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Biomedical subjects

C Okuda

Publications and source records attributed to C Okuda.

At least 55 records · Page 3Linked to original sources
PubMed1989

An antiserum against amyloid beta-protein precursor detects a unique peptide in Alzheimer brain.

An antiserum was raised against an amino acid sequence predicted from the DNA sequence of amyloid beta-protein precursor (ABPP), and it was then affinity-purified. This affinity-purified antibody (anti-GID) intensely stained neurons and dystrophic neurites in plaques of Alzheimer's disease (AD) patients, but marginally stained neurons of age-matched normal individuals. Anti-GID antibody detected a series of protein bands with a molecular weight centered at 100,000 and a second band at 55,000 on a blot of the human brain particulate fraction. It also stained a set of bands with a molecular weight around 95,000 and a doublet of Mr 16,000 in the soluble fraction. A band at Mr 35,000 was detected in the soluble fraction prepared from brain tissue of AD patients but not from control brain tissue. A strong immunostaining of AD sections with anti-GID and the presence of a Mr 35,000 band unique to AD might reflect an altered processing of ABPP in AD brains.

Alzheimer Disease↗
PubMed1989

Fungus invasion of human hair tissue in tinea capitis caused by Microsporum canis: light and electron microscopic study.

Previously, we reported a morphological change of Trichophyton violaceum in hair tissue in black dot ringworm. To investigate the morphology of Microsporum canis in human hais tissue, three cases of tinea capitis by M. canis were examined by both light and electron microscopy. The fungal elements, which were located deeplyin the keratogenous zone, showed nonseptate hyphae in the outer part of the hair cortex. With the upward development of hair tissues, some hyphae invaded the keratinized inner root sheath and were there transformed into arthrospores, which then occupied the large volume of the inner root sheath; each spore was surrounded by an electron-lucent halo. In some affected hair follicles, at the follicular isthmus level, a microabscess composed of polymorphonuclear leukocytes was often formed in the outer root sheath adjacent to the arthrospores in the keratinized inner root sheath. On the other hand, the remaining hyphae in the cortex became degenerated. Fungi did not invade the hair-germinative cells. There is a distinct relationship between the morphological change of fungi and the differentiation of hair cells in tinea capitis by M. canis as well as in that by T. violaceum, although the direction of invasion and pathological roles of fungal elements within hair tissue are significantly different between the two species of fungi.

Child, Preschool↗
PubMed1989

Effects of dibutyryl cyclic AMP on hemodynamics and plasma catecholamine concentrations during ammonium chloride-induced metabolic acidosis in anesthetized dogs.

We investigated, using anesthetized dogs, the effect of dibutyryl cyclic AMP (db-cAMP), a derivative of cyclic AMP (cAMP), on cardiovascular variants and plasma catecholamines during metabolic acidosis. These effects were also compared with those of dopamine. The db-cAMP and dopamine were infused at 200 and 20 micrograms/kg.min, respectively. Metabolic acidosis (pH 7.00, PaCO2 40 torr) was induced by the iv infusion of 1-M ammonium chloride solution (NH4Cl). In the normal acid-base state, both db-cAMP and dopamine significantly increased cardiac output and decreased systemic vascular resistance (SVR). During metabolic acidosis, db-cAMP increased cardiac output by 69 +/- 14% and decreased SVR by 36 +/- 2%, while dopamine did not produce changes in cardiac output and increased SVR. Dopamine caused an elevation of epinephrine and norepinephrine in the normal acid-base state, but db-cAMP did not. During metabolic acidosis, dopamine significantly increased the plasma concentration of epinephrine and norepinephrine, while db-cAMP significantly decreased epinephrine concentration. These results suggest that db-cAMP may have a more beneficial effect on hemodynamics compared with dopamine when therapeutic support is needed during circulatory insufficiency with severe metabolic acidosis.

Acidosis↗
PubMed1989

Pathophysiology of circulatory shock: an overview.

Recent developments in three categories of shock research are discussed. Organ perfusion and humoral pathophysiological responses were investigated first, since the cause of fatal shock is always ischemia, tissue hypoxia and resulting cell damage with abolishment of mitochrondrial function. Both centrally and peripherally administered thyrotropin-releasing hormone (TRH) had vasopressor effects that are mediated by a central cholinergic mechanism. A derivative of TRH, DN-1417, had a longer-acting vasopressor action. TRH content increased in the brain in reversible shock, while amino acids increased in irreversible shock.

Adrenal Cortex Hormones↗
PubMed1989

[The participation of the sympathetic nervous system in thromboxane A2 release induced by limb ischemia].

Our previous studies indicate that the blockade of the sympathetic nervous system by spinal anesthesia or epidural anesthesia inhibits the release of TXA2 induced by limb ischemia with thigh tourniquet in patients with lower limb surgery. The present study was undertaken to confirm this phenomenon in anesthetized dogs. Twenty one anesthetized dogs underwent 60 min occlusion of the abdominal aorta and the inferior vena cava, followed by reperfusion. They were randomized into three groups: no treatment group and pretreatment groups with either 2 ml of 0.5% bupivacaine intrathecally or 4 mg.kg-1 of labetalol intravenously. In no treatment group plasma TXB2 levels were increased significantly after reperfusion. However, prior treatments with bupivacaine intrathecally or labetalol intravenously inhibited the increases in plasma TXB2 levels after reperfusion. These results suggest that limb ischemia stimulates the TXA2 production, which may be influenced not only by endothelial cell damage and the generation of oxygen free radicals but also by the activation of the sympathetic nervous system.

Animals↗
PubMed1988

Involvement of endogenous thyrotropin-releasing hormone in central regulation of the cardiovascular system after bleeding in conscious rats.

The 4th ventricle of a conscious rat was perfused using a push-pull cannula. The concentration of thyrotropin-releasing hormone (TRH) in the perfusate was significantly increased after withdrawal of 30% of the total blood. Administration of antiserum of TRH into the ventricle potentiated and prolonged the hypotension induced by the bleeding. These results suggest that endogenous brain TRH is involved in the central regulation of the cardiovascular system after bleeding in conscious rats.

Animals↗
PubMed1988

Cardiovascular effect of intravenously administered thyrotropin-releasing hormone and its concentration in push-pull perfusion of the fourth ventricle in conscious and pentobarbital-anesthetized rats.

Changes in the concentration of thyrotropin-releasing hormone (TRH) in cerebrospinal fluid (CSF) were examined by the push-pull perfusion method after intravenous (i.v.) administration of the peptide in conscious and pentobarbital-anesthetized rats. The concentration of endogenous TRH in the perfusate was not changed during the 160-min perfusion period and was similar to that in the CSF (0.92 +/- 0.26 ng/ml) collected before the perfusion in conscious as well as in anesthetized rats. After i.v. administration of TRH (5 mg/kg) to the conscious rats, the peptide concentration in the perfusate increased to 42.23 +/- 14.33 ng/ml during the first 20 min and gradually returned to the basal level 2 hr after administration. The total amount of TRH detected in the perfusate was 20.0 ng. It was reduced by 75% in the anesthetized animals. The increases in blood pressure and heart rate, seen after i.v. as well as intracerebroventricular administration of TRH in the conscious rats, was significantly inhibited in the anesthetized rats. These results indicate that systemically administered TRH exerts its cardiovascular effect at central site(s), and that the transportation and the effect of the peptide is suppressed by pentobarbital anesthesia.

Algorithms↗
PubMed1988

Effects of hypothermia on thyrotropin-releasing hormone content in the rat brain.

The thyrotropin-releasing hormone (TRH) content in the brain was determined in normothermic and hypothermic rats subjected to immobilization stress. TRH contents in the hypothalamus, midbrain and cerebral cortex significantly decreased during mild hypothermia (body temperature about 34 degrees C), but not during profound hypothermia (about 24 degrees C). The decreases in the TRH content during mild hypothermia were readily reversed by rewarming the animal. These results indicate that cerebral TRH is involved in the response to a mild body temperature drop when the animal is exposed to a cold environment.

Animals↗
PubMed1988

Fungus invasion into human hair tissue in black dot ringworm: light and electron microscopic study.

In order to investigate the morphology of fungi invading into the human hair tissue, three cases of black dot ringworm caused by Trichophyton violaceum and Trichophyton glabrum were studied by light and electron microscopy. Fungal elements were mainly present in the hair cortex and showed a constant morphologic change during the differentiation of hair layers. The fungal elements, located deep in the keratogenous zone of the cortex, showed less electron dense non-septate hyphae. Distally, the hyphae showed septation and contained several scattered dense bodies in the cytoplasm. At the level where the Huxley's layer was keratinized, the fungal elements were transformed into arthrospores, which occupied the large volume of the cortex; each spore was surrounded by a fiber- and melanosome-free, electron lucent halo. Fungal elements occasionally invaded the keratinized hair cuticle and keratinized inner root sheath in a few hair follicles. Fungi do not invade the hair germinative cells. There seems to be a distinct relationship between the morphology of the invading fungi and the cortical cell differentiation in black dot ringworm; a balance between the fungus proliferation and the cortical cell development may be present.

Aged↗
PubMed1988

Suppression of the pressor effect of centrally administered thyrotropin-releasing hormone under halothane, pentobarbital and flunitrazepam anaesthesia.

Intracerebroventricular (i.c.v.) administration of thyrotropin-releasing hormone (TRH) caused an increase in blood pressure (BP) and heart rate (HR) in conscious rats. The pressor effect was greatly diminished by adrenalectomy as well as after pretreatment with phentolamine, an alpha-receptor antagonist or with mecamylamine, a ganglion blocker, suggesting that centrally administered TRH increases BP mainly by stimulating sympathetic activity. Under halothane (0.8%), pentobarbital (33 mg/kg, i.p.) and flunitrazepam (0.8 mg/kg, i.v.) anaesthesia, the pressor effect of TRH was almost completely blocked. The increase in BP induced by peripheral alpha-receptor stimulation with phenylephrine was not affected by the anaesthetics at these doses. Pretreatment with atropine (50 micrograms, i.c.v.) significantly reduced the pressor effect of TRH. Intracerebroventricularly administered haloperidol and bicuculline also partially diminished the increase in BP produced by TRH, while other neurotransmitter blockers such as phentolamine, propranolol and naloxone did not. These results indicate that the anaesthetics at the doses employed interfere with the central neuronal pathway(s), probably cholinergic pathways, through which TRH exerts its pressor effect.

Animals↗
PubMed1988

Changes in brain thyrotropin-releasing hormone in reversible and irreversible hemorrhagic shock in the rat.

Alterations in thyrotropin-releasing hormone (TRH) content in the brain during hemorrhagic shock were examined in conscious rats, and the results were interpreted in relation to the reversibility of the shock. Two sets of experiments were run. The first one was to establish reversible and irreversible shock models. Hemorrhagic shock was induced by the initial withdrawal of 4 ml of blood followed by 1 ml bleeds at 5, 15, 30, and 60 min to maintain the blood pressure at 40-70 mmHg for 60 min. Blood withdrawn during and 60 min after the end of the shock was used to measure plasma lactate levels and blood gases. Shock was considered to be reversible if the animal survived for 24 hr after the hemorrhage. The plasma lactate levels as well as Base Excess and PaCO2 during and 60 min after the end of the hemorrhage of the surviving rats were significantly different from those of the animals which died within 24 hr. In particular, the plasma lactate levels at 60 min after the end of the hemorrhagic period were good indicators of the mortality of animals; it was predicted that rats whose plasma lactate levels are higher than 3.8 mEq/L would die within 24 hr (0.69% probability of misdiscrimination). The second experiment was to measure brain TRH content during and after hemorrhage produced using the same bleeding procedure as the first. During hemorrhage, brain TRH contents in the medulla oblongata and midbrain were found to be significantly increased compared with the control values. At 60 min after the end of hemorrhage, significantly higher TRH content values were obtained in the medulla oblongata, midbrain, cerebral cortex, striatum, and cerebellum in the rats whose plasma lactate levels were lower than 3.8 mEq/L compared with those of animals having plasma lactate values higher than 3.8 mEq/L. From the results of the two sets of experiments, it is concluded that the surviving animals have more TRH in the brain regions mentioned above than the non-surviving animals after hemorrhagic shock, and it is suggested that brain TRH plays a beneficial role in the course of recovery from hemorrhagic shock.

Animals↗
PubMed1987

The involvement of central cholinergic mechanisms in cardiovascular responses to intracerebroventricular and intravenous administration of thyrotropin-releasing hormone.

Intracerebroventricular (i.c.v.) administration of thyrotropin-releasing hormone (TRH) in a range from 0.1 to 100 micrograms induced a dose-related increase in blood pressure in conscious rats, whereas TRH-free acid (TRH-OH) and histidyl-proline diketopiperazine (His-Pro-DKP), metabolites of TRH, did not. The blood pressure responses to intravenous (i.v.) injection of 5 mg/Kg TRH were similar to those induced by TRH (i.c.v.). Pretreatment with atropine (50 micrograms, i.c.v.) significantly reduced the pressor effect of TRH administered through either route. Hemicholinium-3 (50 micrograms, i.c.v.), an inhibitor of choline uptake, also prevented the increase in blood pressure induced by TRH (10 micrograms, i.c.v.). These results indicate that both centrally and peripherally administered TRH have pressor effects that are mediated by central cholinergic mechanisms, probably by activating cholinergic neurons.

Animals↗
PubMed1987

The interaction of pancuronium and vecuronium with cardiac muscarinic receptors.

The interaction of vecuronium, a monoquaternary analogue of pancuronium, with the cardiac muscarinic receptors in canine hearts was investigated in vitro by [3H] QNB binding assay and compared with that of pancuronium. Both pancuronium and vecuronium, which are nicotinic antagonists of competitive types, inhibited the binding of [3H] QNB to cardiac muscarinic receptors with values of IC50 of 5.41 X 10(-7) mol/l and 3.97 X 10(-6) mol/l respectively. According to the Kd and Bmax values on the Scatchard plot, pancuronium, while not influencing the number of receptors, had a 3-fold greater inhibitory effect than vecuronium on the affinity of the muscarinic receptors. The KI values of vecuronium and pancuronium showed that pancuronium had a 7.3-fold greater affinity with the receptors than vecuronium. We concluded that vecuronium had a direct inhibitory action on the binding of [3H] QNB to the canine heart muscarinic receptors, but this action was much weaker than pancuronium.

Animals↗
PubMed1987

Immunohistochemical demonstration of simple epithelia-type keratin intermediate filament in a case of Merkel cell carcinoma.

A case of Merkel cell carcinoma that developed on the right cheek of a 77-year-old woman is reported. The diagnosis was ultrastructurally made by demonstrating dense-core granules in the cytoplasm of the tumor cells. Immunohistochemically, the tumor cells were shown to possess simple epithelia-type keratin intermediate filaments, but no neurofilaments. This finding was in accordance with that obtained on normal Merkel cells. No bioactive peptides examined could be detected in the tumor cells. Typing of intermediate filaments in tumor cells may be one of the important markers, along with the ultrastructural findings, in diagnosing Merkel cell carcinoma.

Adenocarcinoma↗
PubMed1987

Disseminated cutaneous Fusarium infection with vascular invasion in a leukemic patient.

A 61-year-old male with leukemia manifested multiple cutaneous nodules on his whole body surface, subcutaneous nodules on his arms and a tongue tumor. Septate hyphae were observed microscopically in scrapings from the surfaces of the cutaneous lesions. Fusarium solani and F. anthophilum were isolated from scrapings from the several skin lesions. Histological examination revealed the presence of numerous septate hyphae in the lumina of vessels in the dermis. The fungal elements in the cutaneous tissues were suggested to be Fusarium by an immunoperoxidase method using a genus-specific anti-Fusarium antibody. Although no evidence of fungal infection was found in other organs by clinical examinations, F. solani and/or F. anthophilum were considered to have undergone hematogenous dissemination, because of the presence of thrombi containing abundant fungal elements in the skin lesion. The present case is a case of disseminated cutaneous Fusarium infection, in which fungal elements in skin tissue sections were immunohistochemically regarded as Fusarium, though fungus cultures from biopsied specimens were negative.

Dermatomycoses↗