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Biomedical subjects

K Murase

Publications and source records attributed to K Murase.

At least 163 records · Page 9Linked to original sources
PubMed1994

Thallium-201/technetium-99m-phytate (colloid) subtraction imaging of hepatocellular carcinoma.

UNLABELLED: This paper evaluates the clinical usefulness of 201Tl to image hepatocellular carcinoma (HCC), using 201Tl, 99mTc-phytate (colloid) and a three-headed SPECT camera. METHODS: The tumor-to-nontumor ratios (T/N) of 201Tl for different categories of HCC were generated. Tumors were emphasized by image subtraction (201Tl-99mTc-colloid). Thirty-three lesions in 16 patients (18 studies) with HCC were evaluated. There were 19 untreated nodular, five untreated diffuse, five local recurrent and four necrotic lesions after interventional therapy. RESULTS: The mean T/N were as follows: untreated nodular 1.54 +/- 0.31 (mean +/- s.d.), untreated diffuse 1.28 +/- 0.26, local recurrence 1.50 +/- 0.29 and necrosis 0.22 +/- 0.06. All the tumors (except necrotic areas) were enhanced by the image subtraction. CONCLUSION: Thallium-201 is useful for liver tumor imaging but 99mTc-phytate (colloid) is essential to discriminate 201Tl tumor uptake from normal liver accumulation. Image subtraction (201Tl/99mTc-colloid) is helpful in detecting HCC.

Aged↗
PubMed1994

[A case of subacute stroke with high uptake of 99mTc-HMPAO in the reperfused infarct corresponding to low perfusion area].

We reported a case of subacute stroke which showed high uptake of 99mTc-d,l-hexamethylpropyleneamine oxime (HMPAO) in the reperfused infarct corresponding to slightly decreased perfusion by 133Xe inhalation CBF measurement. In the chronic stage, both SPECT images of 99mTc-HMPAO and 133Xe showed low perfusion in the affected lesion. It was, therefore, considered that the high uptake of 99mTc-HMPAO had represented luxury perfusion. In the subacute stage of stroke, high uptake of 99mTc-HMPAO may imply luxury perfusion but not always hyperperfusion. It is suggested that the fractional fixation of 99mTc-HMPAO temporarily change in the affected lesion and it is essential to take into consideration the clinical stage for the interpretation of SPECT images.

Acute Disease↗
PubMed1993

Effects of oral administration of a stimulator for nerve growth factor synthesis in basal forebrain-lesioned rats.

Nerve growth factor plays an important role in the survival and maintenance of cholinergic neurons in the central neuronal system. In senile dementia of the Alzheimer type, learning and memory are impaired by the loss of neurons in the magnocellular cholinergic neuronal system. It is, therefore, of interest to investigate the role of nerve growth factor in senile dementia of the Alzheimer type. We now found that 6-(4-hydroxybutyl)-2,3,5-trimethyl-1,4- benzoquinone (TMQ) stimulates nerve growth factor synthesis in mouse astroglial cells and that the compound has improving effects on memory and choline acetyltransferase activity in basal forebrain-lesioned rats, an amnesia animal model. TMQ ameliorated amnesia in the water maze and passive avoidance tasks. The compound not only restored the reduced choline acetyltransferase activity in the parietal cerebral cortex, but also increased nerve growth factor content and choline acetyltransferase activity in the hippocampus, although it did not change either of these parameters in any brain region in intact rats. These results suggest that the compound activates cholinergic neurons only in the damaged brain and, further, indicate that nerve growth factor stimulators could be used in clinical trials for the treatment of senile dementia of the Alzheimer type.

Administration, Oral↗
PubMed1993

NGF level of is not decreased in the serum, brain-spinal fluid, hippocampus, or parietal cortex of individuals with Alzheimer's disease.

Although the cause of Alzheimer's disease (AD) is unknown, nerve growth factor (NGF) has gained attention as a therapeutic agent for the disease. Because NGF maintains the magnocellular cholinergic neurons that are damaged in AD, research interests have been focused on the change in NGF level in patients with AD. This is the first reported study in which human NGF levels were accurately measured and compared between normal and AD samples. We measured NGF levels using enzyme immunoassay (EIA) system for human NGF and found no difference in NGF level in serum, brain-spinal fluid, or brain (hippocampus and parietal cortex) obtained from normal people and patients with AD. These results suggest that a decrease in the NGF level is not a causative factor of AD.

Alzheimer Disease↗
PubMed1993

Sequential alterations of [3H]rolipram and [3H]cyclic adenosine monophosphate binding in the gerbil brain following transient cerebral ischemia.

We examined the sequential alterations in the binding of selective cyclic adenosine monophosphate (cAMP)-phosphodiesterase (PDE) and cAMP-dependent protein kinase (cAMP-DPK) in the gerbil brain following transient cerebral ischemia using in vitro quantitative autoradiography. [3H]Rolipram, a cAMP-PDE inhibitor, and [3H]cAMP were used to label cAMP-PDE and cAMP-DPK, respectively. Gerbils were subjected to 2-min or 6-min ischemia. Two-minute ischemia, which caused no morphological neuronal damage, produced no significant changes in either [3H]rolipram or [3H]cAMP binding throughout the recirculation period. The reduction of [3H]rolipram binding in the CA1 subfield of the hippocampus began 6 h after 6-min ischemia. Seventy percent of [3H]rolipram binding was preserved at 4 days, at which time almost all CA1 pyramidal cells had been destroyed. On the other hand, the reduction of [3H]cAMP-binding sites in the CA1 subfield began 1 day after 6-min ischemia. At 4 days, 47% of [3H]cAMP-binding sites in the CA1 subfield were preserved. Furthermore, we observed a transient reduction of [3H]cAMP binding in the dentate gyrus, which is resistant to ischemia, at 1 day and 4 days. These results indicate that marked alterations of cAMP-PDE and cAMP-DPK precede neuronal death in the hippocampal CA1 subfield, and the dentate gyrus also showed a transient alteration of cAMP-DPK.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1993

Tumor necrosis factor stimulates the synthesis and secretion of biologically active nerve growth factor in non-neuronal cells.

Tumor necrosis factor-alpha (TNF) markedly stimulates the synthesis and secretion of immunoreactive nerve growth factor (NGF) in quiescent mouse fibroblasts, which is a result of increase in the NGF mRNA level. NGF produced by TNF-treated fibroblasts has a molecular mass of 13 kDa on SDS-polyacrylamide gel electrophoresis, which is consistent in size with the subunit of mouse beta-NGF, and induces neurite outgrowth in paravertebral sympathetic neurons. Several peptide growth factors such as basic fibroblast growth factor (bFGF) and epidermal growth factor also stimulate NGF production in the cells, but not platelet-derived growth factor. The dose responses of TNF and bFGF to stimulate NGF production in the cells are, respectively, similar to those to induce cell proliferation. However, no correlation is observed between the ability of these growth factors to stimulate NGF production and that to induce cell proliferation. Thus, the stimulation of NGF production in the cells seems to be a specific activity of TNF and some other growth factors. TNF stimulates the synthesis and secretion of NGF also in other cells such as human glioblastoma cells. These findings suggest that TNF plays a role in regulating neuronal cell function through an indirect mechanism by which it stimulates NGF production in glial cells and fibroblasts.

3T3 Cells↗
PubMed1993

Sulfated glycolipids are ligands for a lymphocyte homing receptor, L-selectin (LECAM-1), Binding epitope in sulfated sugar chain.

Specific sugar ligands which bind to rat L-selectin (LECAM-1, lymphocyte homing receptor)-IgG chimera were investigated by thin-layer chromatography-binding assay and ELISA. Rat L-selectin-IgG bound to native sulfated glycolipids such as sulfatide (I3SO3-GalCer), seminolipid, SM3(II3SO3-LacCer), SB2(III3SO3,II3SO3-Gg3Cer), SB1a (IV3SO3,II3SO3-Gg4Cer). The binding activity of the SM2 (II3SO3-Gg3Cer) carrying the internal sulfated Gal was very low, indicating that non-reducing terminal SO3H-3Gal beta 1- structure is essential for the binding. The reactivity of sulfatide was higher than that of sialyl Le(x) [Neu5Ac alpha 2-3Gal beta 1-4(Fuc alpha 1-3)GlcNAc beta 1-3Gal beta 1-4Glc beta 1-Ceramide] either in the presence of 1 mM Ca2+ or 1 mM Ca2+ and 5 mM EGTA. All the non-fucosylated gangliosides including ganglio-series and lacto-series type I and II chains tested gave a negative reaction. Neutral glycosphingolipids tested were all negative. Binding assay using synthetic sulfatide analogs indicated that the L-selectin-binding to its sulfated sugar ligands is position specific and depends on the number of the sulfate group, i.e., (SO3)3-3,4,6Gal- > (SO3)2-3,6Gal- > SO3-3Gal- > SO3-3Glc- > SO3-6Gal- > SO3-2Gal-. Lower reactivity of the chimera to SO3-3Glc-rather than SO3-3Gal- indicates that the chimera recognizes the configuration of hydroxyl group linked to the 4 carbon atom of the pyranose ring in galactose.

Amino Acid Sequence↗
PubMed1993

Limited but evident protective effects of MK-801 and pentobarbital on neuronal damage following forebrain ischemia in the gerbil under normothermic conditions.

The purpose of this study was to examine the protective effects of an N-methyl-D-aspartate receptor antagonist, MK-801, and pentobarbital against neuronal damage in a global ischemia model under controlled body temperature. Gerbils were subjected to 3 and 5 min of bilateral common carotid artery occlusion. MK-801 (1 and 5 mg/kg, i.p.), administered 30 min before ischemia, significantly attenuated the degeneration of hippocampal CA1 pyramidal cells after 3 min of ischemia in a dose dependent manner, but had no such effects after 5 min of ischemia. Pentobarbital (40 mg/kg, i.p.) also protected against CA1 damage after 3 min of ischemia but not after 5 min of ischemia. Thus, we confirmed the protective effects of these agents under normothermic conditions, although these effects were limited to shorter periods of ischemia.

Adenosine Triphosphate↗
PubMed1993

Improvement of brain single photon emission tomography (SPET) using transmission data acquisition in a four-head SPET scanner.

Attenuation coefficient maps (mu-maps) are a useful way to compensate for non-uniform attenuation when performing single photon emission tomography (SPET). A new method was developed to record single photon transmission data and a mu-map for the brain was produced using a four-head SPET scanner. Transmission data were acquired by a gamma camera opposite to a flood radioactive source attached to one of four gamma cameras in the four-head SPET scanner. Attenuation correction was performed using the iterative expectation maximization algorithm and the mu-map. Phantom studies demonstrated that this method could reconstruct the distribution of radioactivity more accurately than conventional methods, even for a severely non-uniform mu-map, and could improve the quality of SPET images. Clinical application to technetium-99m hexamethyl-propylene amine oxime (HMPAO) brain SPET also demonstrated the usefulness of this method. Thus, this method appears to be promising for improvement in the image quality and quantitative accuracy of brain SPET.

Adult↗
PubMed1993

Memory impairment and neural dysfunction after continuous infusion of anti-nerve growth factor antibody into the septum in adult rats.

Nerve growth factor is required for the survival and maintenance of cholinergic neurons in the central nervous system. The direct infusion into the rat's septum of an anti-nerve growth factor monoclonal antibody, which inhibits nerve growth factor bioactivity seven times more strongly than a polyclonal antibody, caused very severe damage to the hippocampal cholinergic system. Anti-nerve growth factor polyclonal antibody also neutralized endogenously occurring nerve growth factor. The infusion of anti-nerve growth factor polyclonal antibody produced a dysfunction of memory and decreased choline acetyltransferase activity and acetylcholinesterase staining in the hippocampus. The cholinergic dysfunction and impairment of memory recovered to the normal level two weeks after cessation of the infusion of the anti-nerve growth factor polyclonal antibody. These results suggest that a deficit of nerve growth factor in the adult brain causes neuronal dysfunction.

Acetylcholinesterase↗
PubMed1993

Alterations in [3H]MK-801, [3H]muscimol, [3H]cyclic AMP, and [3H]rolipram binding in the gerbil hippocampus following repeated ischemic insults.

Using [3H]MK-801, [3H]muscimol, [3H]cyclic AMP, and [3H]rolipram, we performed quantitative in vitro autoradiography to determine sequential alterations in the binding of N-methyl-D-aspartate and GABAA receptors, particulate cyclic AMP-dependent protein kinase, and cyclic AMP-selective phosphodiesterase, respectively, in the gerbil hippocampus following repeated brief ischemic insults. Changes from 1 h to 28 days after three 2-min ischemic insults at 1-h intervals were compared with those after 2 and 6 min of ischemia. We observed no alterations in the binding of all the four ligands throughout the observation period following 2 min of ischemia which produced no histological neuronal damage except for transient reductions in [3H]cyclic AMP binding during the early reperfusion period. [3H]Cyclic AMP binding in the CA1 subfield decreased one day after 6 min of ischemia and four days after three 2-min ischemic insults, and 62-65% of the binding was lost after 28 days. [3H]Rolipram binding in the CA1 subfield decreased one day after 6 min of ischemia and the binding was reduced by 45-50% after four and 28 days. Following three 2-min ischemic insults, [3H]rolipram binding decreased in the CA1 at one day, and decreased by 25-33% after 28 days. Both [3H]MK-801 and [3H]muscimol binding was preserved during the early reperfusion period after 6 min of ischemia and three 2-min ischemic insults. Reductions in [3H]MK-801 binding in CA1 were observed four days after ischemic insults when CA1 neuronal destruction was seen. After one month, approximately 50% of [3H]MK-801 binding was lost in CA1 in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1993

The distribution of excitatory amino acid receptors on acutely dissociated dorsal horn neurons from postnatal rats.

Excitatory amino acid receptor distribution was mapped on acutely dissociated neurons from postnatal rat spinal cord dorsal horn. N-methyl D-aspartate, quisqualate and kainate were applied to multiple locations along the somal and dendritic surfaces of voltage-clamped neurons by means of a pressure application system. To partially compensate for the decrement of response amplitude due to current loss between the site of activation on the dendrite and the recording electrode at the soma, a solution containing 0.15 M KCl was applied on the cell bodies and dendrites of some cells to estimate an empirical length constant. In the majority of the cells tested, the dendritic membrane had regions of higher sensitivity to excitatory amino acid agonists than the somatic membrane, with dendritic response amplitudes reaching more than seven times those at the cell body. A comparison of the relative changes in sensitivity between each combination of two of the three excitatory amino acid agonists along the same dendrite showed different patterns of agonist sensitivity along the dendrite in the majority of the cells. These data were obtained from dorsal horn neurons that had developed and formed synaptic connections in vivo. They demonstrate that in contrast to observations made on ventral horn neurons, receptor density for all the excitatory amino acid receptors on dorsal horn neurons, including the N-methyl-D-aspartate receptor, are generally higher on the dendrites than on the soma. Further, these results are similar to those obtained from dorsal horn neurons grown in culture.

Animals↗
PubMed1993

[Intravascular ultrasound imaging on the endarterectomized coronary arteries in two patients].

Intravascular ultrasound imaging on the endarterectomized coronary arteries in two patients are reported with a review of the literature. Case 1, a 62-year-old male and case 2, a 64-year-old male underwent endarterectomy of the right coronary artery (#3--#4PD, 4AV) combined with coronary arterial bypass grafting. Coronary arteriography (CAG) and intravascular ultrasound imaging (IVUS) were performed one month after operation. CAG revealed bypass grafts and endarterectomized coronary arteries to be patent together, and IVUS revealed endarterectomized coronary arteries had two layers, outer layer to be hyperechoic and inner layer to be heterogenously echoic in both cases. The histological examination of specimens suggests this heterogenously echoic area represents media, thrombus and irregularly proliferated intima. Therefore, anticoagulant therapy after endarterectomy should be strictly performed.

Coronary Artery Bypass↗
PubMed1993

Stimulation of nerve growth factor synthesis/secretion in mouse astroglial cells by coenzymes.

We examined the effect of coenzymes such as PQQ, pyrroloquinoline quinone; TOPA, 3-(2,4,5-trihydroxyphenyl)-DL-alanine, and lipoic acid on nerve growth factor (NGF) synthesis in mouse astroglial cells, BALB c/3T3 cells, and WS-1 cells in culture. These coenzymes had a stimulating effect on NGF synthesis without causing cytotoxicity. Especially PQQ showed the strongest activity of promoting NGF synthesis in astroglial cells, whereas lipoic acid had the strongest effect on BALB c/3T3 cells. The activity may not due to the catechol ring or 1,4-benzoquinone ring, but due to the oxidative or reductive activity. These results suggest that these coenzymes may play a role in NGF synthesis and neuronal survival through the stimulating effect of the NGF synthesis in brain and such compounds are good candidates as NGF inducers.

3T3 Cells↗
PubMed1993

[Emergency operation for complete papillary muscle rupture after myocardial infarction--a case report of 81-year-old patient].

Mitral regurgitation due to complete rupture of the papillary muscles after myocardial infarction has a very poor prognosis, even if diagnosed and operated on at an early phase. Recently, we performed an emergency operation for mitral regurgitation due to complete papillary muscle rupture after myocardial infarction in an 81-year-old patient. This is probably the oldest case in Japan. Operation revealed complete rupture of the posterior papillary muscle, and valve replacement with a Carpentier-Edwards bioprosthesis was performed.

Aged↗
PubMed1992

Human fibroblast cells synthesize and secrete nerve growth factor in culture.

Using our enzyme immunoassay system developed for recombinant hNGF, we examined the synthesis and secretion of human NGF (hNGF) by human fibroblast (WS-1) cells. The amount of the factor secreted by WS-1 cells increased linearly and a significant amount of NGF was detected in the conditioned medium of WS-1 cultures. WS-1 NGF showed properties identical to those of recombinant human NGF in immunoreactivity and molecular weight. An increase in cell density or the withdrawal of serum from the culture medium caused a drastic decrease in the rate of NGF secretion. These results suggest that WS-1 cells are able to synthesize and secrete hNGF in culture and that the synthesis/secretion is regulated in a growth phase-dependent manner.

Cell Division↗