PubMed Health⌕ Search

Biomedical subjects

Y Hayashida

Publications and source records attributed to Y Hayashida.

At least 73 records · Page 4Linked to original sources

Single-trial analysis of P3 in patients with generalized epilepsy.

The latencies and amplitudes of averaged P3, and the latencies, amplitudes and frequency components of single EEG responses to target tones were analyzed in 9 control subjects (CS group), 6 epileptics whose mean IQ was 100 (EP group) and 6 epileptics whose mean IQ was 52 (RE group), using an auditory oddball task. All of the subjects responded to the target tones correctly and there were no differences in the incidence of error in response to the target tones, or in the latencies and amplitudes of the averaged P3 among the three groups. However, the reaction times (RTs) in the RE group were significantly longer than those in the other groups (P < 0.05). Single EEG responses to target tone (single-trial ERPs) were classified into 2 types, those with and those without the P3 component. Type 1 had the P3 component and was observed in 42% of all of the responses in the RE group, significantly less than those in the CS (64%) and EP (61%) groups. The peak latencies of P3 in type 1 were similar among the three groups, but the amplitudes of P3 in type 1 in the RE group were significantly greater than those in the CS and EP groups. RTs in the RE group were significantly longer than those in the other groups, and had no correlation with the P3 latencies of type 1. There was little difference in the results of the frequency analysis among the three groups. These results suggest that all subjects in three groups recognized the target tones correctly, but they did not evaluate every target tone, since the incidence of P3 was almost 60% in the CS and EP groups, and 40% in the RE group. The characteristics of cognition and evaluation in three groups were the same, but the decrease in incidence of evaluation and the dissociation between the cognition and the response execution might be caused by impairment of the subject-environment contact mechanism, which resulted in the decrement of IQ in the RE group.

Acoustic Stimulation↗

Detection of respiratory frequency in the recordings of electrocardiogram, blood pressure or sympathetic nerve activity in the conscious rat.

We extracted the respiratory frequency in conscious rats from variations of blood pressure, electrocardiogram, or renal sympathetic nerve activity by means of a band-pass filter. The frequency derived from any one of these parameters corresponded to directly recorded respiratory chest movements. The method may be useful when respiration and cardiovascular parameters have to be recorded in small animals during steady state when minimal surgical intervention is crucial.

Action Potentials↗

Cerebral blood flow decreases following microinjection of sodium nitroprusside into the nucleus tractus solitarii of anesthetized rats.

The present study was undertaken to examine the effects of microinjection of sodium nitroprusside (SNP), which releases nitric oxide (NO) spontaneously, into the nucleus tractus solitarii (NTS) on cerebral circulation. Cerebral blood flow (CBF) was measured in urethane-anesthetized (1.5 g middle dotkg-1, i.p.), paralysed and artificially ventilated rats using labeled microspheres or laser Doppler flowmetry. The CBF was significantly decreased by microinjection of SNP (5 nmol, n=10, microsphere technique; 0.5 nmol, n=6, laser Doppler flowmetry) into the unilateral NTS. Microinjection of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of the formation of NO, prevented cerebral vasoconstrictor responses induced by microinjection of L-glutamate into the NTS (n=10). Microinjection of NG-monomethyl-D-arginine (D-NMMA) had no effect on the cerebral vasoconstrictor responses induced by L-glutamate (n=11). Unilateral microinjections of L-NMMA into the NTS (n=9), of SNP into the area adjacent to the NTS (n=9), of vehicle solution into the NTS (n=10), and of light-inactivated SNP into the NTS (n=6) had no effect on cerebral circulation. Cerebral autoregulation was well maintained in our protocols (n=9). These results indicate that microinjection of SNP, an NO donor, into the NTS decreases CBF.

Animals↗

Spinal cord lactate concentration during chemical stimulation of the nucleus tractus solitarii in anesthetized rats.

This study was conducted to determine the mechanism of spinal cord blood flow (SCBF) decrease following the nucleus tractus solitarii (NTS) activation. In urethane-anesthetized, paralyzed and artificially ventilated rats, neurons in the NTS were chemically stimulated by microinjection of L-glutamate (1.7 nmol; 50 nl) and the lactate concentration, one of indicators of local neuronal metabolism, in the spinal cord was monitored in real time using an enzyme electrode. Before the chemical stimulation study, the responses of the enzyme electrode and its specificity were tested in vitro and in vivo. The electrode responded to step changes in lactate concentration and a calibration plot and regression line were obtained in vitro. The lactate concentration was significantly (P < 0.01) increased during induced apnea in vivo (n = 8). The lactate concentration in the spinal cord was not significantly changed by chemical stimulation of the NTS when arterial blood pressure (ABP) remained above the lower limit of spinal cord autoregulation (n = 21). When chemical stimulation of the NTS decreased ABP to below the lower limit of autoregulation (n = 18), the lactate concentration in the spinal cord was significantly (P < 0.01) increased. This may only be due to hypotensive effects because the lactate concentration was also significantly (P < 0.01) increased when the ABP was passively decreased below the lower limit of autoregulation by controlled hemorrhage in intact (n = 11) and sinoaortic denervated rats (n = 10). Intravenous lactate injection produced no significant increase in the current from the enzyme electrode in the spinal cord (n = 4). Using the electrode with inactivated enzyme solution, the current from the electrode did not change with the increase in lactate in the spinal cord. These findings indicate that the enzyme electrode can detect rapid changes of lactate, a product of anaerobic metabolism. These results also indicate that the spinal cord vasoconstrictor response elicited by chemical stimulation of the NTS, which was performed above the lower limit of spinal cord autoregulation in our previous study, may be due to neurogenic regulatory mechanism, but not to the secondary effects of changes in metabolism.

Anesthesia↗

Spinal cord blood flow decreases following microinjection of sodium nitroprusside into the nucleus tractus solitarii of anesthetized rats.

This study was undertaken to examine whether or not nitric oxide (NO) is involved in synaptic transmission in the nucleus tractus solitarius (NTS) during control of the spinal cord circulation. Employing urethane-anesthetized, paralyzed and artificially ventilated rats, sodium nitroprusside (SNP), which produces NO, was microinjected unilaterally into the NTS and the spinal cord blood flow (SCBF) was determined using labeled microspheres. Arterial blood pressure (ABP) was decreased by unilateral microinjection of SNP into the NTS, but its value was kept within the normotensive range by blood transfusion, in order to measure SCBF at normotension. After microinjection of SNP into the NTS, the SCBFs of the cervical, thoracic and lumbar cords decreased significantly from 63 +/- 8 (mean +/- S.E.M.) to 49 +/- 7 (P < 0.05), from 54 +/- 7 to 37 +/- 7 (P < 0.05), and from 77 +/- 9 to 58 +/- 8 (P < 0.05) ml/min/(100 g), respectively (n = 10). Prior microinjection of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of the formation of NO from L-arginine, into the NTS blocked the spinal cord vasoconstrictor response produced by microinjection of L-glutamate into the NTS (n = 10). Prior microinjection of NG-monomethyl-D-arginine (D-NMMA), which does not inhibit the formation of NO from L-arginine, did not block the spinal cord vasoconstrictor response elicited by microinjection of L-glutamate (n = 11). Unilateral microinjection of L-NMMA into the NTS exerted no effect on the spinal cord circulation (n = 9). These findings suggest that NO may be involved in the control of the spinal cord circulation in the NTS.

Animals↗

Scalp-recorded direct current potential shifts induced by hypocapnia and hypercapnia in humans.

Shifts in scalp-recorded direct current (DC) potential were studied in relation to the changes in end-tidal partial CO2 (PACO2) or O2 (PAO2) of the expired gas either during hyperventilation (HV), hypoventilation (HYPO) or inhalation of high CO2 content air during HV or HYPO in 10 healthy subjects. The DC potential was obtained through a chopper stabilized type of DC amplifier from Cz referred to linked earlobes. Each session was comprised of 3 min control, 3 min experimental and 5 min recovery periods. HV induced a negative shift of the DC potential of 765.5 +/- 203.0 microV (mean +/- SEM). Inhalation of 6% CO2 air during HYPO induced a positive shift of the DC potential of 280.6 +/- 62.8 microV (mean +/- SEM). The magnitude of the DC potential shifts was linearly dependent on the changes in the end-tidal PACO2 (r = 0.78, P < 0.0001). There was no change in the cephalic inter-electrodes impedance during each experimental session. The results suggest that the scalp-recorded DC potentials reflect the changes in cortical excitability associated with the PACO2 level.

Adolescent↗

Mutations in the TRKA/NGF receptor gene in patients with congenital insensitivity to pain with anhidrosis.

Congenital insensitivity to pain with anhidrosis (CIPA; MIM 256800) is an autosomal-recessive disorder characterized by recurrent episodes of unexplained fever, anhidrosis (absence of sweating) and absence of reaction to noxious stimuli, self-mutilating behaviour and mental retardation. The genetic basis for CIPA is unknown. Nerve growth factor (NGF) induces neurite outgrowth and promotes survival of embryonic sensory and sympathetic neurons. Mice lacking the gene for TrkA, a receptor tyrosine kinase for NGF, share dramatic phenotypic features of CIPA, including loss of responses to painful stimuli, although anhidrosis is not apparent in these animals. We therefore considered the human TRKA homologue as a candidate for the CIPA gene. The mRNA and genomic DNA encoding TRKA were analysed in three unrelated CIPA patients who had consanguineous parents. We detected a deletion-, splice- and missense-mutation in the tyrosine kinase domain in these three patients. Our findings strongly suggest that defects in TRKA cause CIPA and that the NGF-TRKA system has a crucial role in the development and function of the nociceptive reception as well as establishment of thermoregulation via sweating in humans. These results also implicate genes encoding other TRK and neurotrophin family members as candidates for developmental defect(s) of the nervous system.

Amino Acid Sequence↗

Blood pressure variability at annual periodic health examination for employees and cardiovascular risk factors.

The employees with hypertension at the annual periodic health examination (HE) for employees in Japan usually receive a re-examination of blood pressure (BP) on another day and are often found to be normotensive. In this study, we analyzed data from the HE at the workplace to determine whether or not such employees should receive medical care. Two groups of subjects were selected. One group (group 1) was composed of 50 subjects with normotension at the HE (controls). Another group (group 2) was composed of 33 subjects with hypertension at the annual HE but with normotension in re-examinations. Cardiovascular risk factors were significantly higher in group 2 than in group 1: mean values of the body mass index (group 1, 22 +/- 2.7 vs. group 2, 24.3 +/- 3.1 kg/m2, p < 0.01), total cholesterol (group 1, 197 +/- 36 vs. group 2, 222 +/- 42 mg/dl, p < 0.01), and low density lipoprotein (group 1, 118 +/ 32 vs. group 2, 137 +/- 38 mg/dl, p < 0.05). The proportion of the employees with high-normal BP in group 2 (42.5%) was significantly higher than that in group 1 (28.0%) (p < 0.01). These indicate that the employees with hypertension at the annual HE but with normotension in the re-examination require further medical attention and should receive medical supervision. The occupational physician should supervise these employees.

Adult↗

Activation of sympathetic outflow by recombinant human interleukin-1 beta in conscious rats.

The present study was undertaken to determine the effects of interleukin-1 beta (IL-1 beta) on renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), heart rate (HR), and body temperature in conscious rats. Either intravenous or intracerebroventricular administration of IL-1 beta elicited increases in AP, HR, and RSNA accompanied by a rise in body temperature. The maximum changes in AP, HR, and RSNA occurred 10-15 min after intravenous injection of IL-1 beta (100 ng) and 20-25 min after intracerebroventricular injection (5 ng). The responses induced by the intravenous and intracerebroventricular injections lasted for approximately 15-30 min and did not appear when the animals were pretreated with the cyclooxygenase inhibitor indomethacin (10 mg/kg iv). Moreover, intracerebroventricular injection of prostaglandin E2 (1 microgram) produced responses similar to those induced by IL-1 but with shorter latency. Plasma norepinephrine and adrenocorticotropic hormone concentrations were increased after IL-1 beta injection. The results suggested that IL-1 beta augments cardiovascular and sympathetic outflow through the central action of prostaglandin E2 in conscious rats.

Adrenocorticotropic Hormone↗

Growth hormone-independent expression of insulin-like growth factor I messenger ribonucleic acid in extrahepatic tissues of the chicken.

The sex-linked dwarf (SLD) chicken, which lacks GH receptor (GHR), and its normal littermates provide a useful experimental system to investigate GH-dependent cellular responses. The GH dependence of insulin-like growth factor I (IGF-I) expression in tissues was examined in SLD and normal chickens of the Gifu 20 strain. Four weeks after hatching, the most abundant expression of IGF-I messenger RNA (mRNA) was observed in liver of normal chickens, whereas no IGF-mRNA expression was detected in that organ of dwarf chickens. On the contrary, in extrahepatic tissues such as spleen, lung, brain, kidney, heart, intestine, thymus, and muscle, IGF-I mRNA expression was equally observed in normal and GHR-lacking dwarf chickens. In the testis, expression of IGF-I mRNA was enhanced by about 5-fold in dwarf chickens showing an expression level comparable to that in normal liver. On day 16 in the embryonic stage, IGF-I mRNA was expressed in muscle, brain, eye, heart, and lung in both normal and SLD chick embryos. However, no IGF-I mRNA expression was observed in liver or kidney of normal and dwarf chick embryos. These results suggest that in chicken, IGF-I mRNA is expressed in liver in a GH-dependent manner after hatching, whereas in other tissues, mRNA expression is independent of GH and GHR before and after hatching, except for testis, in which GH seems to inhibit IGF-I mRNA expression.

Animals↗

Chemical stimulation of the nucleus tractus solitarii decreases spinal cord blood flow in anesthetized rats.

L-Glutamate was microinjected into the nucleus tractus solitarii (NTS) in anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, and spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres. Unilateral chemical stimulation of the NTS (n = 13) significantly decreased SCBF in the cervical cord from 43 +/- 6 (mean +/- SEM) to 28 +/- 4 (P < 0.05), in the thoracic cord from 35 +/- 3 to 24 +/- 4 (P < 0.01), and in the lumbar cord from 49 +/- 3 to 40 +/- 3 ml min-1 (100 g)-1 (P < 0.05). The decrease in SCBF was not due to the decrease in arterial blood pressure (ABP) because the SCBF during the chemical stimulation of the NTS was significantly smaller (P < 0.05) than the SCBF during controlled hemorrhagic hypotension (n = 11). Chemical stimulation of the NTS did not affect the reactivity of the spinal cord vessels to hypercapnia (n = 5). Microinjection of the vehicle solution into the NTS had no effects on spinal cord circulation (n = 9). These results suggest that the cell bodies within the NTS may play a role in the control of spinal cord circulation.

Animals↗

Sympathetic reinnervation of unilaterally denervated rat lung.

The effect of unilateral sympathetic denervation and reinnervation of the lung on a variety of circulatory parameters was investigated in urethane-anaesthetized rats. The left main stem bronchus together with its surrounding nerves was cut and reanastomosed in 40 rats: 12 intact rats served as controls. Final experiments were performed after 0 days to 10 months: the left stellate ganglion was stimulated. The effect was greatest at 20 Hz. Pulmonary arterial pressure increased significantly (P < 0.05) by 10% and pulmonary flow decreased significantly (P < 0.05) by 16% in the control rats; no effect on these parameters was found in acutely denervated rats. The stimulus-elicited change in pulmonary arterial pressure reappeared 1 week after unilateral hilar stripping and gradually returned during reinnervation. After 10 months, the increase in pressure was significantly (P < 0.05) larger than that of the control by 50%, whereas the noradrenaline content of the reinnervated lung was significantly (P < 0.05) smaller than that of the intact side by 48%. This discrepancy may reflect denervation hypersensitivity of vascular muscle cells. The operations had no effect on systemic circulation: heart rate and systemic arterial pressure increased and aortic blood flow decreased to the same extent in all experimental groups during nerve stimulation. These results suggest that sympathetic reinnervation of the rat lung starts within 1 week but that reinnervation is still incomplete 10 months after unilateral hilar stripping.

Adrenergic Fibers↗

Expression of aberrantly spliced growth hormone receptor mRNA in the sex-linked dwarf chicken, Gifu 20.

The structure and expression of the growth hormone receptor (GHR) gene have been studied in a sex-linked dwarf (SLD) chicken strain, Gifu 20. No gross structural change in the receptor gene was observed by Southern blot analysis, however, a transcript of 5.5 killobases (kb), which was approximately 1 kb larger than the usual chicken full length-GHR mRNA was detected in the dwarf chicken by Northern blot analysis. GHR cDNA was obtained from dwarf chicken liver RNA by reverse transcription-polymerase chain reaction, and nucleotide sequence analysis revealed that it contained an intron sequence of the GHR gene. The unspliced intron showed a single point mutation at the donor site from GT to GC, and an aberrant stop codon was generated in the extracellular domain-coding region. Thus, the mutation resulting in an inappropriate splicing of the GHR gene transcript is considered to be the cause of this dwarf chicken.

Alternative Splicing↗

Deficiency of the E1 beta subunit in the branched-chain alpha-keto acid dehydrogenase complex due to a single base substitution of the intron 5, resulting in two alternatively spliced mRNAs in a patient with maple syrup urine disease.

A patient with maple syrup urine disease (MSUD) associated with a E1 beta subunit deficiency of the branched-chain alpha-keto acid dehydrogenase (BCKDH) complex was investigated at the molecular level. The defect responsible for the deficiency of the E1 beta subunit protein was identified by analysis of cDNA and genomic DNA by polymerase chain reaction. Total RNA isolated from lymphoblastoid cells was transcribed into cDNA and amplified using a set of primers located within exon 3 and exon 9 of the E1 beta gene. Agarose gel electrophoresis of cDNA amplification products revealed two shortened bands as well as a faint band of normal size. Nucleotide sequencing of the shortened cDNA amplification products showed that sequences corresponding to exon 5 and both exons 5 and 6 were absent. Nucleotide sequencing of the proband's amplified genomic DNA corresponding to this region of the E1 beta gene revealed a single base substitution from G to T of the invariant GT dinucleotides at 5' splice site of the intron 5. Analysis of family members using primer-specified restriction map modification showed that the patient is homozygous for this mutation. We postulate that this mutation leads to the skipping of either exon 5 or both exons 5 and 6, thus producing two shortened E1 beta mRNA. The percentage of normal and two shortened transcripts was estimated to be 9, 71 and 20%, respectively. To our best knowledge, this is the first documented example of exon skipping in the E1 beta gene as the cause of MSUD and the novel mutation of the invariant G at the 5' splice site which results in two alternatively spliced mRNA due to the skipping of the preceding exon as well as both preceding and following exon.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

Caudal ventrolateral medullary depressor area controls cerebral circulation via rostral ventrolateral medullary pressor area.

The cerebral blood flow (CBF) was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. Microinjection of L-glutamate (1.7 nmol) into the ventrolateral medullary depressor area (VLDA) produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- S.E.M.) to 48 +/- 9 ml.min-1.(100g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side but not in other structures such as brain stem and cerebellum (n = 9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n = 10). Depression of the ventrolateral medullary pressor area (VLPA) neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase following chemical stimulation of the VLDA (n = 11). Microinjection of the vehicle solution into the VLDA had no effects on systemic and cerebral circulation (n = 7). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.

Animals↗

Cerebral vasoconstrictive response produced by chemical stimulation of the caudal ventrolateral medullary depressor area is mediated via the rostral ventrolateral medullary pressor area and the cervical sympathetic nerves.

It was investigated that the cerebral blood flow (CBF) decrease response elicited by chemical stimulation of the caudal ventrolateral medullary depressor area (VLDA) is mediated via the rostral ventrolateral medullary pressor area (VLPA) and the cervical sympathetic nerve. The CBF was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. (i) Microinjection of L-glutamate (1.7 nmol) into the VLDA produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- SEM) to 48 +/- 9 ml.min-1.(100 g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100 g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side (n = 9). (ii) After cervical sympathectomy, L-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly (n = 10). (iii) After depression of the VLPA neurons with muscimol (GABA agonist), L-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly (n = 14). These results suggest that the pathway from the VLDA to control cerebral vessels may be mediated via the VLPA and the cervical sympathetic nerves.

Animals↗