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T Nagayama

Publications and source records attributed to T Nagayama.

At least 73 records · Page 4Linked to original sources
PubMed1999

[Case report of a long-term home parenteral nutrition patient].

We experienced a patient who received long-term home parenteral nutrition. A 55-year-old woman underwent left adrenalectomy in June, 1992. The histopathological diagnosis was aldosteronism. Abdominal pain and ileus appeared in July, 1993, and an adhesiotomy was conducted. Due to poor appetite and weight loss, fluid was sometimes injected peripherally. After abdominal pain in November, 1996 and April, 1997, the ileus reappeared in July, 1997. A Groshong catheter with a port was then inserted through the subclavian vein to the superior vena cava/right atrial junction. Using this catheter, home parenteral nutrition started. Some time later oral nutrition became possible, but now high calorie parenteral nutrition is continued. The only complications were pain and red skin at the port. A Groshong catheter with port is thus useful for home parenteral nutrition.

Adrenalectomy↗
PubMed1999

Frequency distribution of axon diameters in the left aortic nerve of the rat raised in space--Neurolab Program.

INTRODUCTION: To study development of the aortic baroreflex mechanisms under conditions of microgravity, we carried out the various experiments in the neonate rats aged 25 days raised in microgravity for 16 days (flight: FLT group) in Neurolab program (STS-90, space shuttle Columbia, launch date: Apr 17, '98. Some results of the experiments were already reported. The results of histological examination of the aortic nerve which is the afferent of the aortic baroreflex showed that the number of unmyelinated fibers in FLT was significantly less in than those in two control groups and there was no difference between FLT and each control group in the analysis of myelin. In the present paper, the frequency distribution of axon diameters of the left aortic nerves in FLT was compared to that in two ground control groups to examine the growth of the aortic nerve fibers in space. METHODS: After breeding Sprague-Dawley rats for 16 days in the shuttle in space and in the animal center in the Kennedy space center, a total of 43 deeply anesthetized rats were perfused with 1% parahormaldehyde and 1% glutaraldehyde or 4% parahormaldehyde solution buffered at pH7.4 with 0.12 M phosphate solution. Concerning the control groups, one group was the asynchronous ground control (AGC) group in which the rats were housed in the same cages as those on the shuttle, and the other was the vivarium ground control (VIV) group in which the rats were housed in commercial cages. The cervical region of the left aortic nerve which is a branch of the vagus was cut off and stored in the same fixative as that used for perfusion, and postfixed in the solution of 1% OsO4, for 2 hours within 24 hours after the perfusion. The fixed specimens were embedded in epoxy resin blocks by the usual method for electron microscopy following dehydration. Electron microscopic montages of transverse sections of these nerve trunks were made from the five left aortic nerves in each group. The magnification of the montages was approximately 13400 times. The long and short axes (a and b) of the nerve fibers and the myelin thickness (T) were measured with a caliper and the axon diameters (R were calculated by following formula: R2=[(a-2T)2+(b-2T)2]/2.

Animals↗
PubMed1998

Cyclooxygenase-2 inhibition prevents delayed death of CA1 hippocampal neurons following global ischemia.

The inducible isoform of the enzyme cyclooxygenase-2 (COX2) is an immediate early gene induced by synaptic activity in the brain. COX2 activity is an important mediator of inflammation, but it is not known whether COX2 activity is pathogenic in brain. To study the role of COX2 activity in ischemic injury in brain, expression of COX2 mRNA and protein and the effect of treatment with a COX2 inhibitor on neuronal survival in a rat model of global ischemia were determined. Expression of both COX2 mRNA and protein was increased after ischemia in CA1 hippocampal neurons before their death. There was increased survival of CA1 neurons in rats treated with the COX2-selective inhibitor SC58125 [1-[(4-methylsulfonyl) phenyl]-3-trifluoro-methyl-5-[(4-fluoro)phenyl] pyrazole] before or after global ischemia compared with vehicle controls. Furthermore, hippocampal prostaglandin E2 concentrations 24 h after global ischemia were decreased in drug-treated animals compared with vehicle-treated controls. These results suggest that COX2 activity contributes to CA1 neuronal death after global ischemia.

Animals↗
PubMed1998

The role of BK(Ca) channels in the nitric oxide-mediated regulation of adrenal catecholamine secretion.

We examined whether high conductance Ca2+-activated K+ (BK(Ca)) channels are involved in the modulatory action of nitric oxide (NO) on the secretion of adrenal catecholamines in response to splanchnic nerve stimulation and acetylcholine in anesthetized dogs. The NO donor 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamin e (NOC 7), the BK(Ca) channel blocker charybdotoxin and acetylcholine were administered intraarterially (i.a.) into the adrenal gland. NOC 7 infusion (2 microg min(-1)) inhibited increases in catecholamine output induced by splanchnic nerve stimulation (1-3 Hz) and acetylcholine (0.75-3 microg). Charybdotoxin infusion (100 ng min(-1)) did not affect increases in catecholamine output induced by splanchnic nerve stimulation and acetylcholine. Charybdotoxin blocked the NOC 7-induced inhibition of increases in catecholamine output induced by splanchnic nerve stimulation but not by acetylcholine. These results suggest that NO may inhibit the secretion of adrenal catecholamines induced by splanchnic nerve stimulation through activation of BK(Ca) channels.

Acetylcholine↗
PubMed1998

Induction of caspase-3-like protease may mediate delayed neuronal death in the hippocampus after transient cerebral ischemia.

Delayed neuronal death after transient cerebral ischemia may be mediated, in part, by the induction of apoptosis-regulatory gene products. Caspase-3 is a newly characterized mammalian cysteine protease that promotes cell death during brain development, in neuronal cultures, and in other cell types under many different conditions. To determine whether caspase-3 serves to regulate neuronal death after cerebral ischemia, we have (1) cloned a cDNA encoding the rat brain caspase-3; (2) examined caspase-3 mRNA and protein expression in the brain using in situ hybridization, Northern and Western blot analyses, and double-labeled immunohistochemistry; (3) determined caspase-3-like activity in brain cell extracts; and (4) studied the effect of caspase-3 inhibition on cell survival and DNA fragmentation in the hippocampus in a rat model of transient global ischemia. At 8-72 hr after ischemia, caspase-3 mRNA and protein were induced in the hippocampus and caudate-putamen (CPu), accompanied by increased caspase-3-like protease activity. In the hippocampus, caspase-3 mRNA and protein were predominantly increased in degenerating CA1 pyramidal neurons. Proteolytic activation of the caspase-3 precursor was detected in hippocampus and CPu but not in cortex at 4-72 hr after ischemia. Double-label experiments detected DNA fragmentation in the majority of CA1 neurons and selective CPu neurons that overexpressed caspase-3. Furthermore, ventricular infusion of Z-DEVD-FMK, a caspase-3 inhibitor, decreased caspase-3 activity in the hippocampus and significantly reduced cell death and DNA fragmentation in the CA1 sector up to 7 d after ischemia. These data strongly suggest that caspase-3 activity contributes to delayed neuronal death after transient ischemia.

Amino Acid Sequence↗
PubMed1998

Complete response of esophageal cancer achieved by combination therapy with 5-fluorouracil, low-dose cisplatin, and radiation: report of a case.

To improve the survival rate of patients with esophageal cancer, several protocols of a preoperative combination of chemotherapy and radiotherapy, known as chemoradiation therapy, have been developed, recently characterized by the combination of 5-fluorouracil (5-FU), cisplatin, and radiation. Although some of these combinations have been demonstrated to be effective, the optimal chemoradiation dose and schedule are not yet precisely established. Recent investigations have elucidated that the radiosensitizing effects of cisplatin are able to be achieved more effectively by the daily administration of cisplatin before each fraction of radiation. Based on these investigations, we report herein the case of a patient with esophageal cancer with direct invasion to the trachea, in whom a complete response was achieved by the continuous administration of 5-FU, 600 mg/m2 per day, from days 1-5 combined with the daily administration of low-dose cisplatin, 10 mg/m2 per day before each fraction of radiation, given as 2Gy each time, throughout the entire treatment period of 3 weeks beginning on day 1. The benefits of our preoperative chemoradiation therapy included no severe side effects, down-staging and resectability of the tumor, as well as a pathological complete response, which could prolong the survival time. Our experience of this case prompts us to recommend the concurrent daily preoperative chemoradiation therapy for patients with locally advanced esophageal cancer.

Antimetabolites, Antineoplastic↗
PubMed1998

Effect of cilnidipine, a novel dihydropyridine Ca2+ channel blocker, on adrenal catecholamine secretion in anesthetized dogs.

We investigated the effect of cilnidipine, a novel dihydropyridine Ca2+ channel blocker possessing blocking actions on N-type and L-type voltage-dependent Ca2+ channels (VDCCs), in comparison with the L-type VDCC blocker nifedipine, on adrenal catecholamine secretion in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), the nicotinic receptor stimulant 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. Ca2+ channel blockers and cholinergic agonists were infused and injected, respectively, into the adrenal gland through the phrenicoabdominal artery. Cilnidipine (0.3-3 microg/min) inhibited increases in both epinephrine (EPI) and norepinephrine (NE) output induced by SNS (2 Hz), ACh (1.5 microg), and DMPP (0.2 microg). However, cilnidipine inhibited increase in NE output induced by muscarine (1 microg) without affecting increase in EPI output. Nifedipine (0.3-3 microg/min) inhibited the ACh- and DMPP-induced increases in EPI and NE output without affecting the SNS- and muscarine-induced increases in EPI and NE output. From these results, it seems likely that the inhibition by cilnidipine of the SNS-induced EPI and NE secretion and of the muscarine-induced NE secretion is related to its blocking action on N-type VDCCs.

Acetylcholine↗
PubMed1998

Role of K+ channels in adrenal catecholamine secretion in anesthetized dogs.

We examined the role of K+ channels in the secretion of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. K+ channel blockers and the cholinergic agonists were infused and injected, respectively, into the adrenal gland. The voltage-dependent K+ channel (KA type) blocker mast cell degranulating (MCD) peptide infusion (10-100 ng/min) enhanced increases in CA output induced by SNS (1-3 Hz), but it did not affect increases in CA output induced by ACh (0.75-3 micrograms), DMPP (0.1-0.4 microgram), or muscarine (0.5-2 micrograms). The small-conductance Ca(2+)-activated K+ (SKCa) channel blocker scyllatoxin infusion (10-100 ng/min) enhanced the ACh-, DMPP-, and muscarine-induced increases in CA output, but it did not affect the SNS-induced increases in CA output. These results suggest that KA channels may play an inhibitory role in the regulation of adrenal CA secretion in response to SNS and that SKCa channels may play the same role in the secretion in response to exogenously applied cholinergic agonists.

Acetylcholine↗
PubMed1998

Role of nitric oxide in adrenal catecholamine secretion in anesthetized dogs.

We examined the role of nitric oxide (NO) in adrenal catecholamine secretion in response to splanchnic nerve stimulation (SNS) and exogenous acetylcholine (ACh) in anesthetized dogs. The NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME), NO donor 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamin e (NOC 7), and ACh were administered intra-arterially into the adrenal gland. The increases in catecholamine output induced by ACh (0.75-3 microgram) were enhanced by L-NAME (0.1-1 mg/min) and inhibited by NOC 7 (0.2-2 microgram/min). Inhibition by NOC 7 (2 microgram/min) was observed during treatment with L-NAME (1 mg/min). The increases in catecholamine output induced by SNS (1-2 Hz) were inhibited by L-NAME and by NOC 7. No inhibitory effect of NOC 7 was observed during treatment with L-NAME. These results suggest that NO may play an inhibitory role in the regulation of adrenal catecholamine secretion in response to exogenous ACh.

Acetylcholine↗
PubMed1998

Interferon-alpha-induced thyroid dysfunction in patients with chronic active hepatitis C: a transient, reversible and self-limited dysfunction.

To survey the prognoses of interferon-alpha (IFNalpha)-induced thyroid dysfunction, a total of 100 patients (49 males and 51 females) with biopsy-proven chronic active hepatitis C were studied. Either during or after IFNalpha therapy, 29 patients (33.7%) revealed suppression/elevation of thyroid stimulating hormone (TSH) or both, transient thyrotoxicosis (TSH less than 0.1 microU/ml) or transient hypothyroidism (TSH 5.0-190.95 microU/ml). However, the thyroid function normalized without supplementation of the thyroid hormone in the follow-up period. In the same period, one of the 14 control patients (7.1%) developed thyroid dysfunction. Thyroid abnormalities developed significantly more in patients with IFNalpha therapy than in those without IFNalpha therapy. The findings suggest that the occult autoimmune disorder becomes overt with IFNalpha treatment in patients with pre-existent autoimmune thyroid disease. IFNalpha-induced thyroid dysfunction is transient, reversible and self-limited. It is not necessary to discontinue IFNalpha therapy when thyroid dysfunction develops.

Adult↗
PubMed1998

Histological analysis of the aortic nerve in the rat raised in space (Rapid communication on Neurolab Project).

To study development of the aortic nerve baroreflex under conditions of microgravity, we examined the cross section of the left aortic nerve (LAN), which is the afferent of the baroreflex, in the neonate rats aged 25 days raised in microgravity on the space shuttle Columbia (flight:FLT group) for 16 days. In this paper, we report a part of the result obtained from the data of the myelinated fibers of LAN analyzed with an electron microscope. Two kind of ground control groups were compared to the FLT group; one was asynchronous ground control (AGC) group where the rats were housed in the same cage as that on the shuttle, and the other was vivarium(VIV) group where the rats were housed in a commercial cage. The LANs in each group were extirpated the from rats perfused with a fixative and embedded for histological analysis. We observed the transverse sections of LAN and took pictures of several areas (magnified to x 2K to x 200K). No irregular myelination was found in all fibers of FLT group when they were compared with two control groups. The thickness of myelin of the maximally myelinated fibers were 0.55 +/- 0.17 micrometer in FLT(n=5), 0.45 +/- 0.10 micrometer in AGC(n=5), and O.47 +/- 0.06 micrometer meter in VIV(n=5). There was no significant difference among three groups (unpared t-test). The results suggest that there is no effect of space environment on the myelin formation of each nerve fiber in the aortic nerve.

Animals↗
PubMed1997

Distribution of GABAergic premotor nonspiking local interneurones in the terminal abdominal ganglion of the crayfish.

The inhibitory neurotransmitter of premotor nonspiking local interneurones in the crayfish terminal abdominal ganglion was investigated physiologically and immunocytochemically. Depolarization of a nonspiking interneurone evoked a hyperpolarization in a uropod motor neurone. The amplitude of hyperpolarization in the motor neurone was gradually decreased under low-calcium/high-magnesium saline. Local pressure injection of gamma-aminobutyric acid (GABA) into the neuropil caused a similar hyperpolarization of the motor neurone. These physiological studies suggested a GABAergic inhibitory interaction between nonspiking interneurones and the motor neurones. Premotor nonspiking interneurones are classified into two subgroups ofposterolateral (PL) and anterolateral (AL) interneurones, and AL interneurones are further divided into three subtypes. A combination of intracellular staining from nonspiking local interneurones with Lucifer yellow and immunocytochemical staining with an antiserum directed against GABA revealed that all the PL interneurones sampled in this study showed GABA-like immunoreactivity. A population of cell bodies (n = 6-11) with a small diameter (15-30 microm) packed together forming a cluster showed GABA-like immunoreactivity, and the cell bodies of most PL interneurones were found in this cluster. To compare the number and the pattern of main branches of PL interneurones, cells were classified into three identifiable sets of interneurones, called PL-1, PL-2, and PL-3. By contrast, about one-half of AL interneurones, especially the third subtype of AL interneurones, which have cell bodies located ventrolaterally in the ganglion, did not show GABA-like immunoreactivity. Furthermore, the position of cell bodies of GABA-immunoreactive AL interneurones was scattered compared to that of PL interneurones.

Abdomen↗
PubMed1997

Apamin-sensitive SK(Ca) channels modulate adrenal catecholamine release in anesthetized dogs.

We investigated the role of high conductance (BK(Ca)) and small conductance Ca2(+)-activated K+ (SK(Ca)) channels in adrenal catecholamine release in response to splanchnic nerve stimulation, acetylcholine, the nicotinic receptor stimulant 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. The selective SK(Ca) channel blocker apamin and the selective BK(Ca) channel blocker charybdotoxin were infused into the adrenal gland through the phrenicoabdominal artery, and the cholinergic agonists were injected into the same artery. Splanchnic nerve stimulation (1, 2, 3 and 10 Hz), acetylcholine (0.75, 1.5 and 3 microg), DMPP (0.1, 0.2 and 0.4 microg) and muscarine (0.5, 1 and 2 microg) produced frequency- or dose-dependent increases in catecholamine output as measured in adrenal venous blood. Apamin infusion (1, 3 and 10 ng/min) enhanced the acetylcholine-, DMPP- and muscarine-induced increases in catecholamine output in a dose-dependent manner, but it did not affect the splanchnic nerve stimulation-induced catecholamine response. Charybdotoxin infusion (10, 30 and 100 ng/min) did not affect the increases in catecholamine output induced by the agonists and splanchnic nerve stimulation. Neither apamin nor charybdotoxin affected basal catecholamine output. These results suggest that apamin-sensitive SK(Ca) channels located in adrenal medullary cells may play an inhibitory role in the regulation of adrenal catecholamine release mediated by extrasynaptic nicotinic and muscarinic receptors.

Acetylcholine↗
PubMed1997

Effects of NKH477, a forskolin derivative, and dibutyryl-cyclic AMP on adrenal catecholamine release in response to splanchnic nerve stimulation, acetylcholine, DMPP and muscarine in anesthetized dogs.

The effects of NKH477, a water-soluble forskolin derivative, and dibutyryl-cyclic adenosine monophosphate (dbcAMP) on the release of adrenal catecholamines (CAs) in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), the nicotinic receptor stimulant 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP) and muscarine were examined in anesthetized dogs. NKH477, dbcAMP and the cholinergic agonists were infused and injected, respectively, into the adrenal gland intra-arterially. SNS (3 Hz) or injections of ACh (3 micrograms), DMPP (2 micrograms) and muscarine (2 micrograms) produced increases in CA output determined from adrenal venous blood. Both NKH477 infusion (0.3, 1 and 3 micrograms/min) and dbcAMP infusion (0.1, 0.3 and 1 mg/min) caused dose-dependent enhancement of the SNS-, ACh- and DMPP-induced increases in CA output, whereas they failed to affect the muscarine-induced increases in CA output. Neither NKH477 nor dbcAMP affected basal CA output. Cyclic AMP (cAMP) overflow determined from adrenal venous blood increased during NKH477 infusion. These results indicate that NKH477 and dbcAMP have facilitatory effects on adrenal CA release mediated by nicotinic receptors, but not by muscarinic receptors in the dog, and suggest the selective action of cAMP on nicotinic mechanism.

Acetylcholine↗
PubMed1997

Two types of identified ascending interneurons with distinct GABA receptors in the crayfish terminal abdominal ganglion.

More than half of the identified ascending interneurons originating in the terminal abdominal ganglion of the crayfish received inhibitory sensory inputs from hair afferents innervating the tailfan on the side contralateral to their main branches. Biochemical aspects of this transverse lateral inhibition of ascending interneurons were examined by the use of neurophysiological and pharmacological techniques. Local application of gamma-aminobutyric acid (GABA) and its agonist muscimol into the neuropil induced membrane hyperpolarization of identified ascending interneurons with an increase in membrane conductance. Because the reversal potential of inhibitory postsynaptic potential (IPSPs) in ascending interneurons elicited by the sensory stimulation and GABA injection was similar, and the sensory-stimulated IPSPs of the interneurons were blocked by GABA and muscimol application, this study strongly suggests a GABAergic nature for transverse lateral inhibition of ascending interneurons. According to the response to the GABAA antagonists bicuculline and picrotoxin, ascending interneurons were classified into two types, picrotoxin-sensitive and picrotoxin-insensitive interneurons. Identified ascending interneurons VE-1 and RO-4 showed a pharmacological profile similar to that of the classical GABAA receptor of the vertebrates. Bath application of both bicuculline and picrotoxin reversibly reduced the amplitudes of IPSPs. The other identified ascending interneurons CA-1, RO-1, and RO-2 were not affected significantly by the bath application of GABAA and GABAB antagonists, although bath application of low-chloride saline reversed the sensory-stimulated IPSPs. IPSPs of the picrotoxin-sensitive interneurons had a rather faster time course and shorter duration in comparison with those of the picrotoxin-insensitive interneurons.

Animals↗