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Biomedical subjects

T Hayashida

Publications and source records attributed to T Hayashida.

At least 19 recordsLinked to original sources
PubMed2002

Spinal reconstruction for symptomatic thoracic haemangioma using a titanium cage.

Most vertebral haemangiomas are asymptomatic. A case of spinal reconstruction for symptomatic extraosseous thoracic haemangioma using a titanium cage is reported. Radiographs of the T11 vertebra demonstrated characteristic vertical striations. Magnetic resonance imaging and computed tomography showed spinal cord compression by extraosseous tumour extension. Several tumour feeding vessels were shown by angiography. Through a transpedicular biopsy, a histological diagnosis of cavernous haemangioma was made. Embolisation of feeding vessels was performed using coils before surgery. Laminectomy and subtotal vertebrectomy were performed by a single posterior approach. Rigid stabilisation of the spine was achieved with pedicle screw systems and a cage filled with an autogenous bone graft. Five months postoperatively, stabilisation of the spine was established without loosening of the cage or pedicle screws. Clinical symptoms were improved.

Aged↗
PubMed2002

Ghrelin in neonatal rats: distribution in stomach and its possible role.

Ghrelin, a 28 amino acid peptide, has recently been isolated from the rat stomach as an endogenous ligand for the GH secretagogue receptor. The fact that administration of ghrelin, centrally or peripherally, stimulates both food intake and GH secretion suggests that stomach ghrelin has an important role in the growth of rats. We used immunohistochemistry and radioimmunoassay to determine the age at which ghrelin-immunostained cells begin to appear in the rat stomach. Ghrelin-immunoreactive cells were found to be expressed in the fetal stomach from pregnancy day 18. The number of ghrelin-immunoreactive cells in the fetal stomach increased as the stomach grew. The amount of ghrelin in the glandular part of the rat stomach also increased, in an age-dependent manner, from the neonatal stage to adult. Eight hours of milk restriction significantly decreased the ghrelin concentration in the stomachs of 1-week-old rats, and increased the ghrelin concentration in their plasma. Administration of ghrelin to 1- and 3-week-old rats increased plasma GH concentrations. The daily subcutaneous administration of ghrelin to pregnant rats from day 15 to day 21 of pregnancy caused an increase in body weight of newborn rats. In addition, daily subcutaneous administration of ghrelin to neonatal rats from birth advanced the day of vaginal opening from day 30.7+/-0.94 to day 27.9+/-0.05. These results suggest that ghrelin may be involved in neonatal development.

Analysis of Variance↗
PubMed2002

Role for central ghrelin in food intake and secretion profile of stomach ghrelin in rats.

Ghrelin, a 28-amino-acid peptide, has recently been isolated from the rat stomach as an endogenous ligand for the GH secretagogue receptor. We have reported previously that central or peripheral administration of ghrelin stimulates food intake, and the secretion of GH and gastric acid in rats. In the present study, we investigated how much endogenous centrally released ghrelin is involved in the control of food intake and body weight gain. We also examined the profile of ghrelin secretion from the stomach by RIA using two kinds of anti-ghrelin antiserum, one raised against the N-terminal ([Cys(12)]-ghrelin[1-11]) region and one raised against the C-terminal ([Cys(0)]-ghrelin [13-28]) region of the peptide. The former antibody recognizes specifically ghrelin with n- octanoylated Ser 3 (acyl ghrelin), and does not recognize des-acyl ghrelin. The latter also recognizes des-acyl ghrelin (i.e. total ghrelin). Intracerebroventricular treatment with the anti-ghrelin antiserum against the N-terminal region twice a day for 5 days decreased significantly both daily food intake and body weight. Des-acyl ghrelin levels were significantly higher in the gastric vein than in the trunk. Either fasting for 12 h, administration of gastrin or cholecystokinin resulted in increase of both acyl and des-acyl ghrelin levels. The ghrelin levels exhibited a diurnal pattern, with the bimodal peaks occurring before dark and light periods. These two peaks were consistent with maximum and minimum volumes of gastric content respectively. These results suggest that (1) endogenous centrally released ghrelin participates in the regulation of food intake and body weight, (2) acyl ghrelin is secreted from the stomach, (3) intestinal hormones stimulate ghrelin release from the stomach, and (4) regulation of the diurnal rhythm of ghrelin is complex, since ghrelin secretion is augmented under conditions of both gastric emptying and filling.

Animals↗
PubMed2001

Ghrelin in domestic animals: distribution in stomach and its possible role.

Ghrelin, a novel growth-hormone-releasing acylated peptide, was recently isolated from rat and human stomachs. In rat, peripheral or central administration of ghrelin stimulates the secretion of growth hormone (GH) from the pituitary gland. Recent work suggests that ghrelin plays an important role in energy homeostasis, body weight, and food intake. We examined the distribution of cells immunoreactive to ghrelin in the stomachs of domestic animals and rats, using a polyclonal antibody for the N-terminal fragment of rat ghrelin [1-11]. We measured the plasma levels of ghrelin before and after feeding in cows, and GH levels after central administration of ghrelin in Shiba goats, to elucidate the possible role of ghrelin. Immunostained cells were widely distributed from the neck to the base of the oxyntic gland in all animals. The plasma ghrelin concentration in cows decreased significantly 1 h after feeding, and then recovered to pre-feeding levels. Administration of ghrelin into the third ventricle in Shiba goats dramatically increased the plasma GH concentration dose-dependently. These results suggest that ghrelin plays an important role in GH secretion and feeding regulation in domestic animals.

Animals↗
PubMed2001

Salt-loading elevates blood pressure and aggravates insulin resistance in Wistar fatty rats: a possible role for enhanced Na+ -H+ exchanger activity.

OBJECTIVE: Increased Na+-H+ exchanger activity (NHE) has been reported as an intermediate phenotype in hypertensive subjects, particularly those with insulin resistance. To investigate whether NHE abnormality plays a role in hypertension, Wistar fatty rat (WFR) with overt obesity, hyperglycemia and marked hyperinsulinemia was examined. METHODS: WFR and Wistar lean rats (WLR) as a control (n = 12, each) were fed either with normal (0.38%) or high sodium (4% NaCl) diet for 12 weeks and then sacrificed to examine platelets NHE activity. RESULTS: Mean arterial pressure (MAP) was higher in WFR than in WLR (113 +/- 4 versus 96 +/- 7 mmHg, P < 0.05) under a normal chow. Vmax values of NHE activity were significantly higher in WFR than in WLR. WFR fed with a high sodium diet showed higher MAP than those with a normal chow (128 +/- 3 versus 113 +/- 4 mmHg, P < 0.05). Though Km values were not different between WFR and WLR under a normal chow, both maximal transport rate (Vmax) and half maximal transport (Km) values were significantly higher in WFR with a high salt diet than those with a control diet. Vmax showed significant correlation with MAP, whereas Km values correlated with immunoreactive insulin (IRI) levels. Significant interaction between dietary sodium intake and the strain differences was observed both on blood pressure and on IRI levels by two-way analysis of variance (ANOVA). CONCLUSION: WFR presented salt-sensitive blood pressure elevation. NHE activity was enhanced in WFR in correlation with the blood pressure. These results suggest that augmented NHE activity contributes to the development of salt-sensitive blood pressure elevation in WFR.

Animals↗
PubMed2001

Electrophysiological course of uraemic neuropathy in haemodialysis patients.

The objective of this study was to confirm electrophysiologically both the presence and course of uraemic neuropathy in haemodialysis patients. Nerve conduction studies of the lower extremities were done in 70 haemodialysis patients and 20 normal volunteers. Compared with that in normal volunteers, the distal motor latency in the tibial nerve of patients was prolonged significantly (p<0.05), and the minimal F wave latency in the tibial nerve was also prolonged significantly (p<0.05). Motor conduction velocity in the tibial nerve was reduced significantly (p<0.05), and sensory nerve conduction velocity in the medial plantar nerve also was reduced significantly (p<0.05). These results suggest the presence of uraemic neuropathy in haemodialysis patients. Twenty patients were investigated by a follow up study five years later. Parameters from F wave conduction studies, which were thought to be the most useful in the evaluation of neuropathy, showed no significant differences between the initial and follow up trials. These observations suggest that uraemic neuropathy does not progress during haemodialysis. These results also suggest that most haemodialysis patients showed electrophysiological evidence of uraemic neuropathy, but no remarkable electrophysiological change in uraemic neuropathy during haemodialysis was recognised.

Adult↗
PubMed2001

Stable isotope-labeling studies on the oxidative coupling of caffeic acid via o-quinone.

The formation of ortho-quinone from ortho-diphenol is a key step in its dimerization. An NMR analysis of the oxidation of 3,4-dihydroxycinnamic acid (caffeic acid) by NaIO4 revealed the formation of 3-(3',4'-dioxo-1',5'-cyclohexadienyl) propenoic acid (o-quinone) prior to the formation of furofuran-type lignan 4,8-exo-bis (3,4-dihydroxyphenyl)-3,7-dioxabicyclo[3.3.0]octane-2,6-dione. Both electrolytic and enzymatic oxidation of caffeic acid also generated o-quinone. The yields of o-quinone from caffeic acid were quantified by NMR and HPLC analyses. A stable isotope-labeling study of the formation of lignans directly proved the random radical coupling of semiquinone radicals formed from a set of caffeic acid and o-quinone.

Benzoquinones↗
PubMed2000

Estimation of cervical cord dysfunction by somatosensory evoked potentials.

The purpose of this study was to examine the relationship of abnormal short-latency somatosensory evoked potentials (SSEPs) recorded by a noncephalic reference montage with clinical variables in cervical myelopathy patients and to reexamine the diagnostic utility of SSEPs in such patients. We studied cervical SSEPs elicited by stimulating the median and ulnar nerves in 87 patients. Our grade classification of spinal N13, which is based on the normal limits of latencies or amplitudes, corresponded well with the clinical variables and is of value when trying to localize the cervical lesion segmentally. The N9-P14 interpeak latency in response to ulnar nerve stimulation correlated well with lower extremity function (r = -0.440, P <0.0001). We suggest a combined assessment of N13 amplitude, and N9-N13 and N9-P14 interpeak latencies to estimate dorsal column and dorsal horn function separately in patients with cervical myelopathy.

Adult↗
PubMed2000

Auditory P50 obtained with a repetitive stimulus paradigm shows suppression to high-intensity tones.

We manipulated stimulus intensity and number of frequency bands in auditory stimuli in order to investigate the nature of P50 in human auditory evoked potentials. Pure-tone and mixed-tone conditions were examined. For each condition, four stimulus intensities were used: 55, 70, 85 and 100 dB sound pressure level (SPL). The P50s were obtained at Cz using a repetitive stimulus paradigm. P50 amplitudes increased as stimulus intensities increased up to 85 dB; with 100 dB stimulation amplitudes decreased. The number of frequency bands in the stimulus did not affect P50 amplitude. Considered in terms of P50 suppression under a conditioning/testing paradigm, the results suggest that the P50 wave reflects activity of the sensory gating mechanism in humans.

Adult↗
PubMed2000

Multipoint imprinting analysis in sporadic colorectal cancers with and without microsatellite instability.

Disrupted imprinting is implicated in certain tumorigenesis. Since aberrant methylation has been described for a majority of microsatellite instability (MSI)-positive sporadic colorectal cancers, we have investigated alteration to the imprinting in 55 sporadic colorectal cancers with or without MSI. Loss of imprinting (LOI) of IGF2 and PEG1/MEST was observed in 42% and 35% of informative cancers, respectively. H19 expression was not detected in 24% of informative cancers. SNRPN and NDN retained monoallelic expression in all the cancers examined. These findings indicate no simultaneous disruption of the imprinted genes. LOI of IGF2 and PEG1/MEST was also observed in colorectal mucosa from almost all the patients with LOI in tumor tissue. Moreover, MSI-positive colorectal cancers exhibit LOI of IGF2 with a high frequency compared to MSI-negative cancers (P=0.013). These observations, consistent with a previous report, establish an association between LOI of IGF2 and MSI in colorectal cancers and provide insight into susceptibility of tumor development.

Alleles↗
PubMed2000

[Improvement of obstructive sleep apnea by uvulopalatopharyngoplasty and tonsillectomy in a case of Duchenne muscular dystrophy].

A 10-year-old boy with Duchenne muscular dystrophy (DMD) underwent uvulopalatopharyngoplasty and tonsillectomy for obstructive sleep apnea (OSA). He has snored loudly during nocturnal sleep since infancy, and OSA developed one and a half years after he was wheel chair-bound at 8 years. Magnetic resonance imaging (MRI), conventional spirometry and overnight polysomnography were performed before and after the surgery. MRI before surgery revealed moderate tonsillar hypertrophy and a long uvula which narrowed the upper airway. After the surgery, his vital capacity (VC) was not changed (% VC; from 77 to 78%), but forced expiratory volume (FEV) was improved (FEV 1.0%; from 75 to 86%). A preoperative apnea index of 32.8/hour decreased to 0.8/hour postoperatively. REM-related falls in HbSaO2 improved remarkably. The present case suggests that subjects with DMD with tonsillar hypertrophy and a redundant uvula tend to develop noctrurnal OSA earlier than DMD cases with a normal tonsil and uvula. Assessment of respiratory function, particularly FEV 1.0%, is important for determining surgical indication of OSA in patients with DMD.

Child↗
PubMed1999

TGF-beta1 activates MAP kinase in human mesangial cells: a possible role in collagen expression.

BACKGROUND: Although the pathogenic relevance of transforming growth factor-beta (TGF-beta) to glomerular sclerosis has been established, the intracellular mechanisms by which TGF-beta induces extracellular matrix accumulation are not fully understood. We examined whether the mitogen-activated protein (MAP) kinase pathway is involved in TGF-beta1-induced collagen expression by cultured human mesangial cells. METHODS: The activation of MAP kinase pathways by TGF-beta1 was assessed by immunoblot with anti-phospho-ERK or -JNK antibodies and by transfection of plasmids expressing pathway-specific transcription activators fused to the DNA-binding domain of GAL4, as well as a GAL4 response element-luciferase reporter gene. The role of MAP kinase was assessed using biochemical inhibitors and transiently expressed dominant negative mutant constructs. The effects on TGF-beta1-induced alpha1(I) collagen expression were evaluated by Northern blot and by activation of a transiently transfected alpha1(I) promoter-luciferase reporter construct. RESULTS: ERK and JNK phosphorylation occurred 30 minutes and one hour, respectively, after TGF-beta1 treatment. A biochemical blockade of the ERK pathway inhibited TGF-beta1-induced alpha1(I) collagen expression. A dominant negative mutant of ERK1 but not of JNK decreased alpha1(I) gene promoter activation. Activation of the TGF-beta-responsive p3TP-Lux construct was partially inhibited by cotransfection of an ERK1 dominant negative mutant. CONCLUSION: These data indicate that MAP kinase pathways can be activated by TGF-beta1 in mesangial cells and that the ERK MAP kinase plays a role in TGF-beta-stimulated collagen I expression. Because we have shown previously that SMADs mediate TGF-beta1-stimulated collagen I expression, our findings raise the possibility of interactions between the MAP kinase and the SMAD pathways.

Cells, Cultured↗
PubMed1998

The role of DNA methylation in expression of the p19/p16 locus in human bladder cancer cell lines.

Methylation of CpG sites in the control regions of tumor suppressor genes may be an important mechanism for their heritable, yet reversible, transcriptional inactivation. These changes in methylation may impair the proper expression and/or function of cell cycle regulatory genes and confer a selective growth advantage to affected cells. Detailed methylation analysis using genomic bisulfite sequencing was performed on a series of subclones of a bladder cancer cell line in which a hypermethylated p16 gene had been reactivated by transient treatment with 5-aza-2'-deoxycytidine. Methylation of the CpG island in the promoter of the p16 gene in human bladder cancer cells did not stop the formation of a transcript initiated 20 kb upstream by the p19 promoter but did prevent the expression of a p16 transcript. Furthermore, we show that reactivant clones that expressed p16 at varying levels contained heterogeneous methylation patterns, suggesting that p16 expression can occur even in the presence of a relatively heavily methylated coding region. We also present the first functional evidence that methylation of only a small number of CpG sites can significantly down-regulate p16 promoter activity, thus providing support for the model of progressive inactivation of this tumor suppressor gene by DNA methylation.

Azacitidine↗
PubMed1998

Multifocal electroretinogram indicates visual field loss in acute zonal occult outer retinopathy.

PURPOSE: To report alterations of electrophysiologic tests, including the multifocal electroretinogram, in a case of acute zonal occult outer retinopathy. METHOD: We recorded photopic, scotopic, and single-flash electroretinograms and a multifocal electroretinogram in a 47-year-old woman with acute zonal occult outer retinopathy in the right eye. RESULTS: Her visual acuity was 20/20 in the right eye throughout the follow-up period. The electroretinograms indicated retinal impairment of the right eye, predominantly in the cones. The multifocal electroretinogram showed reduced responses corresponding to the visual field defect of the static perimetry. CONCLUSIONS: In acute zonal occult outer retinopathy, impairment of the retinal area results in a visual field defect. The multifocal electroretinogram can be useful in determining the location of the defect.

Acute Disease↗
PubMed1998

Interleukin (IL)-1 and IL-4 synergistically stimulate NF-IL6 activity and IL-6 production in human mesangial cells.

BACKGROUND: While interleukin (IL)-4 inhibits pro-inflammatory cytokine expression by human monocytes, we have observed that it potentiates IL-6 production by IL-1-activated human mesangial cells (MC). To study the mechanism of this cell-type specific interaction between IL-1 and IL-4 in MC, we examined the effect of both cytokines on the activities of nuclear factor kappa B (NF-kappa B) and nuclear IL-6 NL-IL 6), transcription factors that are essential for IL-6 gene expression. METHODS: We evaluated IL-6 synthesis, mRNA expression, and mRNA stability by ELISA, Northern analysis, and the actinomycin D method, respectively. Activities of NF-kappa B and NF-IL 6 were analyzed by gel shift assay. RESULTS: IL-4 augmented the IL-1 stimulated IL-6 mRNA levels by about threefold without altering mRNA stability. IL-1 treatment rapidly induced the binding activity of NF-kappa B. In contrast, IL-4 did not affect basal and IL-1-induced NF-kappa B activities. Both IL-1 and IL-4 stimulated NF-IL6 activity as early as 30 minutes after treatment. When MC were treated with both cytokines together, marked activation of NF-IL6 was observed at five hours. CONCLUSIONS: These results suggest that simultaneous activation of NF-kappa B and NF-IL6 is essential for IL-6 gene expression and that IL-1 and IL-4 cooperatively stimulate MC IL-6 production through their synergistic activation of NF-IL6.

CCAAT-Enhancer-Binding Proteins↗
PubMed1998

[Myopathology of the intrinsic laryngeal muscles in neurodegenerative diseases, with reference to the mechanism of vocal cord paralysis].

To investigate the mechanism of the vocal cord abductor paralysis (VCAP) in the neurodegenerative diseases, the intrinsic laryngeal muscles (the crycothyroid, the interarytenoid, and the posterior crycoarytenoid muscles) from 41 autopsied cases were histologically examined: 10 cases of amyotrophic lateral sclerosis (ALS), 10 of Parkinson's disease (PD), 9 of multiple system atrophy (MSA), 4 of Machado-Joseph disease (MJD), 4 of progressive supranuclear palsy (PSP), 1 of familial amyloidotic polyneuropathy (FAP), and 3 of cerebrovascular diseases as a control. According to the distribution of the neurogenic changes among above-described three intrinsic laryngeal muscles, three forms were raised: 1. The totally paralytic form showing that all the three muscles developed neurogenic atrophy. This form includes ALS, MJD, and FAP. 2. The posterior muscle-paralytic form showing that only the posterior crycoarytenoid muscle was selectively involved. This form includes MSA. 3. The nonparalytic form showing no morphological abnormalities in any of the intrinsic laryngeal muscles. This type includes PD and PSP. In this nonparalytic form, supranuclear mechanism such as pyramidal or extrapyramidal tract involvement may cause VCAP through the increased laryngeal muscles tone. Considering that VCAP can be seen in any of the above-described forms, our results indicate that the mechanism of VCAP is different among the neurological disorders.

Atrophy↗