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Biomedical subjects

M Funahashi

Publications and source records attributed to M Funahashi.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Sudden death of alcohol withdrawal syndrome--report of a case].

A 50-year-old driver was arrested in a drunken stupor while he was driving a track. He suddenly died after five days of the arrest in a jail. As time went by, various symptoms of alcohol withdrawal appeared. He was in the state of delirium treatments for about a day before he died. Gross and microscopical examination revealed fibrosis and fatty degeneration of liver and heart lesions representing chronic and acute ischemia. We discussed the cause and the mechanism of the death in the case and reviewed those in the previous observations.

Alcohol Withdrawal Delirium↗
PubMed1989

Experimental induction of uterine cancer in rats by N-ethyl-N'-nitro-N-nitrosoguanidine dissolved in polyethylene glycol.

In the present experiment we attempted to experimentally induce uterine cancer in rats by injecting into the uterine cavity N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) dissolved in polyethylene glycol (PEG). Fifty-nine female F-344 rats, 7-8 weeks old, were divided into three groups and each received in the left uterine cavity with laparotomy a single dose of ENNG dissolved in PEG according to the following schedule: Group 1 received 75 mg ENNG/kg body wt.; Group 2 had 20 mg ENNG/kg body wt.: and Group 3 was given only PEG. In Group 1 it was observed that adenocarcinoma and sarcoma were present in the uterine corpus while squamous cell carcinoma occurred in the uterine cervix. In Group 2, although tumors such as adenocarcinoma, adenoma and sarcoma were observed in the uterine corpus, no tumor was present in the uterine cervix. No tumor growth whatsoever was observed in Group 3. From the above results it is apparent that the present method is an efficient means for experimentally inducing uterine cancer and that the site of tumor generation varies according to the concentration of ENNG administered.

Animals↗
PubMed1988

Potentiation of lethality and increase in body temperature by combined use of d-methamphetamine and morphine in mice.

Lethality and change in body temperature in mice were examined after subcutaneous injection of d-methamphetamine and morphine alone or in combination. The LD50 values for methamphetamine and morphine were calculated to be 95 and 670 mg/kg body wt., respectively. When a non-lethal dose of morphine (300 mg/kg) was administered with various doses of methamphetamine, the LD50 for methamphetamine was reduced to 5 mg/kg, indicating a marked potentiation of toxicity by combined use of both drugs. Injection of 5 mg/kg of methamphetamine produced slight hyperthermia, while 300 mg/kg of morphine decreased the body temperature of mice. However, when both drugs were used concomitantly, a marked increase in body temperature was observed. Hyperthermia was also observed when the dose of morphine was reduced to 50 mg/kg. It is postulated that hyperthermia is probably one of the contributory factors in the potentiated toxicity by combined use of morphine and methamphetamine.

Animals↗
PubMed1986

Decrease in d-methamphetamine sensitivity in mice due to ethanol: apparent inhibitory and stimulatory effects of ethanol on d-methamphetamine-induced locomotor activity.

The locomotor activity of mice was recorded after administration of d-methamphetamine-HCl (1.5, 2.5, 5.0 and 7.5 mg/kg body weight) and/or ethanol (0.8 and 1.6 g/kg body weight). Mice injected with lower doses of d-methamphetamine (1.5 or 2.5 mg/kg) showed a marked increase in locomotor activity, while in those with higher doses of d-methamphetamine (5.0 or 7.5 mg/kg), locomotor activity was not further enhanced, but slightly decreased. Administration of ethanol inhibited the stimulated locomotor activity caused by low doses of d-methamphetamine (1.5 or 2.5 mg/kg), while the stimulation of motility after higher doses of d-methamphetamine (5.0 or 7.5 mg/kg) was potentiated by administering ethanol. Although apparent inhibition and stimulation of d-methamphetamine-induced locomotor activity of mice due to ethanol was observed, it is suggested that mice administered ethanol showed the decreased sensitivity to d-methamphetamine by plotting total locomotor activity of mice against doses of d-methamphetamine administered. The half maximum effective dose of d-methamphetamine for locomotor activity was increased from 1.5 mg/kg to 3.0 mg/kg by concomitant administration of 1.6 g/kg ethanol.

Animals↗
PubMed1983

Binding of fibronectin and its proteolytic fragments to glycosaminoglycans. Exposure of cryptic glycosaminoglycan-binding domains upon limited proteolysis.

Binding of intact plasma fibronectin and its proteolytic fragments to glycosaminoglycans immobilized on agarose beads was systematically compared at different ionic strengths. In low ionic strength buffer, intact fibronectin bound to heparin and high sulfated heparan sulfate, but not to low sulfated heparan sulfate, dermatan sulfate, chondroitin sulfates A and C, or hyaluronic acid. Fractionation of the thermolysin digest of fibronectin on the glycosaminoglycan-Sepharoses at low ionic strength revealed that three groups of fragments, i.e. Mr = 150,000-140,000, 24,000, and 16,000 (150K-140K, 24K, and 16K) fragments, were capable of binding to glycosaminoglycans with different specificities and affinities. The 150K-140K fragments exhibited the same specificities as intact fibronectin, binding only to heparin and high sulfated heparan sulfate. However, the 24K fragment bound not only to these two glycosaminoglycans but also to low sulfated heparan sulfate and other glycosaminoglycans as well. The 16K fragments were also capable of binding to most glycosaminoglycans with lower affinity than the 24K fragment. These results suggest that the binding sites in the 24K and 16K fragments are cryptic in the intact protein, but are exposed after limited proteolysis. The binding of fibronectin and its fragments to glycosaminoglycans is dependent on the ionic strength. At physiologic ionic strength, only heparin-Sepharose could bind intact fibronectin. Similarly, only heparin-Sepharose could bind the 150K-140K and 24K fragments, but not the 16K fragments, at the same ionic condition. Other glycosaminoglycan-Sepharoses did not retain significant amounts of any of the fibronectin fragments, suggesting that the affinity of plasma fibronectin and its fragments to heparan sulfate and other glycosaminoglycans, except heparin, is not strong enough to achieve stable mono- (or di-) valent binding under physiologic conditions.

Animals↗
PubMed1981

Formation of arginine and guanidinoacetic acid in the kidney in vivo. Their relations with the liver and their regulation.

A method was developed for evaluating the relative rate of conversion of [14C]-citrulline to [14C]arginine in vivo. By this method it was demonstrated that the conversion was almost completely abolished by functional nephrectomy, but not by functional hepatectomy. It was also demonstrated that functional nephrectomy caused a prompt increase in the citrulline concentration in the serum, while functional hepatectomy caused a rapid decrease in it. On the basis of these findings, it was concluded that the kidney was the main organ for synthesis of arginine from citrulline, which is supplied from the liver. Studies using this method also provided evidence suggesting that arginine formation from citrulline might be controlled by insulin and by negative feedback due to dietary arginine. In addition, in vivo experiments and perfusion experiments on isolated kidney showed that guanidinoacetic acid formation from citrulline was remarkable decreased in diabetic rats. Enzymological studies suggested that this decrease might be due to a change in glycine amidinotransferase [L-arginine:glycine amidinotransferase, EC 2.1.4.1] activity.

Animals↗