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Biomedical subjects

H Ishimaru

Publications and source records attributed to H Ishimaru.

At least 37 records · Page 2Linked to original sources
PubMed1999

Daily time budgets of long-distance commuting workers in Tokyo megalopolis.

In Tokyo Megalopolis, long-distance commuting between residences in the suburbs and work places in the centre of the city was examined. Using a questionnaire, heads of household in two suburbs were asked about the influences of long commuting hours on their daily time budgets. The results showed that on workdays, the workers who spent longer commuting rose and left home for work earlier, and came back home and retired later; accordingly, both time spent on in-home activities on workdays and hours slept on the day before a workday were shorter. Comparison of time budgets between the subjects who work 5 and 6 days per week revealed more vulnerable influences of long commuting hours in the former than the latter. The expected health consequences of these findings are discussed from a biosocial/human ecological viewpoint.

Adult↗
PubMed1999

[Presurgical mapping with functional MRI: comparative study with transcranial magnetic stimulation and intraoperative mapping].

PURPOSE: The accuracy of preoperative mappings in patients with brain tumors near the central sulcus using functional magnetic resonance imaging (fMRI) or transcranical magnetic stimulation (TCS) was evaluated by comparative reference to intraoperative mapping. METHODS: The thumb movement was evoked by TCS for the mapping of the motor cortex. After the placement of the marker determined by TCS on the scalp, fMRI under motor tasks consisting of repetitive grasping was performed. For motor cortex activation, an axial oblique plane to maximize gray matter sampling in the rolandic cortex was employed in order to compare these different mapping techniques more precisely. Sixteen patients with brain tumors were included in this study. RESULTS: In nine patients, fMRI disclosed activation in one restricted gyrus or in the localized area around one restricted sulcus. Of these nine patients, preoperative TCS mapping corresponded closely with fMRI in six, while in the remaining three, the TCS marker fell between 1 and 2 cm apart from the fMRI-activated area. However, in these three patients, intraoperative electrocortical stimulation corresponded with the preoperative mapping with fMRI. In six patients, contigucus two gyri were activated by motor tasks. The TCS marker was disclosed on one of the two activated gyri. Of these six patients, the position of the TCS marker and fMRI-activated site corresponded with each other in four cases. They were found on the same gyrus but there was 1.0-2.0 cm distance between them in two cases. Intraoperative somatosensory evoked potential was monitored in two of these six cases. They corresponded well with the mapping by fMRI and TCS together. In only one patient, no significant activation area was obtained by fMRI because of excessive head motion during motor tasks. The TCS marker in this patient was identical with intraoperative electro-cortical stimulation mapping. CONCLUSION: For presurgical planning in patients with brain tumor near the central sulcus, comparative evaluation with fMRI and TCS is applicable and provides accurate functional mapping.

Adult↗
PubMed1999

Measurement of circulating T cell subsets positive for Fas antigen (CD95) in patients with alcoholic hepatitis.

T cell subsets positive for Fas antigen in peripheral blood of patients with alcoholic hepatitis were measured, using monoclonal antibodies in two colour immunofluorescence assay with flowcytometry. 1) In the patients with alcoholic hepatitis, the ratio of mean +/- standard deviation (M +/- SD) of CD4+ cells positive for CD95 (Fas antigen) in peripheral blood lymphocytes of patients with alcoholic hepatitis tended to increase, but the ratio of CD95-positive cells in CD4+ cells of peripheral blood was almost the same, compared with those of healthy controls. In the alcoholics (overdrink) who did not show alcoholic hepatitis with or without apparent alcoholic damage, the ratio of CD95-positive CD4+ cells in peripheral blood lymphocytes was within normal range, while CD95-positive cells in CD4+ cells of peripheral blood tended to decrease. 2) In the alcoholic hepatitis, the ratios of CD8+ cells positive for CD95 and CD95-positive cells in CD8+ cells of peripheral blood decreased significantly, and in the alcoholics (overdrink) they also tended to decrease. 3) The fluorescence intensity of CD95 on CD4+ cells in peripheral blood of the alcoholics (overdrink) decreased apparently, although the one on CD8+ cells did not. 4) The ratios of T cell subsets, that is, CD4+ and CD8+ cells, positive for HLADR in peripheral blood of the patients with alcoholic hepatitis increased significantly, respectively. These results showed that the ratio of CD8+ cells positive for Fas antigen in peripheral blood of the patients with alcoholic hepatitis decreased. It was suspected that this finding might be due to the direct effect of intaken alcohol to T cell subsets rather than hepatitis, and/or the result of immunological homeostasis in alcoholic hepatitis.

Adult↗
PubMed1998

Direct regulation of acetylcholine release by N-methyl-D-aspartic acid receptors in rat striatum.

The aziridinium ion of ethylcholine (AF64A), a cholinergic neurotoxin, was injected into the right striatum of a rat. The unilateral injection of 10 nmol AF64A reduced the activity of choline acetyltransferase (CAT) and the tissue content of acetylcholine (ACh) in the striatum. The striatal contents of dopamine (DA), norepinephrine (NE), 5-hydroxyindoleacetic acid (5-HIAA) and gamma-aminobutyric acid (GABA) were unchanged. These results suggest that the cholinospecificity in the striatal lesion was induced by the 10 nmol dose of AF64A. The number of N-methyl-D-aspartic acid (NMDA) receptors in the striatum treated with 10 nmol AF64A was determined by a specific binding assay using [3H](+/-)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid ([3H]CPP), a selective ligand for NMDA receptors. The number of the NMDA receptors decreased significantly in the injected area. On the other hand, in a microdialysis using normal rats, the perfusion of 50 microM NMDA into the striatum increased ACh release. The perfusion of 100 microM MK801 which is the specific and non-competitive NMDA receptor antagonist, decreased the basal levels of ACh release and blocked NMDA-elicited ACh release. Taken together, the present results strongly suggest that a population of NMDA receptors exists on cholinergic interneurons within the striatum, and it directly regulates ACh release.

Acetylcholine↗
PubMed1998

NGF delays rather than prevents the cholinergic terminal damage and delayed neuronal death in the hippocampus after ischemia.

Cerebral ischemia induces damage of cholinergic terminals in the hippocampus, which preceded the delayed neuronal death (DND) of the CA1 pyramidal cells. We investigated the effects of nerve growth factor (NGF) on the cholinergic terminal damage after ischemia. Continuous NGF infusion (0.5 microg/7 days) into the lateral ventricle before and after 5 min ischemia prevented a decrease in choline acetyltransferase (ChAT)-immunoreactivity and disturbance of acetylcholine (ACh) release on the 4th day after ischemia, but not on day 7, i.e., NGF infusion caused delay in the progress of the cholinergic terminal damage. These findings show that the cholinergic terminal damage may result from deficiency of endogenous NGF in an ischemic brain. In addition, we investigated whether NGF would prevent the DND after ischemia. NGF infusion also caused delay in the progress of the DND until day 14. Our results suggested that the neuroprotective effect of NGF on the DND may be secondarily yielded by maintenance of communication between cholinergic terminal and the target CA1 cell, and that prevention of cholinergic terminal damage may be useful for the treatment of cerebrovascular disease.

Animals↗
PubMed1998

Changes in presynaptic protein NACP/alpha-synuclein in an ischemic gerbil hippocampus.

We observed temporal changes in NACP (precursor protein of non-Abeta component of Alzheimer's disease amyloid), a presynaptic protein a.k. a. alpha-synuclein, in the hippocampus after 5 min ischemia. Intense NACP immunoreactivity was seen transiently around cerebral blood vessels in the CA1 subfield on day 4, and NACP-positive unusual tubal and chain-like structures developed on month 6. We suggest that the changes in NACP may play an important role in the ischemic pathogenesis.

Amyloid↗
PubMed1998

Stable isotope methodology for kinetic studies of interconversion of cortisol and cortisone in a human subject.

Oral administration of 5 mg each of deuterium-labeled cortisol ([1,1,19,19,19-2H5]cortisol, cortisol-d5) and cortisone-d5 ([1,1,19,19,19-2H5]cortisone) to a human subject on two different occasions four weeks apart provided a useful means of characterizing the kinetics of the interconversion of cortisol and cortisone. From the data on plasma concentration measurements of cortisol-d5, cortisone-d5, cortisone-5, endogenous cortisol and endogenous cortisone by gas chromatography-mass spectrometry, it was demonstrated that (1) the plasma concentration ratio of cortisone-d5 to cortisol-d5 approached a plateau 4-5 h following either the cortisol-d5 or cortisone-d5 administration and the plateau values for the cortisone-d5 and cortisol-d5 administration were almost identical (about 0.43) and (2) dosing with only 5 mg of the deuterium-labeled steroids suppressed the plasma concentrations of endogenous cortisol and cortisone.

Administration, Oral↗
PubMed1998

The role of nitric oxide in striatal acetylcholine release induced by N-methyl-D-aspartate.

Effect of nitric oxide (NO) on striatal acetylcholine (ACh) release induced by N-methyl-D-aspartate (NMDA) was investigated in freely moving rats by means of microdialysis. NMDA caused a significant increase in ACh release in the striatum, which was blocked by the specific NMDA receptor antagonists, (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801), indicating that agonist-evoked increase in ACh release in the striatum was through an NMDA receptor-mediated mechanism. NG-monomethyl-L-arginine acetate salt (L-NMMA; a NO synthase inhibitor) facilitated NMDA-evoked increase in ACh release, while L-arginine (the precursor of NO) inhibited the ACh release. The increase by L-NMMA of ACh release induced by the NMDA was also blocked by L-arginine. These results suggest that NO induced by NMDA receptor-mediated mechanism in cholinergic neurons may mediate an inhibitory regulation of ACh release.

Acetylcholine↗
PubMed1998

Phytoalexins from hairy roots of Hyoscyamus albus treated with methyl jasmonate.

The treatment of hairy roots of Hyoscyamus albus with copper sulfate (Cu2+) and methyl jasmonate (JAMe) produced several phytoalexins having the vetispyrane skeleton. Lubimin and solavetivone were isolated after treatment with Cu2+. Seven sesquiterpenoid phytoalexins were isolated from the culture medium after treatment with JAMe, including lubimin, solavetivone, 3-hydroxysolavetivone and four new compounds (1-4). Structures of the new compounds were elucidated to be (3R,4S,5R,7S,9R)-3-hydroxy-9-tigloyloxysolavetivone (1), (3R,4S,5R,7S,9R)-3-hydroxy-9-(3-methylbutenoyloxy)-solavetivone (2), (3R,4S,5R,7S,9R)-3-hydroxy-9-isobutanoyloxysolavetivone (3); and (3R,4S,5R,7S,9R)-3,9-dihydroxysolavetivone (4). The induction pattern of phytoalexins in hairy roots treated with JAMe was different in those treated with Cu2+, and co-treatment with JAMe and Cu2+ gave only solavetivone.

Anti-Bacterial Agents↗
PubMed1998

Stimulation of rat hypothalamus by microdialysis with K+: increase of ACh release elevates plasma glucose.

The effects of stimulation of the ventromedial hypothalamus (VMH) or lateral hypothalamus (LH) with potassium chloride through a microdialysis probe were studied. The concentrations of ACh and norepinephrine (NE) in the dialysate obtained from the hypothalamic nuclei and plasma glucose concentration were measured. Stimulation of the hypothalamic nuclei, VMH and LH, with potassium increased the plasma glucose level as well as the extracellular concentrations of ACh and choline. Addition of atropine, a muscarinic ACh receptor antagonist, into the potassium solution reduced the increase in the level of plasma glucose. Cholinergic stimulation of these nuclei with neostigmine increased the extracellular concentrations of ACh and plasma glucose. Stimulation of the nuclei with potassium also increased the release of NE. However, stimulation of the VMH or LH with NE and/or pargyline, a monoamine oxidase inhibitor, through the dialysis probe membrane did not significantly increase the plasma glucose concentration. These results suggest that activation of the muscarinic cholinergic or ACh-receptive neurons in the hypothalamic nuclei, VMH and LH, contribute to the elevation of plasma glucose level.

Acetylcholine↗
PubMed1998

[Non-Hodgkin's lymphoma of the spermatic cord: a case report].

A 77-year-old man presented with a 2-week history of a painless lump in the left groin. He underwent left radical orchiectomy under a diagnosis of left spermatic cord tumor. The specimen revealed a 5 x 3 cm solid tumor arising in the spermatic cord at the level of the symphysis pubis. On microscopic examination, the tumor was classified as a diffuse, large cell non-Hodgkin's malignant lymphoma in the Working Formulation, involving a small portion of the upper pole of the left testis. Immunohistochemical stains were positive for LCA and L26. Gallium scan showed increased activity along the left testicular artery in the abdomen. The patient underwent 6 cycles of chemotherapy consisting of cyclophosphamide, vindesine, pirarubicin, prednisone and subsequently the addition of etoposide, which resulted in only temporary improvement. He died with extensive disease 10 months after surgery.

Aged↗
PubMed1997

Neural mechanism of pupillary dilation elicited by electro-acupuncture stimulation in anesthetized rats.

The neural mechanisms to reflex dilation elicited by electro-acupuncture stimulation were investigated in anesthetized rats. Two needles, with 160 microns diameter and about 5 mm apart, were inserted into the skin and underlying muscle of a hindpaw. Repetitive 20 Hz, 0.5 ms electrical pulses at various intensities were used for stimulation for 30s. The pupil size was magnified about 44 times via a microscope and was continuously recorded on a videotape. Electro-acupuncture stimulation at more than 0.5 up to 6 mA induced stimulus intensity-dependent pupil dilation. These responses were abolished by the severance of the sciatic and saphenous nerve of the stimulated hindlimb. Compound action potentials were recorded from the distal cut end of the tibial of a saphenous nerve following electro-acupuncture stimulation of the hindpaw. The mean threshold of the compound action potentials of the myelinated fibers in saphenous nerves was 0.18 mA, while that of unmyelinated fibers was 3.0 mA. The mean threshold of the compound action potentials of the myelinated fibers in the tibial nerve was 0.20 mA of unmyelinated fibers was 3.3 mA. Severance of bilateral trunks did not affect the response, while severance of the third cranial nerves abolished the responses. In conclusion, electro-acupuncture stimulation applied to the hindpaws of the anesthetized rats induced excitation of myelinated or of both myelinated and unmyelinated afferent fibers of the tibial and saphenous nerve, and involved a reflex response of pupil dilation through the third cranial parasympathetic efferent nerve.

Action Potentials↗
PubMed1997

Effects of ventromedial hypothalamus stimulation on glycogenolysis in rat liver using in vivo microdialysis.

In vivo microdialysis was applied to study the effects of ventromedial hypothalamus (VMH) stimulation on liver glycogenolysis under anesthesia. We examined glucose output and norepinephrine (NE) outflow from the liver through analysis of glucose and NE in the liver dialyzate. Stimulation of the VMH increased glucose output and NE outflow from the liver and increased the plasma glucose level. Similar results were obtained on hepatic nerve stimulation. Bilateral adrenalectomy did not abolish the glycogenolysis induced by VMH stimulation. NE outflow increased to a much greater extent in adrenalectomized rats. These data show that VMH stimulation causes glycogenolysis and glucose output from the liver mainly via the hepatic nerves, and that microdialysis is a simple and useful method for the study of liver metabolism in vivo.

Adrenalectomy↗
PubMed1997

Suppression of cholinergic activity via the dopamine D2 receptor in the rat striatum.

The effect of dopamine (DA) D2 receptor on extracellular choline (Ch) and acetylcholine (ACh) levels in rat caudate-putamen (striatum) was investigated by means of microdialysis. The systemic, intraperitoneal (i.p.), injection of (+/-)-2-(N-phenylethyl-N-propyl) amino-5-hydroxytetralin (N-434), a specific DA D2 receptor agonist decreased striatal ACh release in a dose-dependent manner and the i.p. injection of sulpiride, a specific DA D2 receptor antagonist, increased the ACh release in a dose-dependent manner. In contrast, extracellular Ch levels were increased by the agonist and decreased by the antagonist. An increased Ch uptake was observed in sulpiride-treated rats and a decreased Ch uptake was observed in N-434-treated rats. The effects of the D2 agonist on extracellular Ch, ACh and Ch uptake were completely antagonized by the D2 antagonist. These results suggest clearly an inhibition of ACh release by D2 receptor activation, contrasting with previous findings on DA-ACh interaction. The inverse relationship between extracellular Ch and ACh reflects a change in the Ch uptake owing to a change in cholinergic neuron activity via the D2 receptor mechanisms.

Acetylcholine↗
PubMed1997

Effects of MK-801 and pentobarbital on cholinergic terminal damage and delayed neuronal death in the ischemic gerbil hippocampus.

The present study covers both the effects of MK-801, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, and pentobarbital on cholinergic terminal damage and delayed neuronal death (DND) in ischemic gerbil. To study the above effects, in vivo microdialysis, immunohistochemical, and morphological techniques were used. MK-801 (3 mg/kg) or pentobarbital (50 mg/kg) were injected intraperitoneally 1 h or 30 min before 5 min ischemia, respectively. Each estimation was then carried out 4, 7, or 14 days after ischemia. Ischemia induced a significant decrease in acetylcholine (ACh) release and a disappearance of choline acetyltransferase (ChAT)-immunoreactivity in the hippocampus in addition to inducing DND. On day 4, MK-801 protected ischemia-induced DND in the hippocampal CA1 subfield. However, MK-801 had no effect against the decrease in ACh release in spite of protection of the decrease in ChAT-immunoreactivity. On day 7 and 14, no protective effect of MK-801 was observed in all estimations. It became clear that the mechanism of cholinergic terminal dysfunction is different from that involved in pyramidal cell death, i.e., excitative neurotoxicity induced by overabundant extracellular glutamate. Pentobarbital also provided protection against DND. However, protective effects of pentobarbital on the decrease in ACh release and the low ChAT-immunoreactivity were incomplete. Our present study indicated a limitation on the efficacy of NMDA receptor antagonist and barbiturate against cerebral ischemia.

Acetylcholine↗
PubMed1997

Regulation of dopamine D1 and D2 receptors on striatal acetylcholine release in rats.

The effects of dopamine (DA) D1 and D2 receptors on striatal acetylcholine (ACh) releases were investigated by in vivo microdialysis. All drugs were applied via dialysis membrane directly to the striatum. The levels of ACh release were increased by 10(-4) M SKF38393, a D1 receptor agonist. Although 10(-4) M SCH23390, a D1 receptor antagonist, exhibited an increase in the levels of ACh release, the agonist (10(-4) M) induced-increase in the levels of ACh release was suppressed by coperfusion of the antagonist (10(-4) M). In contrast, the levels of ACh release were decreased by the D2 receptor agonist, N-434, in a dose-dependent manner (10(-4) M to 10(-7) M) and increased by the D2 receptor antagonist, sulpiride, in a dose-dependent manner (10(-5) M to 10(-7) M). The agonist (10(-5) M) induced-decrease in the levels of ACh release was suppressed by coperfusion of the antagonist (10(-4) M). Coperfusion of D1 (10(-4) M) and D2 (10(-5) M) agonists blocked both effects of respective drug alone. In order to clarify the effect of endogenous DA, two drugs with different mechanisms for enhancing DA concentration in the synaptic cleft, the DA release-inducer methamphetamine, and the DA uptake inhibitor nomifensine were perfused separately. Both (10(-4) M to 10(-5) M) produced a dose- and a time-dependent decrease in the levels of ACh release. Significant higher levels of ACh release were observed in the striatum of the 6-hydroxydopamine (8 micrograms/10 microliters)-treated rats with significant depletion of striatal DA content. These results suggest that in striatal DA-ACh interaction ACh release, as cholinergic interneuron's activity, is tonically inhibited via the D2 receptor, mainly by dopaminergic input, and the D1 receptor probably modifies the effect of the D2 receptor indirectly.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Hypothalamic cholinergic activity and 2-deoxyglucose-induced hyperglycemia.

To clarify the role of the hypothalamic cholinergic system in the regulation of peripheral glucose metabolism, we investigated hypothalamic cholinergic activities after administration of 2-deoxyglucose (2-DG). Intravenous administration of 2-DG (500 mg/kg) caused neuroglycopenia and marked hyperglycemia; the level of plasma glucose increased to 210% of the initial levels of 20 min. For evaluation of the cholinergic activity, we employed a microwave device and subsequently analyzed the contents of acetylcholine (ACh) and choline after microdissection of the hypothalamic nuclei, ventromedial hypothalamic nucleus (VMH), lateral hypothalamus (LH), and paraventricular nucleus (PVN). In addition, we analyzed fluctuation of extracellular levels of ACh using in vivo brain microdialysis. A decrease in the ACh content, and a corresponding increase in the choline content, was observed in those hypothalamic nuclei min after administration of 2-DG. In the microdialysis perfusate, on the other hand, extracellular level of ACh was increased by 2-DG administration. These data show that ACh release, which is cholinergic activity, was increased after 2-DG administration. Our results suggest the involvement and importance of the hypothalamic cholinergic system in 2-DG-induced hyperglycemia.

Acetylcholine↗