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Biomedical subjects

A Sawa

Publications and source records attributed to A Sawa.

10 recordsLinked to original sources
PubMed1991

[The relationship between the anti-HCV titer and the state of chronic hepatitis C].

By dilution of the serum, we quantitatively analyzed anti-HCV to examine the relation between the anti-HCV titer and the state of chronic hepatitis C, and determined the effectiveness of interferon therapy. The anti-HCV titer was related with the state of chronic hepatitis C, but not as closely as GPT. Cases with blood transfusion had a lower titer of anti-HCV, weaker histological finding and better response to interferon than those without blood transfusion. The anti-HCV titer was not useful for determining the effectiveness of interferon therapy.

Adult↗
PubMed1987

Heterogeneity of postnatal development of ACh levels in brain regions of the mouse.

Acetylcholine (ACh) was measured from birth to the 78th day in 11 mouse brain regions. Three patterns of development emerged: ACh increased rapidly, overshot and returned to the adult level in midbrain-medulla-pons and cerebellum, ACh increased linearly to adult level in neostriatum and olfactory bulb and ACh increased linearly to a plateau and then increased to the adult level in the remaining regions.

Acetylcholine↗
PubMed1979

Calcium requirements for electrically-induced release of an endogenous opiate receptor ligand from the guinea-pig ileum.

Calcium requirements for electrically-induced release of an endogenous opiate receptor ligand in the myenteric plexus-longitudinal muscle strip of the guinea-pig ileum were studied. The naloxone-reversible depression of the electrically evoked contraction caused by stimulation at 10 Hz in normal Krebs solution was markedly reduced by decreasing the calcium concentration in the solution. The depression was greatly diminished by increasing the magnesium concentration in the solution. These results show that the electrically-induced release of an opiate-like material requires calcium ions.

Animals↗
PubMed1976

Effects of narcotic analgesics on serotonin metabolism in brain of rats and mice.

The effects of narcotic analgesics on the brain 5-hydroxytryptamine (5-Ht) and 5-hydroxyindoleacetic acid (5-HIAA) levels of rats and mice were investigated in relation to our preceding data on the effect of humoral modulatorents. The results suggest that morphine accelerates the release of brain 5-HT both in rats and mice, and that neither methadone nor pethidine alters the brain 5-HT and 5-HIAA levels in rats. The morphine-induced increase in brain 5-HT turnover is likely to be involved in the morphine-induced decrease in locomotor activity and hypothermia in rats. The activity-decreasing effects of methadone or pethidine, on the other hand, are mediated by mechanisms different from those which mediate the effects of morphine. In contrast, an increase in brain 5-HT turnover in mice apparently does not play an important role on activity-increasing effects of morphine but rather participates in other pharmacological effects of morphine.

Analgesics, Opioid↗
PubMedDate not supplied

Effects of subchronic soman on avoidance-escape behavior and cholinesterase activities.

Male Sprague-Dawley rats were trained on a discriminated avoidance-escape task. They were administered subchronically saline, 12.7 micrograms/kg (0.125 LD50) soman, or 25.5 micrograms/kg (0.25 LD50) soman. Injections were given 5 days per week for 4 weeks. Injections were given subcutaneously immediately following the avoidance behavior test session. Soman produced a reduction in avoidance behavior efficiency in a dose dependent manner. When soman was discontinued, the rats recovered their pre-soman control baselines. Untrained rats given soman according to the same soman regimen were used to measure acetylcholine in brain and cholinesterase activities in brain, blood, and diaphragm. After 18 soman injections at 12.7 and 25.5 micrograms/kg acetylcholine was reduced significantly only in the amygdala. Blood cholinesterase was inhibited as much as 57% after 12.7 micrograms/kg soman and 74% after 25.5 micrograms/kg. Plasma cholinesterase was inhibited to 24% by the 12.7 micrograms/kg dose of soman and to 38% by the 25.5 micrograms/kg dose. Plasma cholinesterase recovered to control levels 11 days after cessation of soman, and whole blood cholinesterase recovered 25 days after cessation of the higher soman dose. Cholinesterase was inhibited significantly in the hippocampus and amygdala in a dose dependent manner. The cholinesterase activities appear to parallel the soman induced decrement in avoidance behavior and the subsequent recovery to control levels following withdrawal of soman.

Animals↗