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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 847 records · Page 47Linked to original sources

Dural arteriovenous malformation near the left sphenoparietal sinus.

The case of a 14-year-old boy with a dural arteriovenous malformation in the region of the sphenoparietal sinus associated with a markedly dilated dural sinus is reported. The arterial supply was solely via the meningeal branches of the left external carotid artery; venous drainage was through dilated venous channels into the superior ophthalmic vein and pterygoid venous plexus. Treatment consisted of artificial embolization and ligation of the left external carotid artery and excision of the dilated venous sac. The vascular lesions were absent from the post-operative angiogram, except for small angiomatous remnants fed by meningeal branches of the left internal carotid artery.

Adolescent↗

Traumatic arteriovenous fistula between the middle meningeal artery and cortical vein.

A 53-year-old man with a traumatic dural arteriovenous fistula between the middle meningeal artery and the adjacent cortical vein is reported. The lesion was absent on the initial angiogram after his head injury and was first recognized nine months later. It enlarged during the succeeding ten months. Symptoms were convulsions and a transient aphasic episode. Surgical repair was successful.

Arteriovenous Fistula↗

Effects of loperamide on the guinea pig taenia coli.

The effects of an antidiarrhoeal agent, loperamide, were studied using isolated guinea pig taenia coli. Loperamide in concentrations ranging from 10(-7) M inhibited the cholinergic, contractile responses induced by electrical transmural stimulation, nicotine and serotonin, and the nonadrenergic, relaxing responses induced by electrical transmural stimulation and nicotine. However, the adrenergic response to perivascular nerve stimulation was not affected by these concentrations. The inhibitory effects of loperamide were not reversed by washing with a drug-free solution. Morphine (10(-6 M to 10(-5) M) also inhibited both cholinergic and nonadrenergic responses, but the effect was reversible. Naloxone (1o(-6) M) attenuated the inhibitory effects of both drugs. Unlike morphine, loperamide in concentrations higher than 5 x 10(-6) M relaxed the strips and reduced the contractile response to acetylcholine noncompetitively, and these effects were not blocked by naloxone. These results suggest that loperamide at low concentrations acts selectively on the opiate receptors located in both cholinergic and nonadrenergic nerves and at higher concentrations also acts directly on smooth muscle thus producing relaxation of the intestinal tone.

Acetylcholine↗

A neural network model for the development of direction selectivity in the visual cortex.

A neural network model is proposed to explain the development of direction selectivity of cortical cells. The model is constructed under the following three hypotheses that are very plausible from recent neurophysiological findings. (1) Direction selectivity is developed by modifiable inhibitory synapses. (2) It results not from the direct convergence of many excitatory inputs from LGN cells but from cortical neural networks. (3) Direction-selective mechanism is independent of orientation-selective mechanism.--The model was simulated on a computer for a few kinds of inhibitory connections and initial conditions. The results were consistent with neurophysiological facts not only for normal cats but for cats reared in an abnormal visual environment.

Animals↗

Dubin-Johnson syndrome in a neonate.

We described the clinical and biochemical findings in a 32 day-old boy with the Dubin-Johnson syndrome. Only two other patients diagnosed as having the Dubin-Johnson syndrome during neonatal period have been reported in the literature. The ratio of urinary coproporphyrin isomer I of our patient was 97% and that of his parents were carrier level, confirming that increased urinary excretion of coproporphyrin isomer I is of diagnostic value in neonates with the Dubin-Johnson syndrome.

Coproporphyrins↗

Formation of 5-hydroxykynurenine and 5-hydroxykynurenamine from 5-hydroxytryptophan in rabbit small intestine.

In order to clarify the role of indoleamine 2,3-dioxygenase [indole:oxygen 2,3-oxidoreductase (decyclizing), EC 1.13.11.17] in the metabolism of serotonin, DL-5-hydroxy[methylene-(14)C]tryptophan, a precursor of serotonin, was incubated with slices of rabbit ileum. Resulting metabolites were separated by DEAE-cellulose column and polyamide column chromatography and identified by various chromatographic techniques and enzymatic analysis. Metabolites obtained in significant amounts were serotonin, 5-hydroxyindoleacetic acid, 5-hydroxytryptophol, 5-hydroxykynurenine, 5-hydroxykynurenamine, and 4,6-dihydroxyquinoline, representing 13.2, 15.8, 7.0, 21.9, 1.3, and 2.6% of the total metabolites, respectively. The first three compounds were previously reported to be major metabolites produced from 5-hydroxytryptophan by the action of aromatic L-amino acid decarboxylase and monoamine oxidase, whereas the last three are formed by the cleavage of the indole ring by the action of indoleamine 2,3-dioxygenase. In the presence of pargyline, a monoamine oxidase inhibitor, the major metabolites obtained were serotonin, 5-hydroxykynurenine, and 5-hydroxykynurenamine, representing 29.6, 26.6, and 5.4% of the total metabolites, respectively. In the presence of RO4-4602, an aromatic amino acid decarboxylase inhibitor, 5-hydroxykynurenine was the sole major product. These results strongly suggest that the newly discovered metabolic pathway involving the cleavage of the indole ring of 5-hydroxytryptophan operates in vivo to a significant extent and that indoleamine 2,3-dioxygenase plays an important role in the regulation of serotonin levels in the small intestine of the rabbit.

5-Hydroxytryptophan↗

Effect of acetylcholine on the norepinephrine-induced positive chronotropy and increase in cyclic nucleotides of isolated rabbit sinoatrial node.

Transmural stimulation of, or application of nicotine to, the isolated rabbit sinoatrial (SA) node resulted in initial negative and late positive chronotropy. Simultaneous application of acetylcholine and norepinephrine produced a similar biphasic chronotropic effect. These procedures produced an initial increase in cyclic guanosine 3':5'-monophosphate (cyclic GMP) and a delayed elevation in cyclic adenosine 3':5'-monophosphate (cyclic AMP). The initial and late effects on rate and nucleotide levels were inhibited by pretreatment with atropine and propranolol, respectively. Pretreatment with atropine shortened the time of maximum increase in cyclic AMP level and heart rate from 3 to 1 minute after the simultaneous application of acetylcholine and norepinephrine and enhanced the positive chronotropic effect. Physostigmine prolonged the duration of the increase in cyclic GMP and negative chronotropic effect after the simultaneous application. These results suggest that when acetylocholine and norepinephrine are present simultaneously in the SA node region, the former interacts predominantly with muscarinic receptors and stimulates the cyclic GMP system, which in effect delays the cyclic AMP elevation and reduces the positive chronotropic effect of norepinephrine. However, these effects of acetylcholine cannot be explained solely on the basis of changes in the cyclic GMP level, because sodium nitroprusside produced a marked elevation of the cyclic GMP levels without decreasing the heart rate and did not affect the norepinephrine-induced increase in pacemaker rate and cyclic AMP. Sodium nitroprusside may affect cyclic GMP pools other than those susceptible to acetylcholine. These cyclic GMP pools may not exert chronotropic effects.

Acetylcholine↗

Effect of cholera enterotoxin on pacemaker rate and cyclic adenosine 3':5'-monophosphate in isolated rabbit sinoatrial node.

The positive chronotropic effect of cholera enterotoxin on isolated rabbit sinoatrial (S-A) node was investigated. This toxin produced a time and dose-related increase in pacemaker rate and cyclic adenosine 3':5'-monophosphate (cyclic AMP) levels and shifted to the left the dose-response curves of norepinephrine on the pacemaker rate and cyclic AMP content in the S-A node. Thus, the sensitivity of the S-A node to norepinephrine was increased by the toxin. These effects of the toxin were not blocked by propranolol. There was a linear relation between the increases in pacemaker rate and cyclic AMP content after application of both the toxin and norepinephrine. However, the slope of the regression line relating pacemaker rate to cyclic AMP level differed with these two agents. These results suggest that cholera enterotoxin increases pacemaker rate with activation of the adenylate cyclase system in the S-A node, but the mechanism differs from that of norepinephrine.

Adenylyl Cyclases↗

Effects of water-immersion stress on gastric secretion and mucosal blood flow in rats.

The correlation between acid secretion and mucosal blood flow in the rat stomach during stress loading was determined to provide clues to the etiology of the gastric ulceration which thus occurs. The gastric acid output was increased remarkably by water-immersion stress at 23 degrees C, and this increase lasted while the stress was given, yet the mucosal blood flow did not show a corresponding increase. In rats stressed for 3 hr, ulcerative changes were observed in the glandular portion of the stomach. The stress-induced increase in acid output correlated well with the severity of erosions. Pretreatment of animals with atropine 10 microgram/kg, given subcutaneously, or vagotomy, inhibited the increase in acid output and also inhibited the ulcer formation caused by the stress: however, the mucosal blood flow in these animals decreased significantly. These results suggest that when there is an elevation of gastric acid secretion with no parallel increase in mucosal blood flow, gastric ulceration may occur under conditions of stress.

Animals↗