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Biomedical subjects

Y Katayama

Publications and source records attributed to Y Katayama.

At least 397 records · Page 22Linked to original sources
PubMed1995

Effects of an indene-derivative, TN-871, on synaptic transmission in a sympathetic ganglion: presynaptic actions on neurotransmitter release.

Intracellular recordings were made from bullfrog sympathetic ganglion cells to elucidate effects of 2-n-butyl-1-(4-methylpiperazinyl)-5,6-methylenedioxyindene.2 HCl (TN-871) on synaptic transmission. TN-871 at 30 nM augmented cholinergic nicotinic fast excitatory postsynaptic potentials (fast EPSPs), whereas the drug at 3 microM reversibly depressed them, without affecting acetylcholine-induced depolarizations. TN-871 did not affect active and passive electrical properties of the ganglion cells. The quantal analysis method was applied to the fast EPSPs in a 0.54 mM Ca2+/7.56 mM Mg2+ Ringer's solution. The mean quantal content was significantly increased by TN-871 at 30 nM but significantly decreased at 3 microM. TN-871 at 300 nM either increased or decreased the mean quantal content. The mean quantal size of the fast EPSPs was not changed by TN-871 at the concentrations examined. Fast EPSPs in a 0.99 mM Ca2+/4.86 mM Mg2+ Ringer's solution were not affected by nicardipine, but were inhibited in amplitude by omega-conotoxin in a concentration-dependent manner. It is likely that TN-871, in high concentrations, might block omega-conotoxin-sensitive N-type calcium channels in the presynaptic terminals. These results indicate that TN-871 modulates transmitter release from preganglionic nerve terminals without changing the postsynaptic sensitivity of the ganglion cells to ACh.

Animals↗
PubMed1995

Human B lymphocytes respond to Epstein-Barr virus with an increase in intracellular Ca2+ concentration.

Early events in the infection of human B lymphocytes by Epstein-Barr virus (EBV) were examined by measuring calcium ion concentration from fluorescence with fura-2. Intracellular Ca ion concentration ([Ca2+]i) of B lymphocytes increased in response to EBV application. Three types of [Ca2+]i-increase were observed: (1) an early transient [Ca2+]i-increase; and (3) a slow [Ca2+]i-increase without the early transient [Ca2+]i-increase. The early transient increase was observed in the zero Ca2+ condition, but it was suppressed when cells were pretreated with ryanodine before exposure to the virus. The slow sustained [Ca2+]i increase was not observed in Ca(2+)-free extracellular conditions. These results suggest that the early transient [Ca2+]i increase is mediated by Ca2+ release from intracellular Ca storage sites, and the slow sustained [Ca2+]i increase is mediated by the Ca2+ influx through the plasma membrane. Virus receptors on the surface of B lymphocytes were stained with a fluorescence marker, rhodamine, and the capping process after EBV application was observed under a confocal microscope. The capping process and the localization of virus receptors were observed after EBV application. The time course of the capping process seems similar to that of the slow, sustained [Ca2+]i increase.

Adult↗
PubMed1995

[A case of traumatic aneurysm of the thoracic aorta with severe chronic compression of the trachea].

A case of successfully treated traumatic aneurysm of the thoracic aorta with severe major air way compression was reported. A 38-year-old man, who had a history of blunt chest trauma in a traffic accident twenty years ago, complained of asthma-like coughing chest CT scan and angiogram showed a saccular aneurysm of desending aorta compressing the isthmus of the trachea and the esophagus severely. Resection of the aneurysm and prosthetic graft replacement was undertaken successfully with the aid of F-F bypass. The trachea and the esophagus were well decompressed and the patient recovered well with no complaints.

Adult↗
PubMed1994

N-methyl-D-aspartate receptor-mediated, prolonged afterdischarges of CA1 pyramidal cells following transient cerebral ischemia in the rat hippocampus in vivo.

We previously reported the post-ischemic potentiation (PIP) of synaptic efficacy in hippocampal Schaffer collateral/CA1 responses of the rat beginning at 6-8 h following 12 min transient cerebral ischemia in vivo. The present study demonstrated that repetitive stimulation with a relatively low frequency (5 Hz, 6 s), which produced short-lasting afterdischarges (ADs; duration, 4.49 +/- 4.26 s; n = 7) in sham-controls, resulted in prolonged ADs (duration, 26.33 +/- 12.63 s; n = 6; P < 0.001) at the same period after ischemia. The PIP was not affected by 2-amino-5-phosphonovalerate (APV) administered via microdialysis at 7 h post-ischemia. The prolonged ADs in response to repetitive stimulation were, however, reversed to short-lasting ADs (duration, 7.13 +/- 1.44 s; n = 4; P < 0.02) by the same procedure, leaving the response to single stimulation unaffected. These findings suggest that, during the reperfusion period, Ca2+ influx into the CA1 pyramidal cells can be greatly increased through N-methyl-D-aspartate (NMDA) receptor-coupled ion channels if appropriately timed multiple synaptic inputs bombard these cells. Such Ca2+ influx may contribute to delayed death of CA1 pyramidal cells after transient cerebral ischemia if synaptic activity is maintained at relatively high levels during the reperfusion period.

Animals↗
PubMed1994

Receptor-binding affinities of human epidermal growth factor variants having unnatural amino acid residues in position 23.

Ile-23 of human epidermal growth factor (hEGF) has been indicated, by mutagenesis and NMR studies, to be directly recognized by the receptor. In the present study, an unnatural phenylalanine analog, either 2-azaphenylalanine (2aF), 3-azaphenylalanine (3aF), 4-azaphenylalanine (4aF), or 4-fluorophenylalanine (4fF), was incorporated by an in vivo protein synthesis system into position 23 of [Phe23]hEGF, which retains appreciable receptor-binding affinity (about 20% of the wild type). We compared the receptor-binding affinities of the variants with that of [Phe23]hEGF and found that substitution of Phe-23 with 2aF or 3aF raised the affinity, while substitution with 4aF or 4fF remarkably reduced the affinity. The tertiary structure of [Phe23]hEGF was not significantly affected by the substitution of Phe-23 with 2aF, as shown by the two-dimensional nuclear magnetic resonance analysis. In addition, the substitution of residue 23 with His or Tyr produced an hEGF variant with a slightly higher receptor-binding affinity than that of [Phe23]hEGF. Our results suggest that the receptor has an asymmetric hydrophobic pocket for recognition of the side chain in position 23 of hEGF. Furthermore, on the receptor surface, this pocket seems to be adjacent to a less hydrophobic region with a hydrogen-bond acceptor and donor. Thus, the use of unnatural amino acids in addition to the 20 natural ones allows analyses of the structure-function relationship of a protein at a higher resolution than conventional site-directed substitution by only natural amino acid residues.

Amino Acids↗
PubMed1994

Propentofylline administered by microdialysis attenuates ischemia-induced hippocampal damage but not excitatory amino acid release in gerbils.

Systemic administration of propentofylline (PPF), an adenosine uptake inhibitor, has been demonstrated to protect CA1 pyramidal cells from death following transient cerebral ischemia in gerbils. In order to examine the direct effects of this inhibitor, we tested whether or not PPF administered into the hippocampus in situ through a microdialysis probe could attenuate ischemia-induced excitatory amino acid (EAA) release and prevent subsequent death of CA1 pyramidal cells in the gerbil. The EAA release and death of CA1 pyramidal cells observed in the hippocampus were compared with those in the contralateral hippocampus of the same animal into which vehicle alone was administered. The results indicated that pre- as well as post-treatments with PPF inhibited the death of CA1 pyramidal cells after 5-min ischemia in a dose-dependent manner, but did not significantly alter the EAA release during ischemia and reperfusion in the same animals. While the neuroprotective effect of PPF against ischemic damage has commonly been ascribed to attenuation of EAA release during ischemia, other actions of adenosine such as those influencing the synaptic responses, neuronal excitation, and local cerebral circulation, or as yet unidentified actions may be involved in the observed neuroprotective effects of PPF.

Amino Acids↗
PubMed1994

Inhibition of the early phase of free fatty acid liberation during cerebral ischemia by excitatory amino acid antagonist administered by microdialysis.

In order to determine the role of excitatory amino acids (EAAs) in free fatty acid (FFA) liberation during cerebral ischemia, we examined the effect of in situ administration of kynurenic acid, a broad-spectrum antagonist of EAA receptors, by microdialysis on the increase in FFA levels during ischemia in the rat hippocampus. A transient rapid increase in FFA levels, superimposed on a continued slow increase, was observed beginning at 1-2 min after ischemia induction. The early rapid increase in FFAs was profoundly inhibited by kynurenic acid, suggesting that EAAs are critically involved in the early phase of FFA liberation. Development of massive ionic shifts during cerebral ischemia can be delayed for several minutes by kynurenic acid administered by the same procedure, suggesting a vital role for EAAs in the early appearance of anoxic depolarization. The observed inhibition of early FFA liberation may thus be attributable to the delay in development of massive ionic shifts and resultant neurotransmitter release which may activate phospholipase A2 and C.

Amino Acids↗
PubMed1994

Measurement of serum Lp(a) by COBAS MIRA using a latex immunoturbidimetric assay kit.

We had an opportunity to test a reagent kit for serum lipoprotein (a) [Lp(a)] assay, which was based on the latex immunoturbidimetric assay method, and applied it to COBAS MIRA (Roche). Reproducibility of the assay procedure was 0.92-4.0% CV of three samples which contained 12.58-60.4 mg/dl of Lp(a). Minimum detectable concentration was 1.5-2.0 mg/dl. It was confirmed that interference of co-existing substances, i.e. hemoglobin, bilirubin, and intralipid, was negligible. No cross reactivity was seen with plasminogen. Correlation with a ELISA method was excellent. Frequency distribution of Lp(a) in healthy Japanese was similar to that found in white population.

Cross Reactions↗
PubMed1994

Gadolinium DTPA-enhanced magnetic resonance imaging of cerebral contusions.

The morphological characteristics of cerebral contusions in head trauma patients suggest that an increase in cerebrovascular permeability is responsible for the contusion edema which develops within 1-3 days posttrauma. In the present study, 10 patients with cerebral contusions (mean age, 38 years old; 8 males and 2 females) were examined by gadolinium (Gd)-DTPA enhanced magnetic resonance imaging (MRI) at 1-2 days after trauma. Gd-DTPA (0.3 mmol/kg) was infused intravenously over a period of 30 min. MRIs were taken before, and at 2 and 4 hours after initiation of the Gd-DTPA administration. It was found that contusion edema areas were frequently enhanced by Gd-DTPA at 2 hours. The enhancement diminished at 4 hours. These findings appear to be inconsistent with the results of previously reported similar studies in which enhancement was detected at 6-9 days posttrauma but not during the period earlier than 6 days. This discrepancy may be attributable to the presence of a high blood concentration of Gd-DTPA for a longer period of time and a delay in the time at which MRIs were taken in the present study. The present data indicate that an increased cerebrovascular permeability occurs at as early as 1-2 days posttrauma, and suggest that contusion edema which progresses during the initial 1-3 days may be at least partially vasogenic in nature.

Adolescent↗
PubMed1994

Attenuation of hemispheric swelling associated with acute subdural hematomas by excitatory amino acid antagonist in rats.

Acute subdural hematoma (ASDH) gives rise to a mass effect not only by itself but also through unilateral hemispheric swelling. The present study tested the hypothesis that hemispheric swelling is mediated by mechanisms which involve excitatory amino acids (EAAs). After removal of the subdural clot, introduced by homologous blood (0.1-0.2 ml), the % brain water was determined from the formula: ((wet weight--dry weight)/wet weight) x 100. The % brain water of the left hemisphere was significantly greater than that of the right hemisphere during the initial 6 hours after induction of ASDH in animals injected with 0.2 ml blood. A less marked but significant increase was observed in the animals injected with 0.1 ml blood. Systemic pretreatment with kynurenic acid (KYN; 800 mg/kg, i.p.), a broad-spectrum EAA antagonist, attenuated the increase in % brain water in the animals injected with 0.2 ml blood. In order to determine the changes in cerebral metabolism induced by the model of ASDH employed in the present study, we measured the cortical cytochrome oxidase (CYO) activity, a marker of mitochondrial respiration, in a separate group of animals. The CYO activity estimated densitometrically from the histochemical staining was not significantly altered in the animals injected with either 0.1 or 0.2 ml blood, suggesting absence of ischemia. These results indicated that the hemispheric swelling associated with thin ASDHs may be partially mediated by mechanisms other than ischemia, in which EAAs appear to be involved.

Animals↗
PubMed1994

Excitatory amino acid release from contused brain tissue into surrounding brain areas.

The EAA release from contused brain tissue and its effect on the extracellular EAA levels in brain areas surrounding the contusion were investigated with microdialysis technique in the rat. A significant increase in extracellular EAA levels was observed in the contused brain tissue. The EAA increase was significantly greater in the contused brain tissue than in the isolated but non-contused brain tissue. It was further demonstrated that EAAs were released from non-contused brain areas 1-2 mm distant from contused brain tissue. No such EAA release from surrounding brain areas was demonstrated when the cavity was filled with isolated but non-contused brain tissue. The increase in EAAs was attenuated by KYN administered through microdialysis, suggesting that the EAA release from the surrounding brain areas appears to be a consequence that is secondary to the EAA release from the contused brain tissue. Such a diffusion-reaction process is probably mediated by the neurotransmitter actions of EAAs. The results of the present study are of clinical importance, since surgical removal of contused brain tissue and administration of EAA antagonists may serve to protect the surrounding brain areas from EAA neurotoxicity.

Animals↗
PubMed1994

Free fatty acid liberation and cellular swelling during cerebral ischemia: the role of excitatory amino acids.

We previously demonstrated the occurrence of cellular swelling during cerebral ischemia in vivo using microdialysis. 14C-Sucrose was pre-perfused into the extracellular space (ECS) as an ECS marker, and cellular swelling was detected as an increase in extracellular concentration of 14C-sucrose. In the present study, we examined in rats the time courses of the increase in FFA in relation to the occurrence of cellular swelling, and the role of excitatory amino acids (EAAs) in these events. A pair of microdialysis probes were placed in the hippocampus bilaterally. One probe was perfused with modified Ringer solution containing kynurenic acid (KYN, 10 mM), a broad-spectrum EAA antagonist, and the other with Ringer solution as a control. At 30 minutes after the initiation of perfusion, ischemia was induced by decapitation. The brain was subjected to microwave irradiation at 0-8 minutes after decapitation, and the FFA levels in the dorsal hippocampus were measured by high performance liquid chromatography. The time course of cellular swelling was determined in a separate group of animals using the previously described method. It was found that arachidonic and stearic acids began to demonstrate a rapid increase during the period from 1 to 2 minutes following ischemia induction. The levels of oleic and palmitic acids demonstrated similar but less marked increase. The rate of increase became less rapid after 4 minutes, suggesting a transient rapid increase superimposed on a background slow increase. The rapid increase roughly corresponded in timing to the occurrence of the early cellular swelling.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cytochrome oxidase and hexokinase activities in an infusion edema model with preserved blood flow.

Despite numerous investigations, the mechanisms underlying the neurological deficits observed in association with interstitial edema remain unclear. A recent study has demonstrated that the cerebral blood flow (CBF) in edematous white matter is unchanged if the blood flow values are corrected for dilution. In contrast, the cerebral glucose metabolism (CMRgl) has been found to be increased. In order to examine the effects of interstitial edema on the oxidative metabolism, we measured the cytochrome oxidase (CYO) activity, a marker of mitochondrial respiration, and the hexokinase (HK) activity, a marker of glycolysis, together with CBF and CMRgl employing the iodoantipyrine and deoxyglucose autoradiography in an infusion edema model in rats. In agreement with the previous study, CBF was not significantly changed in the edematous hemisphere. No significant alterations in CMRgl and HK activity were noted. In contrast, there was a significant decrease in CYO activity in the edematous hemisphere (-17%; p < 0.01), which was correlated to the edema. These findings suggest that interstitial edema causes a decreased mitochondrial respiratory function despite a maintained circulation. This may be explained by postulating a decreased oxygen delivery and/or accumulation of lactate, both of which have been shown to interfere with mitochondrial respiratory function.

Animals↗
PubMed1994

Effect of a new calcium antagonist (SM-6586) on experimental cerebral ischemia.

SM-6586 (SM) is a new derivative of dihydropyridine with potent calcium blocking activity and inhibitory activity of the Na+/H+ and Na+/Ca++ exchange transport. The effect of SM on survival rate, brain edema and metabolites was evaluated using two different models in spontaneously hypertensive rat (SHR). Global ischemia was induced by bilateral common carotid artery ligation (BLCL) and focal ischemia was induced by middle cerebral artery occlusion. The survival rate after BLCL was higher in the SM-treated group. The brain water content was lower, the ATP level was higher and lactate level was lower in the SM-treated group compared to the control group. In focal ischemia models, the SM-treated group showed a reduction of T1 relaxation time. The brain water content was significantly decreased in the SM-treated group. These results indicate that SM was effective in ameliorating the ischemic insult in global and focal cerebral ischemia models.

Animals↗