risk patients; (2) over-all survival was 65% at 5 years and 59% at 10 years; (3) gastrointestinal bleeding recurred in nine patients, five of whom had major and four minor hemorrhages; (4) portasystemic encephalopathy was seen frequently after shunts had never occurred, and the hepatic encephalopathy was only a sequel of major gastrointestinal bleeding or a manifestation of terminal-stage liver insufficiency; and (5) ascites was not a major clinical problem after this operation; mild esophagitis was an occasional complication.

Esophageal and Gastric Varices↗
PubMed1975

The effect of dimethyl sulfoxide on the neuronal excitability and cholinergic transmission in Aplysia ganglion cells.

The effects of DMSO on single nerve cells of Aplysia were investigated by various electrophysiological methods. 1. Although the increase in permeability of the biological membranes produced by DMSO has been well documented, we found that DMSO at concentration of less than 20% actually decreases the permeability of the neuronal membranes, probably toward potassium and chloride ions. This change in ionic permeability reversibly depolarizes the resting membranes and makes the neurons more excitable. 2. The falling phase of the spike is prolonged by 8% DMSO, because it blocks the active increase in potassium permeability. This change suppresses the high frequency discharge, because the refractory period of each spike is increased. Neither the rising phase nor the absolute firing level is appreciably altered by DMSO when these are examined after the depolarization is cancelled. 3. Dilute DMSO (less than 1%) facilitates cholinergic trasmission because it blocks ACh-esterase activity. DMSO at concentrations of more than 10% ultimately blocks cholinergic transmission entirely, because it also depresses cholinoceptive receptor activity (probably by allosteric interaction). The action of 1-10% DMSO is complicated, because both facilitatory and inhibitory effects take place at the same time. 4. In cholinergic synapses, excitatory transmission is more susceptible to DMSO than inhibitory transmission. This is because the activity of the excitatory receptor is blocked more readily than that of the inhibitory receptor. The depressing effects of DMSO are not specific to the cholinergic system, however, since the activities of GABA and glutamate receptors are similarly depressed.

Acetylcholine↗
PubMed1974

Analysis of hyperpolarizations induced by glutamate and acetylcholine on Onchidium neurones.

1. Four giant neurones, designated G-H cells, in the right pleural ganglion of the marine pulmonate mollusc, Onchidium verruculatum, showed characteristic membrane hyperpolarization during applications of either acetylcholine (ACh) or L-glutamate. In the presence of ACh the membrane was hyperpolarized only transiently, while in the presence of glutamate the response was maintained. Significant increases in membrane conductance accompanied the changes in membrane potential.2. In excess potassium sea water, a slight hyperpolarization occurred when the normal concentration was increased between one- and twofold. However, depolarization usually occurred when the concentration was increased tenfold except on a few occasions when a slight but definite hyperpolarization occurred. These changes were all accompanied by a substantial increase in the membrane conductance. This hyperpolarization was in all probability the result of an increase in chloride ion permeability caused by the release of an ACh-like transmitter from depolarized presynaptic nerve terminals.3. The reversal levels for glutamate- and ACh-induced hyperpolarization respectively were approximately - 20 and - 17 mV with respect to the resting membrane potential.4. By changing the external ion composition, glutamate- and ACh-induced hyperpolarization were shown to be the result of an increased permeability of the subsynaptic membrane to potassium and chloride ions respectively. It appears therefore that inhibition in the same G-H cells can be activated by two different transmitter substances and that each of them activates a change in the membrane permeability to a different ion.5. The relationship between the concentration of glutamate and the membrane conductance change was suggestive of two glutamate molecules reacting with a single receptor site.

Acetylcholine↗