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Biomedical subjects

Y Katayama

Publications and source records attributed to Y Katayama.

At least 703 records · Page 39Linked to original sources
PubMed1987

Transient suppression of event-related evoked potentials produced by mild head injury in the cat.

Studies in humans have shown that sensory stimuli, presented in the context of certain tasks, can elicit a late positive component (LPC), namely P300, in the scalp-recorded evoked potential believed to reflect neural activity related to attentional processes. A similar LPC has been reported in cats and monkeys. In this study, the LPC of the auditory evoked potential (AEP) in the cat was used to detect impairment in attention to a relevant stimulus after low levels of cerebral concussion produced by a fluid percussion device. A hollow screw (for fluid percussion) and stainless steel screws (for AEP recording) were surgically placed in the skull. After recovery from surgery, animals were trained in the paradigm to obtain an LPC. Pupillary dilation was conditioned to tones. A random sequence of two discriminable tones was presented. The lower tone had a probability of 0.1 and was followed by a tail shock (tone-shock). After 400 to 1000 tone-shock presentations, animals attended to the lower tone stimulus as inferred by selective pupillary dilation. In the AEP an early positive component at 50 to 120 msec related to an alerting response was enhanced, and an LPC at 250 to 450 msec appeared in response to the paired tone-shock. Animals were then subjected to cerebral concussion. Complete recovery of normal reflexes, motor coordination, and orienting response was seen within 2 hours after injury. The LPC was suppressed for a period of at least 3 days, suggesting that low magnitudes of brain injury can disrupt higher-order neural activities. This disruption can persist despite recovery of other neurological functions.

Animals↗
PubMed1987

[Determination of antimony in nail and hair by thermal neutron activation analysis].

The concentration of antimony in nail and hair was determined by thermal neutron activation analysis. Samples were collected from the workers of an antimony refinery, inhabitants near the refinery, and residents in control area. They were irradiated by Kyoto University 5 000 kW Reactor for 1 h, and cooled for 30 to 100 days. After cooling, the concentration of Sb in nail and hair was estimated by measuring the intensity of gamma-ray from 124Sb of the samples, then the samples were washed by 0.1% aqueous solution of nonionic surface active agent in an ultrasonic cleaner. The gamma-ray spectrometry was done again (after washing). The concentration of Sb in nail before washing was 730 ppm for the workers, 2.46 ppm for habitants near the refinery, and 0.19 ppm for the control; after washing, it became 230 ppm for the workers, 0.63 ppm for habitants, and 0.09 ppm for the control. The concentration of Sb in hair before and after washing was 222 ppm and 196 ppm for the workers, and 0.21 ppm and 0.15 ppm for the control, respectively.

Antimony↗
PubMed1987

[Different severity of brain ischemia between spontaneously hypertensive rats and Wistar-Kyoto rats induced by internal carotid infusion of arachidonic acid].

Arachidonic acid (AA) is a potent stimulator of platelet aggrgation and is known to induce endothelial cell damage and edema in the brain. An ischemic cerebral infarction model can be produced in rats by an internal carotid infusion of AA. In this study, water content, ATP and lactate in the brain and plasma prostaglandins (thromboxane B2; TXB2 and 6-keto-prostaglandin F1 alpha; 6-keto-PGF1 alpha) were measured and histological observations were made after an internal carotid infusion of AA in two strains of rats; stroke-resistant spontaneously hypertensive rat (SHRSR) and normotensive Wistar-Kyoto (WKY) rats. It is known that the blood pressure of the SHRSR begins to rise at about 8 weeks old. Throughout the study, AA was administered into the internal carotid artery under 2% fluothane anesthesia. In the first study, AA (1.7 mg/kg BW) was administered to 8- and 16-week-old rats and the length of survival was observed. In the second study, water content, ATP and lactate in the brain and plasma TXB2 and 6-keto-PGF1 alpha were measured 3 hours after AA (0.85 mg/kg BW) administration. In the third study, rats were perfusion-fixed 3 hours after the AA (1.7 mg/kg BW) infusion and cerebral arteries were observed by scanning electron microscopy (SEM). During the 6 hour observation period, there was no difference between the two groups in the number of 8-week-old rats which survived. However, the figure became significantly lower in the SHRSR at 16 weeks old. The water content in the bilateral cerebral hemispheres was significantly larger in the SHRSR than in the WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

[Effect of brovincamine fumarate on cerebral ischemia acutely induced by BLCL in SHRSR].

The present study was designed to clarify the effect of brovincamine fumarate (BV 26-723: BV) on the degree of cerebral ischemia acutely induced by bilateral common carotid artery ligation (BLCL) in stroke-resistant spontaneously hypertensive rats (SHRSR). BV was administered to SHRSR by intraperitoneal infusion (I.P.) of 30 mg/kg (BV 30 mg/kg group), 60 mg/kg (BV 60 mg/kg group) and 0.9% saline was similarly injected to SHRSR (control group) before and immediately after BLCL. Cerebral blood flow (rCBF) in the thalamus was measured by hydrogen clearance technique before and until 3 hr of BLCL periodically. The brain metabolites (ATP, lactate, pyruvate) were determined by the enzymatic method and the brain water content was measured by freeze-dry method 3 hr after BLCL. The histopathological changes in brain vessels were observed by scanning electron microscopy (SEM) 3 hr after BLCL. The rCBF of three groups were identical before BLCL. However, the rCBF of BV 30 mg/kg group was statistically higher than in control group until 2 hr after BLCL, and that of BV 60 mg/kg group was significantly higher even 3 hr after BLCL. In measurements of the brain metabolites after BLCL, ATP and pyruvate levels in both the BV 30 mg/kg and 60 mg/kg groups were statistically higher than the control group. And brain lactate concentrations in both the BV 30 mg/kg and 60 mg/kg groups were significantly lower than the control group. The brain water content of BV 30 mg/kg and 60 mg/kg groups were significantly lower then the control group after BLCL.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1987

[Involvement of arachidonic acid cascade in brain edema and cerebral energy metabolism after reperfusion].

The involvements of arachidonic acid metabolites in the development of ischemic brain edema and cerebral energy metabolism were investigated on the experimental ischemia and reperfusion model. The level of arachidonic acid in brain tissue increases especially on the ischemic insult, which is rapidly converted to prostaglandins and leukotrienes after the reperfusion. The drugs which modify the arachidonic acid metabolism were administrated to clarify the effect on ischemic brain edema and cerebral energy metabolism. Male stroke resistant spontaneously hypertensive rats (SHRSR) were subjected to incomplete ischemia for two hours by occlusion of both common carotid arteries with vascular clips, and reperfused for two hours. The drugs used are dexamethasone, indomethacin, trapidil and OKY-046. Indomethacin inhibits cyclooxygenase. Dexamethasone inhibits phospholipases by the production of lipocortin. OKY-046 inhibits thromboxane A2 synthetase. Trapidil inhibits thromboxane A2 synthetase and increases the level of 6-keto-PGF1 alpha. These drugs were administered 18 hours before, just after clipping on (1/2) and off (1/2). Brain water content, cerebral ATP and lactic acid levels were examined. In the saline treated group, the cerebral water content was increased after the reperfusion and reached its maximal level after two hours of the reperfusion. The development of brain edema was prevented by the administration of dexamethasone or trapidil, but not by indomethacin and OKY-046. Administration of trapidil or dexamethasone was found to prevent the decrease in ATP and the increase of lactic acid. In the indomethacin administrated group, only the increase of lactic acid was prevented. 6-keto-PGF1 alpha was high in the trapidil administrated group and low in the indomethacin administrated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

Activation mechanism of human urinary prokallikrein using trypsin as a model activator.

Rapid release of a small peptide from human urinary prokallikrein by trypsin resulted in activation of the prokallikrein. The peptide was identified as the propeptide of the kallikrein from its amino acid sequence. Two large disulfide-linked peptides were also produced very slowly, which accompanied the increase in kallikrein activity. The molecular weights of the two peptides were roughly estimated to be 18,000 and 25,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). N-Terminal amino acid sequences were determined as Ile-Val-Gly-Gly-Trp-Glu-Cys-Glu-Gln-His for the Mr 18,000 peptide and Gln-Ala-Asp-Glu-Asp-Tyr-Ser-His-Asp-Leu for the Mr 25,000 peptide. The N-terminal sequence of the Mr 18,000 peptide was identical to that of the kallikrein. Both peptides contained carbohydrate side chains as judged by staining with periodic acid-Schiff's base. The results indicate strongly that trypsin hydrolyses two specific bonds of human urinary prokallikrein selectively, which are cleaved upon physiological activation to yield the two-chain kallikrein.

Enzyme Activation↗
PubMed1987

[Influence of long-term antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR--protective effect of nicardipine hydrochloride].

We have already reported that the long-term antihypertensive treatment reduced the degree of cerebral ischemia induced by bilateral common carotid artery ligation (BLCL) in stoke-resistant spontaneously hypertensive rats (SHRSR). This antihypertensive treatment was achieved by the combination of captopril and hydroflumethiazide. In this study, nicardipine hydrochloride which is one of the Ca2+ antagonist was similarly administrated to SHRSR for 8-10 weeks (T-SHR). The effect of long-term antihypertensive treatment by this agent on cerebral ischemia induce by BLCL was investigated and compared with untreated SHRSR (U-SHR). The degree of cerebral ischemia 4 hr after BLCL was estimated by the levels of brain energy metabolites (ATP, lactate, c-AMP) and brain water content. The brain metabolites and water content were measured in the forebrain and hindbrain of each hemisphere. And also the histopathological study on brain vessels 3 hr after BLCL was achieved by using scanning electron microscopy (SEM). The blood pressure of T-SHR gradually declined from 185 +/- 10 mmHg (mean +/- S.D.) to 154 +/- 8 mmHg after 8-10 weeks of antihypertensive treatment. However the blood pressure of U-SHR spontaneously changed from 185 +/- 8 mmHg to 206 +/- 12 mmHg after 8-10 weeks. The blood pressure of T-SHR after the treatment was significantly lower than that of U-SHR. The levels of ATP and c-AMP in T-SHR after BLCL were statistically higher than those in U-SHR, and the lactate levels in T-SHR were significantly lower than in U-SHR in the both fore- and hindbrain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

An immunohistochemical study on the river lamprey retina.

The localization of structures immunoreactive to various polypeptides and proteins in the retina of the river lamprey (Lampetra japonica) was investigated by means of an indirect immunohistofluorescence method. In the majority of frozen sections, a subpopulation of amacrine cells showed the immunoreactivity (IR) to one of the examined antisera against corticotropin-releasing factor, glucagon, neuropeptide Y, somatostatin, visinin and 5-hydroxytryptamine, respectively. A few fibers in the inner plexiform layer were immunoreactive to cholecystokinin or substance P antiserum. The visinin-like IR was also found in two types of bipolar cells. The IR was positive in Müller cells against glutamine synthetase but not to glial fibrillary acidic protein. In some flat-mounted preparations, glucagon- and serotonin-like reactive amacrine cells and visinin-like immunoreactive bipolar cells (distally located) could be observed. The results obtained suggest that in the lamprey retina the cytoplasmic property of some cells is similar to, but that of others is different from, vertebrate retinal cells.

Animals↗
PubMed1986

Cystic meningiomas in infancy.

A convexity meningioma associated with a large peritumoral cyst in a 5-month-old girl is reported. Although meningiomas histologically confirmed within the first year of life are quite rare, a review of the cases sporadically appearing in the literature revealed the existence of a group of meningiomas in infants that have unique features in common. The case presented here is a typical example. The clinical characteristics of such a group of meningiomas are discussed.

Brain Diseases↗
PubMed1986

Response of regional cerebral blood flow and oxygen metabolism to thalamic stimulation in humans as revealed by positron emission tomography.

To clarify functional neural pathways originating from the thalamic nucleus ventralis posterolateralis (VPL) in humans, the responses of regional CBF (rCBF) and regional CMRO2 (rCMRO2) to VPL stimulation were investigated by positron emission tomography in five patients who had undergone chronic implantation of electrodes into the VPL for therapeutic purposes. Measurement of rCBF and rCMRO2 under continuous inhalation of C15O2 and 15O2 by steady-state methods revealed significant increases of rCBF and rCMRO2 in the frontal, postcentral, and thalamic regions. The increases in rCBF and rCMRO2 of the postcentral regions were clearly predominant in the stimulated hemisphere insofar as the stimulation produced moderate paresthesia in restricted areas of the body. These results indicate that the VPL relays peripheral somatosensory information, which has previously been demonstrated to be transmitted to the frontal as well as postcentral regions.

Cerebrovascular Circulation↗
PubMed1986

Inhibition of hyperactive trigeminal subnucleus caudalis neurons after experimental trigeminal rhizotomy in response to thalamic sensory relay nucleus stimulation.

The effects of thalamic sensory relay nucleus stimulation on the single neuron activity and field potentials within the trigeminal subnucleus caudalis, which is trigeminal equivalent of the dorsal horn were investigated in intact cats as well as in cats subjected to retro-Gasserian rhizotomy 1-6 months before the experiments. Inhibition of nociceptive neural activity and a positive field potential were evoked by thalamic stimulation in the dorsal horn of the intact animals. A positive field potential followed double pulse stimulation with frequencies ranging up to approximately 50 Hz. The inhibitory periods ranged from 60 to 100 ms. Train pulse stimulation with frequencies ranging from 30 to 50 Hz produced long-lasting inhibition of nociceptive neural activity and a positive shift of the field potentials. Essentially identical inhibition of abnormal neural hyperactivity occurring in the rhizotomized dorsal horn was observed. The positive field potential corresponding to this inhibition also displayed characteristics similar to the field potential seen in the intact dorsal horn. These data indicate that the pathways involved in the inhibitory responses induced by thalamic sensory relay nucleus stimulation, unlike some other pain inhibitory systems, can exert their influence even to the dorsal horn which has undergone reorganization of neural circuits after rhizotomy.

Animals↗
PubMed1986

N-terminal amino acid sequence of human urinary prokallikrein.

The N-terminal amino acid sequences of human urinary prokallikrein and kallikrein have been determined. Their amino acid sequences are as follows. (Formula; see text) The results showed that prokallikrein comprises an additional seven amino acids at the amino terminus of the kallikrein, of which the sequence is (H2N)Ala-Pro-Pro-Ile-Gln-Ser-Arg(COOH). Comparison of the structure of this peptide with those of other proteins revealed extensive sequence identity with the propeptide portions of rat and mouse tissue kallikreins, that were predicted from the preproenzyme-encoded nucleotide sequences. The amino acid sequence of the peptide was also highly homologous to that of the propeptide portion of EGF-binding protein, that was predicted from the nucleotide sequence, and that of the alpha-subunit of NGF. The N-terminal amino acid sequence of kallikrein was completely identical to the reported one (Lottspeich, F., et al. (1979) Hoppe-Seyler's Z. Physiol. Chem. 360, 1947-1950) and shows considerable amino acid sequence homology with the porcine and rat pancreatic kallikreins. As far as the present results are concerned, it is strongly indicated that the inactive kallikrein in human urine is a tissue type prokallikrein which is activated on the release of the N-terminal peptide consisting of seven amino acids.

Amino Acid Sequence↗