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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 649 records · Page 36Linked to original sources
PubMed1985

Giant cell tumor in cervical spine.

A giant cell tumor in the cervical spine of a 67-year-old man complaining of pain in the neck and occipital area is reported. Cervical x-ray films revealed a round destructive lesion in the vertebral body of the fourth cervical vertebra. On the plain cervical computed tomography scan, the most impressive finding was a soap-bubble appearance, which showed a linear high-density area in the mass lesion with destruction of the vertebral body. After embolizing one branch of the artery feeding the tumor, a radical operation was carried out via the anterior approach. The role of cervical computed tomography scanning and computed tomographic myelography in diagnosing and showing the extension of the giant cell tumor is discussed.

Aged↗
PubMed1985

Megadolichobasilar anomaly associated with brain stem infarction: a case report.

A rare case of megadolichobasilar anomaly associated with localized brain stem infarction showing right hemiparesis and disturbance of consciousness is described. The etiologic mechanisms of brain stem infarction in this anomaly are discussed. The tortuosity and dilatation of the basilar artery were thought to play an important role in the pathogenesis of the brain stem infarction.

Aged↗
PubMed1985

A new model of ventricular fibrillation induced by isoprenaline and catechol-O-methyl transferase inhibitor at a high perfusion temperature in isolated rat hearts.

Isolated rat hearts were perfused with various concentrations of isoprenaline (0.01-10 mumol/liter) for 30 min at a constant flow rate (6.5 ml/min) at 37-44 degrees C. The occurrence of ventricular fibrillations was isoprenaline concentration dependent and also perfusion temperature dependent in the combined treatment with various concentrations of isoprenaline and high perfusion temperatures. When the hearts were perfused with isoprenaline (1 mumol/liter) in the presence of tropolone (100 mumol/liter) at 40-41 degrees C, the duration of ventricular fibrillations was significantly prolonged, but the incidence of ventricular fibrillations was similar to that produced with isoprenaline (1 mumol/liter) alone. The antiarrhythmic drugs such as quinidine sulfate, lidocaine hydrochloride, dl-propranolol hydrochloride, carteolol hydrochloride, atenolol, dl-verapamil hydrochloride, and diltiazem hydrochloride, given at a concentration of 10 mumol/liter, significantly suppressed the incidence and duration of such ventricular fibrillations. Bretylium tosylate (10 mumol/liter) significantly suppressed the duration of the ventricular fibrillations but not their incidence. These results indicate that ventricular fibrillation induced by combined treatment with a high concentration of isoprenaline and tropolone at a high perfusion temperature in isolated rat hearts is a more useful experimental model of arrhythmia than conventional models.

Animals↗
PubMed1985

Chromosome heteromorphisms and paternity testing.

Most of the blood group systems have now been applied to paternity investigations. In a complicated case, an alleged father not excluded with blood group testing, could be excluded with only chromosome heteromorphisms. Chromosome heteromorphisms are inherited from parents to offspring as simple Mendelian laws. The authors' paternity testing is presented with the help of chromosome heteromorphism analysis.

Blood Grouping and Crossmatching↗
PubMed1985

Differences in contractile responses to electrical stimulation and alpha-adrenergic binding sites in isolated cerebral arteries of humans, cows, dogs, and monkeys.

The neurogenic responses of cerebral arteries of humans and the monkey were compared with those of the dog. alpha-Adrenoceptors in these cerebral arteries were also characterized by radioligand-binding studies. In human posterior communicating arteries, the contractile response to electrical transmural stimulation was attenuated by treatment with phentolamine in 41% of preparations tested, but not affected by aspirin. The responses in the monkey and canine arteries were not attenuated by treatment with phentolamine, but were reduced by aspirin in 60 and 73% of the cases, respectively. Reactivity and affinity to exogenous noradrenaline were comparable in human and monkey arteries, but greater than those of canine arteries. Radioligand-binding assays revealed binding sites for [3H]prazosin in the human and monkey cerebral arteries; the KD and Bmax values were not significantly different between the two species. Such binding sites were not detected in canine arteries. Binding sites for [3H]yohimbine were present in the arteries of the three species. Thus, the neurogenic contractile response of human cerebral arteries may be at least in part adrenergic in nature, while that of monkey and canine arteries may be due to neurogenically occurring arachidonate. alpha-Adrenoceptors in the monkey arteries are similar to those in humans.

Animals↗
PubMed1985

Biochemical characterization of the nicotinic cholinergic receptors in human brain: binding of (-)-[3H]nicotine.

(-)-[3H]Nicotine was found to bind specifically to membranes of human brains obtained at autopsy. The binding was stereospecific, (-)-nicotine being 40 times more potent than (+)-nicotine in displacing labeled (-)-nicotine. Saturation binding studies revealed the presence of two binding sites with dissociation constant (KD) values of 8.1 and 86 nM, and maximum binding capacity (Bmax) values of 36 and 90 fmol/mg protein, respectively. In competition studies, nicotinic agonists were 1,000 times more potent than ganglionic, neuromuscular, and muscarinic blocking drugs in displacing labeled (-)-nicotine. IC50 values for cholinergic drugs of (-)-[3H]nicotine binding were as follows: (-)-nicotine, 0.51 nM; acetylcholine, 12.6 nM; (+)-nicotine, 19.9 nM; cytisine, 27.3 nM; and carbachol, 527 nM. IC50 values of alpha-bungarotoxin, hexamethonium, d-tubocurarine, and atropine were larger than 50 microM. (-)-[3H]Nicotine binding was highest in the nucleus basalis of Meynert and thalamus and lowest in the cerebral cortex and caudate in the brain regions tested. These results suggest that nicotinic cholinergic receptors are present in human brain and that there are regional differences in the density of these receptors.

Acetylcholine↗
PubMed1985

Activities of a soluble extract from lymphoid cells of MRL mice. Effect on B cell differentiation in vitro.

Soluble extract (sEx) was prepared from lymphoid cells of MRL/Mp-lpr/lpr(MRL/l) mice with early lupus nephritis and also of MRL/Mp-+/+ (MRL/n) mice. sEx from lymph node and spleen T cells of MRL/l mice had an activity for B cells to differentiate into immunoglobulin-producing cells but that of MRL/n mice did not show such an activity. sEx of MRL/l mice also enhanced the in vitro response of B cells to a suboptimal dose of lipopolysaccharide. Implication of these phenomena in the development of lupus nephritis is discussed.

Animals↗
PubMed1985

[Behavioral pharmacology of amantadine with special references to the effect on abnormal behavior in mice and rats].

Behavioral effects of amantadine, especially on abnormal behavior in mice and rats, were reevaluated, in comparison with those of tricyclic antidepressants, methamphetamine and L-DOPA. 1) Amantadine at 10 approximately 50 mg/kg, i.p., tended to decrease ambulation and rearing in rats and mice. The drug at 50 mg/kg, i.p., caused piloerection and hyperirritability and at doses over 80 mg/kg, i.p., it impaired coordinated motor activity in rats. 2) Amantadine inhibited methamphetamine-induced hyperactivity, but apomorphine-induced stereotyped behavior was unaffected in rats. 3) Amantadine was equipotent to imipramine in suppressing haloperidol-induced catalepsy in rats, but L-DOPA was without effect. On the other hand, amantadine was 40 and 400 times as potent as imipramine and L-DOPA, respectively, in suppressing delta 9-tetrahydrocannabinol (THC)-induced catalepsy in rats. 4) Amantadine was as potent as imipramine in suppressing the muricide of olfactory bulbectomized rats, but was 3.5, 8.8 and 225.5 times as potent as methamphetamine, imipramine and L-DOPA, respectively, in inhibiting THC-induced reversible muricide in rats. 5) Amantadine at 50 mg/kg did not elicit circling behavior in the rat with unilateral nigral lesion induced by 6-hydroxydopamine. 6) Amantadine at high doses caused irritable aggression characterized by squealing in rats pretreated with intraventricular 6-hydroxydopamine. The most important characteristic of amantadine is its prominent effect suppressing the THC-induced catalepsy and muricide. This may be a reflection of the feature of amantadine activating the dopaminergic as well as the serotonergic systems.

Aggression↗
PubMed1985

[Behavioral and electroencephalographic effects of lormetazepam].

Behavioral and electroencephalographic effects of lormetazepam were investigated in rats, mice and rabbits, in comparison with those of diazepam, nitrazepam and flurazepam. Locomotor activity of mice in an open-field situation was decreased with large doses of lormetazepam and diazepam, while it was increased with nitrazepam and flurazepam. The anticonflict effect of lormetazepam in rats was much more potent than those of diazepam, nitrazepam and flurazepam. In suppressing the muricide of olfactory bulbectomized and raphe lesioned rats, lormetazepam was more potent than diazepam, nitrazepam and flurazepam. Lormetazepam, diazepam and flurazepam prevented both maximal electroshock and pentetrazol convulsions in mice, the effects on the latter being much more potent than those on the former. Lormetazepam was more potent than diazepam and flurazepam in potentiating thiopental-, ether- and ethanol anesthesia, impairing rotarod performance and in muscle relaxant activity. In conscious rabbits with chronically implanted electrodes, lormetazepam induced a drowsy EEG pattern and suppressed the EEG arousal responses not only to auditory stimulation but also to electrical stimulation of the midbrain reticular formation or hypothalamus. Lormetazepam also inhibited afterdischarges induced by electrical stimulation of the hippocampus and amygdala. These results indicate that lormetazepam has pharmacological properties characteristic of benzodiazepines and that the activity is more potent than those of diazepam, nitrazepam and flurazepam.

Anesthetics↗
PubMed1985

Cerebral edema associated with acute hepatic failure.

The clinicopathological findings of cerebral edema were investigated in patients with acute hepatic failure autopsied at Okayama University Hospital between 1970 and 1980 retrospectively. Nine (64%) of 14 hepatic failure cases were found to have cerebral edema during a post-mortem examination of the brain. Clinical features of the patients with cerebral edema were not significantly different from those of the patients without cerebral edema. However, general convulsions were observed more frequently in patients later found to have cerebral edema. Moreover, the length of time from deep coma to death was much shorter in the brain edema cases with cerebral herniation than without herniation.

Acute Disease↗
PubMed1985

Effects of Goniopora toxin on crayfish giant axons.

The effects of Goniopora toxin (GPT), isolated from the coral Goniopora species, on the crayfish giant axon have been studied by means of microelectrode and sucrose-gap voltage clamp techniques. When applied externally at a concentration of 0.1 microM or higher, the falling phase of the action potential was prolonged markedly. At concentrations over 0.3 microM, GPT gradually depolarized the membrane to 0 mV. The depolarization was not reversed by 1 microM tetrodotoxin or low-Na (1 mM) solution. The amplitude of action potential was slowly decreased in a manner dependent upon the concentration even in the absence of membrane depolarization. Voltage clamp experiments with internally perfused axons have revealed that the falling phase of the sodium current is prolonged markedly and is expressed by two exponential functions. The peak amplitude was first increased and then slowly decreased, and the tail sodium current associated with a step repolarization was slowed. The reversal potential for peak current was not changed by GPT, and the steady-state sodium inactivation was not shifted along the voltage axis. Leakage current gradually increased in the course of GPT action, while the steady-state potassium current was not affected. These effects of GPT were exerted only when it was applied externally and not reversed by washing with toxin-free medium. It is concluded that GPT modifies a fraction of sodium channels to give rise to a prolonged sodium current which is responsible for the prolongation of action potential.

Animals↗
PubMed1985

Dual effects of dynorphin-(1-13) on cholinergic and substance P-ergic transmissions in the rabbit iris sphincter muscle.

In the rabbit iris sphincter muscle, transmural electrical stimulation produces cholinergic and substance P-ergic responses. In the present work, the effects of dynorphin-(1-13), an endogenous ligand of the kappa opioid receptor, on these two neurogenic responses were examined pharmacologically and the data compared to findings in case of other opioid agonists. Dynorphin-(1-13) (10(-7) to 10(-6) M) enhanced the cholinergic responses and attenuated the substance P-ergic response, in a concentration-dependent manner, and these actions of dynorphin-(1-13) were more apparent in the case of low-frequency stimulation. These effects of dynorphin-(1-13) were antagonized by naloxone (10(-5) M). Dynorphin-(1-13) had no effects on the responses to exogenously applied acetylcholine, carbachol and substance P. The augmenting effect on the cholinergic transmission was unique in kappa agonists, as the cholinergic responses were also augmented by other kappa agonists such as dynorphin-(1-17) and ethylketocyclazocine, but attenuated by other opioid agonists (Met-enkephalin, beta-endorphin and morphine) and not affected by SKF-10,047 and nalorphine. On the other hand, the substance P-ergic response was attenuated by all the opioids used. These results suggest that dynorphin-(1-13) presynaptically increases the release of acetylcholine from the parasympathetic postganglionic nerves and reduces the release of substance P from the trigeminal nerve, mediated by kappa type of opioid receptors.

Acetylcholine↗
PubMed1985

Effects of substance P on cholinergically stimulated gastric acid secretion and mucosal blood flow in rats.

Effects of substance P (SP) on gastric acid secretion and mucosal blood flow (MBF) were examined in anesthetized Wistar rats. Intravenous infusion of graded doses of SP (5 and 10 nmol/kg/min) had no effects on either the basal gastric acid secretion or on the MBF. When gastric acid secretion was increased by giving a supramaximal dose of bethanechol (10 micrograms/kg/min), a muscarinic parasympathetic stimulant, SP had no effect on the gastric acid secretion but did decrease the MBF. On the other hand, when gastric acid secretion was increased by left cervical vagus nerve stimulation (0.5 mA, 3 Hz, 0.5 msec duration), SP inhibited both acid secretion and MBF, in a dose-dependent manner. The inhibitory effects of SP on the vagally stimulated gastric responses were not affected by pretreatment with phentolamine (5 mg/kg i.m.), propranolol (10 mg/kg i.m.), mepyramine (20 mg/kg i.m.) or indomethacin (30 mg/kg i.v., followed by 4 mg/kg/hr). These findings suggest that SP acts directly on the gastric vascular system and decreases gastric MBF, and that this substance also acts on the parasympathetic neurons in the gastric wall and inhibits the vagally stimulated gastric acid secretion. The inhibitory effects of SP on the gastric acid secretion do not appear to be mediated by adrenergic or by histamine H-1 receptor-, prostaglandin-involved mechanisms.

Animals↗
PubMed1985

Effects of atropine and pirenzepine on healing of gastric ulcer induced by mucosal excision in rats.

We studied the effects of atropine and pirenzepine on acid secretion induced by electrical vagal stimulation (EVS) and on healing of gastric ulcers after mucosal excision in rats. Both atropine (50, 125, and 250 micrograms/kg/hr) and pirenzepine (2.5, 5.0, and 12.5 mg/kg/hr), administered intraperitoneally, inhibited vagally stimulated acid secretion in a dose-dependent manner. Pirenzepine given at a rate of 0.25 mg/kg/hr had no effect on the acid secretory response to EVS. Either atropine (125 micrograms/kg/hr) or pirenzepine (2.5 mg/kg/hr) given for one week caused an inhibition of approximately 80% in acid secretory response to EVS. The antisecretory dosage of pirenzepine caused a significant reduction in the surface area of the ulcer by the seventh postoperative day, whereas neither the antisecretory dosage of atropine nor the nonantisecretory dosage of pirenzepine significantly affected the size of the ulcer. We conclude that an antisecretory dosage of pirenzepine accelerates the healing of gastric ulcers produced in rats.

Animals↗